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'IIIwIw I" I' ’I;' IIIJNI ’ """VI'I '.'I' I"III'I"'""""'III" 'I"."‘" ”HI/H" "III" I""""" "" "H" II. . ,I'II'fi, I II'WII' 'II'I'I'I 'IIWII III. "III” ' . 'I'f 1""""'I"' """I"' """I _\_:-.: :;—-..“ K 2- .I- ‘II 'J'III 'II I'II‘IIIII‘ II?" 'J'"'.I""‘I‘ . I.'J'I' ' ‘II'H III; I'IEI' I'IIHIIHIIIIIMH' I'II'II'II' IIIII I'zH'II aq- mgws .1 w This is to certify that the thesis entitled The Effects of Submaximal Training Under Hypoxic Conditions Upon Performance at Sea Level presented by Mohammed S. Sanguq has been accepted towards fulfillment of the requirements for M. A. degreein PMSiCfil Education Major professor DateflML d 0-7639 L l’ U 1w; 5-; 1 Michigan State UnivctSiW a ,.p t a ' .1 OVERDUE FINES: 25¢ per day per item RETURNIIKS LIBRARY MATERIALS: 1. _____________._——- V". .‘\"~:‘~\9"” Place in book return to remove .w ~n r"~- '— charge from circulation records THE EFFECTS OF SUBMAXIMAL TRAINING UNDER HYPOXIC CONDITIONS UPON PERFORMANCE AT SEA LEVEL By Mohammed S. Sanguq A THESIS Submitted to Michigan State University in partial fulfillment of the requirements for the degree of MASTER OF ARTS Department of Health, Physical Education, and Recreation 1980 ABSTRACT THE EFFECTS OF SUBMAXIMAL TRAINING UNDER HYPOXIC CONDITIONS UPON PERFORMANCE AT SEA LEVEL By Mohammed S. Sanguq This investigation was conducted to determine the effects of hypoxic submaximal training (simulated high-altitude training) upon performance at sea level. Prime consideration was given to acid-base parameters of the arterialized blood, to oxygen consumption during ex- ercise and recovery as indicators of efficiency in energy metabolism, and to performance time. Eight healthy male students at Michigan State University (22-24 years of age) were used as subjects in the study. The subjects were assigned randomly to one of two treatment groups (n = 4). Group I (normoxic trained while breathing normal air (PO2 = 152 mmHg, 20.7% 02). Group II (hypoxic) trained while breathing air with a reduced oxygen concentration (P02 = 122 mmHg, l6.6% 02). The training consisted of one five-minute run per day on a motor- driven treadmill at 7.0 mph and zero percent grade. The treatment pe- riod lasted three weeks with four days of training during each of the first two weeks and three days of training during the final week. The training was conducted under either normoxic or hypoxic conditions as indicated earlier. Mohammed S. Sanguq Three tests were conducted before and after the treatment period. The first was an all-out run to determine performance time. The tread- mill was Set at 7 mph and 8% grade, and the grade was increased l% per minute after the first two minutes of running. The other two tests were submaximal standard runs, one under hypoxic and one under normoxic conditions. In these two tests gas collection took place during the run and during the first fifteen minutes of recovery. The Douglas bag method was used to determine the oxygen uptake during exercise, the oxygen debt, and the oxygen requirement under each condition. Blood samples were taken before and after the submaximal runs to determine PCO pH, HC03, and BE. 2. Therlood Pco2 was significantly higher in the hypoxic group than in the normaxic group under hypoxic test conditions. There were no other significant differences between the two treatment groups under the two submaximal test conditions. Comparisons of the data obtained before and after training for each group resulted in significant differences only in the performance time of the normoxic group and the oxygen debt of the normoxic group under hypoxic test conditions. ACKNOWLEDGMENTS I would like to eXpress my sincerest gratitude and ap- preciation to Dr. Wayne D. Van Huss for his great assistance and support. Special thanks are extended to Dr. William N. Heusner for his highly respected effort and time. My gratitude is also extended to Dr. Kwok Hai Ho for serving on my Guidance Committee and for his friendly encouragement. iii LIST OF LIST OF Chapter I. II. III. TABLE OF CONTENTS TABLES ......................... FIGURES ........................ INTRODUCTION Statement of the Problem .............. Research Hypotheses ................ Research Plan ................... Rationale for Research Plan ............ Limitations .................... REVIEW OF RELATED LITERATURE .............. Physiological Adaptations to Hypoxia ......... Immediate Response to Acute Hypoxic Exposure . . . . Physiological Adaptations after Prolonged Altitude Exposure ..................... Physiological Adaptations to Submaximal Exercise . . . RESEARCH METHODS .................... Research Design .................. Subjects ...................... Treatment Procedures ................ Gas Mixtures .................... Testing Procedures ................. Performance Time Test .............. Submaximal Run Tests ............... Acid-Base Balance ................. Performance Time .................. 02 Utilization ................... Statistical Analyses ................ iv Page vi 9 9 12 16 20 Chapter Page IV. RESULTS AND DISCUSSION ................. 30 Training Effects Upon Oxygen Utilization ....... 30 Discussion of Oxygen Utilization ........... 31 Training Effects Upon Acid-Base Parameters ...... 38 Discussion of Arterialized Blood PC02 ........ 38 Discussion of Arterialized Blood pH ......... 45 Discussion of Arterialized Blood HCO3 ........ 47 Discussion of Arterialized Blood BE ......... 48 Training Effects Upon Performance Time ........ 48 Discussion of Performance Time ............ 49 V. SUMMARY AND CONCLUSIONS ................ 53 Summary ....................... 53 Conclusion ...................... 54 APPENDICES A. Informed Consent .................... 56 B Gas Mixing Apparatus and Procedures .......... 57 C. Blood Sampling ..................... 65 D Calculation of Oxygen Uptake, Oxygen Debt, and Oxygen Requirement Variables ................ 66 REFERENCES ...................... A ..... 7o LIST OF TABLES Table Page 3.l Subject Characteristics ................ 2l 4.l Means and Standard Errors Before and After Training of 02 U take (V02), 02 Debt (020), and Oxygen Requirement (02R) Under Hypoxic Test Conditions .......... 32 4.2 Means and Standard Errors Before and After Training of 02 U take (V02), 02 Debt (020), and Oxygen Requirement (02R) Under Normoxic Test Conditions ......... 33 4.3 Hypoxic and Normoxic Training Effects on Pre-Run to Post-Run Changes in Arterialized Blood PC02, pH, HCO3, and BE Under Hypoxic Test Conditions ......... 39 4.4 Hypoxic and Normoxic Training Effects on Pre-Run to Post-Run Changes in Arterialized Blood PC02, pH, HCO3, and BE Under Normoxic Test Conditions ......... 40 4.5 Means and Standard Error of Gain Scores in pH, PC02, HCO3 and BE in Pre- and Post-Run Data Obtained Under Hypoxic Test Conditions ................ 43 4.6 Means and Standard Error of Gain Scores in pH, PC02, HCO3, and BE in Pre- and Post-Run Data Obtained Under Normoxic Test Conditions ................ 44 4.7 Means and Standard Errors of Performance Time Before and After Training .................. 49 vi LIST OF FIGURES Figure Page 3.l Research Design .................... 20 3.2 Electrode Placement .................. 23 4.l Result of the Gain Score Comparison of the Two Groups in Oxygen Uptake (V02), Oxygen Debt (020) and Oxygen Requirement (02R) Under Hypoxic Test Conditions . . . . 24 4.2 Result of the Gain Score Comparison of the Two Groups in Oxygen Uptake (V02), Oxygen Debt (020) and Oxygen Requirement (02R) Under Normoxic Test Conditions . . . 34 4.3 Results of Hypoxic Versus Normoxic Training Upon Pre- Run to Post-Run Changes in Arterialized Blood pH, PC02, HCO3, and BE Under Hypoxic Test Conditions . . . 41 4.4 Results of Hypoxic Versus Normoxic Training Upon Pre- Run and Post-Run Changes in Arterialized Blood pH, PC02, HCO3, and BE under Normoxic Test Conditions . . . 42 4.5 Comparison of Performance Time Gain Scores Under Normoxic Test Conditions ............... 50 vii CHAPTER I INTRODUCTION Research on the effects of high altitude training on physical per- formance began early in this century (22). However, it became intensi- fied after the decision to hold the l968 Olympic games in Mexico City (2,300 m above sea level). In regard to training and performance, there are at least three questions to be answered: (a) What are the effects of acute high altitude exposure on performance? (b) Does high altitude training improve or impair performance at high altitude? (c) What are the effects of high altitude training on performance at sea level? The immediate effects of acute high altitude exposure on perform- ance have been studied intensively (36, 40, 66, 94, l43, l49, 186, l87, 2l4). It is well established that hypoxia is the major problem at altitude and, therefore, aerobic performance is negatively correlated with altitude. Although the effects of altitude exposure upon anaerobic capacity have not been precisely determined, no impairments of perform- ance have been reported in those activities which require eXplosive power (i. e. throwing, sprinting, jumping). On the contrary, improve- ments of these activities have been noticed due to other factors such as changes in air resistance and gravity. In respect to the second question, there is general agreement in the literature that performance at altitude is enhanced in athletes who have acclimatized themselves by training at the same altitude (ll, 1 36, 40, 66, 143, 186). The question that has not been fully answered pertains to the ef- fects of altitude training on performance at sea level. Enhanced per- formances have been reported in some studies (13, 14, 15, 62, 67, 139), but another body of literature has failed to support this observation (35, 63, 101, 107, 138, 152). Therefore, there is a demonstrated need to further investigate the effects of hypoxic training on performance at sea level. Several studies have been conducted to determine the effects of high altitude training on maximum performance capability as measured by maximum oxygen uptake (Max. V02). Although the Max. VO2 is an im- portant factor in aerobic work, it does not furnish precise information about the economy of work and the efficiency of energy metabolism (161, 207). Astrand et a1. (9) noted that a submaximal work level provides more accurate information about the subject's aerobic capacity. Thus, 02 consumption and the degree to which a subject is able to approach Max. VO2 for a prolonged period of time are better predictors of en- durance capacity than is Max V02 itself (182). At present, little is known about the changes in blood acid-base balance that occur at sea level as a result of hypoxic-submaximal training. At altitude, however, arterial PCO2 and blood HCO3 were re- ported to increase at rest (76, 106) and to decrease with submaximal exercise as a result of hyperventilation (107, 129, 130). Blood lactic acid has been reported to increase both at rest (80, 107) and during submaximal exercise (10, 80, 107, 112, 124, 130, 160, 195). Blood pH, however, is increased (11, 27, 124, 130). The elevation of the blood lactic acid concentration usually is believed to be a result of insufficient O2 supply (147, 177). From a physiological point of view, acute exposure to altitude, even without exercise, will increase pulmonary ventilation by an in- crease of respiratory rate (37, 159) as a compensatory mechanism in re- sponse to hypoxia. More C02 may be blown off which in turn would raise the blood pH and result in slight alkalosis. It has been reported that alkalosis might reduce the aerobic metabolic capacity (116) by inhibit- ing the activity of cytochrome c (117) and by a decrease of conversion of lactate to glucose in the kidneys (114, 115) and liver (118). However, with submaximal exercise at altitude, alkalosis might not be experienced because of an increased CO2 production, and the ac- cumulation of lactic acid in the blood pH may override the effects of compensatory hyperventilation. The blood pH may fall (11) and slight acidosis would result. It is well d0cumented that acidosis impairs aerobic capacity (60, 71, 204). The question is: to what extent would this shift in blood acid-base balance and low PO2 under hypoxic- submaximal training cause adaptation in the body and, therefore, affect performance at sea level? Statement of the Problem The purpose of this study was to determine the effects of hypoxic submaximal training (simulated high-altitude training) upon performance at sea level. Main consideration was given to acid-base parameters of the arterialized blood, to oxygen consumption during exercise and re- covery as indicators of efficiency in energy metabolism, and to per- formance time. Research Hypotheses 1. Hypoxic submaximal training should help to maintain the blood acid-base balance during standard exercise which is perform- ed at sea level. 2. Hypoxic submaximal training should reduce the O2 utilization for standard exercise which is performed at sea level. 3. Hypoxic submaximal training should prolong the performance time of subjects doing exhaustive exercise at sea level. Research Plan Eight healthy male students at Michigan State University, between 22 and 24 years of age, were recruited as subjects for this study. The subjects were classified as active, but not highly trained athletes. A stress test was administered to determine the subjects' ability to par- ticipate in the study. The subjects were assigned randomly to one of two treatment groups (n = 4). Group I (normoxic) trained while breathing normal air (PO2 = 152 mmHg, 20.7% 02). Group II (hypoxic trained while breathing air with a reduced oxygen concentration (PO2 = 122 mmHg, 16.6% 02). The training consisted of one five-minute run per day on a motor- driven treadmill at 7.0 mph and 0% grade. The training period lasted three weeks with four days of training during each of the first two weeks and three days of training during the final week. The training was conducted under either normoxic or hypoxic conditions as indicated earlier. Three tests were conducted before and after the treatment period. The first was an all-out treadmill run to measure performance time. The treadmill was set at 7 mph and 8% grade, and the grade was increased one percent per minute after the first two minutes of running. The other two tests were submaximal standard runs, one under hypoxic and the other under normoxic conditions. These two tests were used to de- termine the acid-base balance of the blood (pH, PC02, HCO3, BE), the 02 uptake during the exercise, the oxygen debt, and the oxygen require- ment of each run. Standard two-sample t-tests were used to analyze the data. The probability of making a Type I error was set at a = .10, and two-tailed tests were used for all analyses. Rationale for Research Plan A 5 min., 6 mph, 0% grade treadmill protocol was used as a re- producible submaximal test for measuring economy of work. Room air was used during all recovery periods to make comparisons between the oxygen debts and the oxygen requirements of the two groups possible. The first minute of recovery gas was excluded on the assumptions that this period of time was needed to flush the lungs of the hypoxic air mixture and that the effects on the oxygen debt calculations would be approximately the same across all treatment and test conditions. Limitations 1. Exposure to hypoxic air (simulated high altitude) occurred only during the workout period. 2. All recovery data were collected while the subjects were breathing room air. 3. All dependent variables, except performance time, were observed under only one kind of work, at one intensity, and one duration. 4. There was no control over the subjects' living patterns. For example, sleep, diet, and recreational activities were not regulated. 5. The results of the study cannot be generalized to other populations or sub-pOpulations of individuals. Definitions l. Altitude. The term "altitude" refers to the vertical elevation above sea level. The following standard pattern has been used for altitude physiology descriptions. Modest altitude 1,500 to 2,500 meters (4,920 to 8,200 feet) Moderate altitude 3,000 to 3,300 meters (9,840 to 10,500 feet) High altitude 4,000 to 5,000 meters (13,120 to 16,400 feet) Great heights above 5,500 meters (above 16,400 feet) 2. Submaximal Work. Physical work of less than maximal inten- sity or work that can be sustained chiefly by aerobic metabolism is called submaximal work. The submaximal work in this study was considered to be of moderate inten- sity. 3. Normoxic Air. Air with a normal PO2 or normal oxygen con- tent (20.9%) is said to be normoxic. In this study, the subjects breathed compressed air adjusted to the ambient pressure when exercising under normoxic conditions. 10. 11. Room Air. Unmodified ambient air is called room air. In this study the subjects were disconnected from the com- pressed air system and breathed room air during recovery from exercise. Hypoxic Air. Air with a low P02 or a low 02 content is said to be hypoxic. The hypoxic air used in this study was a mixture of compressed N2 and 02. The 02 content was reduced to 16.6 i 0.04%. 02 Uptake. (V02): The volume of 02 (STPO) that is taken in by the body from the inspired air during exercise is called 02 uptake. Oxygen Debt. (020): The term oxygen debt was used in this investigation to indicate the volume of 02 (STPD) used during the last 14 minutes of the 15-minute post-exercise recovery period. Oxygen Requirement. (02R): The total volume of 02 (STPD) used during the entire exercise and recOvery period is called the oxygen requirement. No adjustment of volume was made for basal or resting metabolic rate. Acid-Base Balance. The relative pr0portions of acids and alkali (H+ and 0H" ions) in the blood and tissues deter- mine the acid-base balance. . Blood pH. Blood pH is a measure of the acidity or alka- linity of the blood. Standard Bicarbonate. (HCO3): The amount of alkalizing salts as bicarbonate at PCO2 of 40 mmHg, 38°C and completely 12. 13. 14. Oz-saturated hemoglobin that is available in the blood and body fluid for buffering is referred to as standard bicar- bonate. Base Excess. (BE): The base concentration of whole blood as measured by its titration to pH 7.40 at a PCO2 of 40 mmHg is called BE. It is equal to buffer base minus normal buffer base: therefore normal BE = 0. Alkalosis. A shift of the acid-base balance to the alka- line side when the alkalinity of the blood and tissues is increased (pH increased) is called alkalosis. Acidosis. A shift of the acid-base balance to the acid side when the acidity of the blood and tissues is increased (pH decreased) is called acidosis. CHAPTER II REVIEW OF RELATED LITERATURE This review of literature is focussed in two pertinent areas: (1) physiological adaptations to hypoxia which includes (a) immediate responses to acute hypoxic exposure and (b) physiological adaptations after prolonged altitude exposure, and (2) physiological adaptations to submaximal exercise. Physiological Adaptations to Hypoxia The most apparent physiological adjustments in response to hypoxic exposure at rest and during submaximal physical work are in the oxygen transportation system of the body. The primary stimulus may be the increased demand of oxygen at the tissue level, especially during exer- cise. Therefore, a new homeostasis for transportation of oxygen between the environment and the tissues must be reestablished. Immediate Responses to Acute Hypoxic Exposure Evidence has shown that the immediate responses to acute hypoxic exposure include: (a) respiratory rate is increased (37, 159), (b) minute ventilation is increased (37, 48, 101), and (c) oxygen diffusion capacity in the lungs is increased (103, 171), unchanged (195), or de- creased (100, 216). From a physical point of view, a decrease of oxy- gen diffusion capacity in the lungs is more likely to occur since arte- rial PO is reduced with altitude (99, 76, 215). 2 10 During exercise, pulmonary circulation is markedly increased and the blood circulates through the pulmonary capillaries more rapidly than at rest. Gaseous exchange is not a problem under these conditions at sea level. However, with the reduced arterial PO2 at high altitude, it has been reported that oxygen diffusion capacity may be decreased (100, 216). As a result, the amount of oxygen transported to the work- ing muscles is reduced for a given cardiac output. In some cases, the reduced 02 saturation may be compensated for by an increased cardiac output (7, 83, 108, 144, 195). There is fairly good agreement that heart rate is increased at //rest and during submaximal work at altitude (29, 48, 124). Reports on stroke volume, however, are not consistent (56, 100, 140, 144, 153, 169, 184, 197). It would seem that any increase in cardiac output is pro- duced mainly by an increase in heart rate (106, 197). On the other hand, decreased cardiac output during submaximal work at 3000 m alti- tude and decreased HR following swimming exertion at altitude have been reported (12, 55). 1 Acute hypoxic exposure also causes some adaptations in the blood. Blood hematocrit and relative hemoglobin concentration were reported to increase (100, 106, 142, 170, 197, 200). It is believed that these changes can be attributed to a slight decrease in plasma volume and to an increased kidney secretion of erythropoeitin, a powerful stimulant for red blood cell production (173, 197, 200). Oxygen carrying capac- ity of the blood, therefore, is enhanced due to these changes both at rest and during moderate exerCise (100, 142, 197). .Increases of blood I constituents, such as blood glucose and potassium, also have been 11. reported (87, 134, 198). The adjustments in circulation under hypoxic exposure have not yet been understood completely, especially during exercise. However, a circulatory shunt at tissue level was suggested (16) and shown by Feldman (86) and others (3). Reports of vasodilation in muscle are available (38, 54, 193). There is a shift in the oxyhemoglobin dis- sociation curve toward the right (11, 197, 206). Also, shifting of the extracellular fluid into the intracellular compartment and retention of Na+, Ca++, Mg++, and K+ were noticed (44). In regard to the changes in acid-base balance at altitude, an increase of arterial PC02 and blood HCO3 reported at rest (76, 106). During submaximal exercise the PC02 (107, 129, 130) and the HCO3 were decreased (130) due to hyperventilation (130). Although lactate con- centration has been shown to increase at rest (80, 193) and during sub- maximal exercise (10, 80, 107, 112, 124, 130, 160, 195), the blood pH is increased under both conditions (11, 27, 124, 130). There is an increase in oxygen uptake (V02) at rest (75, 102, 132, 151, 201). With moderate exercise an increase (28, 48, 124, 130), no change (6, 47, 85, 101, 189), and even a decrease (56, 151, 203) in V02 were reported. The conflicting results in V02 during moderate ex- ercise cannot be explained at present. Further controversy comes from reports on the oxygen requirement during exercise under hypoxic condi- tions. No change (89), a decrease (56, 120, 151, 203), and an increase (47, 78) in the oxygen requirement for a given exercise at altitude have been shown. Further research in this area obviously is needed. 12 The respiratory quotient (R0) was shown to be increased during exercise under hypoxic conditions (29, 48, 88, 130, 151). This incre- ment in R0 may be a result of hyperventilation (130) (increased C02 exhalation) and/or a result of increased carbohydrate metabolism at altitude (48). The hormonal responses to acute hypoxic exposure have been studied. An increase in urinary catecholamines was reported at rest (23, 42, 146) and during submaximal exercise (45). Factors other than hypoxia, however, might affect the catecholamine level as was pointed out by Becker (23) and Antel (4). Free fatty acids (130, 198), plasma glucose, cortisol and serum growth hormones also were reported to increase (198). On the other hand, a 50% decrease in the blood insulin level was noted during exercise under hypoxic as compared to normoxic conditions (198). These hormonal changes have been suggested by Sutton (198) to favor fat mobilization and enhanced hepatic gluconeogenisis during submaxi- mal hypoxic exercise. In regard to submaximal performance, it has been reported that a relatively long time is needed to reach steady state (29). This may be due, in part, to the reduced capacity for endurance work in acute hypoxia that was reported by Consolazio (47). Physiological Adaptations after Prolonged Altitude Exposure Acclimatization to high altitude may occur under two circum- stances. So-called "natural acclimatization" is referred to as those physiological characteristics found among people who reside in high altitude all their lives; whereas, "gained acclimatization" consists 13 of those physiological changes that are attained by sea level residents who move to high altitudes. The following review of literature is focussed on the second type of acclimatization. It should be pointed out that acclimatization to altitude occurs gradually and the time need- ed for acclimatization depends upon the altitude and the individual. However, complete acclimatization or "steady state" has not been found even in subjects who have been at altitude for prolonged periods of time (126). An increase of ventilation at rest and submaximal exercise is continued after initial exposure to altitude (29, 158, 159). A new level of pulmonary ventilation, higher than the value observed at ini- tial exposure, may be attained (11). Both an increase (65, 103) and no change (64, 215) in diffusing capacity in the lungs have been observed. It is believed that any in- creased diffusing capacity that does occur is the result of a better perfusion in the pulmonary capillaries and the elevated ventilation (196). Cardiac output gradually decreases and returns to sea-level values (140, 181, 212) or even slightly lower (140) at rest and during submaximal exercise. Reduction in cardiac output during submaximal exercise might be attributed to a decrease in heart rate (17, 85, 211) and/or to a decrease in stroke volume (11). The red blood cell count and the hemoglobin concentration are increased by prolonged altitude exposure (127, 189, 211). The increase of red blood cell production results in an elevated hematocrit (43, 61). In addition, a shift of the oxygen dissociation curve (23, 206, 215) 14 and an increase of 2,3-diph05phoglycerate (11) resulting from altitude acclimatization suggest a possible mechanism for increased availability of oxygen to the working muscles. This might explain the improvement in aerobic work which was reported by Saltin (178) and others (17, 145, 189). Adaptations at the tissue level also occur during prolonged alti- tude exposure. Improved efficiency of oxygen utilization was observed by Barbashova (19). This improved efficiency might be due to an in- crease of myoglobin content in the muscle cell (5, 172), an increase of oxiditive enzyme activity (19, 172), and/or an increase of capillariza- tion in the muscle (210). An increase of capillarization would reduce the oxygen diffusion distance (11, 90). Supporting data on improved oxygen utilization also come from Duckworth's work (77) in which a lower oxygen consumption in isolated diaphragm muscle exposed to hypoxia was observed. It is difficult to explain the increased pulmonary ventilation observed after prolonged altitude exposure since the initially elevated PCO2 (106, 128, 196) and alkaline reserve (11, 76, 106, 128, 196) are decreased with acclimatization. In addition, the blood pH decreases to its normal value (11, 128, 196), and a decrease of the blood lactate level following exercise has been reported (29, 70, 145, 165, 205). The mechanism by which lactic acid is decreased might be explain- ed in connection with the action of the catacholamines. The secretion of catacholamines is increased under hypoxia (23, 93). It is well es- tablished that epinephrine has great glycogenolytic effects in liver and muscle cells. However, epinephrine also may cause glycogenisis 15 particularly in liver cells. Therefore, large amounts of blood lactate may be taken up by the liver to be converted to glucose (51, 52, 53). Glycogenolysis also takes place and an increased supply of blood glucose becomes available for the muscles during exercise (25, 41). Based on this possibility, Tillman (203) suggested that lactate production does not decrease, but that the lower blood lactate level under hypoxia may be due to an increased secretion of catecholamines. Another striking fact is that a reduced oxygen consumption during submaximal exercise has been reported after hypoxic training (29, 56, 160). For example, Tillman (203) observed that his hypoxic-trained subjects used less oxygen for a standard submaximal exercise when breath- ing hypoxic air (16.6% oxygen) than when breathing normoxic air. On the other hand, increased oxygen intake has been observed during hypoxic training (29, 57, 85). Billing (29) suggested that the effects of the intensity of the exercise and the altitude may be interrelated. He observed that oxygen intake did not change with altitude when the inten- sity of exercise was at 2.2 L. 02/min. However, a lower oxygen intake value was found when the intensity of exercise was at 2.5 L. Oz/min. The possible lower oxygen consumption during a given submaximal exercise may indicate either an improved oxidative capacity with alti- tude adaptation (17, 145, 165, 178) or an increased contribution of anaerobic energy metabolism with little change in the phosphagan com- ponent (21). Therefore, from the data of Billing (29) and Bason (21), altitude adaptation may result in an increase of 02 debt capacity. However, reduction in 02 debt capacity with acclimatization to altitude also has been observed (50). 16 It is well known that the total hemoglobin concentration is in- creased with altitude acclimatization (100, 106, 170, 197). Hemoglobin has a function other than the transportation of 02. It is a powerful buffer in the body. In regard to exercise energy metabolism under hypoxia, anaerobic glycolysis may be stimulated and lactate formation is in fact increased. However, due to the effects of catecholamines and hemoglobin, more lactate may be taken up by the liver and more H+ could be buffered. The contribution of anaerobic metabolism in the total energy production is therefore increased (21). The reported lower 02 consumption during a submaximal exercise after altitude accli- matization may be the result of the readjustment of energy metabolism in the body. Physiological Adaptations to Submaximal Exercise Exercise tends to disturb the homeostasis of the body. A series of biochemical, physiological and anatomical changes takes place in the body in order to re-establish a new level of homeostasis as a result of physical training. Once this new level of homeostasis is achieved, the body will function better and less strain will be imposed on the body for any given amount of physical work. Many of the physiological adaptations of the body to submaximal exercise are well established in the literature (11). However, there still are numerous areas that are not completely understood. This might be due to the fact that the effects of submaximal exercise are interrelated with many other factors such as: (a) intrinsic character- istics of the subjects (e. 9., age, sex, hormonal regulation, nutri- tional status, heredity, muscle fiber composition, degree of motivation, 17 physical capacity, etc.) and (b) extrinsic conditions (e. g., environ- ment, time of day, etc.). Therefore, the following literature is in- tended to present a summary of the well-known adaptations to exercise rather than a search for the mechanisms of the adaptations. Cardiorespiratory adjustments are marked by a quicker increase of heart rate (HR) and stroke volume (SV) at the beginning of exercise, but the absolute HR will be lower for a given submaximal work load (91, 179, 180, 185). The cardiac output (0) however, may be unchanged (150) or may be even slightly decreased (3, 81) for a given exercise. Also, resting HR is decreased (92) while SV is increased (157). Cardiac hypertrophy on the left side also has been noticed (157, 162, 176). Respiratory rate is increased at the onset of exercise (11), while a reduced total ventilation has been reported with training (208, 209). Pulmonary diffusing capacity has been reported to be either increased (18) or unchanged (79). Total blood volume and total hemoglobin concentration are in- creased with training (136, 164). It seems to be beneficial for a trained individual to have a higher total hemoglobin content in the blood since this may increase the potential oxygen carrying capacity. It is well established that muscle capillarization is increased after submaximal training (113, 166, 182). However, blood flow to working muscles for a given work load is decreased (98, 120, 137). A reduced oxygen consumption for a given workload also has been reported (11, 208, 209). This decline of oxygen cost with training may reflect a gain in efficiency of energy metabolism as a result of a series of changes at the tissue level. For example, the myoglobin content (164), the number and size of the mitichondria (97, 121, 135), 18 and the concentration and activity of a series of aerobic enzymes in the Kreb's Cycle (20, 24, 121) are all increased with training. In regard to substrate utilization, it is well known that train- ing will result in an increase of fat metabolism during exercise (105, 156). A reduction of R0 during exercise may reflect this shift in sub- strate utilization (32, 208, 209). Along the same line, there are re- ports that indicate glycogen concentration is increased in the muscle (25, 26, 152) and plasma triglycerides are lower after a period of sub- maximal training (30, 31). Regarding hormonal responses, blood catecholamine levels are in- creased during exercise (105), but they are normalized rapidly during recovery (105). With training, blood catecholamine levels gradually decline during a given exercise (213). Glycogen is increased (33, 105), but insulin is decreased during work (109). The lower-than-normal in- sulin level during exercise has been proposed to be the result of an inhibitation by the action of epinephrine since insulin secretion by the human pancreas is virtually shut off during an infusion of epine- phrine (167). This effect may be explained as the result of a direct inhibitory action of epinephrine on the beta cells. However, it is well known that epinephrine will activate phos- phorylase (58, 59) and thus facilitate glycogenolysis in both the liver and the muscles (52, 53). As a result, glucose is released from the liver into the circulation. Also, the fact that insulin in the plasma remains depressed for a much longer time after exercise than do cate- cholamines speaks against the hypothesis that catecholamines are the inhibators for insulin during exercise. An inhibitation of insulin 19 secretion might appear to be a problem for glucose transportation across the muscle cell membrane during exercise. However, it has been reported that glucose uptake by the muscle cells during exercise does not necessarily need the presence of insulin (46, 96, 168, 217). A substance with a similar effect has been postulated to be released by the contracting muscle tissue (95). Growth hormone also has been reported to be increased during submaximal exercise (109, 199) as is Cortisol (109, 199). So it seems that the adjustment of the endocrine system during submaximal exercise is to help the body establish a new level of homeostasis as was suggested by Hartley et al. (109). CHAPTER III RESEARCH METHODS The methods and procedures described in this chapter were used to investigate the effects of hypoxic submaximal training (breathing low P02 air) upon performance at sea level. Main consideration was given to performance time, blood acid-base balance, and 02 consumption during exercise and recovery as estimators of the efficiency of energy meta- bolism and economy of work. Research Design A true experimental design, with two independent comparison groups, was used in this study. The analysis included both pre- and post-treatment data as is shown in Figure 3.1: HYQOXla n = 4 Normoxia n = 4 pre-treatment T1 T1 post-treatment T2 12 Figure 3.1. Research Design The experiment was conducted as a single-blind study. The subjects did not know their treatment groups during the course of the investi- gation. 20 21 Subjects Eight healthy male students at Michigan State University were used as subjects in this study. The subjects were classified as active but not highly trained athletes. Their physical and physiological characteristics are given in Table 3.1. TABLE 3.1 SUBJECT CHARACTERISTICS Height Weight Max in in HR Max V02 Subjects Age in Yrs cm Kg bpm ml/Kg/min. fat % JB 20 176.8 68.8 192 72.63 13.5 KC 22 189.0 82.4 191 65.63 12.5 0H 20 155.4 70.0 186 64.62 11.5 PP 22 155.8 89.4 190 49.42 20.5 SH 27 192.0 97.2 181 47.94 19.5 as 18 173.7 71.8 183 52.56 15.5 US 18 176.8 70.2 195 68.05 13.0 TM 18 182.9 81.6 192 66.59 12.0 Prior to the start of the study, an informed consent statement was obtained from each potential subject (See appendix A) and a modi- fied Bruce protocol (34) was administered as a stress test to determine each individual's ability to participate in the study. In addition, weight, height, age, pre-run heart rate, and blood pressure were taken. Electrodes1 then were placed in a single biopolar V5 electrocardiograph 1Disposable 3M Red Dot Monitoring Electrod-Minnesota Mining Co., 3M Center, St. Paul, Minnesota 55101. 22 configuration2 (see Figure 3.2), and each subject was stress tested under the following conditions: Level I -- 3.4 mph, 12% grade, 3 minutes Level II -- 4.2 mph, 12% grade, 3 minutes Level III - 6.0 mph, 12% grade, 1.5 minutes Recovery 3 minutes (standing) During and immediately after each level, the following data were collected: Heart Rate: Recorded at the end of each minute of exercise and recovery. Blood Pressure: Recorded at the end of each level. ECG: Recorded at the end of each level (5-6 second strip). The following criteria were used to eliminate potential subjects (82): l. Systolic blood pressure over 220 mmHg. Diastolic blood pressure over 110 mmHg. Depression of the ST-segment of the ECG greater than 2 mm. hum Premature ventricular contractions (PVC's) in pairs or with increasing frequency. The eight subjects whose physical condition qualified them to participate in the study were assigned randomly to one of two treatment groups (n = 4). Group I (normoxic) was trained while breathing normal air (P02 = 152 mmHg, 20.7% 02). Group II (hypoxic) was trained while breathing air with a reduced oxygen concentration (P02 = 122 mmHg, 16.6% 02). 2Cambridge 3030 EKG, Cambridge Instrument Co. Inc., 73 Spring Street, Ossining, New York 10562. 23 Figure 3.2. Electrode Placement. 24 Prior to the training period, anthropometric measurements were taken to characterize the subjects. These measurements included height (cm), weight (kg), and biceps, triceps, subscapular, and superailiac skinfolds (mm). Percent body fat was estimated from the skinfold meas- urements by the method of Durnin (79). The physical characteristics of the subjects are given in Table 3.1. All subjects were asked not to change their activity patterns during the course of the study. Treatment Procedures Although a prolonged treatment period might be necessary to de- monstrate all the effects of hypoxic training, the eleven-day training period described by Tillman (203) was used in this study since it had been shown to be effective with two treatment groups similar to those used in this study. The training period was carried out over three consecutive weeks with four days in each of the first two weeks and only three days in the last week. Each subject ran eight times under either normoxic or hypoxic conditions as indicated earlier. The train- ing was conducted on a motor-driven treadmill at 7.0 mph and 0% grade. The schedule was set so that each subject could arrive at the research laboratory ten minutes prior to his exercise session. Baro- metric pressure, temperature, relative humidity, and body weight were taken each day. The subject was seated on a chair on the treadmill and heart rate was determined by palpation of the radial artery for ten seconds. Meanwhile, a reservoir balloon was filled with hypoxic air for a hypoxic subject and with normoxic air for a normoxic subject (see appendix B). This procedure was used to keep the subject from knowing his treatment group. The subject then stood up beside the 25 treadmill, the chair was removed, and a Collins' Triple "J" valve was placed in the subject's mouth. After the subject was prepared, the treadmill was started, and the signal "Ready . . . set . . . go" was given. The subject then ran for five minutes. At the end of the run, a ten-second heart rate was taken while the subject was still standing. Subsequently, recovery heart rates were taken at the end of each minute for five minutes while the subject was seated on a chair. Gas Mixtures The procedures described by Tillman (203) were used to prepare the hypoxic air for this study. Compressed air and nitrogen were mixed together in a SCUBA tank in such a way that the percentage of oxygen in the mixture was 16.60 i 0.04%. This concentration of O2 resulted in a P0 of 120 mmHg (STPD) which is similar to the P02 found in the ambient 2 air of Mexico City (2,300 m) where the 1968 Olympic games were held. The percentage of N2 in the mixture is considered to be biologically safe (203). The normoxic air was prepared by filling a SCUBA tank with com- pressed air in the room adjacent to the laboratory. Both the normoxic and the hypoxic air mixtures were reduced to ambient pressure, moisten- ed, and warmed by the techniques of Tillman (203) before they reached the subject (see appendix B). Testing Procedures The following three tests were conducted before and after the training period: 26 Performance Time Test. An all-out multilevel treadmill run was used to determine performance time. Each subject came to the laboratory dressed in tennis shoes and track shorts. Barometric pressure, tempera- ture, and relative humidity were recorded. The subject was weighed and a pre-run blood sample was taken. ECG electrodes were placed. The subject then warmed up in his own manner (usually about five minutes of running at 6 mph and 0% grade). Since the run was to be terminated by exhaustion, a protective harness was used. The subject put on a head-piece which held a low-resistance Collins' Triple "J" valve through which the prepared air was inspired and expired air was col- lected. The treadmill was set at 7 mph, 8% grade, and the grade was increased 1% per minute after the first two minutes of running. With the signal "Ready . . . set . . . go," the subject ran until he indi- cated exhaustion by raising a hand and/or by grasping the iron railing of the treadmill. The treadmill then was turned off immediately. Two people on the sides supported the subject who straddled the treadmill until it stopped. The harness was removed and the subject was helped to a chair placed on the treadmill. The following data were collected: Performance Time: Recorded in minutes and seconds from the time the subject started running until the treadmill was turned off. Heart Rate: Taken at 30-second intervals during exer- cise and at l, 2, 3, 4, 5, 7, 9, 12, and 15 minutes during recovery. Gas Collection: Obtained at 30-second intervals during exer- cise and at l, 2, 3, 5, 7, 9, 12, and 15 minutes during recovery. 27 Submaximal Run Tests. Two submaximal run tests, one under hypoxic (H) and the other under normoxic (N) conditions were conducted. Stand- ard laboratory procedures described earlier were used. After the warm- up, the Collins' Triple "J" valve was placed in the mouth. The subject then ran for five minutes at 7 mph, 0% grade under one of the predeter— mined conditions (H or N). During and immediately after the run, the following data were collected: Gas Collection: Obtained at 30-second intervals during exer- cise and 1, 2, 3, 4, 5, 7, 9, 12, and 15 minutes during recovery. Blood Sample: Taken at the fifth minute of recovery for the determination of PC02, pH, BE, and HC03. Heart Rate: Taken at 30-second intervals during exercise and at 30 seconds, 12, 15 minutes of recovery. Respiratory Observed each minute (10 second strip during Frequency: exercise) and at 1, 2, 3, 4, 5, 7, 9, 12, and 15 minutes during recovery. Acid-base Balance One hundred and twenty microliters (mml) of arterialized capillary blood were drawn from a pre-warmed, cleaned, and dry finger tip in a heparanized capillary tube (appendix C). This blood sample was used to determine the subject's acid-base status; i.e., pH, PC02, HCO3, and BE were determined. The pH and PCO2 were measured directly by a Radio- meter pH 72 and a Radiometer Microtonometer.1 BE and HCO3 were calcu- lated by the Siggarrd-Anderson Alignment Nomogram using the Astrup Equilibration Method (12, 190, 191, 192). 1Radiometer, 72 Emdrupuei, Copenhagen NJ, Denmark. 28 Performance Time An electrical digital stopwatch, accurate to 1/10 second was used manually to record the performance time. 02 utilization The expired air during exercise was collected by the standard Douglas bag method (49) using a low-pressure Otis-McKerrow valve. A minimum hose length between the subject and the collection bag was used. The percentages of 02 and CO2 were measured by a Beckman Model E2 oxy- gen analyzer and a Beckman Model LB15A Carbon Dioxide analyzer.2 The volume of air in the bag was determined using an American-Meter Company Dry Gas Meter (Model DTM-ll)3 STPD using the gas temperature and the barometric pressure recorded during measurement. All gas analyzers and recording equipment were calibrated daily and, usually, before each run. Helium was used to determine the zero points of the analyzers. Temperature, barometric pressure, and a known standard gas sample (17.78% 02 and 4.311 C02) were used to calibrate the analyzers. The 02 uptake during exercise, oxygen debt, and oxygen requirement were calculated using the method described in Consolazio, Johnson and Pecora (49) (appendix 0). Statistical Analyses Two procedures were used to detect statistically significant dif- ferences in the several dependent variables. Dependent-sample t-tests 2Beckman Instruments Inc., 3900 River Road, Siller Park, Illinois. 3Singer, American Meter Company, 13500 Philmont Avenue, Philadelphia, Pennsylvania. 29 for before (Tl) to after (T2) analyses within each group and independent sample t-tests to compare the gain scores of the two groups under the two environmental conditions. The probability of making a type I statistical error was set at a = .10 for all analyses. The calculations were made by a CDC 6500 computer at the Computer Center of Michigan State University. CHAPTER IV RESULTS AND DISCUSSION The purpose of this study was to determine the effects of hypoxic submaximal training upon performance at sea level. Consideration was given to acid-base balance parameters of arterialized blood, to oxygen utilization as an indication of efficiency in energy metabolism, and to performance time. The data were obtained from observations of the two treatment groups (n = 4) under two test conditions: hypoxic and normoxic. Two types of comparisons were made to obtain the results: first, from prior to after training to examine the separate effects of hypoxic and normoxic training under hypoxic and normoxic test conditions; second, comparisons between the gain scores of the two groups to examine the differences resulting from the two treatments. In addition, the acid- base parameters were compared in pre-run and post-run blood samples before and after training. Training Effects Upon Oxygen Utilization Analysis of t-test results revealed no statistically significant differences from before to after training for the two treatment groups in oxygen uptake (V02) or oxygen requirement (02R) (P > .10). Likewise, the oxygen debt (020) of the hypoxic group was not altered (P > .10). The 020 of the normoxic group, however, was significantly decreased under hypoxic test conditions (P 5_.10). The results are given in 30 31 Tables 4.1 and 4.2. The result of the analyses of gain scores in V02, 020, and 0 R, 2 between the two training groups are shown in figures 4.1 and 4.2. There were no statistically significant differences between the two groups. Discussion of Oxygen Utilization Oxygen uptake during exercise (V02) reflects that part of the energy cost of the work that is not associated with the production of lactic acid. Therefore, V02 increases in proportion to the oxygen de- mand up to a given value known as the maximum oxygen uptake. The individual's VO2 during exercise is determined by several factors (131) such as respiratory rate, oxygen carrying capacity of the blood, loading of oxygen at the tissue level, and minute ventilation. These factors are known to be altered with submaximal training in a direction that serves economical transportation and utilization of oxygen (18, 98, 120, 113, 136, 164). The decline in VO2 during sub- maximal exercise is a reflection of increased efficiency and economy of performance and is well established in terms of exercise physiology concepts. The effects of exercise at high altitudes upon V02, on the other hand, are not clear. No change (6, 47, 85, 101, 189), decreases (56, 151, 178, 203) and even increases (28, 29, 48, 124, 130, 202) in VO2 have been reported. The results of hypoxic and normoxic training upon V02 in this study are given in Tables 4.1 and 4.2 respectively. As was expected, the V02 was lower under hypoxic test conditions than under normoxic test conditions. Furthermore, the small sample size may have masked a tendency under normoxic test conditions for the V02 to be decreased 32 TABLE 4.1 MEANS AND STANDARD ERRORS BEFORE AND AFTER TRAINING OF 0 UPTAKE (V02), 02 DEBT (02D), AND OXYGEN REQUIREMENT (02R; UNDER HYPOXIC TEST CONDITIONS BEFORE TRAINING AFTER TRAINING GROUP ml/kg ml/kg P N 188.8 s 24.0 190.7 s 22.4 NS* v0 2 H 190.0 s 35.1 192.1 e 25.8 NS N 104.6 s 5.83 97.3 s 4.12 s** 0 0 2 H 100.0 s 6.06 102.1 s 6.01 NS N 293.4 s 16.3 288.0 5 14.20 NS 0 R 2 H 290.0 e 23.14 294.2 s 6.22 NS B = Normoxic Training Group (N = 4) H = Hypoxic Training Group (N = 4) *Not SignificantX (P > .10) **SignificantX (P i .10) 33 TABLE 4.2 MEANS AND STANDARD ERRORS BEFORE AND AFTER TRAINING OF 0 UPTAKE (v02). 02 DEBT (020), AND OXYGEN REQUIREMENT (02R UNDER NORMOXIC TEST CONDITIONS BEFORE TRAINING AFTER TRAINING GROUP ml/kg ml/kg P N 215.1 i 12.4 209.2 i 8.3 NS* V02 H 216.3 2 23.5 208.4 2 13.9 NS 0 D N 96.5 t 3.92 92.4 t 0.9 NS 2 H 99.7 i 5.10 94.9 i 1.4 NS 0 N 311.6 i 8.84 301.6 i 2.87 NS 2R H 316.0 2 14.86 303.2 2 7.11 NS N = Normoxic Training Group (N = 4) H = Hypoxic Training Group (N = 4) * Not Significant (P > .10) 34 5 .- 4 '" F——1 3 .- 2 .— 3 -1 - \V V > E ‘2 r -3 .. -4 - -5 .. -6 1- -7 - , ‘9 “ V02 0,0 0,1? Figure 4-1- Result of the gain score comparison of the two groups in oxygen uptake (V0,), oxygen debt (030) and oxygen requirement (02R) under hypoxic test conditions (p> .10) Normoxic Training Group [:1 Hypoxic Training Group 0 \ N N N - 2 h - 3 _. .. 4 .. _ 5 L__ 3' :-6- E _. 7 _ —-—l - a 1- - 9 .- --10 E- -|| h— "2 ‘ vo, 0,0 0,12 Figure 4-2 - Result of the gain score comparison at the two groups in oxygen uptake (V021. oxygen debt (020) and oxygen requirement (0le under normoxic test conditions (p >10) 35 by both types of training. The results of this study are in agreement with data obtained by other investigations using approximately the same procedures (56, 151, 203) and with data obtained at modest altitude (122). When investigations were carried out at varying altitudes and intensities of work load, different results were obtained (29, 48, 202). The intensity of the work load seems to be an important factor in de- termining the V02 at altitude. When the intensity is low, the same or a somewhat increased V02 in comparison to sea level is reported (29, 48, 202). However, it has been observed that a work load which elicits a V02 of 2.5 l/min. or more at sea level can be accomplished with a lower V02 at 3800 m. altitude (29). The comparisons between the gain scores of the two training groups under each test condition are Shown in Figures 4.1 and 4.2. The re- sults indicate that, although the two training regimens altered the V02 in the same direction and to approximately the same extent, perform- ance under the two test conditions produced distinctively different effects on the V02. The phenomenon of a decreased V02 during submaxi- mal exercise under hypoxic test conditions is not new (56, 151, 186, 178, 203). The results might lead one to think that under hypoxia subjects perform more economically and efficiently. However, this hypothesis cannot be accepted without first determining whether or not the subjects reached steady state. Furthermore, both the oxygen debt and the total oxygen requirement of the exercises must be considered. The standard treadmill run used in this study has been Shown to be appropriate for measuring the energy cost of exercise and has been employed by many researchers in the exercise physiology field (207). 36 Therefore, it can be assumed that all subjects did reach steady state during the run. The 020 that is repaid after exercise is divided into two phases or components (11, 150). The lactacid debt or fast component is the amount of oxygen used to resynthesize and restore muscle ATP and CP. This fast component reflects the oxidation delay that occurs at the beginning of exercise. The lactacid debt or slow component reflects the oxidation of the lactic acid that is accumulated during exercise beyond the steady state level. Margaria et al. (148) confirm that the fast component is the only debt present in submaximal moderate ex- ercise. Since submaximal exercise was used in this study and the ac- cumulation of lactic acid was negligible, the alactacid debt was of primary concern. Submaximal normoxic training is known to decrease alactacid debt (110, 111) Since training decreases the time required to reach steady state (110, 111, 122). However, an elevated 020 is always observed during steady state exercise at high altitude (21, 29, 47, 56). The 020 data obtained in this study are given in Tables 4.1 and 4.2 for hypoxic and normoxic test conditions respectively. In general, the results show that the 020 was elevated under hypoxic test conditions and that the value obtained under hypoxic test conditions for the nor- moxic group decreased with training. It is obvious that the lower V02 during exercise under hypoxic test conditions might have been repaid by a higher oxygen uptake dur- ing recovery. In fact, Cerretelli (39) observed that muscle demands an increased amount of oxygen at high altitude; however, this large 37 oxygen demand does not appear during exercise but during the recovery as a large repayment of 020. Furthermore, Astrand (11) suggested that anaerobic processes are incurred at a relatively low work load under hypoxic conditions. Unfortunately, the limitations of this study pre- clude the drawing of any firm conclusions with regard to 020. Transfer of the subjects from the hypoxic gas mixture to room air during the recovery period and not collecting the expired gas during the first minute of the recovery both are factors which may have produced spurious results in the 020 data. The changes in the 02R reflect the changes in VO2 and 020 dis- cussed earlier. Tables 4.1 and 4.2 give the results of the 02R under hypoxic and normoxic test conditions respectively. The decreased 02R under hypoxic test conditions is in agreement with data from previous studies (56, 203). Although definite conclusions are not justified, it is possible that acute exposure to hypoxia reduced oxygen utiliza- tion and increased work efficiency. In addition, Figure 4.2 suggests that the overall effect of training, across both treatment groups, was increased economy of exercise. The lack of Significant differences in the O2 utilization vari- ables between the two training groups under the two test conditions might be the result of the small sample size and/or the short duration of the training period. Support for this hypothesis comes from pre- vious work which suggests a negligible effect for a short period of work at altitude (151). 38 Training Effects Upon Acid-Base Parameters Comparisons between the effects of normoxic and hypoxic training on the changes that were observed during the run in arterialized blood pH, PC02, HCO3, and BE are presented in Tables 4.3 and 4.4 and in Figures 4.3 and 4.4. The only Significant difference (P 5_.10) occurred in PC02 under hypoxic test conditions. Discussion of Arterialized Blood PC02 The normal value of arterialized blood PCO2 fluctuates between 38 and 42 mmHg. This value iS affected by the oxidative processes in the tissues, the blood composition, and the gas exchange rate in the lungs. During mild exercise at sea level, no important changes in PC02 are noticed in either athletes or normal subjects (79, 154). However, with a moderate work load, a slight fall in PC02 is seen until steady state is attained (270). Changes in PC02 with submaximal exercise are Shown in Tables 4.3 through 4.6. The decreases observed between the pre-run and the post- run values are consistent with the literature. The adaptations to the two types of training used in this study, when subjects perform under normoxic test conditions, are Shown in Figure 4.4a. It is obvious from the results that the two submaximal training regimens used in this study did not differentially alter the mechanisms that control PCO2 at sea level. At high altitude, PCO2 has been reported to decrease (76, 106, 107, 130). In lowland subjects who lived one week at an altitude of 3,800 m a decreased PCO2 to 29.2 mmHg was reported (188). Clearly, 39 2:. w A: 28:239.... Aop. A av seeewc_em_a eez a Fm.m+ me.~ - mm. - om.~ e_.e- me.e - o“., mz 00.0- ~.a - om.m - oa.m e.m- o_.R - om._ um mm.m+ oe.~ - o~.e~ om.e~ mm.m- oa.ap mk.m~ m2 ow.o- me.m - me.m_ o~.m~ mm.~- mm.mp om.e~ moo: mpo.o+ mNo.o - mam.“ mme.h meo.o- men.“ m.e.~ «m2 o_o.o+ mmo.o - “we.“ oee.~ meo.o- Nmm.~ mes.“ Ia me.m+ m_._ - oa.am. mo._e mm.e - ma.Nm mu.am @155 .Im moo. - we.op- om.om we._e mo.op- m~.om mu.oe Nova 23m 23¢ a human“ uzsmso 23m 23m eszDD 23m 23m eszquc mezz mmoz: mm oz< .mou: .zn .Noua QOOAm om-¢<~mmhm< 2H mmczI m.v mgm<~ 40 III. A II IIIIIIIIIII IIII I._- I.I- I.I- I.I I.I- I.I- I.I I _\III II I.I- I.I- I.I - I.~ I.N-. I._ - ~.I I II NI.I- NI.I- II..~ II.IN I.I- II.I~ II.I~ I I\III II I II.I- II.I- II.I~ II.IN I.~- I~.I~ II.IN I III III.I- NI. - III.I III.I III.I- III.I III.I I II . III.I- III. - III.I INI.I II.I- II.I III.I I II II.I- II.I- II.II II.II I.m- I.II II.II I III; «mz I- II.I- II.II II.NI II._- I.II II.II I NIII III III I IIIIII IIIIII III III IIIIII III III IIIIIIII IIIIII -IIII -III IIIIII -IIII -III quzH1 mmoz: cmz~F 1E0” 9.5.... ISI BBIV €03.58 36> 05...“. 339.950 .3 .3230: :4 380588 )— II 0.) 59 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. 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 over- shoot 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 mix- ture 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 ob- tain the desired end 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 dr0pped 60 the appropriate amount. Following that step, compressed air was intro- duced 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 end filling pressure was not exceeded. Specific Mixing_Procedures With reference to the apparatus shown in Figure B-l the specific procedures employed were as follows: 1. All valves closed. Oxygen line completely disconnected. 2. Open V1 and read pressure in nitrogen tank on gauge G]. 3. Open V2, V3 and V6 in that order until G1 pressure draps appropriately. 4. Close V2 to check pressure reading. If okay, proceed. Otherwise open and close V2 until desired reading is obtained. 5. Having sufficient nitrogen in mix tank, close V1 and V6' Open V5 to bleed off line pressure completely. Then close V2, V3 and V5. 6. Connect oxygen to SCUBA tank fitting. V7 closed. 7. V10 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 63 and G2 reach desired reading. 9. Close V6 and then V9. lO. Open V7 to bleed line pressure read on G3 and G4. Then close V4. Compressed air supply lead can then be disconnected. 61 11. V4 and V3 closed. Open V6. Then open V5. Obtain sample. Close V5. 12. Close V6. If sample okay, 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. All valves closed. Turn on air compressor. 15. Open V10 to refill compressed air reservoir. 16. Open V9 to read G4 which shows pressure in compressed air reservoir. When full, close V9 and V10. Turn off air compressor. Open V8 and V7 to bleed off line pressure. 17. Close all valves. Table B-1 shows the results of using these procedures while mix- ing the nine tanks of hypoxic air used in the study. End oxygen per- centages and end filling pressures obtained are shown. These may be compared to the goals of 16.60% and 1900 psi. Gas Feed Apparatus The use of compressed gas as a source of inSpired air necessi- tated design and construction of special gas feed apparatus. This ap- paratus was needed to fulfill two functions. Pressure had to be lower- ed to ambient levels in order to avoid forcing air into subjects' lungs. The second function needed was moisturization of the air. The mois- turization was made necessary by the fact that air passing through the compressor was almost completely dried out by a desiccator. The desic- cator had been built into the system to avoid problems which would re- sult from having excess moisture in the SCUBA tanks. 62 TABLE B-1 HYPOXIC AIR MIXING DATA1 . Tank End Filling 2 Mixture No. % 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 1Goal was to obtain 16.60% 02 and an end of filling pressure at 1900 psi. The accuracy required for the oxygen percentage was i 0.2%. 2Pressure readings given were read off of gauges at the end of filling procedures. Pressure capacity of tanks used was approximately 2500 psi. 63 The schematic arrangement and essential components of the gas feed apparatus are shown in Figure B-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 ar- rangements permitted withdrawing gas from either tank. The two gauges indicated in the drawing are both attached to the gas pressure reducing valve. 61 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 permitted 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" 1.0.) through which it was conveyed to a water bath for moisturization and warming. The moisturization and warming were considered necessary to avoid irri- tation of tissues in the respiratory tract. From the water bath the air was passed into a meteorological bal- loon which was used to accomplish final depressurization. The flow rate was controlled such that the balloon was kept flaccid to avoid repres- surization which would be generated in part by the balloon's elasticity. Use of the meteorological 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. mzumgmaam vow» mam we mucmcoqsou meucmmmm new acmswmcmggm orgasmcum .mim «Lamp; mar—.45??? 0mm“. mdo no 241045 UFSzmrom 33> «503.1 9.335 8.5... .3 339.260 M . . - N) 10> .m. s 6 6 .0 N0 80:00 30.31.2832 58 363 33> . ‘ 1...... sec. 32.8 a? 1 V mmZZDm o... APPENDIX C BLOOD SAMPLING Principle It has been shown that arterialized capillary blood very closely approximates arterial blood gas composition. To insure rapid and easy flow of blood, the finger should be warmed (45°C water). The blood must be taken from the middle of rapidly forming blood drops so that the sampled blood does not make contact with atmospheric air. Hepa- rinized capillary tubes must be used to keep the blood from clotting. Procedure 1. The finger was warmed for about two minutes in water (approximately 45°C). 2. The finger was cleaned with alcohol and wiped dry with a sterile gauze pad. 3. The finger was lanced with a long point microlance. 4. The first drop of blood formed was wiped away and then a large pool of blood was allowed to form. 5. The capillary tube was placed in the center of the blood pool and allowed to fill via capillary action insuring that the capillary tube did not take blood from the sur- face of the pool. 65 APPENDIX D CALCULATION OF OXYGEN UPTAKE, OXYGEN DEBT, AND OXYGEN REQUIREMENT VARIABLES Principle The volume of expired gases must be corrected to standard tem- perature pressure dry (STPD) conditions. This can be accomplished using the following STPD correction factor: STPD correction = 76 factor (0.1) where: PB = ambient barometric pressure, PH 0 = the water vapor tension in mm Hg at the 2 temperature of the gasometer, T = the temperature of the gasometer in degrees Centigrade, .0367 = 1 divided by 273 (273 is the conversion factor for convertin temperature in Centigrade to Kelvin). To simplify this computation, a line chart devised by R. C. Darling (Figure D-l) was used. The correction factor is then multiplied by the VE ambient temperature saturated (ATPS) in order to obtain VE (STPD). The volume of oxygen consumed can be found by obtaining the number of ml of oxygen consumed for every 100 ml of expired gas (true 02) and multiplying the true 02 by VE (STPD). Expired gas volume does not equal inspired gas volume unless the respiratory quotient (R0) is 66 67 This figure is an example of a nomogram. >3! 8 ashes—1.4.3 2. may! 03:39.6 w;a.“.«.w..«.w-w.w.m:w.«.m.m.m.m.m.m.m.m.m m... 44464aaqaam«bumpawawwqflmqaammmma«mafiamaquwwawwquflw L FPL.— P EPFLL—l—FFLP—br—PL—LVP—rrrh _p—._rb—b—lP—-EP—P_ _r1_l.1FL LP—Ll—rk—thrhrr—Iprpl—rtrrlf bl ”E .935». m T A). R _..___ d. . .fuium ._.._ . q q u 1 .—.d- 4 +411 1‘11 1 d N—lq l1 . d 4 41‘! <—- al—J J—JJ.il—114A:l 4 14111 (141. a u o. a. u m. a u n u w w a u... aimm&nmw wanmmnwmuneumoe. 63432.. Line chart for determining factors to reduce saturated gas volumes to dry volumes at 0°C and 760 mmHg Figure 0-1. 68 equal to 1.00. The following formula for true 02 corrects for this difference in the inspired and expired gas volume. TRUE 02 = % N2 in expired air X .265 - % O2 in expired air. (D-2) .265 = % O2 in ambient air % N2 in ambient air Where: This computation can be simplified by using the line chart (Figure D-2) by Di11. Procedure 1. An STPD correction factor was obtained for each gas collection bag using the line chart in Figure D-l. 2. The STPD correction factor was multiplied by the total gas volume for the appropriate gas collection bag. 3. True 02 and R0 were obtained from the line chart in Figure 0-2. 4. True 02 was multiplied by corrected VE (STPD) and divided by 100 to get the volume of O2 consumed in each gas collection bag. 5. Oxygen intake during exercise was obtained from the sum of gas volume bags collected during five minutes of exercise. 6. Oxygen debt was obtained by the sum of oxygen intake values for all of the recovery bags in the last 14 of the 15 minutes recovery. 7. Oxygen requirement was obtained from the sum of oxygen intake during exercise and during recovery. Figure D-2. 69 .61 2 0 1- 0.00 00 00 40 v—v—v'vvv 1' fi' fl ‘ 20 v' 6.00 00 00 7 7*11 V~Tw yaw: v 4.0 20 £00 00 00..“ ”I“! "71m. ‘ . 'er'v vv'fi'v'VVVY 60 40 20 3.00 vv'vvv'w—vw'v-v 'vv 00 r'vv'wvv-v" 20 00 WWWY'vwv'V Line chart for calculation R0 and analyses of expired air 00 00 2.00 .611 60" 40" 20" 1 ' I. 8 O 00'- oo- 20- 80*- 60‘- 40 “HI. ”Ill-MI. ‘ 20 V‘UVV. TV 20 " 4:15.00 00 001- true oxygen from REFERENCES 10. 11. 12. REFERENCES Adams, W. C., E. M. Bernauer, D. B. Dill and J. B. Bomar, Jr. "Effects of Equivalent Sea Level and Altitude Training on VOzmax and Running Performance." J. Appl. Physiol., 38:262, 1975. Alexander, J. K., R. F. Grover and L. H. Hartley. "Reduction of Cardiac Output in Man at High Altitude." Clin. Res., 14:121. 1966. 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