PSYCHOGENIC EFFECTS OF ENVIRONMENTAL CUES ON PHYSIOLOGIC RESPONSES TO SUBMAXILMAL WORK UNDER HYEPOXIC CONDITIONS Thesis for the Degree of Ph. D. MICHIGAN STATE UNIVERSITY THOMAS N. TILLMANI 1972 O F I.‘ ‘ ’Fn'- 'wn y... LI.’3R1‘ ,r "I 1" ’ ' &‘ 11:;r.1_ . C - “ ”13:3“ (lg-'3'“ V I to «.41).. (6(5):)! r R . .“ - V" This is to certify that the thesis entitled Psychogenic Effects of Environmental Cues on Physiologic Responses to Submaximal work Under Hypoxic Conditions presented by Thomas N. Tillman has been accepted towards fulfillment of the requirements for PM). degreein Physical Education gig/M éfl ' Major professor ABSTRACT PSYCHOGENIC EFFECTS OF ENCIRONMENTAL CUES ON PHYSIOLOGIC RESPONSES TO SUBMAXIMAL WORK UNDER HYPOXIC CONDITIONS By Thomas N. Tillman The purpose of this study was to determine whether physiologic responses during submaximal work under normoxic or hypoxic conditions are psychogenically influenced by cues pertaining to the presence of those conditions. A subsidiary purpose was to obtain physiologic bases for judging whether the psychogenic influence would be facilitory or inhibitory to the performance of submaximal work. Subjects were 8 male graduate and undergraduate physical education majors ranging in age from 20 to 33 who were recruited on the basis of having reasonable cardiovascular fitness for endurance work performance. Only one, a nation-class mile runner, was an athlete in training. A standard run of 5 minutes at 7 mph and zero grade on a motor driven treadmill was employed as the submaximal work task in each of four test conditions (treatments). Heart rate (by ECG) and respiratory rate were recorded continuously during each 5 minute run and 15 minute recovery period using Douglas bag techniques. Serial samples of expired air were analyzed for 02 and C02 percentages. Thomas N. Tillman The 4 test conditions (treatments) were: 2 l 1 breathing normoxic air when told it was normoxic; Z l 2 breathing normoxic air when told it was hypoxic; :11 I 1 breathing hypoxic air when told it was hypoxic; a: I 2 breathing hypoxic air when told it was normoxic. After 6 pre-experiment training runs (5 minutes at 7 mph and 0% grade) every subject was observed in 4 replications of each of the 4 testing situations with counterbalancing technique employed to avoid biases being introduced by training or treatment order. Testing was con- ducted over a period of 5 1/2 weeks-—each subject running on the same 3 respective days of the week (either MWF or TThS) and at the same respective time of day (either 6:00, 6:30, 7:00, or 7:30 a.m.). Double- blind techniques were employed to the extent practicable. Irrespective of cues provided, the average ventilation, respiratory rate and heart rate measures obtained in exercise and recovery periods were higher for hypoxic runs than for normoxic runs. Oxygen uptakes for hypoxic runs were lower during exercise but higher during recovery than the respective measures for normoxic runs. Hypoxic R.Q.'s were higher than normoxic R.Q.'s during exercise, but the recovery R.Q. measures were not significantly different. No significant differences were found in oxygen requirement, presumably because the amount of work per- formed was essentially always the same. None of these results were con- sidered deviant from expectations. In comparing the effects of hypoxic cues with the effects of normoxic cues, a greater number of significant differences were found under hypoxic conditions than were found under normoxic conditions. Hypoxia cues were found to have altered hypoxic measures toward normoxic measures. This apparent counteracting of hypoxic effects by hypoxic cues was considered Thomas N. Tillman an important fact toward elucidating the physiologic mediation of psycho- genic influence. The tendency of hypoxic cues to raise normoxic exercise R.Q.'s and to lower hypoxic exercise R.Q.'s was also considered to be important. A third fact of interest was that, irrespective of air breathed, hypoxic cues lowered pulse rates and raised oxygen uptakes. Although conducted only to facilitate interpretation of the data, an investigation of training effects revealed interesting and unusual adaptations had taken place. Subjects acquired an ability to perform a given amount of work using less oxygen under hypoxic conditions than was used under normoxic conditions. Due to alternation of hypoxic with normoxic runs, this effect was considered to involve acute response mechanisms. With both long term and acute adaptation evidenced, the specific mechanisms of adaptation could not be identified. Average R.Q. values during exercise and recovery were of interest in that they increased as the study progressed in contrast to the decreases which usually accompany training at submaximal work intensities. These changes were interpreted to indicate a qualitatively different adaptation than is usually observed. When effects of training and cues were considered along with effects of breathing normoxic or hypoxic air, adaptations were apparent which acted to increase the difference between the effects induced by normoxic and hypoxic cues under hypoxic breathing conditions. The adaptation was particularly evident in oxygen uptake and R.Q. variables. Results of the present study indicate that environmental cues can affect physiologic responses during work performance and that the effects produced can be modified by training. Thomas N. Tillman Results of the present study also indicate that, under some circum- stances, adaptation to hypoxic work conditions can be manifested in humans as a reduced oxygen requirement for a given amount of work. PSYCHOGENIC EFFECTS OF ENVIRONMENTAL CUES ON PHYSIOLOGIC RESPONSES TO SUBMAXIMAL WORK UNDER HYPOXIC CONDITIONS By .\__ ‘ 1‘ I Thomas N. Tillman A THESIS Submitted to Michigan State University in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY Department of Health, Physical Education and Recreation 1972 efl’is‘if’t; ACKNOWLEDGEMENTS The writer wishes to express gratitude to the eight students who donated so much of their time while serving as subjects. He is particularly indebted to Dr. John H. Shroyer and to Mr. David Anderson for their gifts of time, effort and talent in serving as members of the data collection and processing team. Gratitude is also due Dr. James Stapleton for graciously given statistical consultation. Special appreciation is extended to Dr. S. Howard Bartley and to Dr. E. Paul Reineke who, as members of the doctoral committee, were constant sources of encouragement and technical advice. The writer is very deeply indebted to Dr. William W. Heusner and to Dr. Wayne D. Van Huss for their invaluable and generous assistance with every phase of this study. Without their help this document would never have been possible. ii TABLE OF CONTENTS Chapter Page I THE PROBLEM. . . . . . . . . . . . . . . . . . . . . . . . 1 STATEMENT OF THE PROBLEM . . . . . . . . . . . . . . LIMTATIONS OF THE STUDY 0 O O O O I O O O 0 O O O 0 DEFINITION OF TERMS. o . . . . . . . . . . . . . . . #450) II REVIEW OF RELATED LITERATURE . . . . . . . . . . . . . . . 8 THE PSYCHOGENIC INFLUENCING OF ATHLETIC PERFORMANCE . . . . . . . . . . . . . . . . . . . 8 PHYSIOLOGIC ADAPTATION TO SU MAX WORK. . . . . . 23 PHYSIOLOGIC RESPONSES TO HYPOXIA AND SUBMAXIMAL WORK . . . . . . . . . . . . . . . . . 3O Acute Hypoxia . . . . . . . . . . . . . . . . . 30 Chronic Hypoxia . . . . . . . . . . . . . . . . 33 III RESEARCHMETHODS.....................38 SUBJECTS . . . . . . . . . . . . . . . . . . . . . . 38 TREATMENTS . . . . . . . . . . . . . . . . . . . . 39 The Standard Tr admill Run. . . . . . . . . . . 39 The Hypoxic Air Mixture . . . . . . . . . . . . 40 The Normoxic Air. . . . . . . . . . . . . . . . 4O Cues. . . . . . . . . . . . . . . . . . . . . . 4O Rationale for Selecting the Four Treatments . . 41 PROCEDURES . . . . . . . . . . . . . . . . . . . . . 42 Pre-Training. . . . . . . . . . . . . . . . . . 42 Psychological Preparations. . . . . . . . . . . 43 Test-Run Procedures . . . . . . . . . . . . . . 44 Data Collection Provisions. . . . . . . . . . . 45 APPARATUS AND EQUIPMENT. . . . . . . . . . . . . . . 47 Hypoxic Air Mixture Apparatus . . . . . . . . . 47 Air Feed Apparatus. . . . . . . . . . . . . . . 48 ANALYSIS OF DATA . . . . . . . . . . . . . . . . . . 49 Experiment Design . . . . . . . . . . . . . . . 49 Training Effects Versus Treatment Effects . . . 52 Statistical Analyses. . . . . . . . . . . . . . 53 IV RESULTS AND DISCUSSION 0 C 0 9 O O O O O O C O O O O O O O 55 RESULTS. . . . . . . . . . . . . . . . . . . . . . . 56 Hypoxic Effects Versus Normoxic Effects . . . . 56 Hypoxic Effects on Individual Variables . . . . 59 Discussion of Hypoxic Versus Normoxic Effects . 59 iii Chapter Effects of Physiologic Adaptation to Experiment Conditions. . . . . . . . Discussion of Normoxic-Hypoxic Adaptations. Psychogenic Effects . . . . . . . . . . . . Discussion of FINAL DISCUSSION . V SUMMARY, CONCLUSIONS AND SUMMARY. . . . . . CONCLUSIONS. . . . RECOMMENDATIONS. . BIBLIOGRAPHY O O O O 0 O O O O O O APPENDICES. . . . . . . . . . . Psychogenic Effects . . . RECOMMENDATIONS . . . . . iv Page 61 71 76 85 101 103 103 106 106 108 118 Table 4-1 4-2 3-4 3-5 3-6 3-7 3-8 LIST OF TABLES Treatment effects as reflected in mean values of 21 physiologic variables . . . . . . . Overall training effects as reflected in pooled mean values per quarterly periods of the experiment . . . . . ANOVA F test and Sign test results obtained from analyz- ing normoxic and hypoxic data separately . . . ,.. . . . Comparisons of effects on dependent variables which were apparently induced by the three main factors in the experiment . . . . . . . . . . . . Treatment effects across run and recovery. . . . . . . . Treatment effects across cycles (training effects) . . . ANOVA summaries for dependent variable ANOVA summaries for dependent variable rate 0 O O O O O 0 O O O O O O O O O 0 ANOVA summaries for dependent variable 02/pu18e O O O I O O O O O I O 0 O O 0 ANOVA summaries for dependent variable ventilation. . . . . . . . . . . . . . ANOVA summaries for dependent variable ventilation. . . . . . . . . . . . . . ANOVA summaries for dependent variable ventilation (run + recovery) . . . . . ANOVA summaries for dependent variable ventilation rate . . . . . . . . . . . ANOVA summaries for dependent variable volume . . . . . . . . . . . . . . . . ANOVA summaries for dependent variable respiratory rate . . . . . . . . . . . peak pulse rate exercise pulse exercise total exercise 0 O O O 0 O 0 total recovery 0 O O O O O 0 sum total 0 Page 57 63 78 86 118 122 126 127 128 129 130 131 132 133 134 Table 3—10 3-11 3-12 3-13 3-14 3-15 3-16 3-17 3-18 3-19 3-20 3-21 C-l ANOVA summaries for dependent variable 0 2 up take 0 O O O O O O O O D O O I O 0 ANOVA summaries for dependent variable ANOVA summaries for dependent variable ANOVA summaries for dependent variable uptake rate. . . . . . . . . . . . . . ANOVA summaries for dependent variable uptake/respiration . . . . . . . . . . ANOVA summaries for dependent variable rate/kg body weight. . . . . . . . . . ANOVA summaries for dependent variable bOdy weight 0 O O O O O O O O O O O 0 0 ANOVA summaries for dependent variable k8 bOdy weight 0 O O O 0 O O I O O O 0 ANOVA summaries for dependent variable extraction . . . . . . . . . . . . . . ANOVA summaries for dependent variable extraction . . . . . . . . . . . . . . ANOVA summaries for dependent variable ANOVA summaries for dependent variable Hypoxic air mixing data. . . . . . . . total exercise 02 debt 0 O I O 02 requirement. exercise 02 exercise 02 O O O O O O O 0 Ex. 02 uptake 02 debt/kg 02 requirement/ exercise 02 recovery 02 exercise R.Q. . recovery R.Q. . Pre-training post-exercise heart rate data . . . . . . . vi Page 135 136 139 140 141 142 143 144 145 146 ‘4 U1 |...| 158 LIST OF FIGURES Figure Page 3-1 Schematic layout of experimental design. . . . . . . . . . 51 4-1 Three comparisons essential to interpretation of data. . . 56 4—2 Comparison of effects of training on ventilation and O2 extraction under normoxic conditions. . . . . . . . . . 64 4-3 Comparison of effects of training on ventilation and O2 extraction under hypoxic conditions . . . . . . . . . . 65 4-4 The effects of training on respiratory gas measures. . . . 66 4-5 Training effects on means obtained under normoxic and hypoxic breathing conditions . . . . . . . . . . . . . . . 68 4-6 Comparison of pulse rate and 02 uptake data showing relative degrees of recovery in first and last cycles. . . 73 4-7a Training effects on means obtained under normoxic and hypoxic truth and lie conditions . . . . . . . . . . . . . 83 4-7b Training effects on means obtained under normoxic and hypoxic truth and lie conditions . . . . . . . . . . . . . 84 4-8 Pulse rate means per treatment plotted against time. . . . 90 4-9 Oxygen pulse means per treatment plotted against time. . . 91 4-10 02 uptake rate per kg. of body weight means per treat- ment plotted against time. . . . . . . . . . . . . . . . . 92 4-11 Ventilation rate means per treatment plotted against time 0 O O O O O O O O O C O O O O O 0 0 O I 0 O O O O O 0 93 4-12 Tidal volume means per treatment plotted against time. . . 94 4-13 Respiratory rate means per treatment plotted against time. 95 4-14 02 uptake per single respiration means per treatment plotted against time . . . . . . . . . . . . . . . . . . . 96 4-15 02 extraction means per treatment plotted against time . . 97 4-16 R.Q. means per treatment plotted against time. . . . . . . 98 vii Figure C-1 C-2 Schematic arrangement and essential components of gas mixj-ng apparatus O O O O O O I O O I O O O O O O O O O O O 148 Schematic arrangement and essential components of gas feed apparatus . . . . . . . . . . . . . . . . . . . . . . 153 Mean environmental conditions during the study . . . . . . 155 viii Appendix LIST OF APPENDICES Treatment Effects Data . . . . . . . . . . . . . Three-Way, Mixed Model ANOVA Summaries . . . . . Gas Mixing Apparatus and Procedures and Gas Feed Apparatus O O O O O O O O O O O O O O 0 O 0 O 6 0 Environmental Conditions . . . . . . . . . . . . Pre-Experiment Instructions to Subjects. . . . . Pre-Training Post-Exercise Heart Rate Data . . . ix Page 118 125 147 155 156 158 CHAPTER I THE PROBLEM Variability in the quality of athletic performance is often attributed to psychogenic influence. While it seems that increments in performance are ascribed to psychogenic influence about as often as are decrements, relatively little has been learned in the way of explaining how either kind of deviation is produced or why, in any given situation, a deviation is psychogenically induced in one direc- tion instead of in the other. Situations in which the kind or direction of variability appears to be associated with intellectual assessment of circumstances attendant to the performance situation are especially perplexing. For example, evidence has been presented that motor performance can be improved by pre-performance warm-up exercises, but only if the indi- vidual believes the warming-up to be beneficial (128). A possible interpretation of such observations is that cortical activity of the CNS may be involved in the regulation of physiologic processes classically thought of as being regulated by peripheral mechanisms for maintaining physiological homeostasis. In theory, at least, an arrangement permit- ting cortical control could act to either enhance or inhibit, directly or indirectly, the processes by which energy is obtained for muscle activity and thereby produce increments or decrements in work performance. 2 Since it has been shown that the CNS contains anatomical provisions for the development of integrated responses involving combinations of autonomic and somatic discharges (112,113), it is reasonable to expect that evidence of psychogenic influence might be detected by monitoring physiologic responses during a given work performance situation in which psychogenic influence is suspected. Observations obtained in this way would, of course, have to be compared to similar observations obtained when the suspected psychogenic influence was not present. Although few investigators have addressed themselves to the problem of assessing physiologic responses during muscular exercise for evidence of psychogenic influence, this would seem a logical first step toward an understanding of how work performance is modified by psychogenic influence. It also would be important to know whether or not intellectual assessment of work performance circumstances affects, to any important degree, the physiologic responses observed under those circumstances. Although now recorded in history, it may be remembered that when preparations were being made for the 1968 Mexico City Olympic games, there was a great deal of concern that the 2300 m. altitude at Mexico City would have detrimental effects on athletes' performances and upon the athletes themselves. Because of this concern, a considerable amount of research was initiated in order to determine the best ways of training and conditioning the athletes so that physiologic effects of altitude would be minimized. Because of the extensive publicity given to the concern over physiologic problems of competing at altitude, Opinions were expressed that detrimental effects might also be caused by pshcho- logical factors (15,120,121). That these opinions may have been well founded was reflected in comments made by a member of the Canadian 3 Women's Olympic Swim Team during a post-games interview.l When asked how the athletes felt about the altitude, she answered, "We continually tried to 'psych' ourselves into believing it wouldn't hurt us. I kept telling myself over and over, 'It won't bother me. It won't bother me.'" Yet, virtually no research was conducted to investigate the psychological aspects of knowing that a condition was present which might detrimentally affect.performance. It is pertinent to ask the question--Just how does a person respond in a work performance situation when informed that a condition is present which might detrimentally affect work performance capability, if not health? While the answer to this question may not be evidenced in parameters of physiologic response, an attempt to determine this through controlled laboratory research would seem warranted. STATEMENT OF THE PROBLEM The purpose of this study was to determine whether physiologic responses during submaximal work under normoxic or hypoxic conditions are psychogenically influenced by cues pertaining to the presence of those conditions. The study was designed to provide answers to three main questions: 1. Can psychogenic influence induced by information relevant to conditions of work performance be detected as alterations in parameters of physiologic response during the work performance? 2. If alterations of response can be detected, how do effects induced by cues that hypoxic air is breathed compare to effects induced by actually breathing hypoxic air? 1Personal communication with Miss M. Corson. 4 3. If alterations in response can be detected, do they appear to be of an incremental or decremental nature with respect to the kind of work performed? LIMITATIONS OF THE STUDY The limitations of this study were as follows: 1. There was no design provision in this study for obtaining obser- vations without cues being provided. 2. Observations were obtained from only one kind of work, at one work intensity, using one duration. 3. Recovery data were restricted to the last 14 minutes of a 15 minute recovery assessment period. 4. All recovery data were collected while the subjects were breathing room air. 5. Exposure to hypoxic air breathing occurred only during the hypoxic air work periods. 6. No basis is seen for extrapolation of these results to a general papulation or to a subpopulation of highly trained, well conditioned athletes. DEFINITION OF TERMS l. Psychogenic influence--influence of intrapsychic origin (39). The term was used here to specify non-volitional, endogenous activity operant in modifying parameters of physiologic function. The term psycholggical influence is considered to be more encompassing with broader implications. 2. Normoxic air--air having a normal P02, or normal oxygen.content (compared to ambient air found at or near sea level). The related phrase, normoxic air condition, is used in the text to indicate specifically the 5 breathing of compressed air reduced to ambient pressures such that the P02 was virtually identical to that of the ambient air. 3. Room air--refers to the ambient air specifically. (Subjects recovered on normoxic room air which means they were disconnected from the compressed air feed system.) 4.- Hypoxic air--air having lowered PO2 or 02 content. The hypoxic air used in this study was a mixture of compressed air and N2 such that the 02 content was reduced to 16.60 i 0.04%. The related phrase, hypoxic air condition, refers specifically to the breathing of the 16.60% 02 mixture. 5. Exercise--as used in this study, exercise refers to running on. a motor driven treadmill at 7 mph for exactly 5 minutes i one treadmill revolution. 6. Recovery--normally refers to a recuperative period following exercise of a duration lasting until the pre-exercise resting level physiologic state is reached. In this study, recovery data were arbi- trarily held to the last 14 minutes of a 15 minute post-exercise period with subjects resting in a sitting position. 7. Submaximal work--customarily refers to physical work of less than maximal intensity and/or work which can be sustained over an extended period of time. As a consequence of the sufficiently low energy use rate, the major portion of energy needed can be supplied by aerobic metabolism. The submaximal work in the present study was considered to be of moderate intensity. 8. Peak pulse rate--the highest pulse rate observed in subjects during exercise. 6 9. Tidal volume--the volume of air (STPD) expired with each breath. Values were calculated from respiratory rate and ventilation measures. 10. .92 extraction--the percentage of oxygen extracted from inspired air. Values were obtained by serial analyses of expired air. 11. '92 uptake--the volume of O2 (STPD) removed from inspired air. Values were obtained by calculation using 02 extraction and ventilation measures. Total exercise 02 uptake denotes total volume of O2 (STPD) removed from inspired air during exercise. Other related phrases are self-explanatory. 12. .Qz_dgb£f-in contrast to normal usage, the term was used here to denote the total volume of O2 (STPD) taken up during only the last 14 minutes of a 15 minute post-exercise recovery period. No adjustment of volume was made for basal or resting state metabolic needs. 13. .92 requirement--the volume of O2 (STPD) removed from inspired air during the entire exercise period and during the last 14 minutes of the 15 minute recovery period. Values thus obtained are inferred to estimate the total amount of oxygen required to perform the given work task. 14. Cyglgr-one-fourth of the 16 treadmill runs made.by each subject. In a cycle subjects were exposed once to each of the four test condi- tions (see Chapter III). 15. Overall adaptation--physiologic adjustment inferred to have taken place during the course of the study on the basis of differences observed between cycle-mean values of the variables under study and inferred to have occurred as the consequence of participation in the study. 7 16. Altitude—-as it is normally used, altitude refers simply to a vertical distance or elevation above sea level. However, for altitude physiology communications, the following standard designations have been adOpted: Modest altitude ------ 1500 to 2500 meters (4920 to 8200 ft) Moderate altitude----3000 to 3300 meters (9840 to 10,500 ft) High altitude ------- 4000 to 5000 meters (13,120 to 16,400 ft) Great heights--------above 5,500 meters (18,040 ft) CHAPTER II REVIEW OF RELATED LITERATURE The literature review is presented in three sections. The first deals with the primary emphasis in the study--the psychogenic influences upon athletic performance in general and upon.physiologic responses to work. In the second section, training adaptations under normoxic con- ditions to the type of work load utilized in this study are reviewed. Physiologic responses to work at modest altitude (2300 m.) are presented last. The latter two sections are more abbreviated summaries of large bodies of literature and were included, primarily, to provide needed perspective. THE PSYCHOGENIC INFLUENCING OF ATHLETIC PERFORMANCE The psychogenic influencing of athletic performance has been a matter of interest for many years. However, even though both increments and decrements in performance are commonly attributed to psychogenic influence, phenomena of this sort are not well understood. While there is agreement that psychological factors do not determine physical or physiological capacities, but act instead to modify the expression of these capacities (73,82), there is still much to be learned about the nature of modification processes involved before it is possible to understand effects which are, or might be, produced in a given situation. (15,81,119,121). 9 From the fact that increments as well as decrements can apparently be induced by psychogenic influence, the existence of separate inhibi- tory.and enhancing mechanisms could be postulated. On the other hand provision for variation in amount of continuously operant influence from either inhibitory or enhancing mechanisms could produce the same results. Ikai and Steinhaus (73) were able to produce modifications of maximal elbow flexion strength in a series of investigations by using hypnotic suggestions, pharmacological agents, and also extrinsic and intrinsic noise production. On the basis of their results, they postu- lated that removal_or reduction of cortical inhibitory influences can_ take place which permits subjects to approach more closely the physio- logic limits of performance capability. However, they limited this thesis to situations in which voluntarily executed, all-out maximal performance is involved. Extrapolation to submaximal effort is there- fore rendered questionable. Of course, the possibility exists that submaximal efforts commence to assume proportions of all-out maximal effort with onset of fatigue. A somewhat different and more specific outlook has been provided by Gellhorn (51). Fionia priori evidence at the time, he stated that emotion causes excitation of the hypothalamus resulting in a state which, by itself, does not elicit movement but acts instead to increase the intensity and complexity of cortically initiated movement. These effects he attributes to summation processes taking place in the spinal cord and also in the motor cortex. In some circumstances, the summa- tions may act to spread efferent impulses to muscles in other extremities. In essence, the thesis of Ikai and Steinhaus on the one hand, and the report of Gellhorn on the other, both imply psychogenic influence~ consisting of neurogenic modifications in cortical control over volitional 10 activity. By the thesis of Ikai and Steinhaus, increments in.performance are explained by reduction or removal of cortical inhibitory mechanisms. Decrements would result from failure to remove continuously operant or newly added cortical inhibitory influence. Interpreting from Gellhorn's report, increments in performance would result from the addition of hypothalamic activity to cortical activity so that increased strength would be applied. Decrements, on the other hand, would be produced as a consequence of activating antagonistic muscles as well as agonistic muscles. In such a case, there would be an impairment of motor skill as well as a reduction in the amount of effective force that could be applied. The principles outlined by Gellhorn not only permit extrapolation to increments or decrements in maximal volitional effort, but also to increments or decrements in submaximal performances. Where submaximal effort is concerned, decrements could begproduced by the loss of coordinated effort which would accompany activation of both agonistic and antagonistic muscles. Decreméhts could also be produced by a reduction in mechanical efficiency occurring consequentially to the activation of additional muscle fibers whether they were of agonistic or antagonistic muscle groups. Since muscle contraction is an energy consuming process, more energy would be consumed with the activity of more muscle fibers. Hence, the likelihood is increased of fatigue setting in earlier than would otherwise be expected. By this same logic, increments in submaximal performance would be enabled through the reduction_or avoidance of the extra energy consuming effects. The factor of efficiency in performance exposes another aspect of volnerability to psychogenic influence. Where athletic performance is concerned, relative efficiency is only of primary importance when, or 11 if, a point is reached at which energy needs commence to exceed supply capabilities. Therefore, influence of processes such as circulo- respiratory functioning which.are involved with energy liberation and energy supply would be a possible way in which submaximal work performance could be particularly affected by psychogenic influence. With regard to circulo-respiratory functioning during exercise, Rushmer (112,113) has shown that anatomical provisions exist by which the motor cortex can activate the circulo-respiratory changes which are needed adjustments to the onset of work performance. In years past, such adjustments were believed to occur through activation of peripheral feedback mechanisms in consequence to exercise induced disturbances of homeostasis. According to Rushmer, the earlier theory became prevalent because of using only anesthetized, thoracotomized laboratory animals for cardiovascular research. Furthermore, cardiovascular and respira- tory changes which accompany, and even precede, onset of exercise occur too abruptly to be accounted for by peripheral adjustment mechanisms. Thus it is indicated that cortical control of volitional movement can also act to control the circulo-respiratory alterations which are needed to accommodate metabolic requirements furing work performance with peripheral mechanisms playing either a complementary or supplementary role. Rushmer's work is interesting in another respect in that he reports observing in dogs the phenomenon of anticipatory heart rate which is well known for its occurrence in humans (43,56,127,l34). This pre- exercise increase in pulse rate was observed to occur when dogs were lifted onto the treadmill and also when dogs already on the treadmill could watch the Operator's hand move to activate the treadmill switch (112). This only occurred after several earlier treadmill bouts. Other 12 investigators (61) have reported increases in liver glycogen and blood sugar accompanied the lifting of dogs onto a treadmill after the dogs had become accustomed to treadmill running by earlier experiences. Such observations challenge the view that biases due to psychological factors can be avoided in physiologic research by using laboratory animals as subjects instead of humans. While Rushmer's results (112) are at least indirectly supportive of the notion that metabolism may be psychogenically influenced, the finding of increased liver glycogen and blood sugar levels in dogs prior to treadmill running (61) is especially supportive of that notion. Further evidence having similar implications has been reported by Rougier and Babin (109). During an investigation concerned with comp paring pre-exercise and post-exercise blood glucose levels, these investigators inadvertently obtained evidence which indicated that sporting exercise (handball) of short and medium duration is accompanied by hyperglycemia to an extent that is directly related to the importance of the match. As pointed out by Gellhorn (51), fatigue from muscular exertion is delayed during emotional excitement, and the delay has been associated with liberation of neurohumors from the adrenal medulla. Since the adrenal catecholamines, and epinephrine in particular, are known to produce hyperglycemia (50,89), it is reasonable to speculate that the increased blood sugar levels observed when dogs were lifted onto a treadmill (61), and as reported in handball players by Rougier and Babin (109), might be explained as the consequence of increased adreno- medullary activity. Support for this viewpoint is seen in the cement- of von Euler (144) that secretion of norepinephrine seems more associated 13 with physical stress whereas epinephrine secretion seems more related to mental stress. While attempting to assess the effect of hypoxia on catecholamine secretion, Becker and Kreuzer (8) noted that at high mountain altitudes there was a significant increase in norepinephrine but essentially no change in epinephrine secretion. However, when a barometric chamber was used to simulate the low oxygen tensions found at altitude, there was a significant increase in epinephrine while the norepinephrine secretion was relatively unchanged. 0n the basis of subjective observations, they attributed this difference in results to the fact that subjects experienced anxiety at being enclosed in the barometric chamber whereas subjects were elated by the experiences in the mountain experiments. Although this evidence was considered to agree with von Euler's views (144), it is particularly supportive of the statement by Ganong (50) that epinephrine secretion is increased when an individual faces an unfamiliary situation whereas norepinephrine secretion is predominant during emotional stresses in familiar circumstances. While attempting to assess the effects of training and of competi- tion on turnover of catecholamines in athletes of various different sports, Nowacki and coeworkers (97), using urinary levels of vanilman- delic acid as the criteria, found catecholamine secretions greater after training than before. Even greater secretions were evidenced before and after competition and were explained as the consequence of emotional influence on the sympatho-adrenal medullary system. On the basis of their results, these investigators concluded that emotional stress is a necessary element enabling athletes to perform at their best. In addition to differences that occur in levels of circulating catecholamines, changes in the ratio of norepinephrine to epinephrine 14 in circulation are of interest for reasons related to differences in. effects produced by each (144) as well as to differences in circumstances by which each is secreted (50,144). Whereas norepinephrine produces strong systemic vasoconstriction and therefore an increase in peripheral resistance, epinephrine causes vasodilatation in skeletal muscle which acts to decrease peripheral resistance. While both act to increase rate and strength of heart beat, the increased peripheral resistance induced by norepinephrine may cause a reflex bradycardia and therefore a relative decrease in cardiac output (7,13,52,133,143). This is in contrast to the reduced peripheral resistance and increased cardiac output caused by epinephrine. Another important difference in effects is that it is epinephrine which is primarily responsible for the pro- duction of hyperglycemia (50,143). If catecholamines are involved in the psychogenic influencing of physical performance, as the bulk of evidence indicates, there are ample provisions for a variety of effects to be elicited. In addition to the differences between effects of epinephrine and norepinephrine, changes in the ratio of one to the other can be brought about through two differing processes of selective secretion. Although epinephrine usually constitutes about 802 of the adrenal effluent (144), it has been shown that the amount of norepinephrine in the effluent can be selectively increased under special circumstances (49) such as hypoxia (50). Otherwise, selective increases in norepinephrine are usually inferred to indicate increases in activity of adrenergic tissues of the sympathetic nervous system (142). Increases of epinephrine, on the other hand, are usually interpreted as evidence of increased adrenomedullaryr activity (142,143,144). The involvement of so many tissues, organs, and functions provides, at the very least, a conceptual understanding of why 15 the same external environmental conditions might have different effects on different individuals, or within the same individual at different chronological periods. Since physiologic responses during various kinds of physical per- formance have been extensively studied for a long period of years, much has been learned in the way of providing physiological explanations of man's ability to adapt to and to perform different physical tasks. It would therefore seem possible to examine various parameters of physiologic. functions for effects which could be attributed to psychogenic influence in order to understand how, why, and when performances are affected either incrementally or decrementally. Somewhat curiously, it would appear from the lack of pertinent material in the literature that very few investigators have attempted such tasks. In the meantime, however, coaches, trainers and even the athletes themselves have adopted a number of empirically devised practices in order to gain what is commonly referred to as a "psychological advantage." It is perhaps needless to say that the relative merit of these practices is open to question. One such practice has been the use of music to either_calm or arouse athletes in accord with needs specific to different situations. To assess the relative worth of this practice, Coutts (32) looked for a relationship between pulse rate and speed of submaximal work performance as a consequence to the hearing of calming or rousing music. No sig- nificant effects were observed, and it was concluded that the particular music used may not have been appropriate or else the practice of employing music in this way is without basis. A factor which was evidently not considered by Coutts is that_his subjects may have been concentrating so intently on the work performance task that they were not even aware music was being played. If such were 16 the case, the failure to obtain significant differences could be con- strued as evidence that a psychogenic effect was observed but of a nature which was not expected. An interpretation of this kind would concur with conclusions reached by Ikai and Steinhaus (73) that weight lifters are able to exclude, or at least reduce, inhibitory influences by means of intense concentration on the task of concern. Certainly it is obvious that no effect would have been expected had the subjects of Coutts been actually deaf. Although sound of a different nature was involved, the shot and shout series of investigations by Ikai and Steinhaus are of interest here in that they too deal with the impingement of stimulus energy upon. auditory modalities in humans. In these studies it was found that a shoult produced by the subjects in simultaneity with pulling effort resulted in increased pulling strength. However, the firing of a shot in simultaneity with pulling effort produced lower than normal pulling strength. These findings seem clearly in support of the mechanistic explanation provided by Gellhorn (51). In the Ikai study, it would seem likely that the effort put into the shoult was more important than the energy of the shoult noise per se. With the shot, however, there is little question that the impingement of sound energy was the important initiating factor. The possibility that exercise per se might overcome or interfere with psychogenic influence on physiologic processes has also been explored. By inducing what he called arousal of fear in subjects per- forming steady state work, Antel (3) observed substantial increases in. pulse rate. From these results he concluded that effects due to emotional stimulation are additive rather than abated or blocked during exercise. In addition, he points out that, since exercise pulse rates can reflect 17 an emotional effect, erroneous conclusions may be derived from just assessing pulse rates to determine physical fitness. Faulkner (43) conducted a study to observe and compare effects of cardiac conditioning on anticipatory, exercise, and recovery heart rates. In the data reported, it is quite evident that training procedures acted to reduce heart.rate in each of the three phases. It is therefore indicated that the reduction in the anticipatory heart rates reflected improvement in cardiac efficiency rather than an abatement of anticipa- tion with training. Faulkner concluded that these results support Rushmer's theory (112) of motor cortical control of the left ventricular response prior to, and in the initial stages of, adjustment to exercise. The principles postulated by Rushmer would seem to also explain.an observation reported by Taylor (134). Prior to the time that a subject fell during steady state running on a motor driven treadmill, his pulse rate had been averaging 120 b.p.m. After arising and regaining steady state while running at the same rate, his pulse rate was obServed to be 150 b.p.m. Since the higher 150 b.p.m. rate persisted in similar subse- quent running sessions conducted overs span of several days, it seems entirely possible that the extra 30 b.p.m. resulted from cortical activity rather than from homeostatic mechanisms. In a discussion related to physiological and performance changes that occur in response to athletic conditioning, Henry (66) notes that psychological factors can have considerable influence on individual scores of endurance or work tolerance performance, but he offers little in the way of explanation. Adams (1), on the other hand, obtained evidence in a complex study from.which he concluded that "will power" accounted for 1.642 of the variance in an endurance test consisting of a run to exhaustion on a motor driven treadmill at 7 mph on an 8.6% grade. Since I! III: [E Ii: I]! [It I f'l' I [I I .I" {I’ll [‘It ll i l I 18 his criterion of "will power" was the length of time an individual could hang by his hands from.an overhead bar, one could conclude that "will power", in this instance at least, consisted of the ability to tolerate pain and/or discomfort. Others might equate this with motivation (or "desire" or "mental attitude"). Nevertheless, it is well known that pain sensations act inhibitorily, apparently as mechanisms to protect the organism from tissue damage. However, as theorized by Ikai and Steinhaus, inhibition by discomfort could be a conditioned response that is established early in the life of an individual. Recognition that psychogenic influence can affect quality of athletic performance, along with an interest in finding ways to improve physical performance in general, has led several investigators to employ hypnosis as a research tool (73,75,76,77,78,87,90,93). Although hypnosis is only poorly understood, even at best, its use has permitted some progress toward understanding the nature of psychogenic influence. Improvement in arm and grip strength as measured by dynamometers, and in endurance, as measured by the length of time one could hang by his hands from.an overhead bar, has been reported as the consequence of using hypnosis. During the hypnotic trance, subjects were told they should (and could) disregard sensations of pain (90). In an earlier study by the same investigator, use of the same techniques produced sig- nificant gains only in arm strength (110). The implication of these findings is that pain causes either voluntary or involuntary cessation of muscular effort. On the basis of teleological reasoning, it is argued that provisions for the perception of pain act to protect an organism from tissue damage. By the thesis of Ikai and Steinhaus (73), the stimulation of pain receptors can act to produce cortical activity of an inhibitory nature in the CNS. 19 Ikai and Steinhaus (73) used hypnosis to suggest increases and decreases in strength and obtained respective increments and decrements in arm pulling strength. On the basis of these results, in addition to their studies using pharmacological agents and noise production in simultaneity with muscular effort, they arrived at their often cited thesis which implies that psychogenic influence consists of cortical activity acting to remove cortical inhibition to varying degrees. Whereas Ikai and Steinhaus (73) were particularly impressed with the increases of pulling strength (elbow flexion) that accompanied hypnotic suggestions of strength improvement, Johnson (76,78) reported that his use of hypnosis was singularly more successful in obtaining decrements in performance than in obtaining increments. Only in one study was he successful in obtaining improvements in endurance performance as measured by repetitions of a supine press (77). It is of interest here that Ikai and Steinhaus failed to obtain an increased expression of strength with a subject who was a weight lifter. They theorized that this particular individual had already acquired the ability to remove inhibitions himself. Thus there was no improvement possible wtihout the inhibitory factor to remove even though the subject was hypnotized for that purpose. Massey and Johnson (87) also used hypnosis in a somewhat different way and obtained results having interesting implications. In order to determine whether pro—performance warmrups have any beneficial effect on muscular performance, hypnosis was used to induce amnesia during a pre- performance period. Theoretically, the subjects were to be unaware of whether or not they had participated in warmrup activities. The rate at which subjects could pedal a bicycle ergometer for 100 revolutions at a fixed load was used as the criterion measure. One group of subjects was 20 put into a hypnotic trance and warmed up. The other group, also in a trance, just rested. No significant differences were obtained in the post-hypnotic performances. In his attempt to explain the failure to find significant effects of warming up, Johnson postulated that if there are any benefits from warm-ups they may be only psychological. It is a possibility, of course, that the absence of effects may have been inherent to the nature of the warmrup activities. On the other hand, Johnson's results tend to support the findings of Smith and Bozymowski (128), who reported benefits were obtained fromwwarming up only if the subjects believed warming up to be beneficial. A study combining and duplicating the procedures of both Smith and Johnson.would seem to be a worthwhile venture. In view of the Smith study, it is possible that Johnson's subjects may not have believed that there would be benefits of warming up. In addition to his other work with hypnosis, Johnson (77) investi- gated the possibility that suggestions presented to a subject during hypnotic trance might be no more effective than the same suggestions presented without the use of hypnosis. Dealing only with an endurance type of performance, it was found that suggestions of greater strength when presented during a deep trance for post-hypnotic performance, or during a light trance for performance while in the trance, were more effective than the same suggestions presented without a hypnotic trance. Statistically, there was no difference between the effectiveness of the two hypnotic suggestion situations. When suggestion was followed by per- formances with the subjects in a deep trance, it did not produce endurance performances that were significantly better than performances without the hypnosis. 21 Another investigation designed to evaluate the relative effective— ness of hypnotic and non-hypnotic suggestion was conducted by Morgan (93). Mbrgan, however, used as a criterion measure, the oxygen uptake response to exercise, rather than a gross measure of the exercise performance itself. Although the actual work task employed was always the same, suggestions were given to the effect that the weights being lifted were heavier, or lighter, than those used in the preceding session. A rotational design was used with four subjects of which the same two were always hypnotized and the other two were not. Effects of "heavy" suggestions and "light" suggestions were compared against control measures that were obtained without any suggestion given. In his results, Morgan found especially interesting the fact that, in response to suggestion of heavier work, the oxygen debts were increased in the simulatory subjects but decreased in the hypnotic subjects. In response to suggestions of lighter work, oxygen debt was decreased in simulatory subjects by increased in the hypnotic subjects. From these observations Morgan concluded support for the hypothesis that central neural mechanisms play a role in regulation of oxygen consumption, and that factors other than physiological need appear to affect oxygen uptake. It should be noted, however, that any inferences drawn from Morgan's work must take into consideration the fact that each subject was eXposed only once to each experimental treatment, and that only four subjects were used. Furthermore, the hypnotized subjects were not observed in a non-hypnotized state with the same suggestions, and the non-hypnotized subjects were not observed under conditions of receiving the suggestions in-a hypnotized 8 tate . Despite the obvious limitations to interpretation of Morgan's results, there are interesting aspects of the study which merit discussion. 22 Where Johnson (77) used suggestions of increased strength, Morgan used suggestions that weights being lifted were_lighter or heavier than before. Since.both were dealing with endurance types of performance, it is conceivable that the differences in suggestion might have different effects on subjects. Internal change is suggested in the one case, whereas external change is suggested in the other. A particularly interesting aspect of Morgan's study was his use of a parameter of physiologic response to exercise as a criterion measure. Obtaining differences in effects on physiologic variables would seem to provide more definitive direction for future research than would merely learning whether a multi-faceted performance was improved or impaired. Moreover, the fact that consistent differences in responses were observed supports the concept of providing control for psychogenic influence in physiologic research. The importance of providing control over psychological factors during physiologic research is more widely recognized now than it was in earlier years. Consequently, controls of some sort are often employed, but only rarely is an attempt made to determine what effects would have been produced had those controls not been employed. Efforts of this kind would, if nothing else, help to verify whether the controls used were effective. While investigating the reputed benefits of adminiStering pure oxygen to athletes before, during, and after performance of endurance work, Miller (91) found only small benefits were gained and only when the oxygen was given during the performance. Although complete details of procedures used were not given, Miller asserted that subjects did not know whether they received pure oxygen or plain air. Even though Miller's conclusions were based on both objective and subjective evidence, his 23 results conflicted with previous reports. In consequence he conducted an adjunctive study in which subjects breathed from'bottles of compressed air marked OXYGEN and AIR, respectively. In this case, the subjects could see fromnwhich bottle they were breathing. Almost invariably, when the bottle marked OXYGEN was used, the subjects reported feeling less fatigued and less distressed. Miller then concluded that the earlier reports may have reflected psychological benefits. PHYSIOLOGIC ADAPTATION TO SUBMAXIMAL WORK Physiologic adaptations to submaximal work performance may be thought of as both short and long term responses precipitated by change in energy requirements. The short term or immediate response accommo- dates provision of the energy needed while, at the same time, acting to maintain homeostatic balances. The long term response consists of more gradual changes which have the end effect of reducing the strain imposed on tissues, organs, and functions by the short term changes in level of physiologic activity. By acting to improve the efficiency and speed of acute adaptation, long term adaptation has a secondary effect of extend- ing capacity for duration and/or intensity of work to an extent that is related to the degree of strain imposed upon capacities for acute adaptive changes. Although much remains to be learned about the adaptation process, many of the adaptations which occur with training at submaximal work intensities are well known. The investigations and respective findings which have elucidated these changes have been reviewed by Astrand (4). Since muscle tissue seems to be limited in capacity for storing oxygen and substrates, capacity for continuance of physical activity is highly dependent upon capacities for mobilizing and transporting these 24 substances to the sites where energy release is needed. As might there- fore be expected, much of the adaptation which takes place occurs in the tissues, organs and systems most concerned with those functions. With onset of exercise, cardiac output is increased by inotrOpic and chronotropic action of the sympathoadrenal medullary system in pro- ducing an increased heart rate and stroke volume (4). With training, cardiac output during steady state work is decreased (2) compared to pro-training measures. Heart rate also is decreased (2,79), but stroke volume is increased (118). Diversion of the cardiac output from less active tissue to the more active muscle tissue has been suggested (5,29,111) as one way in which the increased needs for energy could be met. This has been shown to occur as an acute response by Hartley (64) and by Rowell (111) and to improve with training (2,116). While increased venous return occurs with muscular contractions of work performance, the diversion of blood from the viscera by vasoconstriction also aids in the increase of stroke volume (118) and, hence, the amount of circulating blood available to the aetive muscles. Blood flow through the muscle is further enhanced by local vaso- dilatation which apparently occurs through two mechanisms. In_the process of contracting, muscle releases potassium ions which aretaken up by the blood and apparently help bring about a localized dilatation of capil- laries (29,126,140). It is well known that potassium ion depletion can lead to ineffectuation of muscle contracting ability, but apparently this is at least somewhat offset by an increased storage of potassium in muscle as a consequence of training (96). Vasodilatation can also be brought about in muscle by the action of epinephrine (13) released from the adrenal medulla. Whether or not this latter arrangement is enhanced 25 by training has not been reported. HypertrOphy of the adrenal glands as a consequence of training has been reported (84), but it is generally believed that this is a change in the adrenal cortex rather than in the medulla. The medulla, rather than the cortex, is the source of epinephrine (142,144). The need for increased flow of blood through active muscle tissue is apparently met by still another training effect. As shown by Petren (102), an anatomical change takes place consisting of increased capil- larization in both heart and skeletal muscle. Although respiratory rates are increased with onset of exercise, the rate is apparently not affected by training (4). However, decreases in ventilation as a consequence of training have been reported (138,139). A decline in oxygen uptakes has been reported as well (4,138,139). Since both ventilation and oxygen uptake are knwon to increase with onset of exercise, the decline with training can be considered as a gain in efficiency reflected also by the fact that maximal oxygen uptake is increased (140). In contrast to most reports, Ramos (106) found increased ventilation to occur with training. The change in oxygen uptake continues to be somewhat puzzling, but it is believed to reflect improvement of oxidative processes and O2 transport. The changes in circulation already mentioned could very well play an important role by reducing the size of the tissue to blood oxygen diffusion gradient. As pointed out by Westmark (146), accumulation in blood of metabolites such as lactates lowers the pH of blood, which in turn shifts the oxyhemoglobin dissociation curve to the right, favoring the unloading of oxygen at that site. Since a lowered blood pH also stimulates arterial and neural chemoreceptors, respiratory reflexes are activated which bring about an increased ventilation rate and the 26 "blowing off" of carbon dioxide. The loss of the carbon dioxide, by acting as a buffer, raises the pH which shifts the oxyhemoglobin disso- ciation curve to the left and thereby favors loading of oxygen at lower P02's. Enhancement of the cycle as described by Westmark (146) would seem. to explain the reduction of ventilatory volumes without ventilation rate being affected as previously discussed. The reduction of ventilatory volume could very easily be caused by the increased ventilation rate and might well result in lower alveolar pressures. However, there seems to be some question as to whether or not there is an increase in lactate formation. According to Dill (38) there is an increased lactate forma- tion and accumulation enabled by training. Astrand (4), on the other hand, reports that for a given load, lactate formation is lowered by training. Saiki (115), however, reports that lactates are not produced in submaximal work unless the demand for oxygen is greater than the capacity to supply it. The most likely explanation for these discrep- ancies would seem to be found in the degree to which the work performed is submaximal . Another possibility for the explanation of the decline in oxygen uptakes with training is related to the efficiency of intracellular oxidative processes. Increases in the size and number of mitochondria (55), the site of the oxidative processes, have been reported to occur with training at submaximal intensities. Additionally, increases in the oxidative capacity of individual mitochondria have been reported (69), as have increases in quantity of specific enzymes (101,140). While the changes in enzyme activity would act to speed up the oxidative reactions, increased cellular storage of myoglobin, as reported (100), would act to epeed the intracellular transport of oxygen (65). 27 It is believed that protein plays a very small part in energy metabolism and that fat and carbohydrate are the important fuels used. For this reason R.Q. (Respiratory Quotient) is considered of interest as an indicator of the principal fuel being oxidized--oxidation of carbo- hydrate providing an R.Q. of 1.00 and fat an R.Q. of 0.70 (12). Whereas most studies have reported a reduction in R.Q. with training (12,138, 139), Christenson (20) obtained high R.Q.'s in untrained subjects. From such data the conclusion has been drawn that training brings about a shift toward metabolism.of more fat than carbohydrate during submaximal work. Seemingly antithetical to that notion, evidence has been presented which shows an increase of glycogen in muscle as a consequence of training (9,10). This was suggested as a possible explanation for Rougier's findings (109) that trained athletes have lower resting levels of blood sugar and lessened hyperglycemia during exercise than untrained subjects. However, Rougier based this conclusion on the assumption that the well known hyperglycemia response to exercise indicates a mobiliza- tion of carbohydrate fuel for use by active muscle. It is therefore fair to point out that Rougier's observations could also be explained as an indication that free fatty acids are the preferred fuel thus leav- ing glucose to accumulate in blood. In this respect, the findings of Rottini (108) are interesting even though his study did not deal with training observations. In two sets of untrained, fasting subjects, he found relatively insignificant changes in blood glucose, but a highly significant and extensive drOp in circulating free fatty acids. Moreover, the drop in free fatty acids mirrored almost exactly changes which occurred in blood insulin. When free fatty acids were apparently being removed from.circulation during exercise, insulin was increasing. 28 The role of insulin in energy metabolism during exercise has apparently not been extensively explored. It has been established, however, that catecholamine, and epinephrine, in particular, inhibit the secretion of insulin (147). Since insulin facilitates the transfer of blood sugars across cell membranes, its absence permits accumulation of circulating sugars. Whether or not these phenomena are influenced by training is unclear. According to von Euler (144) there is some evidence to indicate a reduction of catecholamine secretion in trained individuals. Since it has been observed that norepinephrine, in par- ticular, seems to be secreted in accord with the degree of physical stress (143), and since training adaptations appear to reduce stress imposed by exercise, it is reasonable to conclude that a reduction in catecholamine secretion would accompany training. However, Nowacki and co-workers (97) report evidence of increased catecholamine secretion after training. Upon finding evidence of greater catecholamine secre- tion following athletic competitions that were won than after those which were lost, Nowacki and associates concluded that catecholamine secretion is a necessary element to superior performance. Whether catecholamine secretions are increased or decreased by training, the degree of hyperglycemia would likely be affected. Of some enlighten- ment is the additional observation that less catecholamines are secreted during aerobic work than during anaerobic work (37). Since the effect of training at submaximal intensities seems to enhance aerobic metabolism, it is reasonable to speculate that under these conditions catecholamine secretion would be reduced. In addition to the inhibition of insulin secretion, epinephrine has another effect which acts to increase levels of blood sugar. By activating phosphorylase (34,35), glycogenolysis in the liver is 29 accelerated (27,28) so that glucose is released into the blood at a faster rate. Since insulin is known for its property of enhancing cellular entry of glucose from blood, its absence in blood would seem to preclude glucose uptake by muscle. However, it has been shown that insulin is not necessary for glucose uptake by muscle tissue during exercise (21, 53,54,103,l47), apparently because a humor with insulin-like properties is released by contracting muscle tissues (54). By virtue of being a highly labile substance, this humor permits little more than a local effect. It is of further interest that, as shown by Mbrgan (92), with high concentrations of blood glucose, phosphorylation rate is the limit- ing factor to glucose uptake in muscle. Since epinephrine activates phosphorylase in muscle as well as in liver (114) the uptake of glucose would seem unimpeded in muscle. In other tissues, however, the reduced blood flow brought about by vasoconstriction along with the reduction in circulating insulin, would act to conserve the circulating sugar for uptake by the active muscles. Bergstrom's (9) findings that increased glycogen storage occurs only in exercised muscle would seem to be indirectly supportive of the latter concept. From the evidences discussed here, it is clear that much more remains to.be elucidated before exercise metabolism can be more com? pletely understood. It is also clear that discussions pertaining to the substrate used need to consider the condition of the subject (108), the fitness of the subject (20,138), the work rate (19), and, certainly, the environment (80). 30 PHYSIOLOGIC RESPONSES TO HYPOXIA AND SUBMAXIMAL WORK The effects of hypoxia on human and animal physiology have been studied since before the turn of the century, and a considerable body of knowledge has been accumulated. The studies and body of knowledge con- cerned with this t0pic have been extensively reviewed by Barbashova (6) and by Stickney and VanLiere (132). Due to wide differences between experimental methods and in basic nature of the studies conducted to investigate this area of interest, cross-comparison of studies and respective findings is rendered particu- larly difficult, and only limited generalizations are possible. Dif- ferences in effects observed at various altitudes are primarily quanti- tative and appear principally related to differences in P02. Qualitative differences apparently occur only when the individual capacity of one or another adjustment mechanism is reached and other mechanisms and combina- tions of mechanisms must act in compensation. This fact is especially apparent from.the work of Thoden and co-workers (136), who found that the degree of ventilation work is affected by air density only when-the demand for oxygen is sufficiently great to require a ventilation rate of 65 liters per minute or greater. For this reason, the effects from breathing a gas mixture of reduced PO at sea level densities may not be 2 strictly comparable to the effects of breathing air of reduced densities (as found at altitude) even though the POz's may be identical. Acute Hypoxia In general, acute responses to hypoxia are essentially the same as acute responses to submaximal work performance. This is probably due to the fact that, in both situations, there is need for more oxygen at the tissue level, relatively speaking. To meet this demand circulation is 31 enhanced. Heart rate is increased (11,24,25,42,44,58,59,63,88,104,106, 107), as is stroke volume (42) and hence also cardiac output (42). However, a lower heart rate following swimming exertion at altitude has been reported (31). To meet the increased needs for oxygen by active muscle, a circulatory shunt was suggested by Banister (5) and shown by others (2,45). Vasodilatation in muscle vessels has also been shown (17,29,126). Similar changes in blood constituents have been observed in that increased amounts of glucose (80) and potassium( 46) have been found. Hansen found blood lactates increased during rest (63) but decreased during exercise as did others (67,71,83). Except for differences occurring under special circumstances as shown by Thoden (136), hypoxic ventilatory responses resemble those of exercise. Respiratory rate (16,95,107) is increased as is ventilation rate (16,24,25,44,57,58,59,88,95,106,107). Others (95,107), however, reported that reapiratory rate was not_affected by acute hypoxia. Since ventilation rate is virtually always increased, a lack of effect on respiratory rate might be a consequence of increases in tidal volume which have been reported (6,57,95). The findings with respect to oxygen uptake are less clear. Both increases (24,47,57,7l) and decreases (25,44,59,88,99,123) have been reported as acute hypoxic responses. It is considered possible that these differences simply represent differences in subjects which would act to maximize the importance of Thoden's (136) findings. The effects elucidated by Thoden's work would also seem a possible explanation for differences reported with respect to oxygen requirement. An increased exercise oxygen requirement has been reported by Consolazio (24,25) while Flandrois (48) observed no change. Decreases for oxygen requirement are reported in exercising humans by Cronin (30) and in 32 exercising and resting animals by Hill (68). Although they did not report the observation per se, McDavid (88) and Kollias (83) have published data that indicate a lowered oxygen requirement for exercis- ing humans breathing hypoxic air. Increased R.Q.'s have been reported during exercise (ll,24,47,48, 88) but were attributed to hyperventilation. However, an increased BMR (basal metabolism rate) as observed in sojourning humans at altitude (57) seems to indicate that metabolism changes might also be involved in elevation of R.Q. Urinalyses have shown an increase of catecholamine secretion (8, 143). Although von Euler (144) reports a greater percentual increase in epinephrine, others (8,37) have found evidence indicating that condi- tions other than hypoxia may influence the relative amounts of epinephrine and norepinephrine which are secreted under hypoxic exercise conditions. Commenting upon changes in submaximal performance, Billings (11) reported that a longer time was needed to reach a steady state. This seems to be in line with Consolazio's report (25) of reduced capacities for endurance work under hypoxic breathing conditions. Of possible enlightenment to these observations, Pugh (104) found that the exercise heart rate at altitude was decreased by the breathing of air at sea level P02 while ventilation was not affected. At the tissue level, the work of Pappenheimer (98) is interesting in that he observed a reduced oxygen uptake in muscle to which blood supply was diminished by means of electrically stimulated vasoconstric- tion. In another study (99), his use of adrenaline to produce vasco- constriction resulted in an increased oxygen uptake and muscle tempera- ture despite the obtained reduction in blood flow. 33 Chronic Hypoxia Since the effects produced by acute exposure to hypoxia resemble so closely the acute responses to submaximal work, it would be reasonable to expect similar long term adaptations. However, this is not entirely the case. While there are some similarities, there are also important differences. No published explanation was found for the differences, but a possible explanation may reside in the fact that hypoxia, as encountered at altitude, is continuous. It does not cease when one becomes tired as is the case with exercise. As with submaximal training, heart rates during exercise at steady ' state have been found to decrease with time spent at altitudes (44, 141). Unlike submaximal training under normoxic conditions, continuous hypoxia apparently reduces the maximal heart rate which can be atttained (25). Moreover, as reported by Billings (11), the time needed to reach steady state is longer in hypoxic air and is not improved by training or continued exposure to hypoxic breathing conditions. A similar situation exists with respect to oxygen uptakes. During repeated submaximal exercise under hypoxic conditions, oxygen uptakes are gradually reduced as is the case with training under normoxic con- ditions. However, the maximal oxygen uptake which can be attained is decreased with adaptation to altitudes (23), whereas it increases with training at sea level pressures. Although some investigators (11,33,44) have reported increased oxygen uptakes with training, the discrepancy may be due to the relative degree of hypoxic work. According to Billings (11), if work output requires less than 2.2 liters of oxygen per minute at sea level, oxygen uptakes are the same at altitude. How- ever, if the demand exceeds 2.5 liters per minute at sea level, the same amount of wdrk is accompanied by lower oxygen uptakes at altitude. 34 Billings inferred this to mean that higher oxygen debts would be incurred. Yet, Consolazio (23) reported reduction in oxygen debts with acclimatization at altitude. Although no report was found in which a change of oxygen require- ment was reported, Duckworth (40) inferred that a reduced oxygen requirement could occur with adaptation to hypoxia. She based this thesis on her findings of reduced oxygen consumption in strips of dia- phragm muscle removed from acclimatized rats. She also found a reduction of cytochrome "C" in the same tissues, a finding which would indicate reduced oxidative activity. Since it seems to be fairly well established that a circulatory shunt of blood from the viscera to the peripheral musculature occurs with hypoxia (45,111), it is possible that continued shunting of this sort might cause the effects observed by Duckworth (40). If that were the case, a reduction in oxygen requirement for the entire body could not be assumed. Furthermore, the evidence of increased oxidative enzyme activity found by other investigators (6,107) as an acclimatization effect would seem to indicate an enhancement of oxidative activity rather than a diminishment. Yet, an enhancement of oxidative efficiency might very well result in a reduced oxygen requirement for a given work load. A distinct difference in adaptation also occurs in exercise ventila- tion. Training under normoxic conditions usually brings about a reduc- tion in ventilation. Acclimatization to altitude hypoxia, on the other hand, appears to increase ventilation (11,94,95) despite the fact that one investigator reported a decrease (44). It is of further interest that acclimatized residents of high altitude have proportionately reduced ventilations when transported to sea level (57,58) but return 35 to the higher ventilations during both rest and exercise almost immediately when they are returned to altitude. The increase of exercise ventilation with adaptation is of added interest in view of the fact that hyperventilation is known to accompany decreases in blood pH. Hyperventilation is generally accepted to be one mechanism by which blood acidity is reduced as a consequence of the buffering effect gained by "blowing off" extra carbon dioxide. Where endurance types of exercise (submaximal) are concerned, an increased blood acidity is usually related to lactacidemia. Lactates are supposedly produced when there is an insufficient supply of oxygen (85,115), and increased blood lactates are considered to indicate an increased reliance upon anaerobic metabolism for energy (115). Although a decreased pH (63) has been reported as a consequence of chronic exposure to hypoxia, most investigators report decreased blood lactates (18,41). Furthermore, it has been postulated that the inability to accumulate blood lactates upon acclimatization to altitude hypoxia is an important factor which limits endurance performance (18,41) if the performance is of a nature that produces lactic acid. ‘These observations and concepts are quite obviously not in agreement. If blood lactates are decreased with acclimatization, it would seem likely that blood pH should be raised. If blood pH is raised, then what accounts for the increased ventilation? Certainly, other factors could be involved. However, in an obviously hypoxic situation, what accounts for the decreased lactates? Possibly, the interpretations have been wrong. Considering the work of Cori and associates (26,27,28), a potential explanation for the questions that have been raised would seem related to the increased secretions of catecholamines which have been observed 36 under hypoxia (8,50). The glycogenolytic effects of epinephrine in liver and muscle tissue are well known. Enhancement of both glycogenesis and lactate uptake in liver are less well known. According to Cori (26,27,28), epinephrine causes an increased uptake of blood lactates and an increased production of glycogen. However, glycogenolysis also takes place and produces increased blood glucose. Since glucose can be taken up by muscle during exercise (10,19), it would appear possible that lactate formation is not decreased under hypoxia. Rather, the increased catecholamine activity might result in more rapid removal of lactates from the blood. In that way, the removed lactates could be reconverted to glucose in the liver and be returned to the muscle cells as substrate for more energy production. Whether an increased or decreased pH would be observed would then be a matter of when and where blood sampling was effected. The same would be true for blood lactates. This explanation would seem to fit all the evidences reported over many years. Yet, surprisingly, no indication was found that other investi- gators had considered this arrangement as a possible explanation of the phenomenal differences described. Additional differences in adaptation have been found in hemoglobin and hematocrit data. Although neither of these appear to be affected by submaximal training, increases in both have been reported as a consequence of altitude hypoxia adaptation (40,72,123). The effects of alternating exposure to hypoxic breathing conditions with normoxic breathing conditions during exercise have produced results which are both similar and different from chronic exposure effects. According to Faulkner (44) the alternation of conditions appears to speed up acclimatization. Other investigators do not report accelerated acclimatization, but do report increased ventilations, decreased oxygen 37 uptakes during exercise (33,36,94), and decreased heart rates (95). Increased blood lactates (94) have also been reported as a consequence of intermittent exposures and are in contrast with decreases usually reported with chronic exposure. CHAPTER III RESEARCH METHODS The purpose of this study was to investigate the possibility that physiologic responses during submaximal work under normoxic or hypoxic conditions are psychogenically influenced by cues pertaining to the presence of those conditions. Data were sought which would permit answering three main questions: 1. Can psychogenic influence induced by information relevant to conditions of work performance be detected as alterations in parameters of physiologic reaponse during the work performance? 2. If alterations of response can be detected, how do effects induced by cues that hypoxic air is breathed compare to effects induced by the actual breathing of hypoxic air? 3. If alterations in response can be detected, do they appear to be incremental or decremental with respect to the kind of work performed? SUBJECTS Eight male subjects were recruited from among students majoring in physical education at Michigan State University. Of these, six were graduate students and two were undergraduate students. The average age of the subjects was 27, and the average weight was 76.89 kg. A11 would be classified as of medium athletic build. All were athletically active. Only one student was an athlete in training, a mile runner from.the track 38 39 team whose participation in the study was permitted by virtue of temporary ineligibility for competition. These particular subjects were specifically selected on the basis of characteristics mandated by the nature of the investigation: 1. Subjects were needed who were in a relatively stable state of cardiovascular fitness permitting endurance efforts of the sort employed in the testing situations. 2. Subjects were needed who would have a reasonable understanding of exercise physiology principles. 3. Subjects were needed who could be depended upon for full c00pera- tion during the length of the investigation. TREATMENTS Treatments consisted of having the subjects make standard runs on a motor driven treadmill under each of the four test conditions: 1. ( H1) - Breathing hypoxic air with cues provided to indi- cate hypoxic air was being inspired. 2. (H2) = Breathing hypoxic air with cues provided to indi- cate normoxic air was being inspired. 3. (N1) - Breathing normoxic air with cues provided to indi- cate normoxic air was being inspired. 4. (N2) = Breathing normoxic air with cues provided to indi- cate hypoxic air was being inspired. The Standard Treadmill Run An endurance type of work performance was considered necessary to obtain definite differences between effects of breathing normoxic air and effects of breathing the hypoxic air. However, it was also neces- sary to select a task which would not be so taxing as to risk inability 40 of subjects to complete every run. With these factors in mind con— sidered in light of past experience in this laboratory, the standard run of 7 mph at zero grade for a period of 5 minutes was selected. Procedures employed made it possible to hold the distance of the runs to within a tolerance of ill treadmill revolution (approx. 18 ft.). The Hypoxic Air Mixture The hypoxic air used consisted of compressed air diluted with nitrogen such that the percentage of oxygen in the air mixture was reduced to 16.60% 110.04%. Reducing the compressed air mixture to ambient pressures resulted in a P0 of 120 mm. Hg (STPD). This particu- 2 lar value for PO2 was used because it closely approximates the P02 found in ambient air at 2300 m. altitude, the elevation of Mexico City. Comparison with findings from research connected with the 1968 Olympic games would therefore be enabled. Based upon Marotta's work (86), the amount of N2 in this mixture was considered to be biologically safe. The Normoxic Air The normoxic air used was obtained from compressed air tanks filled in a room adjacent to the laboratory. Both normoxic and hypoxic air from the compressed air tanks were reduced to ambient pressure as well as being moistened and warmed before reaching the subjects. Techniques employed to accomplish these tasks will be discussed in a later section. Cues Cues of two types were used, verbal and visual. Each time a sub- ject stepped on the treadmill he was told either, "This is an altitude run. Waggle your hands if you get into trouble,‘ or "This is a regular air run. No difficulty is expected, but waggle your hands if you get 41 into trouble." Visual cues were initially provided by filling, in the presence of the subject, a meteorological balloon used as a reservoir from a tank marked either ALTITUDE AIR or ROOM AIR. Secondly a color coded sign was placed so it would be directly in front of the subjects during the run. The altitude sign read, "Altitude Run - Waggle your hands if in trouble," and was printed in bold letters on red paper. The room air sign was printed in the same size letters on white paper and read, "Room Air Run - Waggle your hands if in trouble." The compressed air tanks were identical in every way except for the labels, which included a coding to indicate what was actually in the tank. The coding consisted of small print and simply read, "Tank 1" or "Tank 2." A "1" indicated that the label (Altitude Air or Room Air) was. correct. A "2" indicated that the labels were reversed. Four tanks were always present, and the tanks were always turned off at the end of the run in the presence of the subjects. Only the experimenter knew what was actually in the tanks. Rationale for Selecting;the Four Treatments In designing this investigation, it was postulated that physiologic responses to the condition of breathing hypoxic air during exercise would reflect psychogenic influence as well as physiologic need if a subject was aware of the hypoxic condition. To test that hypothesis required two situations--awareness of hypoxic conditions and unawareness of hypoxic conditions. To examine the nature of effects, however, required the two normoxic situations. It was reasoned that comparing hypoxic effects with normoxic effects on responses would reveal direction of effects occurring as a consequence of physiologic needs. Comparison of the_"told hypoxic" 42 effects under both normoxic and hypoxic conditions would then reveal the direction of the psychogenic effects. Cross-comparison across all four conditions would provide bases for quantifying relative extent of the different effects. Two important assumptions provide the basis for this logic: 1. It was assumed that all subjects would respond in a quali- tatively same manner both physiologically and psychologically. 2. It was assumed that telling the subjects normal (normoxic) air was breathed would have a psychogenically neutral effect by virtue of the subjects being used to breathing normoxic air. PROCEDURES Pre-Trainigg Each of the subjects completed six training runs under normoxic conditions during the week prior to commencement of the study. Speed, grade, and duration of the runs were identical to those used in the study proper. However, the subjects were not attached to the air feed apparatus except during the last two training runs, and electrodes for monitoring pulse rate were attached only during the last training run. The subjects were seated at the end of the 5 minute run as in the study preper, but only for a period of 5 minutes. Pulse rates were obtained by palpation of the radial artery for 30 seconds at one minute post-exercise (124) in order to obtain a rough estimate of how the subjects were responding to training (Appendix F). The pre-training procedures were used to acquaint the subjects with testing conditions and procedures and to reduce variability in responses which was expected to occur as a consequence of adjustments to test 43 conditions in general and to running on a motor driven treadmill in particular. Psychological Preparations Several precautions were taken in hOpes of gaining at least some measure of uniformity in the subjects' psychological set. As a cover for the actual purposes of the study, the subjects were told that the purpose of the study was to compare their responses during exercise while breath- ing hypoxic air to responses while breathing normoxic air in order to explore possibilities of conducting altitude related studies without a hypobaric chamber. They were also told that, if events transpired as expected, breathing the hypoxic air during exercise would most likely be essentially the same as working harder while breathing normoxic air. In other words, they could expect to feel tired more quickly when breath- ing hypoxic air than when breathing normoxic air. The training sessions were also expected to contribute toward uni- formity of psychological set. Advantage was taken during these sessions to explain how the equipment worked. In addition, all subjects were shown that a tank of pure oxygen was in readiness on the off chance that it might be needed during the hypoxic runs. Other measures taken consisted of providing the subjects with a sheet of printed directions concerning their participation in the study (Appendix E), and of not telling the research assistants what air was actually breathed during the runs. Thus, while the investigation was not a true double blind study, double blind techniques were employed to the extent considered practical. 44 Test-Run Procedures Subjects were scheduled to run only three days a weeks-Monday, Wednesday and Friday or Tuesday, Thursday and Saturday. All runs were scheduled early in the morning, and consequently, the subjects reported in a post-absorptive state. Rigid scheduling was kept whereby each subject ran at the same times and on the same days of the week. Report- ing to the laboratory fifteen minutes before actually commencing to run, subjects had electrocardiograph (EGG) electrodes attached immediately. They then proceeded to the treadmill room to rest in a sitting position for approximately ten minutes. During this time the balloon reservoir was filled, and the subject was cued with respect to the air that would be inspired. When it was time to commence, the subject stood up on the treadmill and donned the headpiece holding the low resistance Collins1 Triple "J" valve through which the prepared air was inspired from the air feed apparatus. The ECG electrode leads were then plugged into the polygraph and both respiratory and pulse rate recordings were checked for approxi- mately one minute while the subject remained standing. The starting signals, "Ready - Set - Go," were then given. On the word "Go," the treadmill was started, the subject started running, and a switch was thrown to commence collection of expired air, all simultaneously. Expired air was collected using Douglas bag techniques (22) except that meteorological balloons were used. A Van Huss-Wells automated switching valve was also employed enabling collection bag switching only during inspiration so that expiratory resistance remained constant. Bags 1Warren Collins Co. 45 were switched every 30 seconds during the run and were immediately trans- ported to the research assistant in charge of making gas analyses and measuring the volumes of collected air. The procedures employed were of such efficiency that analysis and measurement took place within two minutes after collection with very few exceptions. The polygraph record- ing respiratory and pulse rate data was left on continuously. At the fourth minute of the run a countdown for stopping was commenced with the statements, "1 minute to go. 30 seconds remaining. 15 seconds. 10. 5, 4, 3, 2, 1. Stop!" On the word "step," the tread- mill was turned off. The inspiratory hose was disconnected, and the subject was then seated in a chair. Recording of pulse and respiratory rates continued, along with the collection of expired air during the 15 minute recovery period. During the recovery period, the expired air was collected in one bag for the first minute, in another bag for the second minute, and thereafter in separate bags at two minute intervals. At the end of the recovery period, subjects were disconnected from the recording apparatus and air collection apparatus. In every case where a subject had been told he was breathing hypoxic air, he was asked, "Do you feel all right or would you like a whiff of oxygen?" (Only once was this offer accepted.) Subjects then left the laboratory immediately, as had been directed at the outset of the study. Data Collection Provisions 1. Subjects reported for each run in the same running costume and shoes. Prior to each run, body weight was obtained (in running costume) on balance-type scales calibrated in metric units. l'lll-Illlll'llll 46 2. Barometric pressure, humidity, and ambient air temperature were recorded prior to every run. Room temperature was held as constant as possible (68.5° i 3.5° F.) with an air conditioner. No control was exerted over humidity and atmospheric pressure (Appendix D). 3. All gas analysis and polygraph recording equipment was cali- brated daily and, usually, before each run. 4. Gas samples from each bag of expired air were analyzed for oxygen percentage using a Beckman Model E2 Oxygen Analyzer and for carbon dioxide percentage using a Beckman Model LB15A Carbon Dioxide Analyzer. 5. Expired air volumes were measured using a Franz-Muller calori- meter and corrected to STPD using the gas temperature recorded during measurement. 6. Samples of air from the air feed apparatus tanks were analyzed on a daily basis as well as at the time of mixing. 7. Before every run, the air feed apparatus was drained, and thoroughly flushed with the gas scheduled for inspiration. 8. Pulse and respiratory rates were obtained by full counts from polygraph records. 9. Technical difficulties produced numerous artifacts in pulse rate data during the first one-third of the study. Therefore, entire first half pulse rate data were excluded from analysis. 10. The shift from hypoxic air to room air for recovery resulted in artifacts in the gas analysis data due to the time needed for flushing residual hypoxic air from the lungs. On the basis of determinations on these subjects, it was established that the time needed for sufficient flushing to take place was 30 to 45 seconds. Therefore, the first minute of recovery data were excluded from analysis. For the purposes of this 47 study, this practice was judged preferable to the alternative of having hypoxic runs followed by recovery on hypoxic air over a more extended period of time. 11. Treadmill momentum did not permit immediate stOpping. However, a device for recording treadmill revolutions indicated that the pro- cedures used held run distances constant within a tolerance margin of one treadmill revolution. 12. Two trained assistants helped with data collection. All gas analyses were conducted by one of the two—-a highly trained and competent individual. Neither of the two assistants received any more information about the nature of the air inspired than was given to the subjects. APPARATUS AND EQUIPMENT Hypoxic Air Mixture Apparatus Special apparatus was devised to obtain hypoxic air mixtures. In essence this consisted of using an air compressor which was already installed for filling SCUBA tanks, and a tank of compressed nitrogen with apprOpriate valves, gauges, and high pressure tubing (Appendix C). Disregarding the effects of temperature changes on volumes, calcu- lations were made to determine pressure ratios which would come close to providing the specified 02 content of 16.60%. Since a greater pressure head was available from the compressor than from the nitrogen tank, nitrogen was drawn off into the empty tank first, until the desired pressure was reached as estimated by the reduction of pressure in the nitrogen tank. Compressed air was then added according to conservative estimate allowing more compressed air to be added as needed to reach the specified 02 centent. Analyses were then run and small amounts of com- pressed air were added as necessary. 48 On the basis of normal atmospheric pressure variations it was felt that i_0.20% was an acceptable margin for accuracy relevant to the per- centage of oxygen. Although the apparatus and procedures which have been described may seem somewhat crude, subsequent events showed that air could be mixed in this way within an accuracy margin of i 0.04% oxygen. Air Feed Apparatus The procedure of using air from compressed gas cylinders necessi- tated the devising of special apparatus to feed the air to subjects in a way which would not interfere with their running. This apparatus (Appendix C) consisted of apprOpriate valves, gauges and tubing through which air was passed into the bottom of a one gallon plastic water con- tainer. Since air is passed through a desiccator in the compressing process, the water bath was employed to moisten the air to prevent drying out of respiratory passage tissues. Due to the fact that gases cool with reductions in pressure as occurred when air was released from storage tanks, the water bath also served to warm the air. Both warming and moistening were considered necessary to reduce chances of respiratory infection occurring in the subjects. From the water bath, the air was passed through small diameter (5/16" I.D.), flexible, plastic tubing into the center of a meteorological balloon in order to reduce the air to ambient pressure. Rate of flow was controlled so that the balloon remained flaccid. A valve was placed in the top of the balloon to facilitate flow control. Attached_to this valve was another piece of flexible plastic tubing having a 1 1/4" I.D. This large bore tubing was attached directly to the inlet of a Collins Triple "J" valve having inspiratory and expiratory resistance of less than 20 mm H20 at flow rates of up to 20 liters/min. 49 A Collins rubber mouth piece was attached to the inspiratory outlet of the Triple "J" valve. The weight of the valve and attached hoses was supported by a welder's head harness modified for the purpose. Another piece of tubing, 18 inches long of 1 1/4" I.D., was fastened between the expiratory outlet of the Triple "J" valve and the intake outlet of the automated switching valve. The Triple "J" valve was modified to permit attachment of a small. diameter tube to the valve. This hose was attached to a sensitive pressure transducer (Sanborn - Model 268A) to permit continuous monitor- ing of the intra-valve (Triple "J") pressures. From recorded pressure curves, the desired respiratory information could be secured. Rate, resistance, and flow could be determined. Only the rate measure has been used in this study. ANALYSIS OF DATA Experiment Desigg Owing to the nature of this investigation, difficulty was foreseen in obtaining and controlling a large number of subjects. The possibility was also considered that any effects induced by psychogenic influence might be so small, in both an absolute and relative sense, that detec- tion of differences by statistical analysis could be difficult. It therefore appeared wisest to employ a statistical design requiring a relatively small number of subjects, and to use procedures which would enhance the precision of the experiment as much as possible. With these considerations in mind, a Latin Square type of design.was selected using incomplete, between-subject counterbalancing as described by Underwood (137), but modified for replications as recommended by Campbell and Stanley (14). 50 Between-subject counterbalancing permits a small number of subjects to be used with each acting as his own control. The counterbalancing acts to distribute effects due to order and to training more evenly across each cycle of four treatments thereby tending to reduce biases associated with these effects. Since it was known that measures of the sort contemplated have con- siderable day to day variation, even with trained subjects, it was con- sidered necessary to replicate observations to improve reliability of the data obtained. In keeping with the principles outlined by Underwood (137), it was decided that four was the minimum number of replications necessary. Although more repetitions would act to increase reliability even further, it was feared that additional repetitions would jeOpardize the validity of the study with respect to the psychogenic aspects of the investigation. The use of four replications with four subjects necessitated further counterbalancing so that subjects would be exposed to a different treat- ment order in each of the four cycles and so that no two subjects would be exposed to the same treatment order in any one cycle. According to Underwood (137), the minimum number of subjects which can be used in a counterbalancing design corresponds to the number of treatments contemplated. According to Campbell and Stanley (14), the involvement of so few subjects produces odds which are statistically in favor of obtaining a bias specific to those particular subjects. Repli- cation by even one more group, however, changes the odds sufficiently to favor not obtaining a bias specific to the group of subjects. For this reason a total of eight subjects was decided upon so that the second group of four subjects could replicate the experimental procedures used with the first four subjects. 51 The design which was finally selected is presented in schematic form in Figure 3-1. Cycle I II III Iv Run No. l 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 Subject A l 2 3 4 2 4 1 3 3 l 4 2 4 3 2 1 A Subject B 2 4 1 3 4 3 2 1 1 2 3 4 3 1 4 2 Subject 0 3 1 4 2 1 2 3 4 4 3 2 1 2 4 1 3 SubjectD 4321314224131234 Subject E 1 2 3 4 2 4 l 3 3 1 4 2 4 3 2 1 B Subject F 2 4 1 3 4 3 2 l 1 2 3 4 3 l 4 2 SubjectG 3142123443212413 Subject H 4 3 2 1 3 l 4 2 2 4 l 3 1 2 3 4 Figure 3-1. Schematic layout of experimental design. In Figure 3—1, it may be seen that each of eight subjects made a total of sixteen runs on the treadmill. In each cycle of four runs, the subjects were exposed to a different order of the four treatments. The four subjects in group B were exposed to the same orders of treatment as the four subjects in group A. Treatment orders were pre-established and subjects were randomly assigned to group and then to treatment order. The use of this design imposes two disadvantages: (1) There is no flexi- bility permitting missing observations, and (2) The low number of subjects greatly reduces the power of statistical testing. An inherent weakness of the design is that the relative effectiveness of the counterbalancing 52 procedures is dependent upon the relative linearity of training and/or order effects. Training Effects Versus Treatment Effects Attention is called to the fact that this study was not designed to accommodate an investigation of training effects. However, the need for replicated measures on the same subjects imposed the need for considera- tion of training effects in designing the study as well as for planning the analysis of data. As was pointed out, counterbalancing was employed to spread more evenly across treatments the variability expected to occur from training effects. It was haped that this procedure, in conjunction with analysis of variance procedures of accounting for variability, would make it statistically easier to detect effects due to psychogenic influence. Although it was expected that the effects of psychogenic influence would be additive to the effects of exercise under hypoxic or normoxic conditions, there was no basis for predicting the magnitude of effects which might be produced, not of knowing for certain how training influence would act or interact with the postulated effects of psycho- genic influence. It was therefore planned to run three separate analyses of variance where one might otherwise do. The first ANOVA would consider the main effects of treatment, cycle (training) and subject as well as the various sub-effects. The second ANOVA would fulfill the same purpose, except data obtained in the first two cycles would be pooled for compari- son with the pooled data obtained in the last two cycles. A third ANOVA would test normoxic and hypoxic data separately on the grounds that vari- ability inherent to the hypoxic and normoxic effects might very well act to mask what were expected to be the relatively small effects of psycho- genic influence. 53 In addition, it was planned to test the effects of treatments across runs by means of a Sign Test. The use of a Sign Test in addition to ANOVA F Tests might seem unnecessary. However, both kinds of testing were considered essential to the analysis for several reasons. The ANOVA's were considered essential to analysis because they enable determination of effects due to factors other than treatment and also permit analysis for interaction effects. The Sign Test was included because it permits analysis of multiple measures made on a single dependent variable across time regardless of whether the data are linear or curvilinear(:125). Since analysis of variance procedures assume linearity, multiple measures which are curvi- linear cannot be analyzed unless there is only a single representative measure used. Due to the fact that physiologic variables such as heart rate and oxygen uptake vary considerably in a curvilinear fashion from the beginning of exercise to the end of exercise, it is questionable whether a single measure such as the mean value can truly represent all events that take place. Consequently, the analysis of variance using that value is severely limited in sensitivity for detecting small changes such as were postulated would occur in this study as the consequence of psychogenic influence. Statistical Analyses Since subjects were randomly assigned to the different treatment orders, with treatments and cycles being fixed variables, three-way, mixed model ANOVA's were conducted (60). All data were submitted for calculation to a CDC 3600 computer at the Michigan State University computer center. 54 Two tailed testing was employed with the probability of making a Type I error held to the .05 level of confidence. Where F ratios indi- cated significant differences at this level, a Student-Newman-Keuls (SNK) contrasting of means was employed to determine which means were significantly different from one another. The SNK contrasts were also held to the .05 level of confidence. The Sign Test was applied to mean values obtained under each treat- ment across duration of the run and recovery periods. The Sign Test was applied separately to the Normoxic Treatments and Hypoxic Treatments, respectively, and was also applied separately to exercise and recovery data, respectively. The Sign Test is a one tailed test, and here too the probability of making a Type I error was held to the .05 level of confidence. CHAPTER IV RESULTS AND DISCUSSION The purpose of this study was to determine whether physiologic responses during submaximal work under normoxic or hypoxic conditions are psychogenically influenced by cues provided to indicate the presence of those conditions. Quantitative differences in observations were postulated. A subsidiary interest was to obtain physiological bases for judging whether psychogenic influence induced under these circum- stances would be facilitory or inhibitory to the performance of sub- maximal work. The data presented were derived from observations of eight subjects throughout four replications of each of the four experimental conditions. Three main comparisons were deemed essential to the analyses and interpretation of results. As shown schematically in Figure 4-1, these comparisons were between the effects of breathing hypoxic air and the effects of breathing normoxic air; between observations obtained in each of the four cycles of the study; and between effects of being cued that hypoxic air was breathed and effects of being cued that normoxic air was breathed. 55 56 TOLD / NORMCXIC AIR / HY xxc 1 / N2 AR H1 / 2 Figure 4-1. Three comparisons essential to interpretation of data. "'1 .l a, N A; RESULTS The results of the experiment have been organized for presentation into three main categories: hypoxic effects versus normoxic effects; training effects (adaptations to testing procedures); and psychogenic effects. Hypoxic Effects Versus Normoxic Effects The treatment means of the variables studied, the analysis of variance (ANOVA) results, and the post-hoc Student-Newman-Keuls (SNK) contrasts are presented in Table 4-1. Significant ANOVA results at P 5 .05 were observed in all but four variables. The SNK results, also held to P 5 .05, indicate that in every instance where a significant F was obtained, both normoxic means were significantly different from both hypoxic means. 57 Table 4-1. Treatment effects as reflected in mean values of 21 physiologic variables 1 2 3 Treatment Means F Test S-N-K Contrasts of Variable- Units N1 N2 H1 H2 Result. Treatment Means“ * Pegttzulse bpm 160 159 163 164 N2 N1 H1 H2 * Exéapzlse bpm 146 145 148 149 N2 N1 H1 H2 * Ex. 02 ml./ 17.2 17.5 15.2 14.7 H2 H1 N1 N2 pulse bt. Total Ex. liters 322 323 360 360 * N N H H . -1--2 -2-nl vent. Total Rec. liters 217 219 230 234 * N N H H —1——-2 -—1—-—2 vent. Sum Tot. liters 539 542 590 542 * N N H H -<1-—2 -ir-—2 vent. Ex. vent. L./ 64.3 64.6 72.0 72.0 * N N H H -fL-—-2 -—2———l rate min. Tidal vol. L./ 2.00 2.03 2.11 2.13 * 111 N2 311 H2 rsp. Ex. resp. rsp./ 32.8 32.8 35.0 34.6 * N N H H -l 2 ~ih——el rate min. * T035 3:. liters 12.7 12.9 11.9 11.6 H2 H1 -§1 N2 0 debt liters 5.47 5.44 6.03 6.09 * N N H H 2 _. _.___. oz req. liters 18.2 18.3 17.9 17.7 n.s. 2 1 l 2 Ex. 02 up L./ 2.54 2.57 2.37 2.31 * -§2 Hl N1 N2 rt. min. Ex. 02/ m1./ 80.6 82.4 71.4 69.9 * s2 H1 _Nl N2 resp. rsp. * Ex. 02 up m1./ 33.2 33.4 31.0 30.1 H2 H1 ‘El N2 rt./kg. min./ kg. 02 debt/ m1./ 71.0 70.4 78.0 78.6 * 312 N1 :11 H2 kg. kg. 02 req./kg. m1./ 237 237 233 229 n.s kg. Ex. 02 Z 3.99 4.01 3.32 3.24 * H2 H1 ‘EI N2 extract. 58 Table 4-1 (cont'd.) Treatment Meansl F Test2 S-N-K3 Contrasts of Variable Units N1 N2 H1 H2 Result. Treatment Means Rec. 02 z 2054 2.53 2.66 2064 neg. extract. * Ex. R.Q., 832/ .90 .92. 1.04 1.07 N1 N2 H1 H2 Rec. R.Q. 002/ 1.03 1.04 .98 1.00 n.s. O 2 lTreatment symbols: N1,- Breathed normoxic air, told normoxic air. N2 - Breathed normoxic air, told hypoxic air. H1 8 Breathed hypoxic air, told hypoxic air. H2 - Breathed hypoxic air, told normoxic air. 2n.s.'- no statistical significance; * - mean differences sig- nificant at the .05 level. Complete ANOVA summaries are tabled in Appendix B. 3Student-Newman—Keuls post hoc contrast of means. All combina- tions significantly different at the .05 level except those underlined. Means are arranged according to numerically ascending size, lowest values at the left. 59 Hypoxic Effects on Individual Variables The effects derived from breathing hypoxic air in comparison with the effects derived from breathing normoxic air while performing essen- tially the same amount of work have been summarized: ll. 12. 13. 14. 15. 16. 17. The normoxic Peak pulse rate was higher. The average exercise pulse rate was higher. Oxygen pulse (uptake vol./beat) was lower. Pulmonary ventilation during exercise was higher. Pulmonary ventilation during recovery was higher. Total pulmonary ventilation was higher (Reflects 2 #4 and #5). Pulmonary ventilation rate was higher. Tidal volume was greater. Respiratory rate during exercise was higher. The total volume of O2 taken up during exercise was lower. Oxygen debt (recovery oxygen uptake) was higher. Oxygen uptake rate during exercise was lower. Oxygen intake volume per breath was lower. Exercise oxygen intake rate adjusted to body weight was lower. Oxygen debt adjusted to body weight was higher. Oxygen extraction during exercise was lower. Respiratory exchange ratio (R.Q.) during exercise was higher. Discussion of Hypoxic Versus Normoxic Effects data in Table 4-1 reflect a consistent differentiation between and hypoxic breathing conditions. This consistency of response may be attributed, at least in part, to the use of trained subjects; to the provision for repeated testing; and to the procedures used to mains tain control over factors which are known to affect the physiologic 60 variables under observation. (Subjects always ran in a postabsorptive state, at the same time of day, the same days of the week, and in approxi- mately the same ambient temperature.) The fact that significance was not found in four variables is not disturbing. In effect, the oxygen requirement and oxygen requirement per body weight are the same measure and reflect the total amount of oxygen which was taken up during both run and recovery. Obviously, the lower oxygen uptake during exercise under hypoxic conditions was offset by a greater oxygen absorption during recovery. The results clearly indicate the two environmental breathing condi- tions produced distinctively different effects. It is therefore con- sidered appropriate to note_both direction and extent of the changes induced by the breathing of hypoxic gas when making further interpreta- tions of these data. The results of breathing hypoxic air during exercise are similar to those which have been observed by a number of investigators studying individuals at sea level and at actual altitudes where the P02 was similar to that of this study (24,25,44,58,59,94,104,ll7,129). In consideration of this evidence, it appears clear that the use of gas mixtures formulated to reduce PO2 to approximately 120 mm. Hg is effective in producing physiologic effects which are similar to those observed at actual altitudes of approximately 2300 m. The data obtained in this study are also in general agreement with results of investigations in which prepared gas mixtures of low PO2 were inspired during performance of submaximal work at sea level (30,88). Where investigators have studied work at very high altitudes and/or at much lower levels of work load, somewhat different responses have been obtained. Apparently if the work level is low, the O2 uptakes at high altitude may be the same or somewhat increased in comparison to sea 61 level measurements (11,24,136). Billings (11) found that work requiring an 02 uptake of more than 2.5 1./min. at sea level was associated with lower 02 uptake rates at 3800 m. altitude. WDrk loads which required 02 uptakes of less than 2.2 l./min. at sea level were accompanied by essentially the same 02 uptake rate at 3800 m. A possible explanation for these differences may have been found by Thoden and associates (136). In a study which compared ventilation work at various work loads while breathing sea level normoxic air or a 152 O2 in N2 gas mixture at sea level pressures or air of reduced density at altitude (PO2 equiva- lent to the gas mixture P02), they found that ventilation work was sig- nificantly increased when the altitude air was inspired at a ventilation rate in excess of 65 liters per minute. On the basis of their results, they postulated that thoracic compression of inspired air might be a significant factor. If ventilation rate were slow enough as a consequence of low work loads, thoracic compression of air might aid in compensating for low PO2 at altitude. However, this mechanism would be compromised at high ventilation rates. Effects of Physiologic Adaptation to Experiment Conditions Previous studies utilizing repeated treadmill testing have shown that continuing adaptation can be expected even though subjects are pre- trained for running on the treadmill at the same velocity used in the testing situation (138,139). Physiologic adaptations to the conditions of this study were therefore expected and counterbalancing procedures were employed as outlined in Chapter III to minimize statistical biasing associated with adaptation. It is the purpose of this section to show the extent of overall adaptation as well as to compare the effects on test variables of adaptation to the separate conditions of normoxic air and hypoxic air. 62 Overall Adaptation Table 4-2 contains mean values derived from pooling all treatment values in each of the four cycles. The table identifies the variables which were significantly altered during the course of this investigation. The oxygen measures, i.e., oxygen uptake, oxygen debt and oxygen require- ment, all declined as was expected from results obtained in previous studies (138,139). However, ventilation rate, respiratory rate, and pulse rate, as well as variables derived from these measures, were not significantly altered. Since both exercise and recovery oxygen extrac- tion as well as the oxygen uptake per respiration were significantly decreased, it is clear that the adaptation evidenced in the oxygen variables occurred without concomitant and similar alteration in amounts of air breathed. This fact is particularly evident in Figures 4-2 and 4-3, which compare minute ventilations with oxygen extractions through- out the exercise periods in each of the four cycles under normoxic and hypoxic conditions, respectively. The significant increases observed in both exercise and recovery R.Q.'s are worthy of note. Neither of these increases were expected for, in usual circumstances (breathing normoxic air), repetitions of submaximal efforts over a period of time bring about a gradual decline in R.Q. values (138,139). The plotted cycle means of true 02 and true CO2 in Figure 4-4 indicate that, for exercise periods, the mean values of both variables declined. The rate of decline was greater in true 02 than in true C02. In the plots of recovery means, it may be seen that expiration of CO2 held fairly constant whileO2 extraction continued to decline with progress of the study. These evidences, considered together with the fact that ventilations were not found to be significantly 63 Table 4-2. Overall training effects as reflected in pooled meanvalues~ per quarterly periods of the experiment Treatment- * Cycle . F Testl Cycle Variable Units 1 2 3 4&4 Result- Interaction Peak pulse bpm 163 161 161 162 n.s. n.s. rate Ex. pulse bpm Missing 147 148 n.s.» n.s. rate Ex. 02 m1./bt. Data 16.4 15.9 n.s. n.s. pulse Total ex. liters 336 339 343 347 n.s. n.s.‘ vent. Total rec. liters 225 227 224 223 n.s. * vent. Sum tot. liters 562 567 567 570 n.s. * vent. Ex. vent. L./min. 67.3 67.9 68.5 69.3 n.s. n.s. rate Tidal vol. L./r3p. 2.08 2.05 2.05 2.08 n.s. n.s. Ex. resp. Rsp./ 33.3 33.7 34.1 34.1 n.s. n.s. rate min. ' Tot. ex. liters 13.0 12.4 12.0 11.7 *’ * 0 up. 02 ebt liters 6.03 5.79 5.61 5.59 * n.s. 02 req. liters 19.0 18.2 17.6 17.3 * * Ex. 02 up. L./min. 2.59- 2.47 2.39 2.341 * * rate Ex. 02 up./ m1./rsp. 81.7 77.1 73.3 72.3 *- n.s.- rsp. Ex. 02 up. ml./min./ 33.8 33.3 31.1 30.6 * * rate/kg. kg. ' 02 debt/kg. ml./kg. 78.0 75.0 72.5 72.6 * n.s.' Oz req./kg. m1./kg. 247 236 228 225 * * Ex. 02 2' 3.88 3.72 3.53 3.43 * * extract ' Rec. 02 Z 2.69 2.59 2.54 2.55 * n.s. extract Ex. R.Q. COZ/Oz .94 .97 1.00 1.02 * * Rec. R.Q. C02/02 .98 1.01 1.03 1.02. * n.s. n.s. - no significant.differences between tabled means (.05 level). * - significant differences between tabled means. Complete ANOVA summaries are tabled in Appendix B. ' 2n.s. - no.significant treatment-cycle interaction effects. * = treatment cycle interactions significant at .05 level. Complete ANOVA summaries are tabled in Appendix B. 64 .nsOHuauooo owxoahoc Hoes: coauomuuxo No one coaumafluno> so wnflsHmHu mo muoomwo mo nomwumnaoo .Nie ouswwm 3.52.2 $6me $52.: msomwxm as. n... od n.» 0.» cu ad a. o._ no on n... 3. an o.» as o.~ a. 0.. no N d d u q q q u u d F HI 1 u d d u d u u d In! Uw he a.» mfin nu w" a m can 3 n w m c. w M. .II. N a.» O u N _I 3. i w. c... m . N _.c i N... m s . I ... as w. . . c ”.396 9|... V7,! .. I. n 386 I In... .. . 3. N 365 oi... / _ 386 9.-.. a . o... . no 20.54Exm uo 20:44:55 “152.: ml mmqo>o I mz co mawdfimuu mo muummmo mo comaumnaou .muq muawwm mm._.32_2 wmammxm awhbzi mmemxm 0..» of 06. men 0.» ad O.N m». 0.. nd Qm mi 0.? QM O.n 0d 0d r... 0.. 0.0 d 1 AU“ d 11 1 HF? v 386 clue n u on n “.386 I . L ad 0 on w N 386 «ii . z m _ 396 4nd 1 s m n cc .4. I. { C 0 m . 3 w on u 4 C ‘ N n 1 o.n ) mm H. ~ mm mm < a ~QL _ M 8 . . m x) : . N» no .. _drn. 1’. < \w L_n‘m Arr M. v (\‘k/ \N 1 v n 2. / b. 4 n m on . dr!¢\.c.l.dplA/ 71+ 1 m n no (‘nfl ‘ 4 h M 0m 20.8456 No / \ Lo.» 2053.5”; mSzi « P a.» ¢u_ mm40>o I wzI TRUE PER CENT 66 CYCLE MEANS - RESPIRATORY GASES I 2 3 4 I 2 3 4 "2 F fl ' t ‘— 1. T 1 I 4.I - 4.0 I- 0‘ 3.9 r- 0: 3J§r 3.7 _ 00: coz 3.6 - CO; 3.5 I- 14 . EXERCISE 3.3 I- O, 3.2 I- 3u|P 3.0 L EXERCISE 2.9 b 2.8 r 2.7 r- CO, 2.6 - 0: 2.5 P RECOVERY 2.4 I- 4L t _1 4 1 1— 1 l 1 L I 2 3 4 I 2 3 4 CYCLE CYCLE All treatments pooled by cycle: Treatments pooled by hypoxic and normoxic conditions H CO, o—o O, 02 0: CO’QmoxnccozfiI-IYPOXIC Figure 4-4. The effects of training on respiratory gas measures. 67 altered, imply that the increased R.Q. values reflect the presence of phenomena other than hyperventilation. What could cause such observations to be made? A shift toward a greater dependence upon anaerobic metabolism might account for the lower 02 extractions. However, according to Issekutz and Rodahl (74) the expired C02 should be an indicator of blood lactates. If a shift toward anaerobic metabolism was taking place, blood lactates would be expected to increase (18,67,85). Hence, one would expect an increase in 002 values, the exact Opposite of what was observed. Moreover, it may be seen that the C02 values declined to an even greater extent under hypoxic breathing conditions than under normoxic conditions. Whatever the explanation for these data may be, it does not appear to be one which follows contemporary thinking. Adaptations Observed Under Normoxic Conditions Mean values of observations made in each cycle under conditions of normoxic air and hypoxic air, respectively, are presented in graphical form (Figure 4-5) illustrating adaptive changes which took place during the length of the study. With the exception of respiratory rates which evidently held constant, all variables show some degree of change under normoxic conditions. Also, within each variable the changes were fairly consistent with little fluctu- ation noted either in direction or in magnitude. Significant changes,1 1The significance referred to here was detected by an ANOVA which tested for differences between measures obtained in the first two cycles and measures obtained in the last two cycles. The data were plotted by cycle to take advantage of the additional information gained by plotting 4 points instead of 2. Readers are therefore cautioned not to infer that significant differences exist between all points along the plots. resthMn. Figure 4-5. CYCLE MEANS-NORMOXIC AND HYPOXIC CONDITIONS 68 M I 3 4 w o——__4y—fl—***“——° J 3 g,. m- 3 CYCLE and hypoxic breathing conditions. ex. 0, UPTAKE/kg. no ~ \fl I60 *- ‘5I5CI- g NORMOXIC - o E: '40.: HYPOXIC ' A 1: I 2 3 3 O; EST/k0. w WA E 't:1 1 1 .4 I 2 3 4 250 I. O; REQUIREMENT I kg. 240 '- 230 P £22on 6 ~ L 1 1 4 s- I 2 3 4 g 35 ex. 0, WTAKE/minjkg. < 1% E 3014 1 1 I I 2 3 4 EX. R.Q. I . ' P / 1.0 I- t 1 1 1 4 I 2 3 4 LI REC. R.Q. '3) Jz;::::::j;:::::::2::::::::; O. I J 1 1 J I 2 3 4 CYCLE Training effects on means obtained under normoxic 69 however, were detected only in the reductions observed in the exercise oxygen uptake and in the oxygen requirement. Although not statistically significant, the small rises apparent in ventilation and R.Q. variables may have biological implications as they are in sharp contrast to significant decreases reported for these same variables where investigators have utilized repetitions of comparable standard treadmill runs (138). The significant decreases in the oxygen variables, on the other hand, are in agreement with the results of the same investigators and appear to reflect an increased efficiency of performance acquired as a training adaptation. Adaptations Observed Under Hypoxic Conditions The graphical presentations of data in Figure 4-5 imply that under hypoxic conditions at least some degree of change occurred across the four cycles in virtually all variables represented. Whereas direction of change was relatively constant within most variables, conspicuous fluctuation is evidenced in both exercise and recovery ventilation. Respiratory rates held constant after an initial rise in the early part of the study. Of the parameters represented in Figure 4-5, significant decreases were found to have occurred in all of the oxygen variables indicating a change toward increased efficiency of work performance. Changes were not found to be significant in the R.Q.'s nor in the recovery oxygen variables, the ventilation measures or respiratory rate. Adaptations to Hypoxic Air Compared with Adaptations to Normoxic Air Figure 4-5 shows that the adaptations were observed under both normoxic and hypoxic conditions in the same direction. The differences 70 between the slopes of hypoxic and normoxic plots illustrate that, within most variables, a more severe response took place under hypoxic condi- tions than under normoxic conditions, i.e., exercise 02 uptake, 02 requirement, exercise R.Q., and exercise 02 extraction. The differences between normoxic and hypoxic responses account for the significant treatment-cycle interactions recorded in Table 4-2. Where plots remain essentially parallel, as in recovery R.Q. for instance, there were no significant interactions. Magnitude and direction of change from one cycle to the next was essentially the same under both conditions. Comparisons of the normoxic and hypoxic data, respective to the different oxygen variables, show that a gain in efficiency of work performance was realized regardless of the air breathed. When compari- sons specific to the exercise 02 uptake, 02 debt, and 02 requirement are considered together, it is clearly indicated that the subjects' efficiency improved more under hypoxic conditions than when breathing normoxic air. The greater efficiency observed under hypoxic conditions appears to have been brought about by an acute adaptive response. It is clear that long term adaptation took place, but whether acute response mechanisms were affected or whether physiologic processes affected by acute responses were the site of adaptation is not established by these data. The adaptations observed under hypoxic conditions, in particular, were unexpected. When the data obtained under both normoxic and hypoxic conditions are considered together along with the experimental procedures employed in obtaining data, it is apparent that unusual training effects were produced. A discussion of possible physiologic explanations is pursued in the following section. 71 Discussion of Normoxic-Hypoxic Adaptations The results presented in the preceding sections strongly suggest that the procedure of alternating normoxic and hypoxic runs acted to produce unique training effects. The unusualness of these results is that the adaptations indicated by the data seem impossible to explain in terms of the present established concepts of exercise metabolism and physiologic adaptation. In accord with those concepts, reductions of O2 uptakes with con— comitant lowering of O2 debts were expected. Such changes would ordinarily be interpreted as reflections of the enhancement of physiologic mechanisms involved in the uptake and transport of oxygen. Following this logic, one would have expected progressive increases in 02 uptake under hypoxic conditions. Since the O2 debts incurred under hypoxic conditions were respectively greater than 02 debts incurred under normoxic conditions, it is clear that the subjects needed more oxygen than.was taken up during hypoxic runs. If the expected adaptation had taken place, it would have shifted hypoxic response measures toward normoxic response measures. Surprisingly, the oxygen debts incurred under hypoxic conditions did decline at about the same rate as those under normoxic conditions, but the reductions in oxygen uptake were strikingly different. If the O2 debts under hypoxic conditions had not declined, a shift toward anaerobic energy sources might have been an attractive explanation. Since the data appeared markedly unusual, it seemed a reasonable possibility that the 02 debts observed in the hypoxic run data might be artifactual as a consequence of failing to extend the O2 debt assessment period for a long enough time. Contradictory to that notion, recovery data for 02 extraction and pulse rate variables (Figure 4-6) indicate that the degree of recovery reached at the shutoff point was virtually 72 Recovery Means in Cycle I and Cycle 4 PULSE RATE I40 I- HI0H4. 3 N. E '30 " N. \ :3 g I20 I- " no _ Ame HYPOXIC-Cycle I E A—A HYPOXIC-Cycle 4 g IDOL o- -0 NORMOXIC-Cyclo I o——0 NORMOXIC - Cycle 4 3” 90 P .1 3 so - ¥ 1 j 1 L l L l 2 4 6 8 IO l2 I4 RECOVERY MINUTES .eoL "'4 g; UPTAKE H. .75 l- N' \ .70 b "4 .65 I E .60 \\ 2 .55 I. \\ A---A HYPOXIC-Cycle l g . A—A HYPOXlC-Cycle 4 3 .50 I- \‘\ o- -0 NORMOXIC - Cycle I m ‘ o——o NORMOXIC - Cycle 4 § .45 - E :3 .40 .- 03 ° .35 - .303: T l L L 1 l L l 2 4 6 8 IC) l2 I4 RECOVERY MINUTES Figure 4-6. Comparison of pulse rate and O uptake data showing relative degrees of recovery in first and last cycles. 73 identical for both hypoxic and normoxic runs. This fact, of course, does not completely exclude the possibility that long term recovery processes may have had some bearing on the results observed. If the hypoxic condition 02 debts were not artifactual, it becomes more likely that the data indicate progressive development of an acute adaptive response to the conditions of performing submaximal work while inspiring hypoxic air. If such a response did take place, the mechanisms of the acute adjustment might well account for the incongruities which have been described. The observation of acute responses to lowered PO2 resulting in submaximal work being performed with a lower 02 requirement while breathing hypoxic air than while breathing normoxic air is not without precedent (30). In addition, the phenomenon of lowered O2 utilization by muscle tissue is well supported in the literature (6,40,68,98,99). However, to the author's knowledge, continued reduction in 02 requirement accompanying repeated exposure to hypoxic has not been reported. Since the phenomenon has not been reported in the altitude training studies (11,44,141), it is presumed to have been caused by the alternating of hypoxic and normoxic breathing conditions. The results are particularly intriguing in that traditional explanations do not apply. The stimulat- ing challenge is to attempt to identify the physiologic mechanisms responsible for such seemingly paradoxical results. Working with isolated perfused hind limb muscles of dogs, Pappen- heimer (98) obtained a decrease in a—v 02 difference with electrical stimulstion of vasoconstrictor nerve fibers. Using the product of blood flow and a-v 02 difference as an indicator of what he termed "apparent oxygen consumption," he postulated that his observations of a reduction. in "apparent oxygen consumption" were produced by vasoconstriction acting 74 to shunt the blood flow from more active tissues to less active tissues. However, when using injections of adrenaline to obtain a sympathomimetic vasoconstriction, he obtained the vasoconstriction, but found an increased a-v 02 difference instead of the decrease observed with electrical stimulation. The adrenaline injections also resulted in observing a-v temperature differences occur in concomitance with the increased a-v O2 differences (98). In a later extension and modification of the earlier study, Pappen- heimer found that either a mechanically reduced flow of perfusing blood having normal 02 saturation, or an induced reduction of 02 saturation at constant blood flow, produced the same effect--a reduction of 02 utiliza- tion_in the affected muscle. Considering the results of both studies, he concluded that the observed reduction in 02 utilization was caused either by a reduced oxygen diffusion rate or by a direct effect of hypoxia on intracellular oxidative processes or both (99). Apparently out of interest in Pappenheimer's work, Cronin and MacIntosh conducted an investigation to assess responses of moderately exercising humans to different levels of induced hypoxemia. Different levels of hypoxemia were induced by the breathing of normoxic air and hypoxic air (11% 02 in N2) and by the performance of different levels of work on the treadmill (grade changes with speed held constant). These investigators did not specify any training effects, but their report implies an acute response took place with results similar to the data- reportrd in the present study--a given amount of submaximal work was performed at a lower 02 cost when breathing hypoxic air than when breath- ing normoxic air. Although the data obtained by Cronin and Macintosh did not enable to them to identify causal mechanisms, they were able to 75 establish that their results were not the consequence of an insufficient O2 debt assessment period (30). Obtained under somewhat different circumstances, similar phenomena have been reported by Hill (68). Resting adult guinea pigs placed in a thermoneutral hypoxic environment did not show a lowering of Oé con- sumption. However, when the animals were subjected first to a lowering of ambient temperature in a normoxic environment, metabolic rate and rectal temperature increased concomitantly with an-increase in 02 con- sumption. All increases were later ablated by reducing oxygen content of the ambient air. She also noted that, when the degree of hypoxia was extreme (10% 02), the animals coumenced agitated movements without any evidence of incurring an O2 debt. In consequence, Hill concluded that the magnitude of reduction in 02 consumption manifested in a hypoxic environment is related to what she termed "extra metabolism" (above basal state metabolism). Results of the Pappenheimer and Cronin and MacIntosh studies are both interesting and puzzling in that an acute adaptive response was immediately present whereas evidence of a similar response was not immediately apparent in the data of the present study. Hill, on the other hand, did not observe the apparent same response until metabolic rate had first been raised above resting rate. Since the studies all differed, one from another, in important ways, cross-interpretation of results is rendered difficult. Of the four related studies, the experi- mental conditions used by Cronin and MacIntosh most closely resemble those of the study at hand. Yet, less fit subjects performed a similar but less stressful exercise while inspiring more severely hypoxic air during both exercise and recovery. Discrepancies between the results 76 of the different studies and the one at hand are therefore a matter for conjecture. It is nevertheless clear from these results that a training effect was obtained. The effect was particularly manifested in the reduction of oxygen uptakes across cycles under the hypoxic condition. The effect is also reflected in the oxygen requirement across cycles since the oxygen debt decreased in a manner previously observed by Consolazio ( 23). This chronic effect which has resulted in a reduced oxygen requirement for the same amount of work cannot be explained from the parameters measured. Several changes of interest observable in the normoxic measures indicate an alteration of the usual training response to a low intensity steady state work task. Under normoxic conditions across cycles, the R.Q. increased rather than decreased, but the ventila- tion also increased rather than decreased. The ventilation response was in the opposite direction to that usually seen with training under normoxic conditions, but it agrees with findings under hypoxic condi- tions (11,95). Although it would be attractive to suggest greater carbo- hydrate metabolism with training the greater ventilation clouds any such interpretation from the increased R.Q. It would also be attractive to explain the marked changes under hypoxic conditions to lowered arterial PO2 at the muscle (6,98,99) and to altered metabolism within the muscle (6,28,40,68,l4l). However, such speculation is not warranted except to hypothesize for continued study. No definitive explanations are possible from these data. Psychogenic Effects This section has been organized to present data relevant to the detection and assessment of psychogenic influence on the physiologic 77 responses under observation. Considered first are the effects of being cued that hypoxic air is breathed when the air is actually normoxic. Treated next are the effects of hypoxic cues when, in fact, the air is hypoxic. Attention is then turned toward evidence related to adaptation and interaction effects before a discussion of results is pursued. Normoxic data and hypoxic data were subjected to separate analysis of variance F tests and also to a simple Sign Test in order to gain greater sensitivity thought necessary to detect psychogenic effects. The results of F tests and Sign Tests are presented in Table 4-3. The tabled values are the approximate probabilities that resultant F ratios were obtained by chance. The data which were subjected to these tests are presented graphically in Figures 4-7 through 4-16. (Complete ANOVA Tables and raw data may be found in the appendix.) Effects on Normoxic Responses of Being_Cued that Hypoxic Air was Breathed. The relatively high probabilities listed in Table 4-3 under NORMOXIC DATA imply that the provision of cues relevant to conditions of inspired air was without effect. Although the probability listed for exercise R.Q. is sufficiently low to be considered significant, it would seem a more likely possibility that this was obtained by chance, especially in- light of the high probabilities obtained with all the other variables. Results of the Sign Test also seem to indicate that provision of cues had little effect on normoxic responses. The Sign Test does indi- cate significance for exercise pulse rate and oxygen pulse. However, these means are derived from.abservations of pulse rate during only the last half of the study. It is interesting, nevertheless, that both the Sign Test and the ANOVA F Test indicate significant exercise R.Q. 78 ANOVA F test1 and Sign test2 results obtained from analyzing normoxic and hypoxic data separately NORMOXIC DATA HYPOXIC DATA ANOVA Sign. ANOVA Sign. F Ratio Prob. Test F Ratio Prob. Test Sig. Sig. Treat- Inter- at .05 Treat- Inter- at .05 Variable Units ment Cycle action level ment Cycle action level Peak pulse bpm .116 .016 .844 .351 .202 .422 rate Ex. pulse bpm Missing Data * Missing Data * rate‘ Ex. 02, ml./ No ANOVA * No ANOVA * pulse bt. Tot. ex. liters .577 .208 .518 .924 .167 .898 vent. Tot. rec. liters .475 .938 .588 .160 .005 .870 * vent. Sum tot. liters .385 .425 .357 .508 .106 .897 vent. Ex. vent. L./ .577 .208 .518 .924 .167 .8984 * rate min. Ex. tidal L./ .493 .892 .804 .352- .339 .219 * vol. rsp. Ex. resp. rsp./ .995 .841 .490 .092 .158 .545 * rate min. Tot. ex. liters .282 .049 .650 .114 <.0005 .562 02 up. 02 debt liters .860 .229 .616 .581 .012 .822 02 req. liters .679 .077 .429 .428 .001 .534 Ex. 02 up. L./ .282 .049 .650 .114 <.0005 .562 rate min. Ex. 02 up./ ml./ .376 .210 .423 .394 .009 .803 resp. rsp. Ex. 02 up. ml./ .453 .023 .631 .096 <.0005 .634 rate/kg. min./ kg. 02 debt/ ml./ .799 .183 .653 .728 .016 .884 kg. kg. 02 Req./ ml./ .880 .036 .536 .369 <.0005 .640 kg. kg. Ex. 02 Z .432 .1992 .135 .224 .002 .797 extract 0 79 Table 4-3 (cont'd.) NORMOXIC DATA HYPOXIC DATA ANOVA Sign ANOVA Sign F Ratio Prob. Test F Ratio Prob. Test Sig. Sig. Treat- Inter- at .05 Treat- Inter- at .05 Variable Units ment Cycle action level ment Cycle action level Rec 0 02 z o 774 o 019 o 686 o 851 o 019 o 745 extract Ex. R.Q. C02/ .045 .014 .623 * .160 .012 .304 * 02 Rec. R.Q. C02/ .441 .004 .388 * .611 .201 .804 02 1 Tabled values are probabilities of obtaining F ratio by chance. Probabilities 5..05 are underlined. Means tested are tabled in Appendix A, Table A-2. Complete ANOVA summaries are tabled in Appendix 8. 2Sign test was applied only to data dealing with mean treatment differences as reflected in the multiple measures obtained across run. and recovery periods. 80 differences. Furthermore, the Sign Test also indicates significant differences between recovery R.Q.'s. If the Sign Test results are accepted, the effects on normoxic responses of being cued that hypoxic air was breathed are as follows: 1. Pulse rate during exercise was lowered. 2. Oxygen pulse during exercise was increased. 3. R.Q. during exercise was raised. 4. R.Q. during recovery was raised. These effects can also be seen in Figures 4-9 through 4-16. Effect on Hypoxic Responses of Being Cued that Hypoxic Air was Breathed As indicated in Table 4-3, analyses of variance failed to detect any significant differences induced by cues that hypoxic air was breathed when it really was hypoxic air being breathed. Several proba- bilities, however, were sufficiently low to warrant calculating power of the F test. In every case power was on the order of .05. From a statistical point of view, the lower probabilities fall into the range of reserved judgment--the null hypothesis cannot be accepted or rejected. Consideration of Sign Test results with hypoxic data indicate sig- nificant alterations in several variables. If these results are accepted, the effects of being cued that hypoxic air is breathed when it actually is hypoxic air are as follows: 1. Pulse rate during exercise was lowered. 2. Oxygen pulse during exercise was.raised. 3. Ventilation during recovery was lowered. 4. Tidal volume during exercise was lowered. 5. Respiratory rate during exercise was increased. 6. Oxygen uptake during exercise was increased. 81 7. Oxygen uptake per breath during exercise was increased. 8. Oxygen extraction during exercise was increased. 9. R.Q. during exercise was lowered. These effects can also be seen in Figures 4—8 through 4-16. Adaptation and Interaction Effects Adaptation indications in the ANOVA's conducted to consider normoxic and hypoxic data separately are particularly interesting. From the probabilities listed in Table 4-3, it is evident that more variables were significantly affected by adaptation under hyporix conditions than under normoxic conditions. This information, considered with the fact that no significant interactions were found, supports the conclusion drawn in an earlier section that interaction effects noted in the earlier ANOVA were related to the differences between breathing hypoxic air and normoxic air and apparently not to provision of cues. The absence of significant interactions in Table.4-3 might also be interpreted to indi- cate that the counterbalancing techniques were successful in avoiding a bias due to training effects. The fact that more variables show adaptation under hypoxic condi- tions than under normoxic conditions along with the fact that the probe- bilities under hypoxia are, in general, much lower than under normoxia is of much interest. These factors, considered together, seem to imply that the long term adaptation which occurred took place more in conse- quence to the hypoxic exposures than in consequence to the exercise performed. When the plots of cycle means for all four treatments (Figures 4—7a and 4-7b) are examined it may be seen that the truth-lie conditions pro- duced more clearcut differentiation under hypoxic conditions in general 82 CYCLE MEANS: NORMOXlC-HYPOXIC - TRUTH-LIE CONDITIONS ex. VENT./min. 73 4.2 r- ex. 0, EXTRACTION (7.) 4.I - 4.0 - 3.9 r- 3.8 p liters/min. GO! I.9JI' 5: «bl- E 5 CYCLE CYCLE Figure 4-7a. Training effects on means obtained under normoxic and hypoxic truth and lie conditions. 83 CYCLE MEANS: NORMOXIC-HYPOXIC - TRUTH-LIE CONDITIONS 0 DEBT/k9. sz ~ A ‘ .75 F ex. 0, UPTAKE/kg. \ <\ so 78 ITCIP |65 76 Int/kg 235» 230 225 2220 :3 E I LI 2 51: E n.s-«a 1:41 1 1 .41_ J. 1 1 1 I 2 3 4 I 2 3 4 CYCLE CYCLE Figure 4-7b. Training effects on means obtained under normoxic and hypoxic truth and lie conditions. 84 than under normoxic conditions. Furthermore, with the exceptions of exercise ventilatory measures and of recovery R.Q. data, the condition of cueing subjects breathing hypoxic air that hypoxic air was breathed appears to have altered response measures toward values obtained under normoxic conditions. Whereas the truth-lie means retain a fairly consistent relationship across cycles under hypoxic conditions, the pattern is different under normoxic conditions. This difference is clearly evident in the plots of oxygen extraction means during exercise. Where cues that hypoxic air was breathed produced means lower than did normoxic cues during the early part of the study, the hypoxic cues produced higher means than did the normoxic cues at the end of the study. The latter relationship is interestingly the same as the relationship maintained throughout the last three cycles under hypoxic conditions. If only first and last cycle means are observed it is apparent that overall adaptation is evidenced similarly across all four treat- ments. In general, the picture is similar to that usually observed to occur during training at submaximal work intensities. Exceptions are the rises in R.Q. and ventilation measures which are classically reported to diminish with endurance training under normoxic conditions. Observation of oxygen requirement means across cycles is of special interest. The increase in efficiency which was greater under hypoxic conditions than under normoxic conditions is also reflected in the truth- lie means across cycles. However, it is evident that hypoxic cues pro- vided under hypoxic conditions reduced efficiency. Under normoxic conditions, hypoxic cues appear to have had fluctuating effects--at times improving efficiency and at other times reducing it. 85 Discussion of Psychogenic Effects Due to the fact that several factors in this study were simul- taneously Operant to influence the dependent variables, consideration of any one factor such as psychogenic influence is difficult without COD? sidering also, and at the same time, the influence of the other factors. Accordingly, Table 4-4 was arranged to compare the direction in which variables were significantly altered by factors of hypoxia, training, and "told hypoxia." Briefly summarized from Table 4-4, the breathing of hypoxic air acts to increase pulse rate and ventilation measures; to decrease oxygen uptake during exercise; and thereby, to increase oxygen debt. R.Q. is also raised during exercise, but the increase may signify only the decreased oxygen uptake. When the effects of training are considered, it is fair to remember that the usual picture with submaximal effort is a decline in.virtually all variables represented in Table 4-4 (138). Such a decline is generally interpreted to indicate increased efficiency. The fact that significant declines were not observed in pulse rate and ventilation variables may very well be a consequence of the tendency for hypoxic exposure to increase those values. Where hypoxic exposure tends to produce a decrease in values, significance was found in training effects. Presumr ably, the two factors acted in concert to reinforce one another, the single exception being R.Q. during exercise. Possibly the influence of hypoxic exposure was sufficient to overcome the usual normoxic training effect which would have been a reduction in R.Q. representing a shift toward fat metabolism. When the psychogenic effects derived from provision of hypoxic cues are reviewed, it may be seen that, with few exceptions, the significant 86 Table 4-4. Comparisons1 of effects2 on dependent variables which were apparently induced by the three main factors in the experiment 1 2 3 Hypoxia Traininngffects Told Hypoxic Dependent to on on on on Variables Units (Normoxia) Normoxia Hypoxia Normoxia Hypoxia Peak pulse bpm Inc. rate Ex. pulse bpm Inc. Dec. Dec. rate Ex. 02 pulse ml./beat Dec. Inc. Inc. Total Ex. liters Inc. vent. Total rec. liters Inc. Dec. Dec. vent. Sum tot. liters Inc. vent. Ex. vent. L./min. Inc. rate Ex. tidal L./ Inc. Dec. vol. breath Ex. resp. rsp./ Inc. Inc. rate min. Tot. ex. liters Dec. Dec. Dec. 02 up. 02 debt liters Inc. Dec. 02 req. liters Dec. Ex. 02 up. L./min. Dec. Dec. Dec. Incc rate Ex. 02 up./ ml./ Dec. Dec. Inc. resp. breath Ex. 02 up. ml./min./ Dec. Dec. Dec. rate/kg. kg. 02 debt/kg. m1./kg. Inc. Dec. 02 req./kg. ml./kg. Dec. Dec. Ex. 02 Z Dec. Dec. Dec. extract. Rec. 02 % . Dec. Dec. Inc. extract. Ex. R.Q. 002/02 Inc. Inc. Inc. Inc. Dec. Rec. R.Q. 002/02 Dec. Inc. 1Comparison 1 - between breathing hypoxic air and breathing nor- moxic air; Comparison 2 - between earlier and later measures; Comparison 3 - between cues that hypoxic air was breathed and cues that normoxic air was breathed. 2Effects are signified as increases or decreases in the numerical values of measures obtained where differences between means were sig- nificant at .05 level. Cross comparison of effects is therefore enabled. 87 effects observed are opposite to the direction of effects which were produced by actually breathing hypoxic air. This is evidenced across treatment means during runs as well as in treatment means across cycles of the study. Paychpggnic Effects During Runs In the plots of treatment means during runs (Figures 4-8 to 4-16), it may be seen that the patterns are fairly consistent, the essential differences being of a quantitative nature where they are found at all. It is believed that differences, where found, can be explained on the bases of differences in catecholamine activity and to differences between the effects of epinephrine and norepinephrine. However, the participa- tion of other mechanisms cannot and should not be excluded from con- sideration--the action of adrenal corticoids for example. In spite of the fact that no catecholamine data were collected, all evidences-~the nature of this study, the overall results obtained, and the nature of responses observed--appear to fit very closely with the circumstances of secretion and the characteristic effects which have been reported for epinephrine and norepinephrine. It has been reported that epinephrine secretion rates appear to be more related to degree of mental stress, whereas norepinephrine secre- tion appears more related to physical stress (8,145). In the present study, hypoxia and exercise constitute a physical stress, and the hypoxic cues were presumed to have induced at least some degree of mental stress. It has been shown that hypoxia induces a selective increase in secretion of noradrenaline from the adrenal medulla (SO), and the effects of epinephrine on aortic muscle (rabbit) have been found to be qualitatively (reversed) and quantitatively affected by hypoxia (70). 88 In this study a difference was found between the effects of hypoxic cues on normoxic and hypoxic responses. It is known that administration of epinephrine is followed by an immediate, if short lived, increase in oxygen consumption (105,114). ,The psychogenic effects observed in the present study were virtually all in the same direction as normoxic (more oxygen in comparison to hypoxia) response values. Epinephrine has been shown to enhance glycogenolysis in liver and muscle (26,27,28) and is known to inhibit insulin secretion (147) with the result that blood sugar is accumulated (89). In the present study high R.Q.'s were observed which cannot be solely attributed to hyperventilation phenomena. However, they could indicate increased glucose metabolism during exercise. Although admittedly based upon circumstantial evidence, the case for attributing responses observed in this study to changes in catecholamine activity appears sufficiently strong to suggest further investigation along the lines of thought presented. Since psychogenic effects were the primary concern of this study further comments are in order with regard to the oxygen uptake, tidal volume, and respiration rate variables. It is common knowledge that voluntary control can be exerted over rate and depth of breathing. Con- sequently, it was expected that these variables in particular would be likely to show evidence of psychogenic effects. As may be seen in Table 4-4, only the respiratory rate under hypoxic cues and hypoxic exercise was significantly altered. This is interpreted to indicate that the changes in oxygen uptake were apparently not a function of changes in either rate or depth of breathing. It may therefore be inferred that oxygen uptake changes were not brought about by voluntary control of respiration (Figures 4-11, 4-12, 4-13, 4-14, 4-15, and 4-16). PULSE RATE (boots/min) 89 PULSE RATE ,, 3*: '60 " ’ " ‘ I ~| A ’ ° N v - X 3 ‘ I . . / '50 #- a . / / I’ / I’llgR” I40 - I I o I, '/ I3CI- :/ I, 0 I20- I, True ' ' HIH 0’ . Nzo—--o " b A . LIe szma 1 t l l J J l l A 1 l J (15 I.O I15 2L) 2L5 313 315 '4‘) 4L5 51) I00 ,. a: ‘ EXERCISE MIWTES m .1 I50 H.‘ F“ F1 71 \ -I4() N . 95 ~ N' \ «I30 ' \ \ d \‘.\ IZCJ 9Cl- dIIO \ . \ ‘ I00 \ ss - t 5 , . so \ \\\ I A‘ \( \ I ‘ ‘ 8C) 80 C ' I. ‘L 70 4 4 L 1 1 1 1 1 1 1 i’ 2 4 6 8 I0 l2 MIRIRERER RECOVERY MINUTES N: N: H. H: MEANS Figure 4-8. Pulse rate means per treatment plotted against time. O, PULSE (ml/boot) I9 I8 I7 I! F1 90 02 PULSE l 1 l l l J l L l . ”'05 I0 I!) 2.0 2.5 3.0 3.5 4.0 4.5 5.0 EXERCISE MINUTES 1 2 Figure 4-9. J. lo '2 I4 ERERERER 4 6 s RECOVERY MINUTES N. "2 H. ”2 was Oxygen pulse means per treatment plotted against time. 91 40* 02 UPTAKE 35IP 25I- ,. I5 . '3 LI NWT 0 go sz-‘A :§,'CEE .1, 1 1, 1 1 1 1 1 .1 J 0.5 l.O I.5 2.0 2.5 3.0 3.5 4.0 4.5 5.0 3‘“ H, EXERCISE MINUTES 3. I0 I- _ 'I 35 ‘5 6‘ 9+- r'I TI .1 430 3.. -I25 7» ~20 s . - I5 5 . 4 IC) 4 - 5 It I 1 1 1 l 1 1 J .I 2 4 6 3 IO I2 I4”””'* RECOVERY MINUTES NI "2 HI ”2 NEHUWS Figure 4-10. 02 uptake rate per kg. Of body weight means per treatment plotted against time. VENTILATION (liters/min) 92 VENTILATION H __ . a BSI| " : _.— . H. 80 '- 751- , ‘,xr” ; N2 . / - - u, 7TI- I ‘ . I’ 65 -. ’I 60 I- , ,l 55 b I 50 I- / 1- ' °___° ' me 45 - "IA"19 40%- I N:°__° ‘ Lie 35" . Htk‘fi 4L T l l L L L l 1 l L I 0.5 I .O I .5 2.0 2.5 3.0 3.5 4.0 4.5 5.0 II, EXERCISE MINUTES 28 - PI "'1 ~70 24 - r'I . 60 .. 50 20 - - 40 I6 - - 3O -' 20 I. '2 ~ IO 4L l J l l l 4 J E II E II E II E II ‘ 2 4» 6 8 IO I2 I4 RECOVERY MINUTES "I "z "I "a _ MEANS Figure 4-11. Ventilation rate means per treatment plotted against time. TIDAL VOLUME (liters/resp.) 93 TIDAL VOLUME 2.2 l’ A ‘ ‘ ~‘ ‘ H2 {3’ . . . . 2.l » ’I . / ‘ . N. Z'OI I, . \Nz |.9I' ‘ IJB- |.7 - I, True N, o——-o I 5 - II. H I.5I- . Ng°""° "41 O L" n.s-“A T 1 1 1 1 1 0.5 l.0 I.5 2.0 2.5 3.0 3.5 4.0 4.5 5.0 EXERCISE MINUTES L4- I" 1 LB- I... "I 0 III- I.O- 0.9r 0.8b . , . z 11 1 05¢ L L4 . 1 4 1 . , cm;- 2 4 6 8 l0 l2 l4 3"" 'INR EH'EHR RECOVERY MINUTES l 2 I 2 MEANS Figure 4-12. Tidal volume means per treatment plotted against time. 1 1 1 1 1 1 l 22 2.0 I.8 l.6 I.4 I.2 I.O 0.8 RESPIRATORY RATE (reap/min) 94 RESPIRATORY RATE A”: 40- I . H. 38- :’, 4 X’ONZ 36'- : " ‘ ’ . '. ' 'NI I , . . 1’ , 34'- I . ,A’ / 32? ‘ ’I . , 30r- / ; 28 L/ T N.o——o P . r " u. H.H 26L ‘ ° . N2°""" 24" / L's "IA—‘I-A 4L 1 1 A 1 . A. ~ 1 1 L 1 1 J 0.5 I .0 I .5 2.0 2.5 3.0 3.5 4.0 4.5 5.0 EXERCISE MINUTES HI —I 1 'I 35 2I _ H: '1 m N" a 30 2O - NI ‘ I9 I- "\ fir" 4 “~A.‘ d 25 I8 \f' ‘ ‘tx ‘ ‘L - 20 I7 I- 'GE -I I5 d - I 2.8 r! L 1 J 1 L 1 L 1 1 0.5 |.0 L5 2.0 2.5 3.0 3.5 4.0 4.5 5.0 EXERCISE MINUTES F1 1 4.0 2.8 P 2.7 - 2.6 P 2.5 I- 2.4 - T 2.3 J H I. 1 . 1 l l 2 4 6 8 I O l 2 RECOVERY WTES Figure 4-15. 02 extraction means per treatment plotted against time. R.Q. LI5 LIO L05 L00 .95 .90 .85 .80 .75J L25 L20 I.l5 LIO L05 L00 .95 .90 .85 .80 .75 JO II 1 05 L0 97 1 1 1 1 l 1 J 1 L5 20 25 30 35 40 45 50 EXERCISE MINUTES 1 - I.05 - LOO i . LII-21:1? Figure 4-16. 4 6 s IO RECOVERY MINUTES N. ”a “I l I I I J '2 |4ERERERER H2 MEANS R.Q. means per treatment plotted against time. 95 90 85 80 75 7O 98 A final point of interest with regard to the plots of run and recovery means (Figures 4-8 through 4-16) is the slight change which occurs during the last 30 to 45 seconds of the exercise period in many variables. It is believed that these effects resulted from the epxeri- mental procedure of counting down to the stop signal which was commenced with one minute of running time left. Since the treadmill stop swatch was not activated until exactly five minutes after the start, these changes are considered psychogenic effects also. Psychogenic Effects Across Cycles From the data which are presented in Table 4-3 and in graphical form in Figures 4-7a and 4-7b, it is readily apparent that the principal adaptation was related to oxygen uptakes and especially under hypoxic conditions. Since ventilatory variables were not significantly affected, it is unlikely that the changes in 02 uptake were related to changes in ventilation. It therefore seems possible that these effects are attributable to changes in catecholamine activity or to changes in tissues affected by catecholamines. Since most of the significant changes occurred under hypoxic condi- tions it is now possible to see that 02 requirements declined most under normoxic cues. The implication of this observation is that the psycho- genic effect of hypoxic cues was in counterpoise to the training adapta- tion toward greater efficiency. As pointed out in the preceding section, it is known that administra- tion of epinephrine is followed by an increased 02 consumption (114). Furthermore, Raab (105) notes that epinephrine has an "oxygen wasting" effect on cardiac tissue. Thus it could be that the higher 02 uptakes under hypoxic conditions simply represent this "oxygen wasting" effect. 99 If the oxygen is wasted then this should be reflected by the absence of effect on recovery values. Figure 4—10 shows that 02 debts across runs were not affected to any noticeable extent. The decline in 02 uptakes across cycles, however, is not explained unless one postulates decreased secretion of epinephrine. Yet, the gap between the normoxic cue effects and hypoxic cue effects widens across cycles. Other data such as the R.Q.'s are also puzzling for by simply increasing the oxygen uptake, as might happen from epinephrine, and "wasting" the oxygen, R.Q.'s would show a decrease with time. In View of this fact an altered metabolism may have resulted. A shift to carbohydrate metabolism with increasing enhancement could produce the overall lowering of 02 uptake and still permit acute responses of increased 02 uptake. Another possibility of considerable merit would be that which is suggested by Cori's work (26,27,28). Epinephrine not only accelerates glycogenolysis in liver and muscle tissue (26,28) by activating phos- phorylase (34,35), but it also acts to accelerate glycogenesis in liver from blood lactates (26). Thus a cycle is set up. Due to lack of oxygen, increased lactates are produced (67,81). Due to action of epinephrine in stimulating glycogenesis in the liver, the lactates would be removed and turned back into glycogen. Glycogenolysis could then be accelerated by epinephrine and release additional amounts of glucose to active muscle. Under hypoxic conditions increased lactates would be formed and the cycle continued. Changes in liver tissue to accommo— date these processes might then enhance the cycle and therefore require less and less oxygen, yet the "oxygen wasting" could still be permitted. 100 The enhancement or even the operation of this cycle would be a plausible explanation for the reported inability to accumulate blood lactates at altitudes (18,41). The reduced lactates in blood, however, would be interpreted as an increased ability to remove lactates rather than an inability to form them. This kind of an arrangement would explain the CO2 and 02 decline observed in the present study and dis- cussed in a previous section. It would also explain the more marked effects found under hypoxic conditions in the present study as well as the increased R.Q.'s during exercise. During testing runs under normoxic conditions, the subjects would be less stressed than when under hypoxic conditions. Hence, there would be less catecholamines released. With less catecholamines, there would be less glycogenolysis, less carbohydrate metabolism, etc., and it would take longer to establish the response. R.Q.'s during exercise could simply indicate an increased carbo- hydrate metabolism as a consequence of the increased accumulation in the blood of glucose and of lower CO '8 expired due to removal of 2 lactates. The same line of reasoning would seem to provide an explanation of the increased R.Q.'s during recovery. With the mechanisms which have been cited, acting to increase the level of circulating blood sugars, an oversupply would be left after exercise.‘ Then with a resurgence of insulin in response to the decreased catecholamine production and hyper- glycemia, glucose would commence to be converted to fatty tissue while at the same time being used as energy to pay back the oxygen debt-- conditions which have been reported to produce R.Q.'s above 1.00 due to the liberation of small amounts of oxygen during the chemical reactions involved in the conversion of carbohydrate to fat (62). 101 FINAL DISCUSSION In view of the unusual nature of results Obtained in this study it is considered particularly unfortunate that provisions were not made to determine blood lactate and glucose concentrations. Doubtless, urine analyses for catecholamine content would also have been helpful. Without such observations, the possibilities for speculation are almost unlimited. Nevertheless, it does appear indicated that long term adaptation combined with acute adjustment mechanisms to produce conditions whereby the subjects were able to perform submaximal work more efficiencly while breathing hypoxic air (16.60% 02) than while breathing normoxic air. Of all the possibilities considered it is believed most likely that this represented a shift from fat metabolism to carbohydrate metabolism occurring as a consequence of sympathoadrenal medullary reaction to acute exposure to hypoxia. Undoubtedly other response mechanisms were also involved. The nature of the long term adaptation, however, remains obscure. With regard to the nature of the psychogenic influence, this too remains obscure due to the confounding effects of the several factors exerting concomitant influences, due to the limited number of dependent variables which were observed, and due to the lack of data on blood and urine composition. It does seem indicated that the responses were of an emotional nature rather than the product of cortical adjustment (control) mechanisms. If intellectual assessment was involved, it was probably only in the perceiving of a potential threat which may have been so mildly upsetting as to go unnoticed. As to whether or not the psychogenic effects were incremental or decremental with respect to the work task performed, this too is 102 difficult to determine. With reference to the hypoxic exercise situation, the psychogenic influence would seem incremental. By increasing oxygen uptake during exercise, 02 debt was slightly lower. So, it is reasonable to assume that individuals' ability to run for a longer time at the same speed would have been enhanced. From the standpoint of training goals, the psychogenic influence would seem to be decremental under hypoxic conditions by way of reducing the reaction to hypoxia and thereby probably prolonging the training period. On the other hand, there is no way of knowing whether this would have been offset by other benefits or by subsequent events. CHAPTER V SUMMARY, CONCLUSIONS AND RECOMMENDATIONS SUMMARY The purpose of this study was to determine whether physiologic responses during submaximal work under normoxic or hypoxic conditions are psychogenically influenced by cues pertaining to the presence of those conditions. A subsidiary purpose was to obtain physiologic bases for judging whether the psychogenic influence would be facilitory or inhibitory to the performance of submaximal work. Eight male subjects ranging in age from 20 to 33 were recruited from among graduate and undergraduate students majoring in physical education. 0n the basis of regular participation in endurance types of running activities, all were judged to possess reasonably good cardiovascular fitness. Only one, a nation class mile runner, was undergoing regular athletic training. A standard run of five minutes at 7 mph and zero grade on a motor driven treadmill was employed as the submaximal work task in each of the four test conditions (treatments). Heart rate (ECG) and respiratory rate were recorded continuously during each run and at selected regular intervals during the 15 minute recovery periods. All expired air was. collected throughout every run and recovery period using Douglas bag techniques. Serial samples of the expired air were analyzed for O2 and 002 percentages. 103 104 The four test conditions (treatments) were: 2 l 1 breathing normoxic air when told that it was normoxic; Z I breathing normoxic air when told that it was hypoxic; {1'1 I l breathing hypoxic air when told that it was hypoxic; and it: I 2 breathing hypoxic air when told that it was normoxic. After six pre-experiment training runs, every subject was observed in four replications of each of the four testing situations with counter- balancing techniques employed to avoid biases from effects of either treatment order or training. Testing was conducted over a period of 5 1/2 weeks--each subject running on the same respective days of the week (either M{W.F. or T.Th.S.) and at the same respective time of day (either 6:00, 6:30, 7:00, or 7:30 a.m.). Irrespective of cues provided, the average ventilation, respiratory rate, and heart rate measures obtained in exercise and recovery periods were higher for hypoxic runs than for normoxic runs. Oxygen uptakes for hypoxic runs were lower during exercise but higher during recovery than the respective measures for normoxic runs. Hypoxic R.Q.'s were higher than normoxic R.Q.'s during exercise, but the recovery R.Q. measures were not significantly different. No significant differences were found in the measures of oxygen requirement, presumably because the amount of work performed was essentially always the same. None of these results were considered deviant from expectations. In comparing the effects of hypoxic cues with effects of normoxic cues, a greater number of significant differences were found under hypoxic conditions than were found under normoxic conditions. Moreover, results showed that hypoxic cues apparently acted to alter the hypoxic response measures toward values obtained under normoxic conditions. This apparent counteracting of hypoxic effects was considered an 105 important factor for identifying physiologic mechanisms involved in the mediation of psychogenic influence. Another potential factor was seen in the fact that hypoxic cues acted to raise R.Q.'s during normoxic exercise and to lower R.Q.'s during hypoxic exercise. It was of further interest that, regardless of which air was breathed, hypoxic cues acted to lower pulse rate and to raise oxygen uptake during exercise. An investigation of training effects was not intended to be a major thrust of this study. Yet, interesting and unusual adaptations were discovered to have taken place during the course of the experiment. When hypoxic and normoxic data were analyzed irrespective of cues provided, oxygen requirements were found to have declined more under hypoxic conditions than under normoxic conditions. Since the data were obtained by alternating hypoxic and normoxic runs, the greater rate of decline for hypoxic runs was interpreted to indicate that some kind of long term adaptation to acute hypoxic exposure had taken place. Average R.Q. values during exercise and recovery periods as well as average ventilation measures during exercise periods were also of interest in that they increased as the study progressed. Since these values are commonly observed to decline with training, the increases were interpreted to indicate that an adaptation had taken place which was qualitatively different from what is normally observed. When the effects of training and of cues were considered along with the effects of breathing normoxic or hypoxic air, it was found that under hypoxic conditions, adaptation was evidenced which apparently acted to gradually increase the differences in effects induced by hypoxic and normoxic cues. The adaptation was especially evident in oxygen uptake and R.Q. variables. 106 CONCLUSIONS The results of this study have led to the following conclusions: 1. Physiologic responses during submaximal work under normoxic and hypoxic conditions were psychogenically influenced by cues pertaining to the presence of those conditions. 2. The effects, for the most part, of hypoxic cues on physiologic responses were essentially Opposite to the effects induced by the actual breathing of hypoxic air. 3. The evidence obtained in the present study was insufficient to ascertain whether the psychogenically induced effects were of an incre- mental or decremental nature with respect to the specific work task employed in the testing situations. 4. Experimental procedures, possibly the alternation of hypoxic and normoxic runs, produced unique physiologic adaptation permitting subjects to perform a given amount of work at a lower oxygen cost while breathing hypoxic air than when breathing normoxic air. RECOMMENDATIONS The psychogenic and training effects observed in the present study appear to be of greater physiologic complexity than can be properly explained from the kinds of observations which were made. Further investigation of these phenomena is warranted. Based upon insights which were gained in this experiment, the following recommendations are offered: 1. The study should.be duplicated but with provisions made to obtain data from urine and blood analyses. a. Norepinephrine and epinephrine concentrations in urine are needed to determine whether differences in acute responses 107 and long term adaptation are related to the relative amounts of these hormones. b. Determinations of blood pH along with lactate, glucose, and free fatty acid concentrations in circulation are needed to elucidate the effects which were observed on oxygen uptakes and R.Q.'s. If obtainable, arterial and venous measures would be particularly enlightening. 2. 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APPENDICES APPENDIX A TREATMENT EFFECTS DATA 118 .Aoausv hano hnsum mo was: umma aoum mum mumma omasa\~o can mums madam mousse: unwouoxm huo>ooou new can mmouom N m .uonusm aoum OHanHm>m moon guano .vouummoum mum moanmwum> unmuuoeaa umoa OH can mHnON .Aumnnv mnOfiumoaHmou a x muoofinsm m aouw mnmuza o.¢m m.a¢ N.mm m.wm «.mm 0.0m m.mm m.~m o.am m.m~ «.mm mm o.mm m.o¢ «.mm m.wm w.nm m.om m.om <.em o.~m ¢.m~ ~.mm Hm w.~m o.wm m.nm o.mm m.mm m.qm o.mm m.om o.om o.mN m.m~ Nz m.~m m.nm m.om w.mm H.mm o.¢m ~.qm m.am w.om n.5N m.¢~ Hz Anaa\mnummuov comm muoumuammom NH.~ ma.~ N~.~ «N.N mN.N mN.N m~.N ¢~.~ NH.N Hm.H .wm.a mm HH.~ ma.~ H~.~ m~.~ s~.~ .s~.~ -.N mH.~ ou.~ Hm.a Rm.a Hm .mo.N so.m oa.~ NH.N oa.~ ma.~ oa.~ wo.~ oo.~ om.a mm.H Nz oo.~ Ano.u .nH.N HH.N 0H.~ .mH.N HH.N <0.N om.a ,am.a ¢¢.H Hz _ . 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Nmm Hm NNN Nmm oNN NNN Nam Hz Amuouwav .uno> .xm Hmuoe N.sN N.¢N N.ma mama Ne m.NN N.NH N.NH mama Nz N.mH H.mH s.ma Nuammaz Hm N.Na H.NH N.NN Nassau: Hz I Aummn\aav NomNsm cm ass omN mes mama Nm NSN Nee sea some Nz NSN was NeN NaNmmNz Hm oeN NeN msN waammNz Hz Anfla\mumonv momma omaom .xm sou mos sou moN mEN Ne amN ocN mmN Nna Hon Nz meN mos ass «on was a: OOH Hon awn can Non Hz Anaa\mumonv comm madam xmom .>< s m N N .>< e m N a moaomo moaozu puma saxoahm muOQ.Oonauoz Amuoowwm mafiafimuuv Hmoaozo mmouom muummwm unmaummua .~I< manna 123 0N.0 00.N 00.0 0N.0 00.0 N0 00.0 00.0 00.0 00.0 00.0 Nz N0.0 00.0 0N.0 00.0 00.0 00 00.0 00.0 00.0 N0.0 N0.0 Hz ANM coauomuuxm No .xm 0NN 0NN 00N 00N 00N N0 N0N N0N 00N 00N 00N Nz 00N NNN 0NN N0N 00N 0: N0N 00N N0N 00N 00N Hz wa\aavIwM\unmamufiswom No 0.00 0.0N 0.0N N.00 0.N0 N0 0.0N N.N0 N.0N 0.00 0.00 Nz 0.0N N.0N 0.0N 0.0N 0.00 00 0.00 0.00 0.00 0.0N 0.0N Hz .I 000\Nav 00\0000 N0 0.00 0.NN 0.0N 0.00 0.00 N0 0.00 0.N0 0.N0 0.00 0.00 Nz 0.00 0.0N N.00 N.H0 0.00 00 N.00 0.N0 0.N0 0.00 0.00 Hz A00\0aa\050 00\0000 .mmINo .00 0.00 0.00 0.00 0.00 0.0N N0 0.N0 0.00 0.00 0.00 0.00 Nz 0.0N N.00 N.N0 0.NN 0.0N 00 0.00 0.NN 0.NN 0.N0 0.00 Hz A000000\Hav .0000\wm0 00 .00 00.N 00.N 0N.N N0.N 00.N N0 N0.N 00.N 00.N 00.N N0.N Nz N0.N NN.N N0.N N0.N 00.N Hm 00.N 00.N 00.N 00.N N0.N Hz Anfia\mpouwav comm .QD mo .xm N.N0 0.00 0.N0 0.00 0.00 N0 0.00 0.N0 0.00 0.00 0.00 Nz 0.N0 0.N0 0.00 . N.0N 0.00 00 N.0H 0.00 0.N0 0.00 0.00 02 RI Amuoufiav unmaouasdomIeo 00.0 00.0 00.0 0N.0 00.0 N0 00.0 00.0 00.0 00.0 00.0 Nz 00.0 N0.0 N0.0 00.0 0N.0 0: N0.0 00.0 N0.0 00.0 00.0 02 RI 00000000 0000 .0 .>0 0 0 N N .>0 0 0 . N N moaomo mmaohu mono canoe»: mama oaxoauoz 0.0.00000 NI< 00000 ‘0 00.0 00.0 00.0 00.0 00. 00 00.0 No.0 00.0 00.0 00.0 02 00. 00. 00. 00. N0. 0: 00.0 No.0 00.0 ‘00.0 00.0 0z 0No\Nouv .0.0 .000 00.0 00.0 00.0 00.0 00. N0 N0. 00. N0. N0. 00. N2 00.0 00.0 00.0 00.0 00.0 00 00. N0. N0. 00. 00. 0z .. 00000000 .0.0 .00 00.N 00.N 00.N N0.N 00.N N0 00.N N0.N N0.N N0.N 00.NV Nz 00.N 00.N N0.N 00.N N0.N 00 00.N N0.N 00.N 00.N 00.N Hz ANV nowuomuuxm 0o .oom .>0 0 0 N 0 .>< 0 0 N 0 000000 moaoao mama oaxoauoz 0009 00009»: 0.0.00000 NI< 00000 APPENDIX B THREE-WAY, MIXED MODEL ANOVA SUMMARIES APPENDIX B THREE-WAY, MIXED MODEL ANOVA SUMMARIES Notes Three separate ANOVAs were necessitated as reported in Chapter III. a. AOVl tested for main effects b. AOV2 tested first half against last half for training effects and for interactions c. AOV3A tested for truth-lie differences in normoxic data only d. AOVBB tested for truth-lie differences in hypoxic data only. Subjects were the random variable. Treatment and cycle were fixed variables. 23 appearing in the table indicate the error term specific to the effects term appearing immediately above. Where an effects term is not followed immediately by a ”Z", the error term used is identified by Rem. Error (Remaining Error). Tables 372 and B-3 are incomplete due to missing data. AOVl summaries were conducted for data obtained only in the last half of the study. 125 126 Table B-1. ANOVA summaries for dependent variable - peak pulse rate Source of Var. SS df MS F Ratio F Prob. on1 ' A-Treatment 557.78 3 185.93 16.98 <0.0005 Z=AC 229.97 21 10.95 B-Cycle 105.09 3 35.03 1.39 0.272 Z=BC 527.66 21 25.13 C-Subject 17,748.72 7 2535.53 423.81 <0.0005 AC 229.97 21 10.95 1.83 0.176 ABC .505.91 63 8.03 1.34- 0.334 Rem. Error 53.84 9 5.98 Total 19,728.97 127 AOV2 A-Treatment. 557.78 3 185.93 16.98 <0.0005 ZBAC 229.97 21 10.95 B-Cycle 1&2 Cycle 3&4 5.28 l 5.28 0.12 0.744 Z=BC 320.97 45.85 AB 33.41 11.14 1.67 0.203 Z=ABC 139.84 6.66 C-Subject 17,748.72 2535.53 232.27 <0.0005 AC 229.97 10.95 1.00 0.473 BC 320.97 45.85 4.20 0.001 ABC 139.84 6.66 0.61 0.896 D-Replic. 5.28 5.28 0.48 0.489 Rem. 687.72 10.92 Total 19,728.97 AOV3A (Normoxic Data Only) A—Treatment 21.39 1 21.39 4.83 0.116 Z=AC 13.30 3 4.43 B-Cycle 65.05 3 21.68 5.96 0.016 Z=BC 32.77 9 3.64 AB 16.54 3 5.52 0.27 0.844 Z=ABC 182.52 9 20.28 C-Subject 5,619.30 3 1873.10 13.39 <0.0005 Rem. Error 4,476.50 32 139.89 Total 10,427.36 63 AOVBB (Hypoxic Data Only) A-Treatment 8.27 1 8.27 . 1.21. 0.351 Z=AC 20.42 3 6.81 B-Cycle 47.67 3 15.89 1.89 0.202 Z=BC 75.64 9 8.40 » AB 29.67 3 9.89 1.04 0.422 Z=ABC 85.89 9 9.54 C—Subject 3,980.42 3 1326.81 9.38 <3.0005 Rem. Error 4,525.50 32 141.42 Total 8,773.48 63 127 Table B-2. ANOVA summaries for dependent variable - exercise pulse rate Source of Var. SS df MS F Ratio F Prob. AOVl A-Treatment 4,337.72 3 1445.91 7.65 0.001 Z=AC 3,971.78 21 189.13 B-Cycle 540.56 1 540.56 1.61 0.245 Z=BC 2,349.69 7 335.67 C-Subject 128,024.43 7 18289.21 112.31 0.001 AC 3,971.78 21 189.13 1.16 0.523 ABC 4,149.72 21 197.61 1.21 0.505 Rem. Error 488.53 3 162.84 Total 143,862.44 63 AOV2 A-Treatment Z=AC B-Cycle 1&2 Cycle 3&4 Z=BC AB Z=ABC (Missing Data Prohibited Analysis) C-Subject AC BC ABC D-Replic. Rem. Error Total AOV3A (Normoxic Data Only) A-Treatment Z=AC B-Cycle Z=BC (Missing Data Prohibited Analysis) AB Z=ABC C-Subject Rem. Error Total AOV3B (Hypoxic Data Only) ArTreatment Z=AC iggécle (Missing Data Prohibited Analysis) AB Z=ABC C-Subject Rem. Error Total 128 Table B-3. ANOVA summaries for dependent variable - exercise 02/pulse Source of Var. SS df MS F Ratio F Prob. AOVl A-Treatment 95.76 3 31.92 59.38 <0.0005 Z=AC 11.29 21 0.54 B-Cycle 2.84 1 2.84 5.54 0.051 Z=BC 3.59 7 0.51 C-Subject 212.17 7 30.31 107.58 0.001 AC 11.29 21 0.54 1.91 0.330 ABC 12.43 21 0.59 2.10 0.298 Rem. Error 0.85 3 0.28 Total 338.93 63 AOV2 A-Treatment Z=AC B-Cycle 1&2 Cycle 3&4 Z=BC AB Z=ABC (Missing Data Prohibited Analysis) C-Subject AC BC ABC D-Replic. Rem. Error Total AOV3A (Normoxic Data Only) A-Treatment Z=AC B—Cycle Z=BC (Missing Data Prohibited Analysis) AB Z=ABC C-Subject Rem. Error Total AOV3B (Hypoxic Data Only) A-Treatment Z=AC B-Cycle Z=BC AB . Z=ABC (Missing Data Prohibited Analysis) C-Subject Rem. Error Total 129 Table B-4. ANOVA summaries for dependent variable - total exercise ventilation Source of Var. SS df MS F Ratio F Prob. AOVl A-Treatment 41,178.67 3 15,059.56 44.55 <0.0005 Z=AC 7,098.64 21 338.03 B-Cycle 1,805.90 3 601.97 2.32 0.104 Z=BC 5,442.89 21 259.19 C-Subject 134,813.39 7 19,259.06 89.72 <0.0005 AC 7,098.64 21 338.03 1.57 0.245 ABC 12,485.48 63 198.18 0.92 0.612 Rem. Error 1,931.82 9 214.65 Total 208,756.79 127 AOV2 A-Treatment 45,178.67 3 15,059.56 44.55 <0.0005 Z=AC 7,098.64 21 338.03 B-Cycle 1&2 Cycle 3&4 1,409.21 1 1,409.21 17.46 0.004 Z=BC 564.74 7 80.68 AB 731.34 3 243.78 1.71 0.196 Z=ABC 2,998.50 21 142.79 C-Subject 134,813.39 7 19,259.06 77.92 <0.0005 AC 7,098.64 21 338.03 1.37 0.170 BC 564.74 7 80.68 0.33 0.939 ABC 2,998.50 21 142.79 0.58 0.919 D-Replic. 390.78 1 390.78 1.58 0.213 Rem. Error 15,571.53 63 247.17 Total 208,756.79 127 AOV3A (Normoxic Data Only) A-Treatment 38.041 1 38.04 0.39 0.577 Z=AC 293.80 3 97.93 B-Cycle 1,700.04 3 566.68 1.85 0.208 Z=BC 2,751.84 9 305.76 AB « 539.58 3 179.86 0.81 0.518 Z=AB 1,992.59 9 221.40 C-Subject 19,489.31‘ 3 6,496.44 Rem. Error 40,470.16 32 1,264.69 Total 67,275.36 63 AOV3B (Hypoxic Data Only) A-Treatment 1.40 1 1.40 0.01 0.924 Z=AC 394.98 3 131.66 B-Cycle 1,404.69 3 468.23 2.12 0.167 Z=BC 1,983.48 9 220.39 AB 93.42 3 31.14 0.19 0.898 Z=ABC 1,445.62 9 160.62 C-Subject 35,048.31 3 11,682.77 6.68 0.001 Rem. Error 55,970.31 32 1,749.07 Total 96,342.21 63 Table B-5. ANOVA summaries for dependent variable - total recovery ventilation Source of Var. SS MS F Ratio F Prob. AOV1 A—Treatment 6,900.54 2,300.18 4.75 0.011 Z=AC 10,178.17 484.67 B-Cycle 287.85 95.95 0.19 0.899 Z=BC 10,367.01 493.67 C-Subject 219,768.56 31,395.51 255.98 <0.0005 AC 10,178.17 484.67 3.95 0.019’ ABC 6,061.92 96.22 0.78 0.732 Rem. Error 1,103.83 122.65 Total 254,667.89 AOV2 . A-Treatment 6,900.54 2,300.18 4.75 0.011 Z=AC 10,178.17 484.67 B-Cycle 1&2 Cycle 3&4 204.47 204.47 0.28 0.610 Z=BC 5,034.26 719.18 AB 745.51 248.50 5.74 <0.005 Z=ABC 909.93 43.33 C-Subject 219,768.56 31,395.51 181.08 0.0005 AC 10,178.17 484.67, 2.80 0.001 BC 5,034.26 719.18 4.15 0.001 ABC 909.93 43.33 0.25 1.000 D-Replic. 3.27 3.27 0.02 0.891 Rem. Error 10,923.17 173.38 Total 254,667.89 AOV3A (Normoxic Data Only) A—Treatment 41.86 1 41.86 0.66 0.475 Z=AC 189.07 3 63.02 B-Cycle 79.75 3 26.58 0.13 0.938 Z=BC 1,809.40 9 201.04 AB 136.64 3 45.55 0.68 0.588 Z=ABC 605.21 9 67.25 C-Subject 27,182.01 3 9,060.67 5.31 0.004 Rem. Error 54,564.59 32 1,705.14 Total 84,608.53 63 AOV3B (Hypoxic Data Only) A-Treatment 245.31 1 245.31 3.46 0.160 Z=AC 212.63 3 70.88 B-Cycle 1,056.02 3 352.01 8.89 0.005 Z=BC 356.26 9 39.58 AB 119.27 3 39.76 0.23 0.870 Z=ABC 1,526.01 9 169.56 C-Subject 48,339.99 3 16,113.33 4.62 0.009 Rem. Error 111,590.50 32 3,487.20 Total 163.446.00 63 131 Table B-6. ANOVA summaries for dependent variable - sum total ventila- tion (run + recovery) Source of Var. SS df MS F Ratio F Prob. AOVl A-Treatment 86,677.52 3 28,892.51 33.89 <0.0005 Z=AC 17,901.23 21 852.44 B-Cycle 1,048.11 3 349.37 0.28 0.840 Z=BC 26,330.19 21 1,253.82 C-Subject 608,788.95 7 86,969.85 157.41 <0.0005 AC 17,901.23 21 852.44 1.54 0.256 ABC 23,936.34 63 379.94 0.69 0.815 Rem. Error 4,972.58 9 552.51 Total 769,654.93 127 AOV2 ArTreatment 86,677.52 3 28,892.51 33.89 <0.0005 Z=AC 17,901.23 21 852.44 B-Cycle 1&2 Cycle 3&4 540.10 1 540.10 0.47 0.516 Z=BC 8,081.61 7 1,154.52 AB 2,557.21 3 852.40 4.45 0.014 Z=ABC 4,020.97 21 191.47 C-Subject 608,788.95 7 86,969.85 134.88 <0.0005 AC 17,901.23 21 852.44 1.32 0.196 BC 8,081.61 7 1,154.52 1.79 0.105 ABC 4,020.97 21 191.47 0.30 0.998 D-Replic. 465.54 1 465.54 0.72 0.399 Rem. Error 40,621.81 63 644.79 Total 769,654.93 AOV3A (Normoxic Data Only) A-Treatment 159.71 1 159.71 1.03 0.385 Z=AC 464.85 3 154.95 B-Cycle 2,479.11 3 826.37 1.03 0.425 Z=BC 7,237.67 9 804.19 AB 1,03l:27 3 343.76 1.22 0.357 Z=ABC 2,530.87 9 281.21 C-Subject 90,610.83 3 30,203.61 5.80 0.003 Rem. Error 166,567.76 32 5,205.24 Total 271,082.07 63 AOV3B (Hypoxic Data Only) A-Treatment 209.63 1 209.63 0.56 0.508 Z=AC 1,119.96 3 373.32 B-Cycle 2,233.66 3 744.55 2.73 0.106 Z=BC 2,456.62 9 272.96 AB 276.65 3 92.22 0.20 0.897 Z=ABC 4,240.69 9 471.19 C-Subject 143,602.88 3 47,867.63 5.93 0.002 Rem. Error 258,124.59 32 8,066.39 Total 412,264.68 63 ' tion rate 132 ANOVA summaries for dependent variable - exercise ventila- Source of Var. SS df M3 F Ratio F Prob. AOV1 A-Treatment 1,807.15 3 602.38 44.55 <0.0005 Z=AC 283.95 21 13.52 B-Cycle 72.24 3 24.08 2.32 0.104 Z=BC 217.72 21 10.36 C-Subject 5,392.54 7 770.36 89.72 <0.0005 AC 283.95 21 13.52 1.57 0.245 ABC 499.42 63 7.93 0.92 0.612 Rem. Error 77.27 9 8.59 A ~ Total 48,350.27 127 AOV2 ArTreatment 1,807.15 3 602.38 44.55 <0.0005 ZsAC 283.95 21 13.52 B-Cycle 1&2 Cycle 3&4 56.37 1 56.37 17.47 0.004 Z=BC 22.59 7 3.23 AB 29.25 3 9.75 1.71 0.196 Z=ABC 119.94 21 5.71 C-Subject 5,392.54 7 770.36 89.72 <0.0005 AC 283.95 21 13.52 1.37 0.170 BC 22.59 7 3.23 0.33 0.939 ABC 119.94 21 5.71 0.58 0.919 D-Replic. 15.63 1 15.63 1.58 0.213 Rem. Error 622.86 63 9.89 Total 8,350.27 127 AOV3A (Normoxic Data Only) A-Treatment 1.52 1 1.52 0.39 0.577 Z=AC 11.75 3 3.92 B-Cycle 68.00 3 22.67 1.85 0.208 Z=BC 110.07 9 12.23 AB 21.58 3 7.19- 0.81 0.518 Z=ABC 79.70 9 8.86 C—Subject 779.57 3 259.86 5.14 0.005 Rem. Error 1,618.81~ 32 50.59 Total 2,691.01 63 AOV3B (Hypoxic Data Only) ArTreatment 0.06 1 0.06 0.01 0.924 Z=AC 15.80 3 5.27 B-Cycle 56.19 3 18.73 2.12 0.167 Z=BC 79.34 9 8.82 AB 3.74 3 1.25 0.19 0.898 Z=ABC 57.82 9 6.42 C-Subject 1,401.93 3 467.31 6.68 0.001 Rem. Error 2,238.81' 32 69.96 Total 3,853.69 63 133 ANOVA summaries for dependent variable - exercise tidal volume Source of Var. SS df MS F Ratio F Prob. AOVl A-Treatment 0.3562 3 0.1187 9.67 <0.0005 Z=AC 0.2578 21 0.0123 B-Cycle 0.0231 3 0.0077 0.33 0.802 Z=BC 0.4853 21 0.0231 C-Subject 15.0562 7 2.1509 214.76 <0.0005 AC 0.2578 21 0.0123 1.23 0.392 ABC 0.5538 63 0.0088 0.88 0.651 Rem. Error 0.0901 9 0.0100 Total 16.8226 127 AOV2 A-Treatment 0.3562 3 0.1187 9.67 <0.0005 Z=AC 0.2578 21 0.0123 B-Cycle 1&2 Cycle 3&4 0.00001 1 0.00001 0.0003 0.986 Z=BC 0.2321 7 0.0332 AB 0.0346 3 0.0115 0.91 0.451 Z=ABC 0.2653 21 0.0126 C-Subject 15.0562 7 2.1509 218.45 <0.0005 AC 0.2578 21 0.0123 1.25 0.246 BC 0.2321 7 0.0332 3.37 0.004 ABC 0.2653 21 0.0126 1.28 0.221 D-Replic. 0.0000 1 0.0000 0.00 0.983 Rem. Error 0.6203 63 0.0098 Total 16.8226 127 AOV3A (Normoxic Data Only) A-Treatment 0.0092 1 0.0092 0.61 0.493 Z=AC 0.0456 3 0.0152 B-Cycle 0.0151 3 0.0050 0.20 0.892 Z=BC 0.2237 9 0.0249 AB 0.0104 3 0.0035 0.33 0.804 Z=ABC 0.0949 9 0.0105 C-Subject 2.7436 3 0.9145 6.31 0.002 Rem. Error 4.6391 32 0.1450 Total 7.7817 63 AOV3B (Hypoxic Data Only) A-Treatment 0.0045 1 0.0045 1.21 0.352 Z=AC 0.0111 3 0.0037 B-Cycle 0.0617 3 0.0206 1.28 0.339 Z=BC 0.1448 9 0.0161 AB 0.0259 3 0.0086 1.79 0.219 Z-ABC 0.0433 9 0.0048 C-Subject 2.7985 3 0.9328 5.32 0.004 Rem. Error 5.6085 32 0.1753 Total 8.6983 63 tory rate 134 ANOVA summaries for dependent variable - exercise respira- Source of Var. SS df MS F Ratio F Prob. AOVl A-Treatment 135.95 3 45.32 7.25 0.002 Z=AC 131.32 21 6.25 B-Cycle 14.47 3 4.82 0.83 0.494 Z=BC 122.37 21 5.83 C-Subject 4,708.19 7 672.60 166.55 <0.0005 AC 131.32 21 6.25 1.55 0.254 ABC 218.27 63 3.46 0.86 0.668 Rem. Error 36.35 9 4.04 Total 5,366.92 127 AOV2 A-Treatment 135.95 3 45.32 7.25 0.002 Z-AC 131.32 21 6.25 B~Cyc1e 1&2 Cycle 3&4 11.05 1 11.05 1.39 0.277 Z=BC 55.53 7 7.93 AB 5.76 3 1.92 0.48 0.694 Z=ABC 82.53 21 6.93 C-Subject 4,708.19 7 672.60 180.71 <0.0005 AC 131.32 21 6.25 1.68 0.059 BC 55.53 7 7.93 2.13 0.053 ABC 82.53 21 3.93 1.06 0.416 D-Replic0 2.10 1 2.10 0.56 0.455 Rem. Error 234.49 63 3.72 Total 5,366.92 127 AOV3A (Normoxic Data Only) A-Treatment 0.00 1 0.00 0.00 0.995 Z=AC 12.29 3 4.10 B-Cycle 7.67 3 2.56 0.28 0.841 Z=BC 83.11 9 9.23 AB 4.76 3 1.59 0.87 0.490 Z=ABC 16.32 9 1.81 c—Subject 234.66 3 78.22 1.22 0.320 Rem. Error 2,057.27 32_ 64.29 Total 2,416.08 63 AOV3B (Hypoxic Data Only) A-Treatment 3.11 1 3.11 5.97 0.092 Z=AC 1.56 3 0.52 B-Cycle 33.91 3 11.30 2.20 0.158 Z=BC 46.34 9 5.15 AB 4.48 3 1.49 0.76 0.545 Z=ABC 17.72 9 1.97 C-Subject 292.88 3 97.63 1.29 0.294 Rem. Error 2,418.01 32 75.56 Total 2,817.99 63 135 Table B-lO. ANOVA summaries for dependent variable - total exercise 02 uptake Source of Var. SS df MS F Ratio F Prob. AOVl A-Treatment 38.08 3 12.69 19.24 <0.0005 Z=AC 13.86 21 0.66 B-Cycle 28.14 3 9.38 14.67 <0.0005 Z=BC 13.43 21 0.64 C-Subject 177.07 7 25.30 33.71~ <0.0005 AC 13.86 21 0.66 0.88 0.619 ABC 19.98 63 0.32 0.42 0.977 Rem. Error 6.75 9 0.75 Total 297.30 127 AOV2 A-Treatment 38.08 3 12.69 19.24 <0.0005 Z=AC 13.86 21 0.66 B-Cycle 1&2 Cycle 3&4 21.77 1 21.77. 45.33 <0.0005 Z=BC 3.36 7 0.48 AB 5.14 3 1.71 5.03 0.009 Z=ABC 7.15 21 0.34 C-Subject 177.07 7 25.30 62.84 <0.0005 AC 13.86 21 0.66 1.64 0.068 BC 3.36 7 0.48 .1.19 0.320 ABC 7.15 21 0.34 0.85_ 0.656 D-Replic. 5.51 1 5.51 13.68 <0.0005 Rem. Error 25.36 63 0.40 Total 297.30 127 AOV3A (Normoxic Data Only) A-Treatment 0.24. 1 0.24 1.71 0.282 Z=AC 0.42 3 0.14 B-Cycle 4.68 3 1.56 3.91 0.049 Z=BC 3.59 9 0.40 AB ‘ 0.19 3 0.06 0.57 0.650 Z=ABC 1.00 9 0.11 C-Subject 48.77 3 16.26 9.18 <0.0005 Rem. Error 56.69 32 1.77 Total 115.58 63 AOV3B (Hypoxic Data Only) AJTreatment 1.35 1 1.35 4.90 0.114 Z=AC 0.83 3 0.28 B-Cycle 29.48 3 9.83 17.55 <0.0005 Z-BC 5.04 9 0.56 AB 0.55 3 0.18 0.73 0.562 Z=ABC 2.27 9 0.25 C-Subject 35.03 3 11.68 5.29 0.004 Rem. Error 70.68 32 2.21 Total 145.23 63 136 Table B-ll. ANOVA summaries for dependent variable - O2 debt Source of Var. SS df MS F Ratio F Prob. AOVl A-Treatment 11.89 3 3.96 7.92 0.001 Z=AC 10.51 21 0.50 B-Cycle 3.98 3 1.33 3.44 0.035 Z=BC 8.09 21 0.39 C-Subject 119.18 7 17.03 210.39 <0.0005 AC 10.51 21 0.50 6.18 0.004 ABC 9.25 63 0.15 1.81 0.169 Rem. Error 0.73 9 0.08 Total 163.63 127 AOV2 A-Treatment 11.89 3 3.96 7.92 0.001 Z=AC 10.51 21 0.50 B-Cycle 1&2 Cycle 3&4 3.10 1 3.10 5.51 0.051 Z=BC 3.94 7 0.56 AB 0.241 3 0.08 0.50 0.685 Z=ABC 3.39 21 0.16 C-Subject 119.18 7 17.03 98.58 <0.0005 AC 10.51 21 0.50 2.90 0.001 BC 3.94 7 0.56 3.26 0.005 ABC 3.39 21 0.16 0.93 0.552 D-Replic. 0.51 1 0.51 2.94- 0.091 Rem. Error 10.88 63 0.17 Total 163.63 127 AOV3A (Normoxic Data Only) A-Treatment 0.01 l 0.01 0.04 0.860 Z=AC 1.08 3 0.36 B-Cycle 1.86 3 0.62 1.74 0.229 Z=BC 3.22 9 0.36 AB 0.26 3 0.09 0.63 0.616 Z=ABC 1.24 9 0.14 C-Subject 17.46 3 5.82 6.58 0.001 Rem. Error 28.30 32 0.88 Total 53.42 63 AOV3B (Hypoxic Data Only) A-Treatment 0.08 l 0.08 0.38 0.581 Z=AC 0.60 3 0.20 B-Cycle 2.51 3 0.84 6.67 0.012 Z=BC 1.13 9 0.13 AB 0.08 3 0.03 0.30 0.822 Z=ABC 0.81 9- 0.09 C-Subject 39.50 3 13.17 7.84 <0.0005 Rem. Error 53.70 32 1.68 Total 98.40 63 Table B-12. ANOVA summaries for dependent variable - 02 requirement Source of Var.‘ SS MS F Ratio F Prob. AOVl A-Treatment 7.71 2.57 1.92 0.157 Z=AC 28.07 1.34 B-Cycle 53.03 17.68 11.16 <0.0005 Z=BC 33.25 1.58 C-Subject 458.56 65.51 68.97 <0.0005 AC 28.07 1.34 1.41 0.307 ABC 42.24 0.67 0.71 0.800 Rem. Error 8.55 0.95 Total 631.40 AOV2 A-Treatment 7.71 2.57 1.92 0.157 Z=AC 28.07 1.34 B-Cycle 1&2 Cycle 3&4 41.30 41.30 27.70 0.001 Z=BC 10.44 1.49 AB 7.28 2.43 3.52 0.003 Z=ABC 14.46 0.69 C-Subject 458.56 65.51 76.10 <0.0005 AC 28.07 1.34- 1.55 0.092 BC 10.44 1.49 1.73 0.118 ABC 14.46 0.69- 0.80 0.709 D-Replic. 9.36 9.36 10.87 0.002 Rem. Error 54.24~ 0.86 Total 631.40 AOV3A (Normoxic Data Only) A-Treatment 0.14 1 0.14 0.21 0.679 Z=AC 2.02 3 0.67 B-Cycle 12.24 3 4.08 3.19 0.077 Z=BC 11.49 9 1.28 AB 0.72 3 0.24 1.02 0.429 Z=ABC 2.11 9 ‘ 0.23 C-Subject 123.65 3 41.22 10.90 <0.0005 Rem. Error 121.01 32 3.78 Total 273.38 63 AOV3B (Hypoxic Data Only) A-Treatment 0.78 1 0.78 0.83 0.428 Z=AC 2.82 3 0.94 B-Cycle 47.65 3 15.88 16.56 0.001 Z=BC 8.63 9 0.96 AB 0.97 3 0.32 0.78 0.534 Z=ABC 3.74 9 0.42 C-Subject 142.14 3 47.38 10.49 <0.0005 Rem. Error 144.50 32 4.52 Total 351.23 63 Table 3'13 0 138 ANOVA summaries for dependent variable - exercise 02 uptake rate Source of Var. SS df MS F Ratio F Prob. AOVl A-Treatment 1.5233 3 0.5078 19.24 <0.0005 Z=AC 0.5543 21 0.0264 B-Cycle 1.1255 3 0.3752 14.67 <0.0005 Z=BC 0.5371 21 0.0256 C-Subject 7.0828 7 1.0118 33.71 <0.0005 AC 0.5543 21 0.0264 0.88 0.619 ABC 0.7990 63 0.0127 0.42 0.977 Rem. Error 0.2702 9 0.0300 ' Total 11.8920 127 AOV2 A-Treatment 1.5233 3 0.5078 19.24 <0.0005 Z=AC 0.5543 21 0.0264 B-Cycle 1&2 Cycle 3&4 0.8710 1 0.8710 45.33 <0.0005 Z=BC 0.1345 7 0.0192 AB 0.2058 3 0.0686 5.04 0.009 Z=ABC 0.2858 21 0.0136 C-Subject 7.0828 7 1.0118 62.84 <0.0005 AC 0.5543 21 0.0264 1.64 0.068 BC 0.1345 7 0.0192 1.19 0.320 ABC 0.2858 21 0.0136 0.85 0.656 D-Replic. 0.2202 1 0.2202 13.68 <0.0005 Rem. Error 1.0145 63 0.0161 Total . 11.8920 127 AOV3A (Normoxic Data Only) A—Treatment 0.0096 1 0.0096 1.71~ 0.282 Z=AC 0.0168 3 0.0056 B-Cycle 0.1870 3 0.0623 3.91 0.049 Z=B 0.1435 9 0.0159 AB' 0.0076 3 0.0025 0.57 0.650 Z=ABC 0.0401 9 0.0045 C-Subject 1.9508 3 0.6503 9.18 <0.0005 Rem. Error 2.2678 32 0.0709 Total 4.6233 63 AOV3B (Hypoxic Data Only) A-Treatment 0.0541 1 0.0541 4.90 0.114 Z=AC 0.0331 3 0.0110 B-Cycle 1.1790 3 0.3930 17.55 <0.0005 Z=BC 0.2015 9 0.0224 AB 0.0220 3 0.0073 0.73 0.562 Z=ABC 0.0909 9 0.0101 C-Subject 1.4014- 3 0.4671 5.29 0.004 Rem. Error 2.8271 32 0.0883 Total 5.8091 63 139 Table B-14. ANOVA summaries for dependent variable - exercise 02 uptake/respiration Source of Var. SS df MS F Ratio F Prob. AOV1 A-Treatment 3,842.13 3 1,280.71 13.90 <0.0005 Z=AC 1,934.68 21 92.13 B-Cycle 1,763.52 3 587.84 7.01 0.002 Z=BC 1,760.36 21 83.83 C-Subject 45,214.14 7 6,459.16 109.83 <0.0005 AC 1,934.68 21‘ 92.13 1.57 0.248 ABC 2,015.94 63 32.00 0.54 0.921 Rem. Error 529.31 9 58.81 Total 57,060.09 127 AOV2 A-Treatment 3,842.13 3 1,280.71 13.90 <0.0005 Z=AC 1,934.68 21 92.13 B-Cycle 1&2 Cycle 3&4 1,410.50 1 1,410.50 18.61 0.004 Z=BC 530.64 7 75.81 AB 266.77 3 88.92 2.26 0.111 Z=ABC 824.91 21 39.28 _ C-Subject 45,214.14 7 6,459.16 145.97 <0.0005 AC 1,934.68 21- 92.13 2.08 0.013 BC 530.64 7 75.81 1.71 0.122 ABC 824.91- 21 39.28 0.89 0.606 D-Replic. 248.60 1 248.60 5.62 0.021 Rem. Error 2,787.73 63 44.25 Total 57,060.09 127 AOV3A (Normoxic Data Only) ‘ A-Treatment 51.31 1 51.31 1.07 0.376 Z=AC 143.19 3 47.73 B-Cycle 287.36 3 95.79 1.84 0.210 Z=BC 468.65 9 52.07 AB 79.72 3 26.57 1.03 0.423 Z=ABC 231.59 9 25.73 C-Subject 8,780.54 3 -2,926.85 5.29 0.004 Rem. Error 17,709.53 32 553.42 Total 27,751.89 63 AOV3B (Hypoxic Data Only) A-Treatment 37.74 1 37.74 0.99 0.394 Z=AC 114.72 3 38.24 B-Cycle 1,893.17 3 631.06 7.16 0.009 Z=BC 792.94 9 88.10 AB 32.60 3 10.87 0.33 0.803 Z=ABC 294.49 9 32.72 C-Subject 7,622.06 3 2,540.69 5.51 0.004 Rem. Error 14,767.41 32 461.48 Total 25,555.12 63 Table B-15. rate/kg body weight 140 ANOVA summaries for dependent variable - Ex. 02 uptake Source of Var. SS df MS F Ratio F Prob. AOV1 A-Treatment 249.44 3 83.15 19.96 <0.0005 Z=AC 87.46 21 4.16 B-Cycle 191.89 3 63.96 16.11 <0.0005 Z=BC 83.35 21 3.97 C-Subject 427.12 7 61.02 11.79 0.001 AC 87.46 21 4.16 0.80 0.677 ABC 128.71 63 2.04 0.39 0.985 Rem. Error 46.57 9 5.17 Total 1,214.55 127 AOV2 A-Treatment 249.44 3 83.15 19.96 <0.0005 Z=AC 87.46 21 4.16 B-Cycle 1&2 Cycle 3&4 150.93 1 150.93 42.47 <0.0005 Z=BC 24.88 7 3.55 AB 37.04 3 12.35 5.38 0.007 Z=ABC 48.15 21 2.29 C-Subject 427.12 7 61.02 24.70 <0.0005 AC w 87.46 21 4.16 1.69 0.058 BC 24.88 7 3.55 1.44 0.206 ABC 48.15 21 2.29 0.93 0.559 D-Replic. 33.87 1 33.87 13.71 <0.0005 Rem. Errdr 155.66 63 2.47 Total 1,214.55 127 AOV3A (Normoxic Data Only) A-Treatment 0.59 1 0.59 0.74 0.453 ZaAC 2.41 3 0.80 B-Cycle 31.78 3 10.59 5.27 0.023 Z=BC 18.09 9 2.01 AB 1.57 3 0.52 0.60 0.631 Z=ABC 7.86 9 0.87 C-Subject 25.79 3 8.60 1.56 0.218 Rem. Error 176.17 32 5.51 Total 264.26 63 AOV3B (Hypoxic Data Only) A-Treatment 11.43 1 11.43 5.77 0.096 Z=AC 5.95 3 1.98 B-Cycle 200.90 3 66.97 19.22 <0.0005 Z=BC 31.35 9 3.48 AB 4.20 3 1.40 0.60. 0.634 Z=ABC 21.16 9 2.35 C-Subject 91.12 3 30.37 2.80 0.056 Rem. Error 346.75 32 10.84 Total 712.87 63 weight 141 ANOVA summaries for dependent variable - 02 debt/kg body Source of Var. SS df MS F Ratio F Prob. AOVl A-Treatment 1,865.25 3 621.75 7.99 0.001' Z=AC 1,633.64 21 77.79 B-Cycle 645.57 3 215.19 3.31 0.040 Z=BC 1,363.05 21 64.91 C—Subject 5,229.78 7 747.11 54.04 <0.0005 AC 1,633.64 21 77.79 5.63 0.006 ABC 1,590.08 63 25.24 1.83 0.166 Rem. Error 124.42 9 13.82 Total 12,451.78 127 AOV2 A-Treatment 1,865.25 3 621.75 7.99 0.001 Z=AC 1,633.64 21 77.79 B-Cycle 1&2 Cycle 3&4 503.47 1 503.47 4.96 0.061 Z=BC 710.52 7 101.50 AB 33.48 3 11.16 0.41 0.748 Z=ABC 572.83 21 27.28 C-Subject 5,229.78 7 747.11 25.65 <0.0005 AC 1,633.64 21 77.79. 2.67 0.001 BC 710.52 7 101.50 3.49 0.003 ABC 572.83 21 27.28 0.94 0.549 D-Replic. 67.95 1 67.95 2.33- 0.132 Rem. Error 1,834.87 63 29.12 Total 12,451.78 127 AOV3A (Normoxic Data Only) A-Treatment 4.78 1 4.78 0.08 0.799 Z=AC 184.61 3 61.54 B-Cycle 293.87 3 97.96 2.01 0.183 Z=BC 437.85 9 48.65 AB 48.57 3 16.19 0.56 0.653 Z=ABC 258.69 9 28.74. C-Subject 87.75 3 29.25 0.38 0.767 Rem. Error 2,451.33 32 76.60 Total 43,767.45 63 AOVBB (Hypoxic Data Only) A-Treatment 6.39 1 6.39 0.15 0.728 Z=AC 131.46 3 43.82 B-Cycle 415.57 3 138.52 5.93 0.016 Z=BC 210.33 9 23.37 AB 11.98 3 3.99 0.21 0.884 Z-ABC 168.22 9 18.69 C-Subject 845.37 3 281.79 1.79 0.169 Rem. Error 5,040.93. 32 157.53 Total 6,830.26 63 142 Table B-17. ANOVA summaries for dependent variable - 02 requirement/ kg body weight Source of Var. SS df MS F Ratio F Prob. AOVl ArTreatment 1,364.25 3 454.75 1.91 0.159 Z=AC 5,007.39 21 238.45 B-Cycle 8,908.37 3 2,969.46 11.53 <0.0005 Z=BC 5,408.64 21 257.55 C-Subject 2,732.62 7 390.37 2.37 0.113 AC 5,007.39 21 238.45 1.45 0.289 ABC 6,861.79 63 108.92 0.66 0.836 Rem. Error 1,479.88 9 164.43 Total 31,762.95 127 AOV2 A-Treatment 1,364.25 3 454.75 1.91 0.159 Z=AC 5,007.39 21 238.45 B-Cycle 1&2 Cycle 3&4 7,033.29 1 7,033.29 24.96 0.002 Z=BC 1,972.31 7 281.76 AB 1,263.44 3 421.15 3.72 0.027 Z=ABC 2,380.15 21 113.34 C-Subject 2,732.62 7 390.37 2.85 0.012 AC 5,007.39 21 238.45 1.74 , 0.047 BC 1,972.31 7 281.76 2.06 0.061 ABC 2,380.15 21 113.34 0.83 0.676 D-Replic. 1,394.31‘ 1 1,394.31 10.20 0.002 Rem. Error 8,615.19 63 136.75 Total 31,762.95 127 AOV3A (Normoxic Data Only) A-Treatment 2.77 1 2.77 0.03 0.880 Z=AC 310.49 3 103.50 B-Cycle 2,025.21 3 675.07 4.42 0.036 =BC 1,374.93 9 152.77 AB 130.30 3 43.43 0.78 0.536 Z=ABC 503.87 9 55.99 C-Subject 409.36 3 136.45 0.80 0.502 Rem. Error 5,448.40 32 170.26 Total 10,205.33 63 AOV3B (Hypoxic Data Only) A—Treatment 206.71 1 206.71 1.11 0.369 Z=AC 557.17 3 185.72 B-Cycle 8,050.72 3 2,683.57 16.94 <0.0005 Z=BC 1,425.41 9 158.38 AB 182.02 3 60.67 0.58 0.640 Z=ABC 933.521 9 103.72 C-Subject 1,046.44 3 348.81 1.40 0.262 Rem. Error 8,000.86 32 250.03 Total 20,402.85 63 143 Table B-18. ANOVA summaries for dependent variable - exercise 02 extraction Source of Var.- SS df MS F Ratio F Prob.. AOVl A-Treatment 16.8861 3 5.6287 77.73 <0.0005 Z=AC 1.5207 21 0.0724 B-Cycle 3.7057 3 1.2352 18.05 <0.0005 Z=BC 1.4374 21 0.0684 C-Subject 15.7531 7 2.2504 31.49 <0.0005 AC 1.5207 21 0.0724 1.01 0.521 ABC 2.3752 63 0.0377 0.53 0.931 Rem. Error 0.6433 9 0.0715 Total 42.3214 127 AOV2 A-Treatment 16.8861 3 5.6287 77.73 <0.0005 Z=AC 1.5207 21 0.0724 B-Cycle 1&2 Cycle 3&4 3.1680 1 3.1680 110.38 <0.0005 Z=BC 0.2009 7 0.0287 AB 0.3360 3 0.1120 3.22 0.043 ZzABC 0.7295 21 0.0347 C-Subject 15.7531 7 2.2504 43.95 <0.0005 AC 1.5207 21 0.0724 1.41 0.146 BC 0.2009 7 0.0287 0.56 0.785 ABC 0.7295 21 0.0347 0.68 0.838 D-Replic. 0.5011 1 0.5011 9.79 0.003 Rem. Error 3.3261 63 0.0512 Total 42.3214 127 AOV3A (Normoxic Data Only) ArTreatment 0.0045 1 0.0045 0.82 0.432 Z=AC 0.0166 3 0.0055 B-Cycle 0.9919 3 0.3306 10.36 0.003 Z=BC 0.2874 9 0.0319 AB 0.1759 3 0.0586 2.41 0.135 Z=ABC 0.2193 9 0.0244 C-Subject 3.8212 3 1.2737 7.55 0.001' Rem. Error 5.3997 32 0.1687 Total 10.9165 63 AOV3B (Hypoxic Data Only) A-Treatment 0.1101 1 0.1101 2.34 0.224 Z=AC 0.1411 3 0.0470 B-Cycle 3.1274 3 1.0425 10.82 0.002 Z=BC 0.8672 9 0.0964 AB 0.0537 3 0.0179 0.34 0.797 Z=ABC 0.4749 9 0.0528 C-Subject 4.6492 3 1.5497 9.52 <0.0005 Rem. Error 5.2099 32 0.1628 Total 14.6334 63 144 Table B-19. ANOVA summaries for dependent variable - recovery 0 extraction 2 Source of Var. SS df MS ' F Ratio F Prob. AOVl A-Treatment 0.4133 3 0.1378 2.57 0.082‘ Z=AC 1.1276 21 0.0537 B-Cycle 0.4616 3 0.1539 3.13 0.047 Z=BC 1.0319 21 0.0491 C-Subject 6.6624 7 0.9518 62.44 <0.0005 AC 1.1276 21 0.0537 3.52: 0.028 ABC 1.1761 63 0.0187 1.22 0.397 Rem. Error 0.1371 9 0.0152 Total 11.0101 127 AOV2 A-Treatment 0.4133 3 0.1378 2.57 0.082 Z=AC 1.1276 21 0.0537 B-Cycle 1&2 Cycle 3&4 0.2885 1 0.2885 3.53 0.102 Z=BC 0.5728 7 0.0818 AB 0.0372 3 0.0124 0.63 0.602 Z=ABC 0.4109 21 0.0196 C-Subject 6.6624 7 0.9518 42.28 <0.0005 AC 1.1276 21 0.0537 2.39 0.004 BC 0.5728 7 0.0818 3.64 0.002 ABC 0.4109 21 0.0196 0.87 0.628 D-Replic. 0.0794 1' 0.0794 3.53 0.065 Rem. Error 1.4180 63 0.0225 Total 11.0101 127 AOV3A (Normoxic Data Only) A-Treatment 0.0026 1 0.0026 0.10 0.774 Z=AC 0.0796 3 0.0265 B-Cycle 0.3330 3 0.1110 5.61 0.019 Z=BC 0.1782 9 0.0198 AB 0.0258 3 0.0086 0.51 0.686 Z=ABC 0.1520 9 0.0169 C-Subject 1.8043 3 0.6014 9.12 <0.0005 Rem. Error 2.1088 32 0.0659 Total 4.6842 63 AOV3B (Hypoxic Data Only) A-Treatment 0.0021 1 0.0021 0.04 0.851 Z=AC 0.1521 3 0.0507 B-Cycle 0.2122 3 0.0707 5.62 0.019 Z=BC ‘ 0.1132 9 0.0126 AB 0.0279 3 0.0093 0.42 0.745 Z=ABC 0.2004 9 0.0223 C-Subject 3.0794 3 1.0265 15.42 <0.0005 Rem. Error 2.1302 32 0.0666 Total 5.9173 63 145 ANOVA summaries for dependent variable - exercise R.Q. Source of Var.- SS df MS F Ratio F Prob. AOVl ' A-Treatment 0.7080 3 0.2360 37.48 <0.0005 z-AC 0.1322 21 0.0063 B-Cycle 0.1255 3 0.0418 10.46 <0.0005 Z=BC 0.0839 21 7 0.0040 C-Subject 0.7278 7 0.1040 20.55 <0.0005 AC 0.1322 21 0.0063 1.24 0.382 ABC 0.2312 63 0.0037 0.73 0.783 Rem. Error 0.0455 9 0.0051 Total 2.0542 127 AOV2 A-Treatment 0.7080 3 0.2360 37.48- <0.0005 Z-AC 0.1322 21 0.0063 B-Cycle 1&2 Cycle 3&4 0.1002 1 0.1002 30.52 0.001 Z=BC 0.0230 7 0.0033 AB 0.0314 3 0.0105 3.69 0.028 Z=ABC 0.0596 21' 0.0028 C-Subject 0.7278 7 0.1040 26.41 <0.0005 AC 0.1322 21 0.0063 1.60 0.078 BC 0.0230 7 0.0033 0.83 0.563 ABC 0.0596 21 0.0028 0.72 0.796 D—Replic. 0.0239 1 0.0239 6.06 0.017 Rem. Error 0.2480 63 0.0039 Total" 2 .0542 127 AOV3A (Normoxic Data Only) A-Treatment 0.0050 1 0.0050 11.09 0.045 Z=AC 0.0013 3 0.0004 B-Cycle 0.0196 3 0.0065 6.22 0.014 Z=BC 0.0095‘ 9 0.0011 AB 0.0021 3 0.0007 0.61 0.623 Z=ABC 0.0103 9 0.0011 C-Subject 0.0914 3 0.0305 6.15 0.002 Rem. Error 0.1584 32 0.0050 Total 0.2976 63 AOV3B (Hypoxic Data Only) A-Treatment 0.0104 1 0.0104 3.44 0.160 Z=AC 0.0090 3 0.0030 B-Cycle 0.1312 3 0.0437 6.53 0.012 Z=BC 0.0603 9 0.0067 AB 0.0181 3 0.0060 1.41 0.304 Z=ABC 0.0388 9 0.0043 C-Subject 0.2379 3 0.0793 4.55 0.009 Rem. Error 0.5583 32 0.0174 Total 1.0640 63 Table B-21. 146 ANOVA summaries for dependent variable - recovery R.Q. Source of Var. SS df MS F Ratio F Prob. AOVl A-Treatment 0.0666 3 0.0222 2.28 0.109 Z=AC 0.2045 21 0.0097 B-Cycle 0.0432 3 0.0144 7.01 0.002 Z=BC 0.0431 21 0.0021 C-Subject 0.4034' 7 0.0576 30.02 <0.0005 AC 0.2045 21 0.0097 5.07 0.008 ABC 0.2153 63 0.0034 1.78 0.177 Rem. Error 0.0173 9 0.0019 Total 0.9934 127 AOV2 A-Treatment 0.0666 3 0.0222 2.28 0.109 Z=AC 0.2045 21 0.0097 B-Cycle 1&2 Cycle 3&4 0.0286 1 0.0286 12.97 0.009 Z=BC 0.0154 7 0.0022 AB 0.0026 3 0.0009 0.22 0.876 Z=ABC 0.0804 21 0.0038 C-Subject 0.4034 7 0.0576 19.06 <0.0005 AC 0.2045 21 0.0097 3.22 <0.0005 BC 0.0154 7 0.0022 0.73 0.648 ABC 0.0804 21 0.0038 1.27 0.233 D-Replic. 0.0014 1 0.0014 0.45 0.506 Rem. Error 0.1905 63 0.0030 Total 0.9934 127 AOV3A (Normoxic Data Only) A-Treatment 0.0039 1 0.0039 0.78 0.441 Z=AC 0.0150 3 0.0050 B-Cycle 0.0260 3 0.0087 9.13 0.004 z-BC 0.0085 9 0.0009 AB 0.0115 3 0.0038 1.13 0.388 Z=ABC 0.305 9 0.0034 C-Subject 0.1117 3 0.0372 6.38 0.002 Rem. Error 0.1868 32 0.0058 Total 0.3939 63 AOV3B (Hypoxic Data Only) A-Treatment 0.0036 1 0.0036 0.32 0.611 Z=AC 0.0338 3 0.0113 B-Cycle 0.0188 3 0.0063 1.90 0.201 Z=BC 0.0297 9 0.0033 AB 0.0042 3 0.0014 0.33 0.804 Z=ABC 0.0381 9 0.0042 C-Subject 0.1114 3 0.0371 3.95 0.017 Rem. Error 0.3007 32 0.0094 Total 0.5404 63 APPENDIX C GAS MIXING APPARATUS AND PROCEDURES AND GAS FEED APPARATUS W if APPENDIX C GAS MIXING APPARATUS AND PROCEDURES For reasons of economy and certainty of adequate supply, tanks of hypoxic air needed for the study were obtained using laboratory facilities to mix compressed air with compressed nitrogen. Although an air compres— sor and other equipment needed for filling SCUBA tanks were already installed, it was necessary to design and assemble an apparatus for transferring compressed nitrogen from a full tank to an empty compressed gas cylinder. The schematic arrangement and essential components used for the purpose are shown in Figure C-l. Parts labeled V or G were valves or gauges, respectively. All equipment, valves, gauges and hydraulic tubing had been manufactured to handle gas and gas flow at high pressures (3000 psi) and were obtained from commercial suppliers. GENERAL MIXING PROCEDURES Although temperature changes invariably accompany compression and decompression of gases, the effects of such changes on the volumes of gas being mixed were ignored. Instead, it was assumed that cooling during decompression that occurred while gas was entering the empty cylinder would be offset by heating as the cylinder became full. Mixing to specific concentrations was based solely on pressure changes until the end pressure sought was approached. At that time, a sample was drawn off and analyzed for oxygen content. This was always done conservatively so that more compressed air could be added to raise the oxygen content to the desired level. 147 148 .msumuwnna madame mam mo muaoaomaoo Howucommo was uaoaowuuuum ofiumaonom .Huo «usage mabdmdama‘ 0232.2 93 m0 Sammie G..—.Szmrow 880588 c:‘ xcop 22.2.2 3.9.60 .850 :4 :82 8:38 / .> $.98. N 96> 95:... return” .28. :5... 38m . c6230”. mph. 2, o oommmcano €009.22 > N0§ . 00.2” \I/ l _ 25E .28 BamV > co_a:ool\ l/ocfia... o_£xo_ml\‘- o_> x030 F , hwv «F & L: AV «> > a> no 6 149 As may have been inferred from the preceding statement, nitrogen was always introduced into the mixture tank first because the nitrogen pressure available in the nitrogen reservoir tank was always lower than that available in the compressed air reservoir. Since the nitrogen reservoir tank was the same size as the gas mixture tank, a point was soon reached where sufficient nitrogen had been drawn off. At that time filled mixture tank pressure also exceeded that of the nitrogen tank. Since flow direction is from high to low pressure, it would not have been possible to get more nitrogen into the mix tank. An overshoot in addition of compressed air to the mix tank would therefore result in loss of the gas mixture. In order to obtain the greatest accuracy with the least amount of sampling trials, an end filling pressure was selected for the gas mixture tank. This was conservatively below the tank's pressure capacity (approx. 2200 psi) and below the capacity pressure of the compressed air reservoir and air compressor. It was then possible to calculate the partial pressure of nitrogen which would be needed to obtain the desired partial pressure of oxygen. Next a calculation was made of the drop in pressure of the nitrogen tank that would be needed. This was added to the partial pressure of nitrogen in compressed air to obtain the desired and partial pressure of nitrogen in the filled mixture tank. The procedure then was simply one of draining nitrogen into the mixture tank until the pressure reading in the nitrogen tank drOpped the appropriate amount. Following that step, compressed air was introduced into the mixture tank until the desired end filling pressure was reached. At that time, a sample was drawn off and analyzed. Since the tank heated up considerably during the filling, addition of compressed air was always conservative so long as the pre-determined and filling pressure was not exceeded. 150 SPECIFIC MIXING PROCEDURES With reference to the apparatus shown in Figure C-l the specific procedures employed were as follows: 1. A11 valves closed. Oxygen line completely disconnected. 2. Open V1 and read pressure in nitrogen tank on gauge 61' 3. Open V2, V and V6 in that order until Gl pressure drops 3 apprOpriately. 4. Close V2 to check pressure reading. If OK, proceed. Other- wise open and close V2 until desired reading is obtained. 1 and V6. Open V5 to bleed off line pressure completely. Then close V2, V3 5. Having sufficient nitrogen in mix tank, close V and V5. 6. Connect oxygen to SCUBA tank fitting. V7 closed. 7. Vlo closed. Open V9 and read pressure in oxygen reservoir on G4. 8. Open V8, V4.and V6 allowing compressed air to flow into gas mixture tank until 03 and G2 reach desired reading. 9. Close V6 and then V9. 10. Open V7 to bleed line pressure read on 03 and G4° Then close V4. Compressed air supply lead can then be disconnected. 11. V and V closed. Open V Then Open V Obtain sample. 4 3 6' 5' Close V5. 12. Close V6' If sample OK, open V5 to bleed line pressure. Close V5 and disconnect tank. If not, add additional compressed air and obtain analysis samples as before. 13. Valve V8 and V9 closed. 14. A11 valves closed. Turn on air compressor. 15. Open V to refill compressed air reservoir. 10 I! A 5-45.. D u I‘- 5m .1 1 "ad "a 151 16. Open V9 to read G4 which shows pressure in compressed air reservoir. When full, close V and V 9 10. Turn off air compressor. Open V8 and V7 to bleed off line pressure. 17. Close all valves. Table C-l shows the results of using these procedures while mixing the nine tanks of hypoxic air used in the study. End oxygen percentages and end filling pressures obtained are shown. These may be compared to the goals of 16.60% and 1900 psi. Table C-l. Hypoxic air mixing data1 —.——~— r V Tank H A ' I End Filling Mixture No. Z 02 (STPD) Pressure Reached 1 16.60 1902 psi 2 16.59 1951 psi 3 16.61 .1921 psi 4 16.62 1903 psi 5 16.59 1951 psi 6 16.59 1966 psi 7 16.59 1967 psi 8 16.63 1894 psi 9 16.62 1953 psi 1 Goal was to obtain 16.60% 02 and an end of filling pressure at 1900 psi. The accuracy required for the oxygen percentage was;i 0.22. 2Pressure readings given were read off of gauges at the end of filling procedures. Pressure capacity of tanks used was approximately 2500 psi. 152 GAS FEED APPARATUS The use of compressed gas as a source of inspired air necessitated design and construction of special gas feed apparatus. This apparatus was needed to fulfill two functions. Pressure had to be lowered to ambient levels in order to avoid fbrcing air into subjects' lungs. The second function needed was moisturization of the air. The moisturiza- tion was made necessary by the fact that air passing through the com- pressor was almost completely dried out by a desiccator. The desiccator had been built into the system to avoid problems which would result from having excess moisture in the SCUBA tanks. The schematic arrangement and essential components of the gas feed apparatus are shown in Figure C-2. V's indicate valves and G's indicate gauges. In essence, this apparatus consisted of a manifold with fittings at one end for simultaneous attachment to two tanks. The other end of the manifold was connected to a gas pressure reducing valve so that gas could be released at substantially reduced pressures. Valve arrangements permitted withdrawing gas from either tank. The two gauges indicated in the drawing are both attached to the gas pressure reducing valve. 01 shows pressure of the gas in the tank from.which gas is withdrawn. Gauge G2 shows the pressure at which the gas is released.. Release pressure is adjustable by opening or closing valve V4. Valve V5 per- mitted further control over flow rates. After passing through the reducing valve and flow rate control valve, the air entered small bore flexible tubing (1/4" I.D.) through which it was conveyed to a water bath for moisturization and warming. The moisturi- zation and warming were considered necessary to avoid irritation of tissues in the respiratory tract. .‘r'. ‘4 ‘ 92' .Clhn-I..}J’ m .maumummmm vmmm mow mo muamaomaoo Hmfiuaommm paw usuamwnmuum ofiumamnom .Nlo shaman makdmdn—ad 0mm... 93 .10 2554.0 oCSzwzom M>_o> 3831 2:8ch 9.5:. .__< commuter—coo coo. _om TD 620295222 3 5 .I. .2 CES. £8 .20; 36> ‘ 1. =9. 29: 258 as l V muzznm O... 154 From the water bath the air was passed into a meteorological balloon which was used to accomplish final depressurization. The flow rate was controlled such that the balloon was kept flaccid to avoid repressurization which would be generated in part by the balloon's elasticity. Use of the meterological balloon as the final depressurization chamber had an additional advantage in that it could literally be wrung out and milked dry of gas. This simplified the process of clearing gas from the apparatus as was done to avoid contaminating the next mixture used. APPENDIX D ENVIRONMENTAL CONDITIONS anruvrsm 4- "§,"- 1: 155 ENVIRONMENTAL DATA 72 t AV. TEMP. PF) 70- 68~ 66- 750 AV. BAR. PRESS. (mm Hg._) 740 W 730 AV. REL. HUM. (‘36) ‘ 58~ 56r- 54- 52*- 50- 48+- . 46- 44. 42- - 40-- 38- 36h- 34r- 32+- 30 rllr L l 1 L I 2 3 4 P I 1 L L J 1 1 1 J l J 6789|Ol||2|3l4|5|6 RUNS CYCLE I CYCLE 2 I CYCLE 3 CYCLE 4 Figure D-l. Mean environmental conditions during the study. APPENDIX E PRE-EXPERIMENT INSTRUCTIONS TO SUBJECTS APPENDIX E PRE-EXPERIMENT INSTRUCTIONS TO SUBJECTS ALTITUDE SIMULATION STUDY Subject Instructions PLEASE READ CAREFULLY: By now most of you have a fair idea of what this study is about. What you may not fully realize is that complete cOOperation from each subject will be critical to the success Of the experiment. In fact, it was the belief that you peOple in particular could be depended upon for such COOperation which was a major consideration in seeking your help as subjects. Basically, what we are attempting to show is that a compressed air mixture can be used to simulate altitude respiratory conditions if proper techniques and apparatus are employed. If the study is successful, it will Open the door to many research projects which before now did not appear possible in this laboratory. The nature of this experiment is such that we are dealing with several unknowns. Thus it was decided as preferable to use the fewest number of subjects needed for statistical analysis. An important conse- quence of this decision is that statistical analysis is rendered almost 7’ impossible if any subject misses a single session or even part Of a a session. -1 That particular statistical vulnerability made it necessary to select a minimally aerobic type of run when we should really have a highly aerobic type of run for the study. While this gives reasonable assurance that every subject will be capable of completing every "run" it has the consequence of making it imperative to obtain all observations with the greatest possible precision. Another consequence is that, since such small differences will be expected and the need is so great for precision of measurement, even minor "psychological" influences could very easily distort the data. To offset such possibilities you are all asked to: r‘ he. lk‘ 'W)'A .m' ‘2' -. v 1. Try to think of the run as a tedious, but necessary, job that must be done so that you will feel like showing up on time, making the run, and then be able to just forget it until the next time. 2. Do not request any information about how you or the others are doing at any time Of any Operator until the 5 week collection period is over. (It is unlikely we will have the data sufficiently analyzed to know anything until then anyway.) 156 157 3. Avoid discussing the runs with anyone. HOpefully this will avoid many things, but particularly motivation differences. We especially do not want you to compare notes with other subjects in the study. It is believed the competition urge much too strong to ignore except in complete ignorance. Obviously we don't even want you to compete with yourself. 4. In short it is hoped you can put the study out of your mind com— pletely except when you actually participate. Tough to do - but you are asked to try (in hopes that knowing why will make it easier). One last point of interest is that the late modification of design (the addition of the water bath to the inspired air system) might produce some unpredictable results. Specifically, the variability in the humidity from run to run could conceivably alter partial pressures of oxygen just enough that on occasion the simple compressed air might seem more stress- ful than the altitude air mixture. Preliminary checking to date indicates there should be no problem, but it seemed prudent to warn you in advance so you won't panic, thinking that something has gone wrong with you when it hasn't. Finally, be assured that every conceivable precaution has been taken to protect your health and well being in planning and devising this study. Oxygen has even been provided for the extremely unlikely possi- bility of need after an altitude run. Thank you many times over for your help and cooperation! General Instructions 1. Try not to upset or change your daily routines. 2. Follow normal breakfast habits as possible before each run. 3. Wear shorts and the same shoes for each run. 4. Please take whatever measures are necessary to assure your ability to show up 15 minutes before you are scheduled to run. 5. Towels will be provided to permit showering after finishing each run. 9." 4.5” "' '-? ‘2'! c APPENDIX F PRE-TRAINING POST-EXERCISE HEART RATE DATA '1! .- I APPENDIX F PRE-TRAINING POST-EXERCISE HEART RATE DATA Table F-l. Pre-training post-exercise heart rate data Pre-Experiment Training Runsl Subjects 1 2 3 4 “,5, 6 No. Initials Heart rates at 1 min. after exercise‘ 1 MG 130 141 116 122 122 123 2 DK 120 120 110 124 122 121 3 JR 120 130 134 132 128 122 4 CB 128 134 128 124 120 120 5 AR 116 112 120 120 120 134 6 RR 110 116 116 124 130 125 7 DD 70 74 84 70 84 68 8 JA 110 130 120 126 134 126 1Pre-experiment training runs were conducted on six successive days, 1 run per day, during the week immediately preceding the experi- ment. Runs were made on motor driven treadmill for five minutes at 7 mph and zero grade. 2Heart rates were Obtained at 1 minute after cessation of the runs with subjects resting in a sitting position. Measures were Obtained by palpation of the radial artery. 158 0 NEW? L I! v- II VI III N“ R" E“ VI" NI” 3177 84 s‘afljmnufl f flUlWUl