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(914.....-.....v...ln..fi.zl .59.; u... 12:.-- . . . .. ....rl... . ,. ...”...mm ...... .. _ .... . ..lit.ct......r!nv.z..lz££5...u~mwmu. 5.1.3171. .Iihliti itk‘;.¢§.i... . aflxuwfi...hrn.Nb.... 1............:. , ...h...........rr., >412: i . a s ... ....z.......-..........E..;., . ‘II l.‘ . ($.- ‘II. .LI 4' . .. 1f...........nn..r...........uu..5. ...... , ......n...!.....: . 4.-.... . Ill]”I!!!MIWHIHIIMMIJI”MIMI! JIBRARY iii-£35.57: igvan State University This is to certify that the thesis entitled THE EFFECTS OF SELECTED SODIUM BICARBONATE SUPPLEMENTATION AND DIETARY REGIMENS UPON ACID-BASE STATUS AND PERFORMANCE CAPACITY DURING HEAVY INTERMITTENT MULTI-STAGE WORK presented by Asghar Khaledan has been accepted towards fulfillment of the requirements for Ph.D. degnwin Physical Education W Major professor [Mew 0-7 539 OVERDUE FINES ARE 25¢ PER DAY PER ITEM Return to book drop to remove this checkout from your record. THE EFFECTS OF SELECTED SODIUM BICARBONATE SUPPLEMENTATION AND DIETARY REGIMENS UPON ACID-BASE STATUS AND PERFORMANCE CAPACITY DURING HEAVY INTERMITTENT MULTI~STAGE WORK By Asghar Khaledan A DISSERTATION 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 1979 ABSTRACT THE EFFECTS OF SELECTED SODIUM BICARBONATE SUPPLEMENTATION AND DIETARY REGIMENS UPON ACID-BASE STATUS AND PERFORMANCE CAPACITY DURING HEAVY INTERMITTENT MULTI-STAGE NORK BY Asghar Khaledan The purpose of this study was to determine the effects of the ingestion of NaHCO3 (.065 gm/kg) under high CH0 and fat-protein dietary conditions upon acid-base balance and performance time in trained long distance runners during an intermittent multi—stage treadmill run to exhaustion. Eight healthy male distance runners 20-40 years of age were volunteer subjects in this study. The subjects were stress tested, informed of the aim of the study and randomly assigned to four different conditions. The conditions, measured in four successive weeks, included: (a) NaHCO plus CHO 3 (SC), (b) NaHCO3 plus fat-protein (SFP), (c) placebo plus CHO (PC), and (d) placebo plus fat—protein (PFP). Each condition was preceded by three days of the relevant dietary regimen. Each subject received a list of standard American foods con- tained in the high carbohydrate or high fat—protein diets. Prior to each test a dietary recall was conducted to determine the percentage of carbohydrate, fat and protein that were consumed. Two hours before the exercise test the supplement was taken orally. Asghar Khaledan The exercise consisted of six different levels with speeds "of 6, 7, 8, 9, TO and 10 mph and 5, 6, 7, 8, 9 and l2% grade, respec- tively. Each level consisted of 3 minutes of exercise followed by 3 minutes of rest. On each test the subject ran to exhaustion. Recovery was standardized at 15 minutes. Heart rate, respiratory rate, and energy metabolism measurements (Douglas bag method) were measured throughout the work and rest intervals and the recovery period. Blood gases (Astrup method), various acid-base parameters, and blood lactic acid (Enzymatic method)‘were obtained from blood samples taken pre-work, following each work load, and at 5, l0 and 15 minutes of recovery. The maximum time the subject could continue to work was recorded. Data were analyzed using a repeated measures ANOVA and the Sign test was used in instances where there were continuous curvilinear measures. No statistically significant differences were observed in performance time, V02 max, gross 02 debt or oxygen uptake among the four treatment conditions. Ventilation values were highest under the fat-protein condition. Significant bicarbonate effects were observed in the pre-run pH values (P = .09) and in the differences between the pH values at the end of exercise and at five minutes of recovery (ALS-Rl, P = .03). The pH values were consistently higher following NaHCO3 supplementation under both dietary conditions (P = .Ol). With supplementation of NaHC03, the PC02 values were significantly lower under both dietary treatments. The P02 measure- ments were consistently higher under the CHO (P = .002) and SC condi- tions (P = .002). The HCOQ and base excess values showed a supple- ment effect from the termination of exercise to the first five Asghar Khaledan minutes of recovery (ALB-RT) (P = .07 and .Ol). HCO3 and base excess values were lower under the CHO dietary condition (P = .02 and P = .09). Only the supplement differences in lactate between levels 5 and 15 minutes of recovery (ALS-R3) were significant (P = .09). the lactate differenCes were highest following bicarbonate supple- mentation. The following conclusions were drawn: l. The oral ingestion of sodium bicarbonate, in the dosage of .065 gms/kg of body weight, alters the acid-base status of the blood of trained distance runners toward greater alkalinity. 2. In the absence of supplementary sodium bicarbonate intake, a high carbohydrate diet changes the acid-base status of the blood of the trained distance runners toward greater alkalinity. 3. The oral ingestion of sodium bicarbonate two hours before work does not significantly increase the maximum performance time of trained distance runners. 4. A high carbohydrate diet does not significantly increase the maximum performance time of trained distance runners. 5. The effects of sodium bicarbonate supplementation and a high carbohydrate diet are not synergestic in trained distance runners. 6. There are no significant improvements in maximum oxygen intake or oxygen debt following either NaHCO3 or carbohydrate diet treatments, and there are no interactions between the two treatments. DEDICATION To my wife, Farideh; my lovely children, Fariba and Farzad; my mother; and to the memory of my father. 11' ACKNOWLEDGMENTS I wish to express my sincere appreciation to Dr. Wayne 0. Van Huss, my academic advisor, and Dr. William Heusner, for their invaluable guidance and advice during my graduate program and throughout the course of this study. I wish also to thank Dr. Robert Pittman and Dr. Peggy Reithmiller for their contribution on the guidance committee. Special thanks are due to Dr. Kwok-Wai Ho for suggestions during the preparation of this dissertation. Thanks are also extended to Dr. Gary Hunter for his guidance during the pilot study. The author is especially grateful to Shokr Fallah Bosjin, Ali Motaghi, Peter Rodin and Dwight Gaal for their constant assistance during data collection. Acknowledgment is also made of the encouragement and assistance rendered by David Anderson and other members of the staff of the Human Energy Research Laboratory at Michigan State University. TABLE OF CONTENTS Page LIST OF TABLES . . . . . . . . . . . . . . . . vii LIST OF FIGURES . . . . . . . . . . . . . . . . ix LIST OF APPENDICES . . . . . . . . . . . . . . . xi Chapter I. THE PROBLEM . l Statement of the Problem 6 Significance of the Study 6 Research Hypotheses 7 Limitations . 7 Definitions 8 Acidosis . . 8 Alactacid Oxygen Debt . 8 Alkaline Reserve 8 Alkalosis . 8 Base Excess (BE) . 8 Bicarbonate— Carbon Dioxide System (HCO3/CO2 ) 9 Buffer . . 9 Buffer Base . 9 Carbonic AnhydraSe . . 9 Glycogen Super Compensation . . . . . . . . 9 Gross Oxygen Debt . . . . . . . . . . . . l0 Intermittent Work . . . . . . . . . . . . l0 Lactacid Oxygen Debt . . . . . . . . . . . l0 Lactate . . . . . . . . . . . l0 Maximum Oxygen Uptake (V0 max) . . . . . . . l0 PC 2 l0 Performance Time . : : : Z : Z : : : : I TO PFK. . . . . . . . . . . . . . . . . l0 PFP . . . . . . . . . . . . . . . . TO Phosphagen (PG) . . ._ . . . . . . . . . . ll Plasma Bicarbonate (HCO3) . . . . . . . . . ll SC . . . . . . . . . . . . . . . . . ll SFP. . . . . . . . . . . . . . . . ll Total CO2 (TCOZ) . . . . . . . . . . . . ll iv Chapter Page II. REVIEW OF RELATED LITERATURE . . . . . . . . . 12 (a) Anaerobic Energy Metabolism . . . . . . . . 12 (b) Aerobic Energy Metabolism . . . . . . . . 16 (c) Energy Metabolism During Recovery . . . . 19 (d) Limiting Factors in Anaerobic and Aerobic Work . 20 (e) Measurement of Aerobic and Anaerobic Capacity . . 22 (f) Acid-Base Balance and Anaerobic Metabolism . . . 28 (g) Acid-Base Balance and Aerobic Metabolism . . . 31 (h) Acid-Base Balance and Performance . . . . . . 33 (i) Effects of Diet on Muscular Performance . . . . 35 (j) Effects of Diet on Acid-Base Balance . . . . . 36 III. RESEARCH METHODS . . . . . . . . . . . . . 39 Experimental Design . . . . . . . . . . . . 39 Subjects . . . . . . . . . . . . . . . . 41 Exercise Test . . . . . . . . . . . . . . 41 Measurement Procedure . . . . . . . . . . . 44 Respiratory Frequency . . . . . . . . . . . 44 Heart Rate . . . . . . . . . . . . . . 45 Blood Sampling . . . . . . . . . . . . . 45 Lactate Analysis . . . . . . . . . . . . 47 Acid-Base Parameters . . . . . . . . . . 47 Energy Metabolism Measures . . . . . . . . . 48 Dietary Measures . . . . . . . . . . . . 49 Test Protocol . . . . . . . . . . . . . 51 Statistical Analysis . . . . . . . . . . . . 53 IV. RESULTS AND DISCUSSION . . . . . . . . . . . 54 (a) Performance Time . -. . . . . . . . . . 54 (b) Maximum Oxygen Uptake (V02 max) . . . . . . 54 (c) Gross Oxygen Debt . . . . . . . . . 57 (d) Oxygen Uptake (V 02). . . . . . . . . . . 57 (e) Ventilation (VE) . . . . . . . . . . 57 (f) Heart Rate . . . . . . . . . . . . . 62 (9) Respiratory Rate . . . . . . . . . . . 62 (h) Respiratory Quotient . . . . . . . . . . 67 (i) pH . . . . . . . . . . . . . . . 67 (j) PCO2 . . . . . . . . . . . . . . . 73 (k) P02. . . . . . . . . . . . . . . 73 (1) Total C02. . . . . . . . . . . . . . 80 (m) Bicarbonate . . . . . . . . . . . . . 84 (n) Base Excess . . . . . . . . . . . . . 88 (o) Lactic Acid . . . . . . . . . . . . . 88 Discussion . . . . . . . . . . . . . . . 96 Chapter Page V. SUMMARY, CONCLUSIONS, AND RECOMMENDATIONS . . . . . 103 Summary . . . . . . . . . . . . . . . . 103 Conclusions . . . . . . . . . . . . . . . 107 Recommendations . . . . . . . . . . . . . 107 APPENDICES . . . . . . . . . . . . . . . . . 108 REFERENCES . . . . . . . . . . . . . . . . . 150 vi Table 2.1 :bPfi-b-P-h-b 03 LIST OF TABLES Relative Contribution of Anaerobic and Aerobic Energy Metabolism to Total Energy Output During Maximal Exercise of Different Durations . Previous Studies: Effects of Alkalyzer upon Performance and Related Physiological Parameters . Supplement and Diet Conditions Treatment Conditions . Test Sequence of Latin Square Design Characteristics of Subjects and Their Responses to the Stress Test . . . . . . . . . . Speed, Grade, Work and Rest Intervals in the Multi- Stage Intermittent Treadmill Test . Mean, Standard Deviation and Percentage of Carbohydrate and Fat-Protein Dietary Conditions Statistical Results, Performance Time (secs) V02 max (ml/kg) and Gross Oxygen Debt (liter) . Statistical Results, Oxygen Uptake (liter, min) . Statistical Results, Ventilation (liter) Statistical Results, Heart Rate (min) Statistical Results, Respiratory Rate (min) Statistical Results, Respiratory Quotient (RQ) Statistical Results, pH . Statistical Results, PCO2 (mmHg) . Statistical Results, PO2 (mmHg) vii Page 25 29 39 4O 4O 42 43 50 56 59 61 64 66 69 72 76 79 Table 4>J> ‘T'l 'T13>J>3>-i>-i> 'fi‘f'l 13 14 Statistical Results, TCO2 (mM01/L Plasma) Statistical Results, Bicarbonate (mEq/L Plasma) Statistical Results, Base Excess (mEq/L Blood or Plasma . . . . . . . . . . . Statistical Results, Lactate (mMol/L) Changes and Statistical Results of Blood Parameters . High Carbohydrate Diet High Fat—Protein Diet . Summary of Food Intake of an Individual Subject Performance Time (secs), VO2 max (ml/kg) and Gross Oxygen Debt (liter) . . . . . . . . . . Basic Data, Oxygen Uptake (V02) (l/min) . Basic Data Ventilation (VE)(liter per minute) (STPD) . . . . . . . . . . . . Basic Data, Heart Rate (HR) (per minute) Basic Data, Respiratory Rate (RR) (per minute) Basic Data, Respiratory Quotient (RQ) Basic Data, pH Basic Data, PCO2 (mmHg) Basic Data, P02 (mmHg) Basic Data, TCO (mMoL/L plasma) 2 Basic Data, Bicarbonate (HC03)(mEq/L plasma) Basic Data, Base Excess (mEq/L Blood) Basic Data, Lactate (mMol/L) viii Page 83 87 91 94 95 110 111 112 132 133 135 137 139 141 143 144 145 146 147 148 149 Figure 2.1 .10 .11 .12 .13 .14 h-D-h-b-b-b-b-b-b-b-b-bbb £0 .15 LIST OF FIGURES Schematic Representation of the Various Energy Sources for Muscular Work . . . . Glycolytic Pathway Cytric Acid Cycles and Electron Transport Pathways . Single Bipolar V5 Electrocardiograph Configuration . Results: (a) Performance Time, (b) Maximum Oxygen Uptake, (c) Gross Oxygen Debt . . . Diet and Supplement Effect on Oxygen Uptake Diet and Supplement Effect on Ventilation . Diet and Supplement Effect on Heart Rate Diet and Supplement Effect on Respiratory Rate Diet and Supplement Effect on Respiratory Quotient . Diet and Supplement Effect on pH . pH Changes under Different Conditions Diet and Supplement Effect on PCO2 PCO2 Changes under Different Conditions Diet and Supplement Effect on P02 P02 Changes under Different Conditions . Diet and Supplement Effect on TCO2 TCOZ Changes under Different Conditions Diet and Supplement Effect on Bicarbonate . ix Page 13 15 17 46 55 58 6O 63 65 68 7O 71 74 75 77 78 81 82 85 Figure Page 4.16 HCOé Changes under Different Conditions . . . . . 86 4.17 Diet and Supplement Effect on Base Excess . . . . 89 4.18 Base Excess Changes under Different Conditions . . 90 4.19 Diet and Supplement Effect on Lactate . . . . . 92 4.20 Lactate Changes under Different Conditions . . . . 93 8.1 Effect of Oral NaHCO3 Ingestion on Arterial Blood pH and Base Excess . . . . . . . . . . . 115 8.2. Effect of Two Doses of NaHCO3 on Arterial Blood pH and Base Excess . . . . . . 116 0.1 Siggaard-Andersen Alignment Nomogram . . . . . . 123 LIST OF APPENDICES Appendix A. Diets 8. Timing of Supplementation C. Exercise Stress Test D. Blood Measures Blood Sampling Acid-Base Measures . Lactate Determinations . E. Energy Metabolism Determinations F. Basic Data xi Page 109 113 117 120 121 122 124 127 131 CHAPTER I THE PROBLEM Methods of increasing an athlete's performance have long been of research interest. Maximum performance involves intricate and complex adjustments of the body systems. Biomechanics, psychological factors and physiological adaptations are all involved. Since the entire Spectrum of performance-related factors is too broad for in- depth study, it is necessary to narrow the scope. In the present study, emphasis has been placed upon the effects of manipulation of acid-base status Upon performance. Changes in blood gases, acid-base balance, and lactic acid level during exercise and recovery have been studied extensively since the classic work of Hill et al, (118), Margaria et_al, (190), and Fletcher and Hopkins (84). The accumulation of blood lactate has been considered to be an indication of anaerobic metabolism during muscular effort with a high level being associated with exhaustion (94, 104, 155). This interpretation is not applicable to continued low-intensity work in which other factors, such as depletion of energy stores, are more closely related to the end point of exercise (12, 14, 26, 49, 95, 121, 136, 229, 231). The highest levels of lactic acid are found in young individuals who are highly trained for high intensity work of durations between one and five minutes (261). Hill gt_al, (118) and Margaria gt_al, (190) demonstrated that there is a positive correla- tion between the blood lactate level and the amount of O2 debt at the end of exercise. The higher the blood lactate at the end of work, in general, the higher the oxygen debt in the same individual (115, 190). Between individuals, however, this correlation is not high. Since it has long been observed that there may be little lactate in the blood with four- to six-liter oxygen debts (15, 189), the debt was divided by Margaria into alactacid and lactacid components (189, 190). The blood lactate level is dependent on the rate of lactic acid formation in the working muscles, the rate of its intracellular reconversion to glucose, the rate of its diffusion into the blood and adjacent tissues (255), the rate of its utilization by skeletal and cardiac muscle (39, 149, 150, 174, 176), and the rate of its removal by the liver (21, 66, 222). The intracellular pro— duction of lactic acid is related to the intensity and duration of muscular work (69, 109, 206). During anaerobic work, in which glycogen is metabolized, lactic acid is the end product. Since the pK of lactic acid is 3.86, it dissociates into lactic and H+ rapidly, resulting in the accumulation of the H+ ions. The accumulation of H+ ions will cause the tissue pH to fall (106, 115). An almost direct linear relationship has been shown between the blood pH and muscle pH (155, 206). Intra-muscular pH has been proposed as the main limiting factor in anaerobic exercise (70, 87, 113, 117, 207). This low pH alters both the intracellular and blood acid—base status which may affect a series of biochemical reactions (3, 4, 54, 87, 99, 113, 213, 227, 269). Katz (163) suggested that defects in cardiac contractility and the occurrence of myocardial ischemia may result from intracellular H+ accumulation. It is believed that elevated H+ concentrations reduce the binding capacity of Ca++ to troponin and therefore inhibit acto- myosin formation in muscular contraction (87, 233). Also, the activity of phosphofructokinase (PFK), one of the regulatory enzymes in the glycolytic pathway (64, 101, 178, 180, 256, 260), is inhibited by high concentrations of ATP (180, 208, 256), citrate, isocitrate (180, 208, 216) and by a low pH (64, 116, 185, 260, 262). It has been reported that lactate concentrations up to 32 mM/l will cause severe metabolic acidosis in the blood as indicated by a low blood pH of 6.80 and a low plasma bicarbonate concentration of 2.6 mEq/l (54, 206, 269). The H+ ion can be buffered by the HCOé ion to form carbonic acid which then dissociates into carbon dioxide and water. There are other buffers, including hemoglobin and phosphate, in addition to bicarbonate. The linear relationship between the plasma bicarbonate level and the buffering capacity of the body indicates that the blood base excess (BE) is a good estima- tion of the total body buffering capacity (32, 94, 206, 267). Since the increased H+ ions associated with lactate can be buffered by bicarbonate, it is reasonable to hypothesize that ingestion of alkalyzing agents such as sodium bicarbonate could result in increased buffering capacity and, therefore, enhanced performance. The effect of the ingestion of alkalyzing agents has been the subject of numerous studies. The results are controversial. Some show enhanced performance (71, 72, 147, 148, 245, 257), others no change (145, 162, 187). There also is evidence of negative effects (67). Supplementation with different doses of bicarbonate to increase the alkaline reserve has been used during heavy work (l8, 19, 71, 72, 137, 147, 148, 245, 257). Dennig §t_al, (72) claimed that 02 debt is lower for standard work under alkalotic conditions induced by ingestion of bicarbonate. A statistically nonsignificant (about 23 percent) but directional increase in total work output was observed by increasing bicarbonate to .13 gm/kg body weight and the base excess to 4.1 mEq/l before the start of high intensity anaerobic work (18, 19). These studies suggested that anaerobic glycolysis and performance might be facilitated by a Slightly alkalotic extracellular medium in the body. In fact, under con- trolled conditions, the conversion of glucose to lactate is enhanced in a relative alkaline state (18, 19). Transformation of inactive phosphorylase b to active phosphorylase a may be facilitated by an increase of cellular pH (56). By giving oral doses of sodium bicarbonate or ammonium chloride, Jones gt_al, (147) and Sutton et_al, (257) produced either alkalotic or acidotic conditions in their subjects before work on a cycle ergometer. They found that the acidotic subjects had low venous blood lactate levels and short performance times while the alkalotic subjects had high venous blood lactate concentrations and long performance times. Muscle biopsy samples taken at rest and at 70% of V0 max also were obtained by these investigators to assess 2 the effects of intracellular pH on lactate production in the muscle cells and lactate transportation into the extracellular fluid. Since the lactate changes in muscle and blood were parallel, they hypothesized that decreases in intracellular pH may reduce lactate production in the muscles as a result of the inhibition of anaerobic glycolysis at the level of glycogen phosphorylase. The ventilatory response to simultaneous hypercapnia and moderate to severe hypoxia exceeds the sum of the responses to each stimulus applied alone (82). This interaction of hypoxic and hypercapnic stimulation was absent following both CO2 exposure and bicarbonate ingestion. An increase of buffering capacity under metabolic alkalosis is believed to be the reason. Furthermore, intravenous infusion of sodium bicarbonate stimulates ventilation in spite of a fall in interstitial H+ concentration (195). The early experiments of Christensen and Hansen (50) and Krogh and Lindhard (177) showed endurance performance capacity to be significantly greater when the subjects ate a high carbohydrate diet. As a result of the original work of Bergstrom and Hultman (27), it is believed that loading the body with carbohydrate for some days before strenuous exercise results in an accumulation of muscle glycogen which is of real benefit to the endurance athlete (112, 134, 164, 231). However, in addition to glycogen super-compensation following "carbo- hydrate loading” there is evidence of myoglobinuria (22, 237), heaviness and stiffness in the muscle (27), angina-like pain, and electrocardiographic abnormalities in the hearts of marathon runners (193). Recently the diet has been Shown to be related to acid-base levels with higher pH, bicarbonate, base excess and lactate values under high-carbohydrate dietary conditions (26, 28, 29, 30, 112, 133, 134, 137, 192). Preliminary data for the present study has also shown that performance time may be increased using bicarbonate sup- plementation with no change in a timed recovery. The differences in results observed may be due to the type of subjects studied (i.e., trained vs. untrained), the type of fitness the subjects possess (i.e., power or endurance), and the type of diet the subjects are eat- ing. The present study was designed to control for training level and type of fitness as diet and bicarbonate ingestion are manipulated. Statement of the Problem The purpose of this investigation was to determine the effects of oral ingestion of sodium bicarbonate (.065 gm/kg) under different dietary conditions (carbohydrate and fat-protein) upon acid-base equilibrium and performance time in healthy, fit, long- distance runners during an intensive intermittent multi-stage treadmill run to exhaustion. Significance of the Study This investigation is the initial effort in which diet and bicarbonate ingestion have been manipulated in endurance athletes. The resulting data are unique. The significance of the study rests in obtaining new information regarding diet-related alterations in performance and acid-base parameters in a carefully described study population. Research Hypotheses 1. The oral ingestion of sodium bicarbonate in the dosage of 0.065 gms/kg body weight will alter the acid-base status of the blood toward greater alkalinity. 2. The ingestion of a high carbohydrate diet will alter the acid-base status of the blood toward greater alkalinity. 3. The ingestion of sodium bicarbonate two hours before work will increase maximum performance time. 4. The ingestion of a high carbohydrate diet will increase maximum performance time. 5. The effects of sodium bicarbonate supplementation and a high carbohydrate diet will be synergistic. 6. Enhanced performance times will be achieved with little or no differences in the maximum oxygen intake or oxygen debt. Limitations 1. It was not possible to supervise the supplement and diet programs of the subjects. Reliance was placed on the word of the subjects. 2. The results of this study can be applied only to male long-distance and marathon runners, between 20 and 40 years of age, under similar supplement and diet conditions. 3. There is no way to know with certainty that each subject ran to exhaustion on each run. Definitions Acidosis. The condition in which excess H+ is present in the body. An increase in H+ concentration decreases the pH of the blood, which in turn tends to deplete the body's alkali reserve and alters the acid-base balance. Alactacid Oxygen Debt. That portion of the recovery oxygen used to resynthesize and restore phosphagen (ATP + CP) in muscle following exercise. Alkaline Reserve. The amount of alkalizing salts and protein buffers that are available in the body for buffering H+ ions. Alkalosis. The condition in which the concentration of H+ is reduced in the body. The decrease in H+ increases the pH and alters the acid-base balance. Base Excess (BE). The titratable base minus the titratable acid, when titrating the extracellular fluid (ch = blood plus interstitial fluid) to an arterial blood plasma pH of 7.40 at a PCO2 of 40 mg Hg at 370 C. It is expressed in terms of :_meq/L, indicating the accumulation of non-volatile acid or base in the blood (17). Bicarbonate-carbon Dioxide System (HCOg/COO), Bicarbonate is the most important buffer in the blood. It acts as a buffer to decrease H+ via the following reaction: + H +HC0'F’HC0PC0 +H 3 23 2 20 Only a very snmll amownzof combined H+ + HCOé remains as H2C03. Most of the H2C03 is converted to CO2 and water at equilibrium. Increased lung ventilation removes carbon dioxide and causes the reaction to move to the right. This allows increased amounts of hydrogen ion to be excreted. Decreased lung ventilation does the reverse. Carbon dioxide is elevated causing an indirect increase in hydrogen ion concentration. Buffer. A chemical substance which, when present in a solution, causes resistance to pH change. In blood, buffers consist of weak acids and their conjugate bases (180, 256). Buffer Base. The cation equivalent of the sum total of buffer anions. It is expressed in terms of meq/L of whole blood (17). Carbonic Anhydrase. The enzyme that speeds up the reaction of carbon dioxide (C02) with water (H O) to produce HCO3. 2 Glycogen Super Compensation. Above normal deposition of glycogen in muscle following exhaustive work and a high carbohydrate intake. 10 Gross Oxygen Debt. The total amount of oxygen utilized during recovery from work. For practical purposes constant timed recovery periods are frequently used. Intermittent Work. In the present study this is the tread— mill exercise of varied workloads carried out with alternate work and rest intervals of three-minutes duration. Lactacid Oxygen Debt. That portion of the recovery oxygen used to remove accumulated lactic acid from the blood following exercise. Lactate. The salt of lactic acid (CH3CHOHCOOH). Maximum Oxygengyptake (V02 max). The maximal rate at which oxygen can be consumed per minute, or maximal aerobic power. PC, The experimental condition in which a placebo (dextrose) was ingested following a high carbohydrate diet. Performance Time. The total period of time, in seconds, which each individual performed on the treadmill. The subjects were expected to run to exhaustion under each condition. .355. Phosphofructokinase, the rate-limiting allosteric enzyme which catalyzes the reaction between fructose 6-phosphate and fructose 1,6-diphosphate in the glycolytic pathway. .353. The experimental condition in which a placebo (dextrose) was ingested following a high fat-protein diet. 11 Phosphagen (PG). Collectively refers to adenosine tri- phosphate (ATP) and creatin phosphate (CP) (186). _Pi. Inorganic phosphate. Plasma Bicarbonate (H003). The bicarbonate ion concentra- tion in the plasma of fully oxgenated whole blood which has been equilibrated to a PCO2 of 40 mm Hg at 37°C (17). SC. The experimental condition in which sodium bicarbonate (NaHCO3) was ingested following a high carbohydrate diet. SFP. The experimental condition in which sodium bicarbonate (NaHCO3) was ingested following a high fat-protein diet. Total CO2 (TCOZ). The sum of actual bicarbonate plus carbonic acid. Since the latter is equal to 0.03 x PCO2 (where 0.03 is a constant which relates the partial pressure of CO to 2 the sum of dissolved CO2 and H2C03 in plasma), total CO2 = (HCOE) + (0.03 x PCOZ) expressed in terms of mM/L of plasma (l7). CHAPTER II REVIEW OF RELATED LITERATURE The related literature pertinent to this investigation has been categorized in ten sections: (a) anaerobic energy metabolism, (b) aerobic energy metabolism, (c) energy metabolism during recovery, (d) limiting factors in anaerobic and aerobic work, (e) measurement of aerobic and anaerobic capacity, (f) acid-base balance and anaerobic metabolism, (9) acid-base balance and aerobic metabolism, (h) acid-base balance and performance, (i) effects of diet on muscular performance, and (j) effects of diet on acid-base balance. (a) Anaerobic Energy Metabolism The contraction of skeletal muscle represents the trans- formation of chemically-bound energy to mechanical energy. That is, body movement is dependent upon the breakdown of adenosine tri- phosphate (ATP). For muscular contraction to continue for more than a few seconds, the level of ATP in the muscle must continually be replenished via the anaerobic and/or aerobic pathways (Figure 2.1). The immediate source of energy for muscular work is provided by the splitting of high-energy phosphate bonds--adenosine tri- phosphate (ATP) and creatinephosphate (CP) or, in general, high- energy phosphate (Figure 2.1a and b). Collectively, ATP and CP are 12 13 (ATPose) w?“ A. ATP ADP+Pin+En -, (CPK) // 8. CP C + Pin + En oxid. \\\ C. Food + 02 002 + H20 + En phosph. onoen D. Glycogen LA + En (or glucose) . glycolysus Figure 2.1. Schematic representation of the various energy sources for muscular work. A, B, C and 0 correspond to the different reactions as indicated in the modified Lohman scheme (44). called phOSphagen (PG) (186). These primary energy-rich compounds are found in varying concentrations in all living cells, particu— larly in muscle cells. The average concentrations of ATP and CP in human skeletal muscle are about 4 and 16 moles Kg'1 of wet muscle, respectively (135, 156, 159, 175). Although the total amount of muscular stores of PG is negligible--only about 0.3 moles in females and 0.6 moles in males (85), when PG is broken down (i.e., when the phosphate group is removed) a large amount of energy is produced. At rest the ATP concentration is at its highest, but with the initiation of contraction ATP is split to form ADP and Pi. Since 14 there are limited amounts of ATP in the muscle cells, its supply would be exhausted after a few contractions, and longer work would be impossible, if ATP was not resynthesized continuously at nearly the same rate that it is split. Several investigators have reported a linear relationship between work intensity and the reduction in muscular PG. They showed that PG is approximately 80% depleted after working at 75% of V0 max with only a slight additional decline 2 occurring at the highest work load. Karlsson and Saltin (159) reported that oxygen deficit is closely related to the PG depletion. In muscular work lasting longer than a few seconds at an intensity higher than 80% of V0 max, ATP is resynthesized via 2 anaerobic glycolysis, the end product of which is lactic acid (44, 94, 108) (Figures 2.1d and 2.2). This mechanism can adequately maintain the ATP and CP levels in the working muscles for several minutes during heavy exercise. The rate and magnitude of degredation of muscle glycogen for anaerobic metabolism are governed by the intensity of exercise (94). During heavy exercise, when the work load is higher than 100% of V0 max, glycogen depletion takes place rapidly and the muscle 2 lactate levels may be high. Under these conditions the degradation of glycogen represents a significant source of energy for muscular activity. However, exercise of this intensity produces exhaustion before the glycogen stores of the muscles are completely depleted. Factors other than the glycogen supplies of Umamuscle appear to limit work capacity at these intensities (94). l5 Glycogen Phosphorylase l Glucose Hexok inose ATP ADP Glucose G-phosphate ll Fructose G-phosphate ATP Phosphofructo- kinose ADP Fructose I,6-diphosphate C 1 Dihydroxyacetone L ~ Glyceroldehyde phosphate 3-phosphate Glyceroldehyde 1K NAD+ + Pi 3- phosphate dehydrogenase NADH ... Ht 1,3-Diphosphoglycerate l < ADP ATP 3- Phosphoglycerote 2- Phosphoglycerate 1F Phosphoenolpyruvate Pyruvate ADP kinase ATP Acet I COX *—-— Pyruvate Lactate NADHZ Dehydrogenase NAD Lactate Figure 2.2. Glycolytic Pathway. 16 The importance of the liver in the removal of lactate during work has been postulated by several investigators (21, 66, 222). According to Rowell et_gl, (223, 224, 225) approximately 50% of the total amount of lactate eliminated is metabolized by the liver during exercise. Furthermore, it has been shown that skeletal muscle fibers have Uracapacity to metabolize lactate during the course of muscular work (114, 139, 149). A negligible amount of lactate also is eliminated in sweat and urine (174) or is metabolized by the myocardium and resting skeletal muscles (39, 150), as well as by other tissues (174, 176, 255). (b) Aerobic Energy Metabolism At relatively low work intensities (less than 70% of V02 max) energy needs for the regeneration of ATP and CP may be provided by oxidative metabolism via the tricarboxylic acid or Krebs cycle (Figures 2.1c and 2.3). The longer the exercise duration, the more oxidative phosphorylation reactions are utilized to meet energy demands and the less anaerobic glycolysis is involved (77, 164). The most important substrates for aerobic energy production are carbohydrates and the fatty acids, including their intermediate degradation products such as pyruvate and ketone bodies. To a lesser extent, amino acids also can be oxidized. The relative contribution of these substrates to the total energy-delivery is dependent upon the intensity, duration and type of exercise as well as upon the diet and the conditioning of the subjects (15, 26, l65,l66,167,l69). The efficiency of these processes is relatively high. For example, Mobilization of acetyl -CoA The tricarboxylic acid cycle Electron transport and oxidative phosphorylation 17 Amino Fatty acids Glucose acids Pyruvate 2H C02 Acetyl - CoA Citrate Oxaloacetate (cis - Aconitate) Malate lsocitrate F marate U C02 a - Ketoglutarate l Succinate Succinyl - CoA \- C02 NAD+ Flavoprotein ADP + P,- Coenzyme Q C— “1's: Cytochrome b ADP + Pi Cytochrome C C— “no ADP + P,- Cytochrome 03 C- l A—P 2H++ go A H20 Figure 2-3. Cytric Acid Cycles and Electron Transport Pathways. 18 glucose can generate approximately 13 times more ATP per gram mole aerobically than anaerobically (180, 256). In submaximal exercise, if the rate of ATP formation via oxidative phosphorylation is sufficient to cope with the amount of ATP and CP split, the indi- vidual will reach a so-called "steady state" in which the 02 uptake and the O2 requirement are equal. The application of a training program can alter the indi- vidual's oxygen uptake and modify the energy turnover (164). Usually, the oxygen consumption is slightly lower at the same absolute work level following training (80, 146). In both animal and human studies, it has been shown that the quantity and activity of aerobic enzymes are increased after endurance training (20, 23, 94, 125, 197, 263). A good correlation has been found between the aerobic function of a muscle and its content of mitochondria (20, 88, 125, 126, 142, 179, 197, 199, 205). An increase in the number of mitochondria in skeletal muscle is associated with an increase in the ability of the muscle to generate ATP (124, 125). Within the same individual, the most active muscles have the highest respiratory capacity (125, 142, 179). Endurance training has been shown to increase V02 max capacity which is the maximal amount of oxygen capable of being transported to and consumed by the working muscles (79, 80, 146, 230). The magnitude of the increase depends upon the individual's initial level of training and the intensity as well as the duration of the exercise program. This increase is in the range of 10 to 20% for programs of 6 to 12 weeks duration (15). Larger increases have 19 been reported for programs of 2 to 3 years (79). The improvement in V02 max is accompanied by increases in cardiac output, stroke volume and in the arteriovenous oxygen difference (79, 80, 230). Although the maximum oxygen intake has been recognized for its importance in endurance exercise, it is likely that the maximum work level at which the individual can maintain steady state is more important. This maximal percentage level of V02 max would represent the rate at which the lactic acid accumulation is at its highest level without causing cessation of work. In terms of endurance work the maximum level of steady state that can be achieved may be the most critical. (c) Energy Metabolism During Recovery Margaria et_gl: (189, 190) divided the 02 debt into alactacid and lactacid portions. The alactacid portion is believed to correspond to the amount of oxygen required to rebuild the PG stores depleted during exercise (Figure 2.1a and b). Thus, the restoration of muscle PG by an increased oxygen consumption during the early portion of the recovery period following exercise is called the alactacid oxygen debt (46, 75, 76, 107, 189, 190, 191, 270). The maximal depltion of ATP in skeletal muscle following muscular work is about 40% that of the resting level (94). In con- trast, the CP supplies can be depleted during exercise. The restoration of ATP and CP stores in the muscles during recovery costs energy which is derived from complete oxidation of carbo- hydrates and fats. The replenishment of the phosphagen stores has 20 been shown to be a rapid process. Based on the muscle biopsy tech- nique, after continuous submaximal work for twn minutes the half- time for PG replenishment ranges between 20 and 30 seconds (85). Lactacid O2 debt is believed to reflect the oxygen used to remove accumulated lactic acid from the blood and muscle during recovery following exercise (74, 75, 189, 190). The maximal capacity of the lactacid O2 debt of the young male and female has been reported to be 220—250 cal/Kg body weight (45). This value, however, decreases with age (45) and with changing environmental conditions, particularly in chronic hypoxia (43). (d) Limiting Factors in Anaerobic and Aerobic Work One of the classical questions within the field of work physiology is to postulate the factors which limit V02 max and per- formance. The traditional concept presented by Hill et_gl, (119, 120), Christensen (48), Margaria et_gl, (190), Nielsen and Hansen (204) and included even in recent reviews on circulatory adaptations to severe exercise is that a given V02 max requires a fixed heart rate, stroke volume and cardiac output (79, 228, 253). This whole idea, however, was challenged recently partly due to new knowledge of the adaptive modification in skeletal muscle and the cardio- vascular system (127) and partly due to the failure of skeletal muscle to exhibit better performance following oxygen administration (150). 21 Evidence suggests that lactic acid production, not oxygen consumption, may be the rate-limiting factor during muscle contrac- tion (217). The assumption that the muscles produce lactate because of insufficient oxygen to maintain electron transport in the mito- chondria is invalid since mitochondrial NAD/NADH has been shown to go toward the oxidized state with both twitch and tetanic contrac- tions of isolated frog and toad muscle and in situ mammalian muscle (143, 144, 250, 251). This suggests that the electron transport system is blocked somewhere between the cytoplasm and the mitochon- drial NAD. There is electron accumulation in the cytoplasm which contributes to lactate production, but oxygen does not appear to be the rate-limiting factor. However, the fact that the oxygen supply does not appear to be the rate-limiting process in muscles does not indicate that 02 transport may not play a critical role in deter- mining maximal performance (251). The oxygen supply can be shown to be critical if insufficient oxygen results in impaired tissue mito- chondrial capacity (150, 154). Several studies have reported a relationship between lactic acid accumulation and fatigue (10, 25, 84, 155). Recent studies on cardiac muscle (163) and skeletal muscle (87) also have provided evidence indicating that an elevated H+ ion concentration might affect the myosin-actin interaction during the process of muscular contraction. This could be a limiting factor during overall heavy work (87, 233). On the other hand, pH values of circulating blood below 7.1 may affect the neuromuscular transmission and the reaction of skeletal muscle to acetylcholine (70), and cause an increased 22 tension in solutions containing high lactate and low HCO3 levels (207). The possibility was considered that there is an increased mobilization of intracellular Ca++ at low pH. These observations suggested that blood pH might be the limiting factor in work to exhaustion. Various investigators have shown that the glycogen content of muscle decreases in relation to the duration and intensity of exercise and may finally become a limiting factor in endurance work (112, 134, 164, 231). It was reported that the concentration of hexose monophosphates were very low during heavy exercise indicating that either a lack of glycogen (24, 172) or the inability to utilize the glycogen in glycogen-filled fibers (172) was a limiting factor for work performance. (e) Measurement of Aerobic and Anaerobic Capgcity The energy needs for muscular work are derived from both anaerobic and aerobic sources. The relative contribution of these two energy-liberating processes depends upon the type of work, the intensity of work, and the duration of work. During prolonged exercise of relatively low intensity, most of the energy is derived from oxidation of carbohydrates and fat; whereas, during short exhaustive exercise, the energy needed is derived mostly from anaerobic processes (PG and anaerobic glycolysis). According to the relationship between energy metabolism and 0 consumption, an indi- 2 vidual's capacity for aerobic work may be measured in terms of 02 uptake. 23 Holmgren (128) suggested that V02 max depends on the func- tions of the pulmonary and cardiovascular systems which include the diffusion capability of the lungs and the 02 transport by the blood to the active tissues. Considering only the cardiovascular system in 02 transport, its contribution is shown in the Fick equation (228): V02 = heart rate x stroke volume x arteriovenous 02 difference To measure the maximal oxygen uptake the subject need not be involved in an all-out test to the point of exhaustion. Following warm up of at least five minutes duration, the V02 max may be obtained in high-intensity work of less than two minutes duration or in extended work in which the load is gradually increased (15). Astrand (15) found a linear increase in 02 uptake with increased work loads up to the level of the maximum oxygen uptake which he called the "maximal aerobic power." Two main criteria were used to identify the V02 max: (a) the 02 uptake level does not change in spite of increasing work loads, and (b) the concentration of blood lactate is above 70 to 80 mg/100 ml of blood with a signi- ficant increase of the hydrogen ion (H+) concentration. Both trained and untrained individuals usually can perform continuous work at 60 to 70 percent of their V02 max (168). Surprisingly, in the same people, the values obtained at different intensities and durations for the same type of work (i.e., running, swimming, etc.) vary little (l3, 16). However, different V02 max values can be 24 obtained when using exercises in which more car less muscle mass is involved (246, 254), the work posture is changed (230), the type of apparatus is altered (83, 111), or the physical condition of the subject is changed (230). In general, among athletes the highest V02 max values are obtained in their chosen sport. That is, swimmers obtain higher V02 max values while swimming than when 00 a treadmill or a bicycle ergometer, and distance runners' V02 max values are higher on a treadmill than when swimming or riding a bicycle (l3, 16). On the other hand, there are no generally accepted methods by which the anaerobic energy release can be calculated quantita- tively. The relative contributions of these two important energy systems, therefore, cannot be determined exactly. However, it is possible to estimate the amount of energy released through anaerobic processes by measuring the changes in concentration of ATP, CP, and lactate in the muscles during and after work. According to Karlsson (155) it is reasonable to assume a total maximal energy output of about 30 K cal by anaerobic sources. Based on the results from this study and others (25, 108, 135, 159), the relative contribution of the anaerobic and aerobic systems to total energy liberated during exhaustive work of various durations can be estimated as shown in Table 2.1. Asmussen (9) reported the efficiency of anaerobic work to be between 40 and 50 percent that of aerobic work. Christensen and Hogberg (51) found this value to be around 40 percent. 25 TABLE 2.1.--Relative Contribution of Anaerobic and Aerobic Energy Metabolism to Total Energy Output During Maximal Exercise of Different Durations. Energy Output Relative Contribution (K cal) (%) Work Time, Maximal Anaerobic Aerobic Anaerobic Aerobic Exercise Processes Processes Total Processes Processes 10 sec. 20 4 24 83 17 l min. 30 20 50 60 4O 2 min. 30 45 75 4O 6O 5 min. 30 120 150 20 80 10 min. 25 245 270 9 91 30 min. 20 675 695 3 97 60 min. 15 1200 1215 l 99 Based on the enzymatic reactions of lactic acid production LDH (pyruvic acid + NADH+ efi' lactic acid + NAD+) and the concept of “excess lactate" (LX), Huckabee (130, 131) reports that it is unwarranted to use lactate change as an indication of inadequate oxygen in the tissues. Since a change in the pyruvate concentration may affect lactate production as much as oxygen deficiency, he notes that pyruvate concentration should be considered in evaluating the XL concentration which he believes is a better measure of anaerobic metabolism than is lactate. However, according to the concept of alactacid and lactacic 02 debt, Margaria (190) proposes that venous 26 or arterial blood lactate concentration are good estimators of anaerobic metabolism in short-duration high-intensity exercise. It should be noted that a high correlation has been found between oxygen debt and arterial lactate (5, 68). Furthermore, several studies have reported high relationships between the arterial lactate level and the work load (38, 68, 210). Karlsson (155) also reported that a close linear relationship exists between the arterial blood lactate level during recovery and the muscle lactate concentration immediately after work. The arterial blood lactate concentration ranges between 11 and 14 mM/l for young, moderately trained subjects; whereas, it may be as high as 30 mM/l in highly trained, motivated, middle-distance runners (15). Several investigators (37, 129, 190, 272) recommended the use of arterial blood rather than venous blood in studies of acid- base change since it is difficult to evaluate any modification of the blood after it has passed through the capillaries of non- exercising muscles. Furthermore, there is a marked arterial-venous difference when a part of the lactate produced is metabolized in skeletal muscles. If lactate is metabolized by non-exercising muscles, the alkalinity of the venous blood could be increased since it would decrease the H+ concentration. Osnes and Hermansen (206) and Bouhuys et 31, (32) observed a linear relationship between arterialized capillary blood lactate and the arterialized capillary blood H+ level in muscle biopsies taken during exercise. A very high relationship also was reported 27 between arterialized capillary blood and muscle pH in exercising human muscles (32, 108, 110). There is a negative relationship between base excess and lactate concentration in arterial blood (32, 206). Bouhuys et_gl, (32) found a BE value of -14 mEq/l in a group of twenty-seven male subjects aged 22 to 30. The change in BE (pre-work to post-work) was 15.6 mEq/l. The same relationship existed between plasma bicarbonate and the concentration of lactate in the blood (72, 94, 267). The plasma bicarbonate was shown to be zero with an elevation of lactate of about 30 mM (94). In aerobic work the net alactacid 02 debt appears to be linearly related to the 02 consumption at steady state (157, 190, 212) which is about 20 ml/kg/min during maximal aerobic exercise in young fit non-athletic subjects (74, 75). This has been judged to correspond to the splitting of about half of the total phosphagen content of the resting muscle (155). About two minutes following exercise, the phosphagen resyntheses has been found to be complete (135, 212). Other investigators have reported different magnitudes of the 0 debt varying from 4 to 5 liters up to 20 to 22 liters of O2 2 (108, 118, 188, 202, 226). This variation is due to (1) duration of measurement time, (2) determination of the metabolic baseline, (3) elevation of body temperature after exercise, and (4) elevated O demands of respiratory muscles and the heart (15, 150, 173, 268). 2 Several recent studies have attempted to determine if the oxygen intake during recovery can be attributed to chemical , L a 28 repayment of energy sources that were ”borrowed” during work. Stainsby and Barclay (252) determined that an oxygen debt of 5 liters in an 80 kg man could be accounted for as follows: 10 per- cent to replenish blood oxygen stores; 2-5 percent for repayment of tissue 02, dissolved 02, and full saturation of muscle myoglobin; and 70 percent for the reconversion of ATP from high energy phosphate bonds. About 15 percent of the recovery oxygen intake was unexplained. (f) Acid-Base Balance and Anaerobic Metabolism Maximal exercise of 2—4 minutes duration results in the formation of lactic acid in the muscle cells. This intracellular lactic acid diffuses into the blood where it lowers the extracellular pH and is associated with changes in the acid-base status of the blood (165, 227). Elevation of lactic acid production in an alkaline environ- ment and a decrease of the lactic acid level in an acidotic environ- ment have been demonstrated (90, 91, 260). In addition, increased 02 debt capacity and changes of blood parameters in alkalotic con- ditions have been reported (71, 72, 147, 148, 257) (Table 2.2). However, a uniform relationship between acid-base changes and the blood lactate level has not been found (100). This lack of a uniform relationship between acid-base changes and blood lactate has made some investigators look for reasons other than changes in H+ ion levels to account for increases in blood lactate. It was suggested that these acid-base changes are related to an increase or decrease 29 mmvotoxm umoa ob wca soc» mwocmzu n < emowLo:_ oceo_e_co_m n . mocwcmeewv oz u o mmmmgumu u - mmomLocw u + o 9.26 SN. m 82:3 53973 :3 2 2 2 - o .rz w 3:5 oi. 8:; :58: 2; L35: :2 + + ox\:b moo. mmecag mucoumwo m | 8.: .+ + + o - o e. .wL; m oX\Em m. ouzcz PFWEGooLA mouopzuo-coz ._o.qu mocon hump m LoomEooLm Aumwv + . .32 m 9:5 0m. 8va 633; 33256-82 fl ale 5:3 £2 Louweoogw Anvpv + . 1 .3: m 9:5 8. m8:62 223; 83256-52 flflu 35.. £2 e... EN. 355 x 3.8 1 .2: we .5 om. 88:62 BEE 865.36. 2.2% are: 2; 225m 9:: ..5 E. 35.6 2 m LmumanLm Am—V + + + .mL; N mx\=o MM. ouzaz o_u>oam wmumpcuoicoz angouu< asap 0 o S m .N 885 S. 38.33 5.6288 l 1 E: o o .L; «\H e M moec _u oz prEvomL» mtmccsc vocwagu x—ouugmvo: .—o no negomgax cum— 0 o 50 Pm. ouzoz mgmccac vmcwagh .5 m.» 39;: S. 9.25: E: 0 .mL; q so m.m mouxez zgucaou mewcczc mucoum'a gun—m a comccon mmwp so m mamgo_u oz «mega l l a: o +< .2 + + + - - + + .3: cm 32,5 of. mouzoz 2.263..» mmuo—sumicoz ...m aw 3:ch on: w... mm. .m. M M m M M. m. 20 M. to: 380m 2:23 L322; Sop Co on? 33.33 .353 .80» 3 O 0 O 2 J {50:35: 1. cc . 7. 2 0 T: . e a o :o_omucesopan:m 3 O. J 3 19 w P U 3 a .mtmooEQLea .co_oo_o_mx;a woumpwa ecu mucustoeeoa cog: Lm~mexF< eo muomuuw .YNLC.LLNVNUENHIII 1‘ "mmmuaum maoe>wga--.~.~ u4m60%) and more acidic blood following a high fat-protein diet (about 50% fat and 30% protein). Ingestion of a high-carbohydrate or vegetable-based diet also has been shown to increase the P002 value of the blood about 2 to 3 mm Hg (102, 103, 184, 198, 242). Bischoff et_gl: (29) and Moller (198), respectively, found lower and higher bicarbonate of the blood following a high protein diet. Siggaard-Andersen (242) have reported an elevation of base excess (BE) of about 3 to 4 mEq/L following a heavy meal. CHAPTER III RESEARCH METHODS This study was designed to investigate the effects of oral ingestion of sodium bicarbonate (NaHC03) administered, under high carbohydrate and high fat-protein dietary conditions, prior to an intermittent multi-stage treadmill run upon: (a) performance time, (b) maximum oxygen uptake, (c) gross oxygen debt, and (d) acid-base parameters. Experimental Design A Latin square design with eight subjects exposed to four different treatment conditions was used in this study (Tables 3.1, 3.2 and 3.3). The four treatments consisted of oral doses of sodium bicarbonate or a placebo (dextrose) taken under high carbohydrate or high fat-protein dietary conditions. Supplements were administered in a single-blind method two hours before the exercise test. TABLE 3.1.--Supplement and Diet Conditions. Treatment gm/kg. 0f Conditions Supplement Body Weight Diet 1 Sodium bicarbonate 0.065 Carbohydrate 2 Sodium bicarbonate 0.065 Fat-protein 3 Placebo (dextrose) 0.05 Carbohydrate 4 Placebo (dextrose) 0.05 Fat-protein 39 40 TABLE 3.2.--Treatment Conditions. O 8 Sta g a UJ .1 2 8 8° 3 35 “-0 “’ 6‘6 .9 (1) DIET f High Fat Protein High Carbohydrate Condition Condition 4 3 (PFP) (PC) Condition Condition 2 I (SFP) (SC) TABLE 3.3.--Test Sequence of Latin Square Design. Subjects SF BR DA 03 CC BM BK GS Treatment Order 3 4 l 2 2 3 4 I l 2 3 4 4 l 2 3 I 4 3 2 4 3 2 I 3 2 I 4 2 l 4 41 The subjects were randomly assigned to two equal groups, A and B, consisting of 4 individuals each. The subjects in Group A were asked to adhere to a given diet on Mondays, Tuesdays, and Wednesdays, and were tested on Thursday each week for four weeks. The subjects in Group B were scheduled to diet on Tuesdays, Wednesdays, and Thursdays and were tested on Fridays. Subjects The subjects were eight physically-fit, male, long-distance runners, ages 20 to 40, engaged in endurance training (Table 3.4). A personal medical history and informed consent were obtained from each subject. Prior to initiation of the study, each subject was stress tested utilizing a modified Bruce protocol (81) in which the treadmill speed and grade were progressively increased every three minutes (Appendix C). Heart rate (HR), blood pressure (BP) and an electro- cardiogram record (ECG), were monitored after each level (Table 3.4). In addition, the economy of endurance performance was evaluated from the HR responses of each subject while running on the treadmill at six miles per hour, zero grade, for five minutes (Table 3.4 and Appendix C). Exercise Test The exercise test consisted of a multi-stage (level), inter- mittent, treadmill run with a rest interval between each work interval and a standardized, l5-minute recovery period at the end. A maximum 42 .xpwuw_m> wfinm:o_umm:c mo me wcsmmmga voopn UAFOHmmev xtozipmoq och u e :3; prCM xpmHMwumEEH u m< e _m>6o Laee< n A see e< est meeeee e:e_xez u a: _ Fm>mo mcoemm u 4 Amp am :5; meowmm N am ou\o_m ow\omp ¢o~ _n_ mo o.¢N on _ ow ma om\omp om\o_F mm ow_ AA m.©o cm A mm xm ON\oom ow\omp mm om_ mu m.me ON _ Fm 2m oo—\omp om\oPF we mm_ mm o.mm mm P am ow ow\omp ou\o_fi mm Nm_ Nm w.em No A mm mo om\omp om\o_F mm o@_ um N._m mm _ mm <9 om\omp ow\op_ em Nm_ cu N.©© mm A mm mm om\mw_ mN\omr ow QNF om o.mo om P om mm A see L< o om_ um Lq as am Amxv mempmeweemu mambo: mm< mpumhesm Age_oemeeo\oeeoememv am apex Beam: peeve: “gave: .1 .pmwe mmmcpm esp oo mmmcoammm Lease ecu mpomwnsm mo mowpmwgwpomgmguii.¢.m momLm>oomm o m e m N P mpm>m4 .umee _PAEeemee “empoweLeeeH weeem-23_=z ago :2 m_e>tmee2 puma see 3263 .meaeu .eawam--.m.m momqe 44 of six levels was possible. The durations of the work and rest periods were held constant at three minutes. The treadmill speed and grade were increased progressively as shown in Table 3.5. On each test day the subject ran to exhaustion. The test was carried out on all the subjects under the same conditions. With a few exceptions, scheduling was maintained whereby each subject was tested at the same time and on the same day each week. The subjects were tested between 1:00 p.m. and 6:00 p.m. A light-weight safety harness was worn by the subjects to enable them to run to exhaustion without the threat of falling. The environment of the treadmill room was maintained relatively constant. The temperature varied between 22-25° C and the relative humidity fluctuated between 45% and 52%. Measurement Procedures Respiratory Freguency The respiratory frequency was detected utilizing a Sanborn pressure transducer (Model 268A) which was connected into an Otis- McKerrow respiratory valve1 by a flexible plastic tube. The cycle from the transducer was recorded on a Sanborn Twin-Visa Recorder2 as follows: a. During the middle 10 seconds of each minute of work. b. During the middle 10 seconds of each minute of rest. 1Otis-McKerrow, Warren Collins Company, Braintree, Mass. 2Sanborn Company, Twin Visa Recorder, Cambridge, Mass. 45 The recorded pressure differences per respiration were counted and converted to minute values. Heart Rate Disposable electrodes3 were placed on the subject in a single bipolar V5 electrocardiographic configureation (81) (Figure 3.1). The results were recorded on a Cambridge 3030 ECG unit.4 The heart rate was recorded as follows: a. During the first three levels of run, HR was recorded during the last 10 seconds of every minute. b. During the last three levels of run, HR was recorded during the last 10 seconds of every 30-second period, c. During the rest interval after each level of run, HR was recorded at the end of the first and third minutes. d. During recovery, HR was recorded during the last 10 seconds of each minute for the first three minutes, then at the end of every two minutes from minute four to minute nine, and at the end of every three minutes from minute 10 to minute 15. Blood Sampligg Two hundred and twenty microliters (pl) of arterialized capillary blood were collected anaerobically in two capillary tubes (120 pl heparinized, 100 p1 unheparinized) from a prewarmed, clean, dry finger tip (17, 240-244)(Appendix D). The finger was prewarmed for a minimum of three minutes in 45° C water in a rubber bag pulled on over the hand. Blood samples were taken at the following times: 33M Red Dot Electrodes, Minnesota Mining & Manufacturing Company, St. Paul, Minn. 4 New York. Cambridge Instrument Co., Inc., 73 Spring St., Ossining, 46 Figure 3.l.--Single Bipolar V5 Electrocardiograph Configureation 47 a. Prior to exercise. b. Immediately after the completion of each work level during the rest interval. 6. Immediately following the termination of the exhaustion work level and at 5, 10, and 15 minutes during the standard recovery period. The two blood samples were collected to determine blood lactate and the acid-base parameters. Lactate Analysis The lOO-ul blood sample that was collected in the unheparin- ized capillary tube was mixed with 200 pl of cold 8% perchloric acid and centrifuged at approximately 32 gs. The mixture of plasma and per— chloric acid was drawn in labeled disposable syringes5 and stored at O-3°C for 3-6 days before analysis for the determination of lactate by the enzymatic method (196). A Sigma lactic acid chemical kit6 was used for the enzymatic reaction and a Gilford Stasar II Spectra-photometer7 was used for the analysis of NADH at 340 nm (Appendix D). Acid-Base Parameters The 120-ul blood sample that was obtained in the heparinized capillary tube was used for direct determination of pH, PC02 and P02 using the Radiometer blood micro system.8 The HCOé, TCO2 and BE were 5Becton-Dickinson Co., Rutherford, N.J. 6Sigma Chemical Co., Box 14508, St. Louis, Mo. 7 8Radiometer PHM75, MK2 and BM53, EMDRVPVEJ, Copenhagen, N.V., Denmark. Gilford Instruments, Oberlin, Ohio. 48 determined indirectly by the Astrup Equilibration Method for acid- base variables (17, 240-244) using the Siggaard-Andersen Alignment Nomogram (Appendix D, Figure 0.1). Blood samples used in these determinations were stored at 0-3° C and were analyzed within two hours following collection (240). Energngetabolism Measures The expired gas was collected by the standard Douglas bag method (55) using neoprene weather balloons (89). The remainder of the circuit, which had a total resistance of less than 20 mm H20 at 227 l/min. flow, consisted of an Otis-McKerrow respiratory valve connected to 18 inches of corrugated hose (1% inch 1.0.) attached 9 to a five-way, automated switching valve. Continuous serial collection of the respiratory gas bags was made from the start of the first work level according to the following plan: a. During the first three levels of work, bags were changed every minute (one-minute bags). b. During the last three levels of work, bags were changed every 30 seconds (30-second bags). c. During the rest interval between work levels, bags were changed after the first minute (one-minute bags) and the third minute (two-minute bags). d. During recovery, bags were changed following each minute for the first three minutes (one-minute bags), then every two minutes from minute four through minute nine (two-minute bags), and finally every three minutes from minute 10 through minute 15 (three-minute bags). 9Van Huss-Wells Automated Switching Valve. 49 The filled, labeled bags were transferred from the treadmill room for the immediate determination (<5 min) of volume and content of the expired gas in the bags. The percentages of CO2 and 02 were determined simultaneously using the Beckman LB-2 and OM-ll analyzers respectively.1O Bags were evacuated and pumped through a dry DTM-ll gas meter11 at a rate of 50 l/min. All energy metabolism measures were calculated as described by Consolazio, Johnson and Pecora (55). (Appendix E). Helium was used to set the zero points of the analyzers. Room air and a known standard gas sample were used to calibrate the analyzers. Oxygen and carbon dioxide concentrations of the standard gas sample were verified using a Haldane Chemical Analyzer.12 The energy metabolism variables consisted of the following: ventilation (VE), oxygen uptake (V02), maximum oxygen uptake (V02 max), oxygen debt (02 debt) and respiratory quotient (R.Q.). Dietary Measures The individual subjects received instructions prior to each week. They were given lists of standard American foods (Appendix A) to be eaten during that week. The foods were those contained in either high fat-protein (HF) or high carbohydrate (HC) diets. Subjects were asked to keep the total caloric intake relatively 10Beckman Instruments Inc., 3900 River Road, Schiller Park, Illinois. nAmerican Meter Co. (Singer). 12 Arthur H. Thomas Company, Philadelphia, Penn. 50 1.00. N a :00. N a 1.00. N a e_meoea pea ozo mm.m~ u L Fm.om n L oe.mm u L <>oz< e.m em.e A.m ea.~ ma.m w.e o.“ Fe.m e.__ m.m _.e m.op om o.mN o.me 2.2m 2.42 m.em N.mm m.FN O.Ne e.mm m.e_ o.em N.~m .m eweeoea Bea ozu evapora pea ozu eeeooea pea ozu eeaeeea pea ozu e e e e e e e e e e e e Aaaav Aoav Aaamv Aumv eeaeoea-eea 0:8 cemeoea-eea ozu + + m + m + oeeee_a oeaueea oozez oozez .mcowowncou xcmpmwo cwmpocaipmu saw: new mumgnzsoncmu cor: smug: geopoea vcm pea .mpmguzsoncwo Co mumpcmocma vcm cowumw>wo ucmccmpm .cmmzii.mum mom42% fat, >21% protein, <34% carbohydrate) or the high carbohydrate diet (<34% fat, <15% protein, >53% carbo- hydrate) (Table 3-6). Test Protocol Immediately prior to initiation of work, the subject stood over the treadmill in the straddle position. The ECG was checked to determine if the electrode application was adequate. A ceiling mounted safety harness was adjusted to prevent the subject from falling, while allowing freedom of movement for the run. A rubber bag and covering bag, containing water at temperatures slightly higher than 45° C, were placed on the hand not used for the pre-work blood sample. A mouthpiece and a noseclip were attached. The expired gas during this time was vented to the room through the 5-way valve. When the subject was ready, the treadmill was started (6 mi/hr, 5% grade). Simultaneously, an automated gas-bag switch was pushed to initiate collection of the expired gas and the first 13 was started. 13 timer Universal Timer, Model 172, Dimco-Gray Co., Dayton, Ohio. 52 During the work interval the gas bags were changed at one- minute or 30-second intervals (depending on the work level) and were removed for immediate analysis. Time was called out during the run, and at 15 seconds prior to the end of each work level the subject was informed that the treadmill would stop. For better control, about five seconds before work termination the subject grasped the safety railings of the treadmill. At the time of work termination the subject would hop to a straddle position over the belt until it came to a complete stop (following treadmill adjustment to the next level). Also at the end of the work time, a second timer was started auto- matically for the rest interval. During the rest interval the subject sat on a high stool over the treadmill. Gas collection continued during the three-minute rest interval in one- and two-minute collections. During this period the rubber water bag was removed from the hand, the finger was dried and sterilized with alcohol, and the blood samples were taken using a lancet. The blood samples were immediately removed and prepared for analysis. The finger was wiped with alcohol and taped. The rubber water bag was filled with water slightly about 45° C and placed on the other hand. Heart rate and respiratory rate were monitored throughout. About 30 seconds before the end of the rest interval the stool was removed, the subject straddled the treadmill, and the first timer was reset. Identical procedures were used at each work level to the point of exhaustion when the treadmill was stopped. The subject 53 then sat on the stool for 15 minutes with continuous gas collection and monitoring of heart and respiration rates. Blood samples were taken from alternate hands using the procedures described at 0, 5, 10, and 15 minutes of recovery. At the end of recovery all equipment was removed and the fingers were carefully cleaned. The subject then was oriented for the following week's test. Statistical Analysis A two-way repeated measures analysis of variance (ANOVA) was run with supplement and diet as independent variables (35, 59, 92, 249, 271), Separate analyses were employed for each of the independent variables. The Statistical Package for the Social Sciences (SPSS) system (203) was used on a Control Data 405 computer. In selected instances with continuous data of a curvi- linear nature, as in exercise responses across time, the Sign test was used (239). CHAPTER IV RESULTS AND DISCUSSION The results of this investigation are presented initially in this chapter. The presentation of results is followed by a discussion. The order of presentation is as follows: (a) performance time, (b) maximum oxygen uptake, (c) gross oxygen debt, (d) oxygen uptake, (e) ventilation, (f) heart rate, (9) respiratory rate, (h) respiratory quotient, (i) pH, (j) P002, (k) P02, (T) TCOZ, (m) Hcog, (n) base excess, and (a) lactate. (a) Performance Time The performance time under various dietary and supplementary conditions is shown in Figure 4.1a, Table 4.1a, and Appendix F.1. No statistically significant differences in performance times were observed under any of the treatment conditions. Although the best scores were observed under the SC condition, no conclusions are warranted. (b) Maximum Oxygen Uptake (V02 max) The maximum oxygen uptake values for the different conditions are presented in Figure 4.16, Table 4.1b and Appendix F.1. There were no statistically significant differences observed. Again, the 54 875 850 825 800 775 750 PERFORMANCE TIME (360.) 725 H?! 87.5 85.0 82.5 80.0 77.5 V02 max, (NIL/kg.) 75 .0 72.5 r T 16.5 16.0 15.5 15.0 14.5 GROSS DEBT (1.) 14.0 13.5 I I Figure 4.1.--Results: 55 (0) PERFORMANCE TIME T T I I __1_ __ .I I .L l. .- I l. .I _. J I T l I T l I T SC SFP PC PFP c FP CONDITIONS DIET (b) MAXIMUM OXYGEN UPTAKE 1 I I l _. It. ..I. .11. .11. .JL AL .1. .L ..I T T T .T T T T SI SI SC SFP PC PFP C FP CONDITIONS DIET (C) GROSS OXYGEN DEBT ._L .J- I. .1- J1. J- J- "J— .I. ‘. .1. J T T T T T T T '1' SC SFP PC PFP c FP CONDITIONS DIET (a) Performance Time, (b) V0 (c) 02 Debt, under Different Condition S P SUPPLEMENT T 41 .I .L .I T T ;T S P SUPPLEMENT T I .TI. " d- T SLIT T S P SUPPLEMENT g.1'IlaX, coeuomewucH n H ”pmeo n 0 ”AcmEmFEaam u m 56 00.0 F0.m 00.0 mm._ om 00.0 0N.0 00.0 00.0? mn.0~ 00.0— m_.m— .x pawn cmmxxo mmoe0 A60 cm.“ 00.: 070 00.0 00 00.0 00.0 :0 0.0m 00.2 00.2 00.00 M memmwlqu. 0.00 0.0: 0.0: 0.02 00 0.0 00.0 00.0 0503 00.00m 00K? 00.20 x wave mocmELowLmq Amv a a a Aaeav Auav Aaamv Aumv mbpeeeee> H o m eta-oma ozo eta-bea ozu + + 0 + m + 6666a_a ebbbeea oozez oozez <>0z< mucmemmgk .Aebb__0 pnwo cwmxxo mmogw 0cm A0x\_ev x65000 Amommv wave mocmeeowgmm .mppzmmm Fmowpmwumpmiu.F.¢ 000 9 10 1-1 1 . . 2 2 , : I r-fi ' 250: 51..“ .11 .7 . I , , 1 1 ' J 5 6 1 11 I . 1 1 3 1 1 1 1 I o o T I T T T T I T I T ITV I I I I T I o 3 6 12 15 1 21 24 27 3 6 9 12 15 o 12 18 21 12 15 wmwmwmwm wmwmwm W L1 1 L3 L4 L5 RECOVERY L. L3 L3 L4 L3 RECOVERY TIME (min) TIME (min) (a) SODIUM BICARBONATE (b) PLACEBO . Supplement Effect 8y D1e1 I000 1'- 1 9 , O—OSC ' 0---0 PC I 75.0 _ E E :- ‘ SPEED m 500 ~ ‘. (MPH) .> 10 _.1 9 \‘ ”—1 ‘ 8 25.0 »— ’fi 1 ' r_: 7 —L ——] ‘- . ' . l 1 6 I ' 1% I - . . L i i j I O I I I I I I I I I I T I I I T T T I I 0 3 9 12 15 18 21 24 27 3 6 9 12 15 o 3 6 9 wmwmwm R1w WRIWRIWRIWRIW L I 1 L3 L. L5 RECOVERY L p L3 L3 L. L; RECOVERY TIME (min) TIME (mm) (c) CARBOHYDRATE (d) FAT-PROTEIN 1 Pooled Results 100.0 — 1 I 9 , HS ‘, HC : o---oP I o---oFP - 1 . q 1 75.0 >- 11 . E . 1 E .; oi 2 r, 61 GRADE SPEED L 50.0 I— x ‘ 1%) (MPH) -> ;——1 r—I 9 I0 1‘1 TI 1 . ._ *1 I : 3 Z . . I ; . ' . 25.0 I- : .- ; 1 ‘ i {—j y ; 1 - 6 7 J‘ [—l l l I j 1 ' ‘ ~ r——T i ‘ I . 5 6 T T I l T I I I I I I I I I I T I I T T I I T I I I I I I 03692151621242 3691215 03691215182124273691215 wmwmwmwmw wmwmwmwmw . 1., L, L. 1.° RECOVERY L. z 1.3 1.. 1.. RECOVERY TIME (min) TIME (min) (a) SUPPLEMENT (f) DIET Diet and Supplement Effect on Ventilation. Variables Min 61 Level I: Pl Level 2 3 RI Level 3 3 RI Level 5 3 Recover! ——J 2-3 2-3 6-7 8-9 IO-IZ ><| >d ><| XI XI XI ><| ><| XI XI >d >d >d XI (1" 1) 62. 36. c 74. 43. 52. 87. 55. 59. 60. 96. 60. 48.1 66. (II I\) (.J ()1 LII \1 62. 34. 77. 43. 48. 98. El. 56. 76. 89. 56. 94. 52. 62. 57. 47. 67. NaHCO1 + - Fat-Fro (SFP) 05 ‘ I2 9I : 9. 52 : 9 28 : I5 69 : 9 70 : I0 77 : I9 20 : IE 08 : I3 38 : IO 30 : I6 70 : I8 50 : I4 53 : 25 99 : I3 I2 : 8 9I : I3 43 : 4 99 2 8. 94 : 8. .46 : 9. L) U1 UI est Irterval; lacebo Iacebo + + CHO Fat-Pro (PC) (PFP) 62.53 : 8 64 l6 : 7 33.I4 : 7 35 I8 : 9 43.56 : ll 44 00 : 7 76.59 : I4 83 l: : l3 43.04 : IO. 44 82 : 9 47.59 : l6. 48.73 : 8 92 O7 : 18 l00 26 : 22 59.32 : l4 64 99 : l2 60.2l : l9 66 38 : II 55.0 : ll. 55.20 : 9 7I.50 : I7 78.77 : II 8l.80 : 22. 95 ‘6 : 2l 60.00 : 8 55.29 : 9. 89.80 : 26 83 Al : 22. 53.29 : I3. 55.5I : I9 43 03 : 8 44.30 : ll 63.02 : l: 67 59 : 22 56.69 : I? 57 96 ; 12 47.33 : 9.5 54.28 : 25 6l '3 : ll 64.39 : 9 59.40 : 2l 60.82 : l6 1'51 I = Ioteraction S P 5 0.7" 4 3.62 .l 7 0.47 4 0.77 .4 l 0.67 3 0.43 .9 2 0.85 5 0.82 .l 5 0.83 7 0.37 .3 7 0.69 l .O 6 0.39 L) .88 .97 .39 1.93 .75 .28 .6l l’\) \I .7l .74 .97 .26 .93 .28 .66 62 under the carbohydrate dietary condition (Figure 4.3b, P = .00l). The supplementation of NaHCO3 under the carbohydrate diet (SC) resulted in consistently higher ventilation values than when no supplement was given (Figure 4.3c, P = .02); whereas, when supple- mentation was combined with the fat-protein (SFP) diet, the ventila— tion values were lower than when no supplement was given (Figure 4.3d, P = .00l). It can be concluded that NaHCO supplementation in con- 3 junction with the carbohydrate diet (SC) results in slightly increased ventilation values. This effect was expected. With a greater quantity of bicarbonate ions available a greater stimulus to respiration from carbon dioxide levels should result. However, under the fat-protein dietary conditions with supplementation the ventilation values were lower not higher. This result was unexpected. (f) Heart Rate In Figure 4.4a-f, Table 4.4 and Appendix F.4 the heart rate results are presented. In the ANOVA analysis a statistically sig- nificant interaction effect was observed for the ten to fifteen- minute recovery data (P = .07). Since no other significant values were obtained and no clear trends are evident from the data, the significant interaction is likely due to chance. No conclusions appear warranted from these data. (9) Respiratory Rate The respiratory rate results under different supplementary and dietary conditions are shown in Figure 4.58-f, Table 4.5 and Appendix F.5. A statistically significant NaHCO3 supplement effect HEART RATE (Iminl HEART RATE (lmm) HEART RATE (lmm) I80 I60 I40 l20 l00 80 60 ISO 160 140 |20 I00 80 60 |80 |60 I40 I20 63 mm Effect By Supplement 1 I I O—OSC I O—oPC I o——-o SFP I o---oPFP I I I | GRADE SPEED - - (°/.) (MPH) . r——I 9 '0 1 l I 8 9 r1 I 1 ' ' I—I 1 1 7 8 ,———‘ I 1 . ' I I I I 'I I . I I I 6 7 1 I I I i I I I ' I I I l I I T 5 6 . 1 I 1 1 i 1 I I 1 P4 ' I I o o T TTI I I I I I I I I I I I I T I I I I I T ITI T l I I I I o 3 6 9 12 15 I8 2124 27 3 6 91215 O 3 6 9121516 21 427 3 6 91215 wmwmwmwmw RIWRIWRIWRIW L. L1 L3 L‘ La ECOVERY L. L3 L3 L4 L5 RECOVERY TIME (mm) TIME (mm) (o) SODIUM BICARBONATE (b) PLACEBO Supplement Effect By Def 1 o—csc o——osFP o——-oPC ch--oPFP GRADE SPEED - 1%) (MPH) 9 10 8 9 7 8 6 7 . 5 6 1 I . I I . ' 1 . I I 7 ' ' ' o o T I I I f I T I I I TI I I I V I T T I I TV I I r I I I I I I 03691215182124273691215 0369115182124273691215 wmwmwmwmw RIWRIWRIWRIW L, L, L, L. L, RECOVERY L. L, L, L. L, RECOVERY TIME (min) TIME (mm) (c) CARBOHYDRATE (d) FAT-PROTEIN Pooled ReSultS . | : o—os ¢——oc . o—--oP o---o FP I 1 ‘ . I , 1 1 GRADE SPEED 1' ' ' --o-- 1%) (MPH) r—-<: r—-J_ 9 l0 .— 1" y . 5 . 2 3 ' . 1 I I‘fl I 1 1 I I I I ‘ '. g . ; 23$ 6 I l I . I I 1 I I - I I I L L 1 . 1 o o 7 If I I I T I T I T I I I T T T T T I I T T I I I T I 03691215162124273691215 03691215182124273691215 wmwmwmwmw RIWRIWRIWRIW L. L, L, L. L. RECOVERY L. 1., 1.3 L. 1.ll RECOVERY TIME (min) TIME (mm) (e) SUPPLEMENT (f) DIET Figure 4.4. Diet and Supplement Effect on Heart Rate. 64 TABLE 4.4.--Statistica1 Resu1ts, Heart Rate (min). — '—-————""-‘—:;:‘=:;___.:__:...: :5::_:""— __‘._'_‘="'—'-':.__.:_'=:-::L7==_-m.:::::::__ Conditions ANOVA NaHCO3 NaHCD3 Placebo Placebo + + + + CHO Fat-Pro CHO Fat-Pro S D I Variables Min X SD (SC) (SFP) (PC) (PFP) P p p LeveI 1 I 1 i 5 136.5 5 7.9 137.1 5 8.0 136.5 5 5.5 137.9 5 10.3 0.35 0.38 0.32 55 2 I 5 139.7 5 8.4 141.9 5 7.5 139.4 5 5.1 140.2 5 10.5 I 3 I‘5 139.0 5 8.2 143.0 5 10.8 140.4 5 7.1 140.9 5 10.6 ; 1 I 5 080.0 5 9.2 088.0 5 15.2 079.0 5 15.6 073.1 5 13.9 0.23 1.00 0.95 ""l ”I 2.3 x 5 089.4 5 11.3 085.4 5 15.1 079.9 5 24.1 080.9 5 20.4 Leve1 2 I 1 I 5 151.4 5 6.8 152.2 5 6.3 150.7 5 7.7 149.1 5 7.6 0.97 0.84 0.82 :3I 2 I 5 155.1 5 7.8 154.7 5 8.5 155.2 5 8.0 157.4 5 9.0 I 3 i'5 155.6 5 8.4 158.5 5 8.0 157.6 5 7.9 157.0 5 7.0 I 1 I 5 093 2 5 12 3 099 5 5 15 8 093.7 5 15 8 095 0 5 17 3 0 65 0 84 o 68 5? 2-3 I 5 095.5 5 12.7 094.7 5 14.6 102.7 5 18.6 099.6 5 7.8 Leve1 3 1 1 Y 5 160.6 5 9.3 165.0 5 7.3 162.9 5 8.8 161.1 5 8.9 0.32 0.34 0.35 55' 2 I 5 166.9 5 9.9 168.7 5 8.4 168.5 5 9.5 168.4 5 1.0 3 I 5 168.9 5 13.0 172.2 5 7.6 171.1 5 9.0 169.4 5 11.7 I 1 2': 105.0 5 10.5 110.7 5 16.6 107.0 5 10.4 106.1 5 14.4 0.31 0.34 0.35 aI 2-3 I 5 106.3 5 7.0 107.2 5 10.9 105.7 5 9.3 104.5 5 12.4 LeveI 4 I 1 I 5 168.0 5 12.4 170.5 5 8.5 169.2 5 11.0 168.9 5 9.0 0.56 0.55 0.24 :2I 2 I - 173 0 5 1o 1 173 0 5 14.9 176 7 5 8 8 175 3 5 7 5 I 3 I 5 176.3 5 9.3 177.3 5 10.1 178.0 5 9.6 179.0 5 9.0 _. 1 7 5 137.0 5 27.4 135.8 5 29.3 135.2 5 28.5 131.3 5 19.3 0.65 0.69 0.15 a: 2-3 Y 5 111.0 5 19.1 122.7 5 15.9 113.7 5 10.1 115.9 5 22.2 LeveI 5:31 1 I 5 163.0 5 21.0 167.3 5 22.0 172.0 5 7.0 169.7 5 17.5 0.43 0.95 0.64 Recovery 1 I 3 131.3 3 12.2 131.2 1 13.1 131.2 5 16.0 127.2 : 18.2 0.15 0.16 0.17 2 I 5 109.0 5 10.6 110.9 5 7.8 110.4 5 12.3 106.7 5 18.5 3 I 5 103.6 5 10.2 104.0 5 9.7 102.7 5 8.0 101.5 5 10.8 4-5 7'5 100.8 5 10.9 99.5 5 7.6 97.6 5 7.9 98.0 5 9.1 0.14 0.13 0.13 6-7 7 5 100.0 5 8.4 99.0 5 9.9 99.4 5 7.5 99.1 5 11.6 8-9 I 5 99.2 5 8.0 97.1 5 9.9 100.0 5 8.0 98.5 5 6.5 10-12 I 5 101.7 5 6.9 96.2 5 9.3 100.0 5 7.2 97.7 5 11.8 0.57 0.51 0.07* 13-15 I 5 100.2 5 6.0 100.0 5 8.0 99 4 5 7.0 99 0 5 7 1 w = Work; R1 = Rest Interva1; S = SuppIement; D = Diet; 1 = Interaction; * StatisticaI significance. RESPIRATORY RATE (Imm) RESPIRATORY RATE Umin) RESPIRATORY RATE (Imm) 65 D1et Effect By Supplement 500 450 ' ' PC 400 350 SPEED 300 (MPH) 10 250 9 8 200 7 6 0 w L. L, L, L. L. L. L, L, L. 1., TIME (mm) TIME (mm) (o) SODIUM BICARBONATE (b) PLACEBO Supplement Effect By 0191 500 450 400 350 SPEED 300 (MPH) 10 250 9 8 200 7 6 0 L3 TIME (mm) TIME (mm) (C) CARBOHYDRATE (d) FAT—PROTEIN Pooled ReSUIts 500 I— —'——— 450 400 1— 35.0 e GRADE SPEED 300 >— (°/o) (MPH) 9 IO 25.0 '- 8 9 7 8 20.0 - 6 7 j. 5 6 L . o o 27 wmwmwmwmw wmwmwmwmw L1 L2 L3 L4 L5 L1 L: L3 L4 L8 TIME (min) TIME (min) (a) SUPPLEMENT (f) DIET Figure 4.5. Diet and SuppIement Effect on Respiratory Rate. RESPIRATORY RATE (Iv-nun) RESPIRATORY RATE (lmin) RESPIRATORY RATE (lmm) 65 D1et Effect By Supplement 500 45.0 PC 400 550 GRADE SPEED 300 (7.1 (MPH) 9 10 250 8 9 7 8 200 6 7 5 6 1 O O 27 L1 L2 L3 L4 L5 L. L2 L; L. L3 TIME (mm) TIME (mm) (o) SODIUM BICARBONATE (b) PLACEBO Supplement Effect By Dnet 500 r- o—o SFP ‘50 o---o PFP 400 350 1 I SPEED 300 Q (MPH) I0 250 9 8 200 7 6 O 15 R1 1711 R1 w L. L2 L; L‘ L5 L. L2 L3 L. L9 TIME (mun I TIME (mm I (c) CARBOHYDRATE (d) FAT — PROTEIN Pooled ReSults 500 450 400 35,0 GRADE SPEED 30 0 (°/o) (MPH) 9 10 25,0 8 9 7 8 200 6 7 5 6 O 0 W RI W RI W RI W W RI W RI W RI W RI W L: L: Lo L9 L1 L2 La L. La TIME (min) TIME (mm) (a) SUPPLEMENT (f) DIET Figure 4.5. Diet and SuppIement Effect on Respiratory Rate. (56 TABLE 4.5.-—Statistica1 ResuIts. Respiratory Rate (min). Conditions ANOVA NaHCO3 NaHCO3 PIacebo PIacebo + + + + _ CHO Fat-Pro CHO Fat-Pro S D I VariabIes Min x 50 (56) (569) (PC) (PFP) “F““‘B“““F‘ Levei 1 I 1 Y : 27 : 7.1 27 : 5.1 25 : 5.2 24 : 5.0 0.06- 0.15 0.52 3 ; 2 7 t 33 1 7.0 29 z 3.7 30 : 5.2 27 t 4.1 I 3 Y : 32:5.4 32:7.0 30:4.7 30:5.7 g 1 7 : 29 : 4.7 26 z 7.0 24 : 4.8 27 : 5.4 0.60 0.95 0.38 5&2 Y: 22:30 22:7.1 24:43 23:70 I 4 3 7 : 21 : 2.7 21 1 4.7 23 : 5.4 24 : 5.4 !1 T: 32:91 32:66 31-6.6 29:55 057037034 332 Y: 33:63 34:4.3 33:56 33:64 ;3 i: 37:47 36:4.3 36:57 36:71 ; 1 I : 28 : 6.4 31 : 6.3 26 : 3.7 24 : 3.0 0.10 0.39 0.26 :22 T: 26:4.8 24:5.7 25:5.6 23:54 E 3 Y : 23:4.0 23:7.0 23:4.0 21:3.1 , 1 i : 35:5.1 35:13.0 31:4.1 33:95 0.48 0.33 0.99 27,2 Y: 39:54 41:3.7 37:42 40:77 53 Y: 4142 44:5.0 43:72 44:80 I 1 Y : 32 : 3 3 34 : 5 7 31 : 4.1 30 : 6 0 0 92 0 71 0 71 E ; 2 Y : 25 : 2 a 25 : 8.2 29 : 5 6 27 : 8 1 I3 Y: 27:41 25:5.6 26:77 29:97 | _ v 1 x : 3a : 4 2 42 : 5 7 39 : 6.2 40 : 9 2 o 65 o 39 0 9a 3 I 2 7 : 45 : 4 4 46 : e 3 43 : 6 1 45 - 6 9 I 13 Y: 47:67 47:7.1 44:72 50:76 I _ l 1 x : 35 : 6.0 40 : 5.8 35 : 5.3 40 : 2.0 0.88 0.33 0.67 E: I 2 X : 30 + 2 I 20 + 4 3 32 : 4 6 32 : 3 3 I 3 i : 29:4.4 29:5.6 31:5.1 30:6.1 I 1 7 : 46 : 0.0 49 : 4.6 47 : 5.3 49 : 7.6 0.50 0.45 0.55 3 2 X : 50:6.1 52:7.0 49:6.3 52:00 I 3 i z 56 : 00 54 : 3.5 48 : 00 4a : 00 u = Hark; R1 = Rest IntervaI; S = Supplement; D = Diet; 1 = Interaction; * = StatisticaI significance. 67 was evident in the first IeveI of exercise (P = .06). This did not extend into the higher IeveIs of exercise. The physioIogicaI mechanism operating is not cIear. (h) Respiratory Quotient (R.Q.) In Figure 4.6a-f, TabIe 4.6 and Appendix F.6, the R.Q. vaIues are presented for the various conditions. In neither the ANOVA nor the sign test anaIyses were any significant differences observed. No concIusions can be drawn concerning the R.Q. data presented in this study. (1') L“ The bIood pH resuIts are shown in Figures 4.7a-f, 4.8, Tables 4.7a-i, 4.14a and Appendix F.7. In the ANOVA anaIysis sig- nificant NaHCO3 suppIement effects were observed (i.e., higher pH vaIues) in the pre-run measure (P = .09) (TabIe 4.7a) and in the difference between the measures taken at the end of exercise and at five minutes of recovery (ALS-RI) (P = .03) (TabIe 4.14a). None of the other ANOVA resuIts were significant. In Figure 4.7c, d and e, 'it shouId be noted that aII of the pH vaIues under the bicarbonate conditions are higher than those under the pIacebo condition. UtiIizing the sign test for each graphicaI comparison it can be concIuded that a significant bicarbonate effect (P = .01) upon pH is evident under both dietary conditions. The pH was higher at aII coIIection points when bicarbonate was ingested. It aIso is evident from the ANOVA resuIts and from Figure 4.7a, b and f that diet did not affect the pH in these subjects. R.Q. R0 R0. 105 I I 1.00 095 >— 090 - 065 ~ 030 I 0.75 — o 70 ~ 065 — 0.60 105~ lOOr- ossI— 0.90— 0851- 080»- 0.75— 070.. 0.651- 0.60‘ FIT 1.05 — I00 1— 0.95 I- 090 1— 085 I- 080 *- 0 75 I— 070 r- O 65 - 0.60}: 68 Diet Effect By Supplement o—o so o---o SFP H PC o-—-oPFP GRADE SPE ED I70) (MPH) 9 IO 8 9 7 8 r—~ 6 7 -— ‘ 5 6 1 1 r 1 1 1 1 1 i 1 1 1 1 1 1 1 1 1 T O 0 O 9 l2 I5 I8 2| 24 27 3 6 9 I2 I5 6 9 I2 I5 W RI W RI W RI W RI W W L1 L; L. L5 RECOVERY L1 L3 L3 L4 L. RECOVERY TIME (mm) TIME (min) (0) SODIUM BICARBONATE (b) PLACEBO Supplement Effect By Duet o——o SC o---o PC pc’ .1, ,1 SPEED / . 9 .o {—- b 8 9 ‘r—--. 7 8 r——— I 6 7 —— I I r— 5 6 1 1 1 1 1 1 1 1 1 1 1 1 T‘V i I 1 1 1 1 1 T 1 1 1 1 1 1 1 O O 3 6 9 l2 I5 I8 2| 24 27 3 6 9 I2 I5 3 6 9 I2 I5 I8 2I 24 27 3 6 9 I? I5 W RI W RI W RI W RI W W RI W RI W RI W RI W L1 L3 L3 Lg L5 RECOVERY L1 L2 3 L4 L5 RECOVERY TIME (mun) TIME (min) (C) CARBOHYDRATE (d) FAT-PROTEIN Pooled Results 0—05 o—vC o--—oP I o---o FP GRADE SPEED (Ola) (MPH) ...... 9 IO OUIOINICD 001400 1 1 1 1 1 1—1 1 1 1 1 1 1 T 1 11 1 1 1 1 1 1 1% 1 1 1 1 T 0 6 9 12 IS IS 2| 24 27 3 6 9 I2 I5 0 3 6 9 I2 IS IS 2| 24 27 3 6 9 I2 l5 W RI W RI W RI W RI W W RI W RI W RI W R L. L, 1., L. L, RECOVERY 1.. 1.2 L, L. 1.5 RECOVERY TIME (min) TIME (min) (e) SUPPLEMENT (f) DIET Figure 4.6. Diet and SuppIement Effect on Respiratory Quotient. :m—W .——f 69 TABLE 4.6.--StatisticaI ReSuIts. Respiratory Quotient (RQ). Conditions ANOVA NaHCO3 NaHCO3 PIacebo PIacebo + + + + CHO Fat-Pro CHO Fat-Pro S D I VariabIes Min x 50 (SC) (SFP) (PC) (PFP) P p P Levei 1 1 7': 0.70 : 0.06 0.66 : 0.08 0.70 : 0.06 0.64 : 0.07 .3 2 7 : 0.74 : 0.05 0.71 : 0.07 0.74 : 0.06 0.74 : 0.05 3 7 : 0.77 : 0.04 0.75 r 0.05 0.80 : 0.05 0.76 : 0.03 0.85 0.30 0.84 1 7 : 0.75 : 0.08 0.75 : 0.06 0.80 : 0.05 0.74 : 0.06 55 2-3 7 : 0 82 : 0.11 0.82 : 0.06 0.83 : 0.06 0.82 : 0.09 LeveI 2 . 1 7 : 0.76 : 0.03 0.73 : 0.05 0.77 : 0.09 0.73 : 0.03 :3. 2 7 : 0.76 : 0.05 0.76 : 0.06 0.77 : 0.05 0.77 : 0.03 A 3 7 : 0.81 : 0.05 0.80 : 0.07 0.80 : 0.04 0.80 : 0.02 0.90 0.97 0.77 1 7 : 0.82 : 0.04 0.80 : 0.04 0.81 : 0.03 0.81 : 0.02 '"‘ 2-3 7 : 0.87 : 0.07 0.87 : 0.05 0.86 : 0.05 0.86 : 0.10 LeveI 3 1 7 : 0.71 : 0.10 0.77 : 0.07 0.76 : 0.07 0.76 : 0.02 :3’ 2 7 : 0.81 : 0.04 0.81 r 0 07 0.81 : 0.05 0.81 : 0.03 3 7 : 0.85 : 0.05 0.85 : 0.06 0.85 : 0.05 0.85 : 0.04 0.84 0.84 0.89 1 7 : 0 87 : 0.04 0 87 : 0 08 0.90 : 0.05 0.87 : 0.04 '7 2-3 7 : 0.90 : 0.05 0.89 : 0.05 0.90 : 0.06 0.87 : 0.08 LeveI 4 . 1 7 : 0.80 : 0.06 0.80 : 0.07 0.80 : 0.07 0.78 : 0.05 2’ 2 7 : 0.87 : 0.05 0.85 : 0.05 0.83 : 0.07 0.86 : 0.04 3 7 : 0.93 : 0.07 0.92 : 0.05 0.91 : 0.06 0.93 : 0.06 0.66 0.82 0.91 1 7 : 0.98 : 0.07 0.95 : 0.05 0.94 : 0.12 0.98 : 0.10 :7: 2-3 7 : 1.01 : 0.07 0.98 : 0.06 1.00 : 0.10 1.00 : 0.13 Recovery 1 7': 0.96 : 0.07 0.99 : 0.04 0.98 : 0.04 0.92 : 0.09 0.28 0.31 0.36 2 7 : 1.05 : 0.07 1.06 : 0.04 1.04 : 0.05 1.01 : 0.10 3 7 : 0.96 : 0.08 1.00 : 0.05 0.96 : 0.06 0.92 : 0.13 4-5 7 : 0.89 : 0.07 0.94 : 0.05 0.94 : 0.20 0.89 : 0.11 0.31 0.35 0.39 6-7 7 : 0.89 : 0.16 0.89 : 0.03 0.84 : 0.06 0.85 : 0.07 8-9 7 : 0.82 : 0.07 0.83 : 0.07 0.81 : 0.04 0.80 : 0.07 10-12 7 : 0.77 : 0.09 0.78 : 0.06 0.74 : 0.06 0.75 : 0.08 0.31 0.32 0.32 13-15 7 : 0.71 : 0.07 0.70 : 0.03 0.69 : 0.07 0.69 : 0.07 w = work; R1 = Rest IntervaI; S = SuppIement; D = Diet; I = Interaction 70 0181 Effect By Supplement 745 {- no I- o—o sc o—o Pc o---o SFP o---o PFP 7 35 - 730 P g GRADE SPEED 725 P (961 (MPH) 9 I0 720 » a 9 7 a 7 15 - —— , 6 7 A; — Q r—— 1 5 6 --—w——+—HP—H—fiP-1R41 1 1 1 -—r—4—A1—+P—H—ar 1 1 4P: rv o 0 PW o 3 6 9 12 15 5 IO 15 PW O 3 6 9 12 15 5 IO 15 l-I L2 L3 Ll L3 L. La ' L. 3 WORK RECOVERY ~ WORK RECOVERY TIME (m1n.) TIME (mm) (o) SODIUM BICARBONATE (b) PLACEBO ”5 Supplement Effect By Dlet 74oF o——o sc o—o SFP l I o-—-o PC o-——o PFP 7 35 ‘1- 7 30 r- g I GRADE SPEED 7 25 1- 19.1 (MPH) 9 I0 720 —— e 9 .—- 7 8 7 IOI —— 1 1— 6 7 I _- _ ‘ r.— 5 6 —1—1—4. P—I I——I I—II 1 1 1 1 —1——r——1 I—i I—I I——I ‘r 1 1 1 1 0 0 P11 0 3 6 9 12 15 5 IO 15 Pw o 6 9 12 15 5 lo 15 L1 L2 L3 L4 L9 L1 L2 L9 L4 L5 WORK RECOVERY WORK RECOVERY TIME (mm) TIME (mm) (c) CARBOHYDRATE (a) FAT—PROTEIN ”SI Pooled ResOlts 7.40 >- 0—4 s o—o c o---o P o—--o FP 735 ~ 7.30 ~ :5 SPEED 725 ~ (MPH) 9 10 720 r >0 8 9 I 7 8 7 '5 7 | 6 7 I. ' 5 6 '[-—r—4—Hr—4P—H—R;g 1 1 19* 1 1 1 o 0 PW o 3 6 9 I 1 5 l0 5 IO 15 WORK RECOVERY RECOVERY TIME (min) TIME (mm) (0) SUPPLEMENT (1) DIET Figure 4.7. Diet and SuppIement Effect on pH. a ApH ApI-I 71 DIFFERENCES IN pH A PRE WORK TO LEVEL 5 A PRE WORK TO RECOVERY I 0.30 .- 025 - __ 0.20 P _ F O.I5 - 0. IO 1- 0.05 *- 0.00 b sc SFP PC PFP 0 PP s P so SFP PC PFP c FP s P COIIDITIONS DIET SUPPLEMENT CONDITIONS DIET SUPPLEMENT A PRE WORK TO RECOVERY 3 A LEVEL 5 TO RECOVERY l 0.30 - 0.25 *- O.20 - 0 I5 1- r— F—I '—1 0.10 1- 0105 P I—I—I ....I , Th1 l I‘I I—I—1 sc SFP Pc PFP 0 FR 9 P sc SFP PC PFP c FP s P CONDITIONS DIET SUPPLEMENT CONDITIONS DIET SUPPLEMENT A LEVEL 5 TO RECOVERY 3 0.30 - 0.25 I- 020 - ApH O 31 I 0.05 r 0'00 sc SFP ’Pc PFP c PP s P CONDITIONS DIET SUPPLEMENT Figure 4.8. pH Changes under Different Conditions. 72 TABLE 4.7.--Statistical Results, pH. Conditions ANOVA NaHCO NaHCO Placebo Placebo 3 3 + + CHO Fat-Pro CHO Fat-Pro S D I Variables (SC) (SFP) (PC) (PFP) P P P (a) PW 7 7.43 7.44 7.42 7.41 0.09* 0.90 0.19 SD 0.02 0.03 0.03 0.02 (b) LI 7 7.41 7.42 7.40 7.38 0.12 0.71 0.57 SD 0.04 0.03 0.03 0.06 (c) L2 7' 7.42 7.4l 7.40 7.39 0.15 0.55 0.93 SD 0.04 0.04 0.04 0.06 (d) L3 7 7.39 7.38 7.35 7.36 0.17 0.88 0.73 SD 0.04 0.07 0.06 0.06 (e) L4 7' 7.30 7.3l 7.28 7.26 0.25 0.73 0.63 SD 0.07 0.09 0.08 0.09 (f) L5 7' 7.23 7.24 7.23 7.l8 0.28 0.48 0.30 SD 0.07 0.07 0.05 0.07 (9) RI 7' 7.l9 7.21 7.18 7.20 0.7l 0.38 0.84 SD 0.06 0.05 0.09 0.09 h R2 7' 7.26 7.25 7.26 7.23 0.60 0.33 0.72 SD 0.05 0.06 0.07 0.08 1 R3 7' 7.31 7.29 7.29 7.26 0.37 0.39 0.75 SD 0.05 0.07 0.07 0.ll PW = Pre-work; Ll - L5 = Level l-5 of work. R1 R3 = Five, ten and fifteen minutes of recovery. 3(- "III Statistical Significance Supplement; D = Diet; I = Interaction 73 (.1) 8992 The P002 results are shown in Figures 4.9a-f, 4.l0, Tables 4.8a-i, 4.l4b and Appendix F.8. The ANOVA analyses across treatments at selected levels of work and recovery indicate significant dietary effects (i.e., lower PCO2 values under the CHO diet) at levels 2 and 3 during exercise (Figure 4.9a, b and f; P = .02, P = .09). When it was possible to consider all points simultaneously, as in the sign test, a clearly significant pattern emerged. The PCO2 was significantly lower following the carbohydrate diet than it was when the fat-protein diet was used (Figure 4.9a, P = .09; Figure 4.9b, P = .002; Figure 4.9f, P = .02). With supplementation of bicarbonate, the PC02 was significantly lower under both dietary conditions and obviously when the data were pooled (Figure 4.9c, P = .002; Figure 4.9d, P = .002; Figure 4.9e, P = .002). From these results it can be concluded that the FCC values are lowered by a high 2 carbohydrate diet and by a Dre-exercise bicarbonate supplement. (7) 292 The P02 results are presented in Figures 4.lla-f, 4.l2, Tables 4.9a-i, 4.l4c and Appendix F.9. The P0 increased with the 2 intensity of exercise up through level 3. In most instances, it dropped slightly during level 4 and then started to rise again during level 5 of exercise. During recovery, the P02 decreased but never returned to the base line. Utilizing ANOVA, there were no statisti- cally significant supplement, diet or interaction effects. Figure 4.lla, however, shows that the P02 measurements were consistently pC0, (mm Hg) pCOg (mm HQ) 400 — O—o SC o---o SFP 35 O - SPEED 30 0 - (MPH) 9 IO ,9 8 9 r— l stzs‘;* 7 a 25 O I- I 6 7 .. I. I _ _ l- 5 6 I 1 I I l —T—+—‘I I—'—I I'—'I I—_I1 1 1 1 1 —T—T_I I—I I—'I I‘_II 1 1 1 1 0 0 PW 0 3 6 9 l2 I5 5 IO I5 PW 0 3 6 9 l2 l5 5 I0 l5 L. L2 L3 I-a L5 L1 L1 L3 L4 I-s WORK RECOVERY WORK RECOVERY TIME (mm) TIME (mm) (a) SODIUM BICARBONATE (b) PLACEBO Supplement Effect By 01et H SC ~——o SFP o----o PC o----o PFP 35.0 >- GRADE SPEED 30 o L (9.) (MPH) 9 IO ,0 O——-..°___._o o.—--O” a 9 k——-O——o I 7 8 25 O I- I—' I 6 7 It r—— r— ' I 5 6 —-r— P o—---o FF 6 7 i I ' | 1 5 e f—‘E I—'I I—I I'"_II I I I I fi—I: I—‘I I'_‘I I—I rL T I I I O 0 PW O 3 6 9 12 15 5 IO 15 PW O 3 6 9 12 15 5 IO 15 LI L2 L3 L4 L5 Ll L2 L3 L. L5 WORK RECOVERY WORK RECOVERY TIME (mm) TIME (mm) (e) SUPPLEMENT (1‘) DIET Figure 4.11. Diet and SuppIement Effect on P02. A P0, (mm Hg) A p01 (mm Hg) 20.0 16.0 8.0 4.0 00*- 24.0 200 160 80 4.0 0.0 h A PRE WORK TO LEVEL 7 8 DIFFERENCES IN P02 5 A PRE WORK TO RECOVERY I _ 7 I 47 r— '—7 SC SFP Pc PFP c FF 9 P CONDITIONS DIET SUPPLEMENT A LEVEL 5 TO RECOVERY I j fl sc SFP Pc PFP 0 FF 9 P CONDITIONS DIET SUPPLEMENT A LEVEL 5 TO RECOVERY 3 RUTH—“fl 5C SFP PC PFP C PP S P CONDITIONS DIET SUPPLEMENT A PRE WORK TO RECOVERY 3 H F—I SC SFP PC PFP C FP S P CONDITIONS DIET SUPPLEMENT 24.0 I- 20.0 '- " I6.0 *- E' E .5 12£)~ N C Q a 80 I" 4.0 F 0.0 L SC SFP PC PFP CONDITIONS Figure 4.12. PO 0 PP S P DIET SUPPLEMENT 2 Changes under Different Conditions. 79 TABLE ZI.9.--Statistica1 Resu1ts, P02 (mmHg).* Conditions ANOVA NaHCO3 NaHCO3 P1aceb0 P1aceb0 + + + + CHO Fat-Pro CHO Fat-Pro S D I VariabIes (SC) (SFP) (PC) (PFP) P P P (a) P 7’ 80.57 77.60 77.46 80.47 0.94 0.91 0.16 SD 5.8 3.7 7.5 4.7 (b) L 7 85.50 79.15 85.06 84.70 0.48 0.35 0.40 SD 12.5 6.0 12.4 7.5 Ic) L2 7' 92.77 82.66 91.78 87.48 0.73 0.19 0.59 SD 19.4 5.8 20.0 12.0 (0) L3 7' 94.80 85.85 88.56 95.78 0.74 0.88 0.16 SD 21.2 10.8 15.0 15.0 (9) L4 7 91.02 84.72 87.37 90.18 0.84 0.61 0.22 SD 6.5 12.0 8.1 13.2 (f) L5 7' 93.23 88.62 90.08 92.22 0.99 0.80 0.49 SD 13.5 10.1 14.6 6.0 ( R1 7' 101.00 95.00 99.34 100.02 0.81 0.45 0.43 SD 9.0 7.5 16.1 15.6 h R2 7' 99.33 94.21 90.54 96.57 0.31 0.89 0.12 SD 10.0 9.2 8.8 10.3 1 R3 7’ 97.29 88.28 92.86 94.62 0.90 0.58 0.40 SD 19.3 13.5 20.0 14.8 PW Pre-work; L1 - L5 = Leve1 1-5 of work R1 R3 = Five, ten and fifteen minutes of recovery Supp1ement; D-= Diet; I = Interaction The10w vaIues of P02 cannot be exp1ained. U) 11 III II 80 high under the carbohydrate condition (sign test, P = 0.002). The p001ed resuIts in Figure 4.11f a1so show that the carbohydrate va1ues were higher than the fat—protein vaIues at most of the IeveIS during both work and recovery (sign test, P = 0.09) In generaI, the P02 va1ues are Tower than expected. The reasons for this are not c1ear. The PO2 was consistentIy highest under the SC condition (Figure 4.11a and c; sign test, P = 0.002). The p001ed resu1ts show that the P02 was Towered by bicarbonate supp1ementation during work and post-exercise recovery (sign test, P = 0.09; Figure 4.11e). According to Figure 4.12, the most noticeab1e changes occur f0110w- ing a carbohydrate diet. On the basis of these data, it c0u1d be conc10ded the P02 is decreased by bicarbonate and is increased by a carbohydrate diet. (1) TotaI C02 The tota1 CO2 (TCOZ) resuIts are shown in Figures 4.13a-f, 4.14, Tab1es 4.10a-i, 4.14d and Appendix F.10. The TCO2 is the sum of the actua1 bicarbonate p1us the carbonic acid (TCO2 = (HCOé) + (0.03 x PCOZ) expressed in mMo1/L of p1asma. The ANOVA program showed significant dietary effects at 1eve1 2 of exercise (P = .07). In addition, the suppIement difference between the end of 1eve1 5 and five minutes of recovery (ALS-RI) was statistica11y significant (P = .06; Tab1e 4.14d). The greatest decrease was evident with bicarbonate supp1ementation (Figure 4.14). When a11 measurement points were compared in Figure 4.13a, the TCO2 was significant1y Iower with 11ch03 ingestion fo11owing a carbohydrate diet than foIIowing a fat-protein diet (Sign test, 81 Diet Effect By Supplement 50.0 A 0—0 SC 0—0 PC 2 25-0 0----o sPP o----o PPP 8 a g 20 0 § GRADE SPEED .5, 1%) (MPH) <5- 15 0 [p ’0 9 I0 I3 , ’ 8 9 0" "<7 7 8 I00 6 7 5 6 l T T11 1 1 T O 0 5 10 I5 5 10 I5 WORK RECOVERY RECOVERY TIME (min) TIME (mm) (0) SODIUM BICARBONATE (b) PLACEBO Supplement Effect By Diet 300 H 5C 0—0 SFP ’g 25.0 O-'--O PC o----o PPP 8 a :‘ 200 g GRADE SPEED E (‘79) (MPH) ~ 15.0 9 10 O \ U \ ,/ 8 9 I— , I l ,r I R <>- 7 a 10.0 6 7 .. I—l I I I 5 6 I I—fiF—fihfit I I I I ——r—4:;P—n—AP—M~I I I I o 0 PW o 3 6 9 I2 I5 10 I5 Pw 0 3 6 9 12 I5 5 10 I5 L. Lz L, L. L. L| L2 L3 L. , w0RK RECOVERY WORK RECOVERY TIME (mm) TIME (min) (0) CARBOHYDRATE (d) FAT-PROTEIN Pooled Results 300 I _ A I o—-o s o——o C E 250 I o----o P o-—--o PP E I 9 I S 20.0 I § GRADE SPEED g I 1%) (MPH) ~ I . 9 10 £3 50 [/0 /° 9 9 I— I x’ — 7 8 I I I I 6 7 PP: r— I r— I 5 6 | I —'1_I:I I—I I——'I I—II I I f l _I—; I"'—I I—I I II I I I O 0 PW o 3 6 9 12 Is 5 10 I5 PW 0 3 6 9 12 I5 5 10 I5 L. L2 L3 L. L. L. Lz L, L. L5 w0RK RECOVERY w0RK RECOVERY TIME (mm) TIME (171an (e) SUPPLEMENT (f) DIET Figure 4.13. Diet and Supp1ement Effect on TCOZ. A Tco: (mMoI/I. plasma) A Tco, ImMoI/I. plasma) 16.0 — I2.0 - 8.0 - 4.0 '- 0.0 I- 16.0 12.0 8.0 4.0 0.0 L 82 DIFFERENCES IN TCO2 A PRE WORK TO LEVEL 5 A PRE WORK TO RECOVERY I __ _1—‘ 77* fl sc SPP PC PFP 0 PP S P so SPP PC PFP 0 FF 6 P coNDITIoNS DIET SUPPLEMENT CONDITIONS DIET SUPPLEMENT A PRE WORK TO RECOVERY 3 A LEVEL 5 TO RECOVERY 1 ”TI—— — I— H I—I mmFI—Ifl—I sc SPP PC PFP 0 FF 9 P so SPP PC PFP c PP s CONDITIONS DIET SUPPLEMENT CONDITIONS DIET SUPPLEMENT A LEVEL 5 TO RECOVERY 3 I6.0I- ’6 E I2.0I- O 3 S ‘23 8.0I- .5, N O I_‘:’ 4.0+- Q I—F—I I—fl 6.6 SD 1:11 90 SPP Pc PFP c PP CONDITIONS DIET SUPPLEMENT Figure 4.14. TCO2 Changes under Different Conditions. TABLE 4.10.--Statistica1 ResuIts, TCO 83 (mMoI/L P1asma). 2 Conditions ANOVA NaHCO3 NaHCO P1acebo P1acebo + + + + CHO Fat-Pro CHO Fat-Pro D I Variab1es (so) (SFP) (PC) (PFP) P P Ia) PM 7‘ 27.00 27.40 26.94 26.40 .67 .93 .71 50 3.7 3.4 4.2 2.2 6) LI 7' 22.25 24.01 22.47 23.27 .87 .43 .76 so 3.9 2.5 5.9 5.0 (c L2 '7 21.70 24.57 20.80 24.01 .65 .07* .92 $0 3.7 3.1 6.4 4.0 (d) L3 7' 19.65 20.82 18.91 22.16 .87 .23 .57 50 4.6 3.7 5.4 6.4 {e} L4 7’ 15.20 16.67 15.29 15.60 .77 .60 .73 so 3.1 6.7 4.1 4.5 (f) L5 7' 12.71 13.38 12.87 12.23 .69 .98 .58 $0 2.6 2.6 2.4 3.7 (g) R1 7' 10.80 11.30 11.09 11.83 .65 .50 .90 $0 2.1 1.3 3.0 3.5 (h) R2 7' 12.66 12.19 12.90 12.05 .96 .41 .82 50 1.9 1.3 2.4 3.0 (1 R3 7' 13.90 14.77 13.56 14.53 .84 .51 .97 50 2.87 5.53 2.34 3.82 PW Pre-work; L1 - L5 = Leve1 1-5 of work. R1 R3 = Five, ten and fifteen minutes of recovery. II- II II I 11 Supplement; Statistica1 Significance D = Diet; I = Interaction 84 P = .02). No differences were evident when suppIement effects were compared under the two diet conditions (Figure 4.13c and d). The p001ed resu1ts show that the TCO2 was significant1y Tower with a carbohydrate diet than with a fat-protein diet (Figure 4.13f, P = .02). The p001ed supp1ement resu1ts were not significant (Figure 4.13e). Fo11owing study of a11 of the data, particuTarTy the graphs, it was determined that the significant P va1ue obtained for ALS-RI was 1ike1y due to chance. It wou1d appear that a carbohydrate diet may 1ower the TCOZ. The data presented herein, however, do not appear to be sufficientIy c1ear to warrant such a conCIUsion. (m) Bicarbonate The va1ues for bicarbonate (HCOé) are given in Figures 4.15a-f, 4.16, Tab1es 4.11a-i, 4.149, and Appendix F.11. During exercise the HOD; 1eve1 dec1ined. It started rising at the termina- tion of the work but had not returned to the base Tine after fifteen minutes of recovery. The ANOVA resu1ts show a supp1ement effect (P = 0.07) from the termination of exercise to the first five minutes of recovery (AL5-R1; Tab1e 4.14e). The greatest differences occurred under the suppIement condition. Figure 4.15a shows that the concen- tration of HOD; was Iower after the carbohydrate diet than after the fat-protein diet both before and during exercise (sign test, P = 0.02). This resu1t was not expected due to the higher pH va1ues observed by Hunter (137) under high carbohydrate diet conditions. The supp1ement resu1ts are 1ess c1ear. HCO,’ (mEq/l pIosmo) HCO,’ (mEq/l. plasma) HCO,‘ (mEq /1. p105mo) 85 DIet Effect By Supplement 30.0 I— 0—0 SC 0—0 PC 2510 - 0----o SPP 0----o PFP’ 20.0 >- GRADE SPEED 1%) (MPH) IsoL 9 .6 ,9 e 9 ’ __o’" 7 8 10.0 I- I ‘ 6 7 I r— I . 5 6 —1—_'T—'I H H I—‘I I I r f 7 I I I O 0 PW O 3 6 9 12 15 5 IO 15 5 IO 15 LI L2 L3 L. L5 L1 L2 L3 L‘ 5 WORK RECOVERY WORK RECOVERY TIME (m1n.) TIME (mm) (o) SODIUM BICARBONATE (b) PLACEBO Su lement Effect 8 DIet I o———o SC 0—0 SFP 25-0 o----o PC 0----0 PFP 20.0 GRADE SPEED (90) (MPH) 15 0 9 IO 8 l 9 ,0 1’»- ", 7 —l— 8 10 o ’ 6 7 F— I I 5 6 I I I I —I'—I—‘I I——I I—‘I I—I F I I T 1 O 0 IO 15 PW O 3 6 9 12 15 5 10 15 L. Lz L, L. L, WORK RECOVERY WORK RECOVERY TIME (mm) TIME (mm) (C) CARBOHYDRATE (d) FAT-PROTEIN Pooled ReSUlts 30 o F , —— : s ' ._—o c 25-0 " o—---0 P 0--—-o FP 20 0 ~ GRADE SPEED (‘76) (MPH) 15 o I 9 Io _ 8 9 S” M 7 8 10.0 - r——— ‘ 6 7 41- I—i . I—— ' ‘ 5 6 ‘T—T‘fl I'_'I I—_‘I I‘—_I I_T I I I '—I'_‘I'—I I——1 I—I I—_I Iif I I 7 O 0 PW O 3 6 9 I2 15 5 IO 15 PW O 3 6 9 12 15 5 IO 15 L. Lz L, L. L, L. L. L; L. L, K RECOVERY WORK RECOVERY TIME (mm) TIME (mm) (9) SUPPLEMENT (f) DIET Figure 4.15. Diet and Supp1ement Effect on HCO 3. A HCO,‘ (mEa/I plasma) A HCO,‘ ImEq/I. plasma) 120'- 80*- 00- 160- 12.0 '- 80- 40~ 0.0 - 86 DIFFERENCES IN HCO3_ A PRE WORK TO LEVEL 5 A PRE WORK TO RECOVERY 1 PL. 7* ”751 sc SPP PC PPP C FP s P so SPP PC PFP c FP s P CONDITIONS DIET SUPPLEMENT CONDITIONS DIET SUPPLEMENT 0 PRE WORK TO RECOVERY 3 A LEVEL 5 TO RECOVERY 1 F__~—— F—_-m F_WL-I mflmgfi sc SFP PC PFP c PP S P sc SFP PC PPP 0 PP CONDITIONS DIET SUPPLEMENT CONDITIONS DIET SUPPLEMENT A LEVEL 5 TO RECOVERY 3 160~ '5 g 12.0» 0 a t g 8.0- E I n 8 4.o~ I C o.0-IIII[:IJ:I:1_I;I:L sc SPP PC PFP C FP CONDITIONS DIET SUPPLEMENT Figure 4.16. HCOé Changes under Different Conditions. 87 TABLE 4.11.--Statistica1 Resu1ts, Bicarbonate (mEq/L p1asma). Conditions ANOVA NaHCO3 NaHCO3 P1acebo P1acebo + CHO Fat-Pro CHO Fat-Pro S 0 IL VariabIes (so) (SFP) (PC) (PFP) P P P (a PH 7 25.81 26.21 25.78 25.20 0.67 0.92 0.69 so 3.6 3.2 4.0 2.12 (b) L1 7 21.25 23.07 21.44 22.15 0.81 0.42 0.72 so 3.8 2.5 5.7 4.9 (c) L2 7 20.83 23.50 19.81 22.15 0.63 0.07* 0.87 so 3.6 3.1 6.2 4.9 (d) L 7 18.68 19.86 18.1 21.01 0.88 0.25 0.62 so 4.5 3.6 5.2 6.18 (e) L4 7 14.22 15.64 14.29 14.50 0.74 0.62 0.73 so 3.1 6.6 4.1 4.4 (f) L5 7 11.71 12.40 11.90 11.17 0.68 0.95 0.55 so 2.5 2.6 2.4 3.6 (9) R1 7 9.81 10.29 10.10 10.76 0.70 0.56 0.92 so 2.1 1.3 3.0 3.8 (h) R2 7 11.7 11.21 12.33 11.50 0.56 0.40 0.82 so 1.9 1.3 2.6 2.8 (1) R3 7 12.97 13.84 12.62 12.91 0.65 0.67 0.83 so 2.8 5.5 2.3 3.8 Pw = Pre-work; L1 - L5 = Leve1 1-5 of work R1 R3 = Five, ten and fifteen minutes of recovery, ‘- lllll Statistica1 Significance Supp1ement; D = Diet; I = Interaction 88 (n) Base Excess The base excess (B.E.) resu1ts are presented in Figures 4.17a-f, 4.18, Tab1es 4.12a-i, 4.14f, and Appendix F.12. In the ANOVA statisticaI comparisons, on1y the difference from the termina- tion of exercise to the first five minutes of recovery (ALE-RT) for the suppTement was statistica11y significant (P = 0.01: Tab19 4.14f). In Figure 4.17a, b, and f, the base excess vaIues were con- sistentIy 1ower during work f011owing a carbohydrate diet than foIIowing a fat-protein diet. The differences, using the sign test, were significant (P = .09). On the basis of these data, aIthough not higth conc1usive, the resu1ts indicate that the B.E. tends to be Towered by a carbohydrate diet. Figure 4.17e shows that, when the supp1ementary data were p001ed, the base excess va1ues were significant1y increased (sign test, P = .02) at the various 1eve1s of work and at 10 and 15 minutes of recovery by sodium bicarbonate supp1ementation. (o) Lactic Acid The Tactic acid resuIts are presented in Figures 4.19a-f, 4.20, Tab1es 4.13a-i, 4.149, and Appendix F.13. In the ANOVA ana1yses on1y the supp1ement differences between those taken after 1eveI 5 and those taken at the 15th minute of recovery (ALB-RB) were statistica11y significant (Figure 4.20 and Tab1e 4.149; P = .09). This was one of ten ana1yses and no other comparisons approached significance. In the ALS-R3 comparison the Tactate differences were greatest with bicarbonate supp1ementation. 89 DIet Effect By Supplement Figure 4.17. 3 I 0 0 ' o——o SC 0—0 PC o----o SFP o---o PFP E —5.0 U “2’ V GRADE SPEED : —IO 0 ('l.) (MPH) 9 IO 8 9 - 15 O 7 a 6 7 5 6 1 1 1 1 ‘1 l o o 5 IO 15 5 10 15 RECOVERY RECOVERY TIME (mm) TIME (mm) (0) SODIUM BICARBONATE (b) PLACEBO 30 Supplement Effect By DIet 0.0 O—-o sc 0—0 SFP o----o PC ou-o PFP E -50 U “E " GRADE SPEED : - 10.0 (°/.) (MPH) 9 IO ’20 e 9 —15_o — ’ 7 a 6 7 5 6 1 1 I 1 1 1 O O 10 15 5 IO 15 RECOVERY RECOVERY TIME (mm) TIME (min) (c) CARBOHYDRATE (d) FAT-PROTEIN Pooled Results 3 O — I ‘— 0 0 ” I 0—0 5 0—4 C I on-o P 0----0 FP .. I : -5.OI- I U E 1 ‘f GRADE SPEED : -I0.0 .. I (°/o) (MPH) 9 IO \ 8 9 —I5.0 - I )7 7 3 I—— I I 6 7 I I 5 6 —1'_E ("—1 I—_I I""I I I I I T I 0 0 PW O 3 6 9 12 1 5 IO 15 5 IO 15 L. L2 L, L. L, WORK RECOVERY RECOVERY TIME (min) TIME (min) (6) SUPPLEMENT (f) DIET Diet and Supp1ement Effect on Base Excess. A B.E. (mEq/I.) A B.E. (MEG/l.) 9O DWEERENCESIN BASE EXCESS A PRE WORK TO LEVEL 5 A PRE‘WORK TO RECOVERYI s<>r 0.0 - -Ioc>L b‘ L_1—— 5J__‘ L" ..E“ LJr—‘ —15.0r- Lt— -20.0 *- sc SPP Pc PFP c PP s P sc SFP Pc PFP c FF 3 P CONDITIONS DIET SUPPLEMENT CONDITIONS DIET SUPPLEMENT A PRE WORK TO RECOVERY 3 A LEVEL 5'TO RECOVERY I 5.0 - - 5.0 P- -— 10.0 v- — [5.0 b— --2o.c>L sc SPP Pc PFP 0 PP s P so SPP Pc PFP c FF 5 P CONDITIONS DIET SUPPLEMENT CONDITIONS DIET SUPPLEME NT A LEVEL 5 TO RECOVERY 3 5.0 r- °°” I H LI 1 LII w E; w - 5.0 " 5' m ad - 10.0 >- d - I5.0 [ —20.0 b _— ..__ sc SFP Pc PFP c FF 5 P CONDITIONS DIET SUPPLEMENT Figure 4.18. Base Excess Changes under Different Conditions. 91 TABLE 4.lZ.--Statistical Results, Base Excess (mEq/L Blood or Plasma). Conditions ANOVA NaHCO3 NaHCO3 Placebo Placebo + + + + CHO Fat-Pro CHO Fat—Pro D I Variables (sc) (SFP) (PC) (PFP) P P (a PM 7 +160 +2.18 +1.46 +0.72 .49 0.92 0.56 so 38 2.6 3.6 2.0 (b Ll Y -2.24 -o 79 —2.68 -2 31 .50 0.54 0.72 so 3.6 2 1 5.2 4 8 (c L2 '1? -2.20 -o.34 -3 74 -1.37 .41 O.l8 0.87 so 3.8 3.2 57 3.7 (d) L3 31’ -5.15 -4 09 -6.44 -3 82 .78 0.32 0.68 so 4.4 4 1 5.6 6 2 1e) L4 7 -10.9 -9.59 -11.25 -11.14 .64 0.73 0.77 so 4.3 7.8 5.3 6.8 (f) L5 '1? -l4.63 -13.7o -l4.58 -l6.3 .44 0.77 0.40 so 3.4 3.6 3.0 4.8 (9) RI 7 -17.41 -l6.30 -17.10 -16.17 .89 0.50 0.96 so 3.4 2.3 5.0 5.7 (h) R2 7 -13.61 -14.52 -13.49 -14.91 91 0.32 0.82 so 2.5 2.4 3.0 4.5 (1) R3 7 -11.69 -12.16 -12.42 -13.23 .61 0.72 0.92 so 3.3 5.6 3.1 6.5 PW R1 Pre-work; U) 11 Supplement; Ll - L5 = Level l-5 of work; R3 = Five, ten and fifteen minutes of recovery D = Diet; I = Interaction LACTATE (mMol/I.) LACTATE (mMol/I) LAC TATE (mMOI /I I 75 50 2.5 00 150 92 D1et Effect By Supplement GRADE SPEED 1%) 9 e I O—OSC o—o Pc 7 I o—---o SFP o----o PFP 6 5 I—fih—iF—H*i* 1 1 1 r 1 1 0 Pwos 591215 1015 51015 L. Lz L, L. L, WORK RECOVERY RECOVERY TIME (mm) was (mm) (o) SODIUM BICARBONATE (b) PLACEBO Supplement Effect By Um I l 1 q\ l nx‘x (o/O) l l 5 , l ' ° 5‘3 I H SFP 7 ’ I o----o Pc I o--—-o PFP 6 --.rd’ I ””” J 5 -—fi——4-dE-dF—dP—i%h1 1 1, r—— P—H—fit—dt 1 1 1 1 0 PW O 3 6 9 12 15 5 1o 15 Pw o 3 6 9 1215 5 1o 15 L. L2 L3 L. L5 L. L, L, L. L5 WORK RECOVERY WORK RECOVERY TIME (mm) TIME (mm) “Igfiflgflflflflé (d) FAT - PROTEIN Pooled Re5ults TIME (mm) (e) SUPPLEMENT Figure 4.l9. o——o s o———-O C o---o P o-—--O FP r 1 1 n 1 1 5 IO 15 5 IO 15 RECOVERY WORK RECOVERY TIME (171111.) (1) DIET Diet and Supplement Effect on Lactate. (MPH) IO omumw GRADE SPEED (MPH) 1 0 0014(1)“) SPEED (MPH) IO 004$“) A LACTATE (mMoI/l.) A LACTATE (mMoI/l.) H10 P 15 — 5.0 '- 013b 1013— 151- 501— 251- 0.0 L- 93 DIFFERENCES IN LACTATE A PRE WORK TO LEVEL 5 I—Ir— sc SFP PC PPP CONDITIONS c PP DIET S P SUPPLEMENT A PRE WORK TO RECOVERY 3 I—I— SC SFP PC PFP CONDITIONS 3 O 2 5 1.1.1 1- <1 1— Q d .J C Figure 4.20. 100 15 5O 25 00 c FP DIET r__. S P SUPPLEMENT A PRE WORK TO RECOVERY I F‘— r I— h I—. sc SPP Pc PPP c FF 5 P CONDITIONS DIET SUPPLEMENT A LEVEL 5 TO RECOVERY l I—IWJ—LDEEEI SC SPP Pc PFP c PP CONDITIONS DIET SUPPLEMENT A LEVEL 5 TO RECOVERY 3 sc SFP Pc PPP CONDHWONS C FP 8 DIET SUPPLEMENT Lactate Changes under Different Conditions. 94 TABLE 4.l3.--Statistical Results, Lactate (mMoL/L). Conditions ANOVA NaHCO3 NaHCO3 Placebo Placebo + + + + CHO Fat-Pro CHO Fat-Pro D I Variables (3C) (SFP) (PC) (PFP) P P (a) w T 1.07 1.04 1.04 1.24 .74 0.76 .69 SD 0.9 0 7 0.7 0 5 (b) LI 7' 2.23 l 41 l.57 l.6l .65 0.44 .40 SD 2.4 0 4 0.6 0.8 (c) L2 7 1.88 1.71 2.33 1.80 .45 0.32 .60 SD l.3 0.4 0.7 0.9 (d) L3 71' 3.08 3.36 4.76 3.12 .37 0.40 .23 SD 2.3 1.3 2.4 1.8 (e) L4 Y' 6.45 6.62 6.20 5.50 .56 0.82 .7l SD 4.5 2 7 l.6 3.0 (f L5 7' l0.l9 10.37 7.00 8.52 .34 0.76 .80 SD 4.7 7.4 4.6 5.5 ( RI 7' l0.84 ll.4l l0.02 8.48 .26 0.77 .53 SD 4.l 4.4 2.7 5.3 (h) R2 7' 9.92 9.42 7.66 9.25 .37 0.69 .44 SD 2.5 4.0 2.0 4.6 (i R3 7 7.92 7.66 6.53 7.28 .48 0.80 .67 SD 2.6 1.7 2.8 2.3 Pw = Pre-work; Ll — L5 = Level l5 of work. Rl - R3 = Five, ten and fifteen minutes of recovery S = Supplement; D = Diet; I = Interaction 95 TABLE 4.14.--Changes and Statistical Results of Blood Parameters. Conditions ANOVA NaHCO3 NaHCO3 Placebo Placebo + + + + CHO Fat-Pro CHO Fat-Pro S 0 Variables (SC) (SFP) (PC) (PFP) P P aLH PH - LS 0.20 0.20 0.19 0.23 0.41 0.55 0.39 PM - R1 0.24 0.22 0.24 0.21 0.91 0.30 0.89 PR - R3 0.12 0.14 0.12 0.15 0.58 0.29 0.94 L5 - R1 0.04 0.03 0.05 0.02 0.03* 0.31 0.96 L5 - R3 7.08 0.06 0.07 0.08 0.77 0.81 0.95 IELJJEEQ Pw - LS 9.69 9.61 10.28 9.71 0.51 0.75 0.65 Pw - R1 11.35 13.11 12.50 12.83 0.84 0.73 0.69 Pu - R3 11.27 11.74 12.64 12.00 0.85 0.80 0.48 L5 - R1 1.66 3.50 2.22 3.13 0.99 0.50 0.89 L5 - R3 1.58 2.13 2.36 2.30 0.25 0.99 0.69 c 5P02 Pw - L5 12.66 11.02 12.62 11.75 0.90 0.72 0.55 PR - R1 20.43 17.40 21.88 19.55 0.66 0.55 0.80 PR - R3 16.72 10.63 15.40 14.15 0.61 0.81 0.96 L5 - R1 7.77 6.38 9.26 7.80 0.62 0.98 0.95 L5 - R3 4.06 0.34 2.78 2.40 0.93 0.90 0.83 (d) ATCO2 PH - L5 14.29 14.02 14.07 14.17 0.88 0.96 0.87 PR - R1 ~16.20 16.10 15.85 14.56 0.33 0.32 0.74 Pw - R3 13.10 12.63 13.38 11.87 0.96 0.50 0.57 L5 - R1 1.91 2.08 1.78 0.39 0.06* 0.68 0.76 L5 - R3 1.19 1.39 0.69 2.30 0.79 0.45 0.57 M5 Pw - L5 14.10 13.81 13.88 14.03 0.99 0.91 0.82 Pw - R1 16.00 15.92 15.68 14.42 0.30 0.28 0.64 PH - R3 12.84 12.37 13.16 12.29 0.75 0.75 0.86 L5 - R1 1.90 2.11 1.80 0.41 0.07* 0.74 0.69 L5 - R3 1.26 1.44 0.72 1.74 0.62 0.61 0.75 (f) ABE Pw - L5 ~13.07 -11.50 -13.12 -15.58 0.81 0.81 0.65 PM - R1 -15.80 -14.10 -15.60 -15.45 0.40 0.29 0.82 PR - R3 ~10.10 —09.96 ~10.93 «12.51 0.77 0.68 0.87 L5 - R1 -2.78 -2.60 -2.50 - 0.13 0.01* 0.51 0.74 L5 - R3 -2.93 -1.54 -2.17 -3.07 0.54 0.77 0.94 (g) ALactate Pw - LS 9.12 9.33 5.96 7.28 0.32 0.74 0.83 Pw - R1 9.77 10.37 8.98 7.24 0.16 0.93 0.64 PR - R3 6.85 6.62 5.49 6.04 0.66 0.97 0.99 L5 - R1 0.65 1.04 3.02 0.04 0.80 0.76 0.12 L5 - R3 2.27 2.71 0.47 1.24 0.09* 0.55 0.46 PR = Pre Hork L5 = Level 5 of work R1 - R3 = Five, ten and fifteen minutes of recovery 5 = Supp1ement; D = Diet; I P Interaction; * - Statistical significance. 96 In Figure 4.l9a-f, when all points were considered, no sig— nificant differences were observed using the sign test. In Figure 4.19a, b, and f, in which the dietary conditions are compared, no observable differences are evident. In Figure 4.l9c, d, and e, in which sodium bicarbonate and placebo supplements are compared, there appears to be several trends. The lactate change point appears most distinct at level 2 under the placebo condition, whereas under sodium bicarbonate supplementation there were change points at both levels 2 and 3. Further, under NaHCO3 supplementa— tion, after level 3 the lactate values were higher both at levels 4 and 5 as well as during recovery. Although the statistical analyses used were not adequate to test the differences between the lactate curves for the supplement data (Figure 4.l9c, d, and e), it is evident that the curves appear different. No decision as to statistical significance can be drawn from these graphs. However, when considered with the AL5—R3 ANOVA difference, one can conclude that high lactate values are obtained following sodium bicarbonate supplementation and that this lactate is reduced quite rapidly. Figure 4.19e, in particular, reflects these differences. Discussion The purpose of the present study was to investigate the effects of oral ingestion of NaHCO3 administered prior to an inter- mittent multi-stage treadmill run, under high carbohydrate and high fat-protein dietary conditions, upon performance and acid—base parameters. The experimental design insured that each subject 97 carried out an identical exercise protocol under the four different conditions. It is proper at this point to review the six related research hypotheses that were formulated prior to this study: 1. The oral ingestion of sodium bicarbonate, in the dosage of 0.065 gms/kg. of body weight, will alter the acid—base status of the blood toward greater alkalinity. The data support this hypothesis. The pH values were con- sistently higher following NaHCO3 administration (Figure 4.7c, d, and e) at all collection times. Also, base excess values were consistently higher following NaHCO3 supplementation (Figure 4.17, c, d, e and 4.18). The serum bicarbonate values were less inter- pretable (Figures 4.15a-f, 4.16). In this study the PC02 levels were not increased by an alkalizing agent as was observed by Jones and Sutton (147, 148) and Dennig (71, 72). Nevertheless, on the overall basis of the data collected, it can be concluded that the oral ingestion of sodium bicarbonate in the dosages of 0.065 gms/kg. alters the acid-base status of the blood of marathon runners toward greater alkalinity. 2. A high carbohydrate diet will Change the acid-base status of the blood toward greater alkalinity. The data collected in the present study do not support this hypothesis in its entirety. The pH values appear to be slightly elevated under the high carbohydrate diet (Figure 4.7b and f, P = .09) when no bicarbonate supp1ement was given or when the diet 98 data were pooled. If the supplement was given, however, the diet effect was not evident (Figure 4.7a). Under this condition the carbo- hydrate and fat-protein diets yielded similar results. Thus it can be concluded that, in the absence of supplementary sodium bicarbonate intake, a high carbohydrate diet changes the acid—base status of the blood of marathoners toward greater alkalinity. In the presence of supplementary sodium bicarbonate intake (0.065 gm/kg), the diet effect is not evident. 3. The ingestion of sodium bicarbonate two hours before work will increase maximum performance time. The data from the present study neither support nor refute this hypothesis (Figure 4.1a and Table 4.1a). The present data are in agreement with the results of Johnson and Black (145), Margaria et_al, (187), and Karpovich and Sinning (162) who also were unable to demonstrate significantly increased performance times in their endurance athletes following oral ingestion of alkalizing agents. The present results are in disagreement with the results of Dennig (71, 72), Jones gt_al, (147, 148), and Simmon and Hardt (245). These investigators all found definite increases in performance times following oral ingestion of NaHC03. The present results are in the same direction, but the magnitude of the difference in time is con- siderably less. Thus, the hypothesis is not supported but also cannot be refuted. It would appear from the data that the acid-base status of marathon runners may be more stable than that of less trained subjects. 99 This could account for the differences in results obtained by various investigators. Other data obtained in this laboratory tend to con— firm this position as the subjects of both Hunter (137) and Boosharya (31) were untrained. The differences obtained by these earlier investigators were much greater than the performance dif- ferences observed in the present study. 4. The ingestion of a high carbohydrate diet will increase maximum performance time. The findings of the present investigation do not support this hypothesis. Inspection of Figure 4.1a, however, shows that the subjects did work slightly longer when eating a carbohydrate diet than when eating a fat-protein diet. Therefore, due to the direction of the means and the small number of cases, the hypothesis cannot be refuted. The magnitude of difference attributable to the high carbo- hydrate diet in the present study is small compared with the results of Christensen and Hansen (50), Bergstrom_et_al. (26, 27, 28), Hultman (133) and Saltin and Hermansen (231). The difference in results could be due to the fact that the subjects in the present study were highly trained marathoners or that it was not possible to induce the marathoners to actually partake of a truly high fat- protein diet. Finally, it may be the differences in diet were not sufficiently great to obtain the expected difference. 5. The effects of sodium bicarbonate supplementation and a high carbohydrate diet are expected to be synergistic. 100 There are not data to support this hypothesis. In fact, it may be refuted as the effects of the NaHCO3 supplement and the high carbohydrate diet were not even additive in action. 6. Enhanced performance times are expected with little or not differences in the maximum oxygen uptake or oxygen debt. The lack of significant improvement in performance time under either sodium bicarbonate or carbohydrate conditions, and the lack of any interaction between the two treatments, resulted in no significnat increases in the values of both maximum oxygen intake or oxygen debt in the present study. Therefore, this hypothesis cannot be accepted. The preceding discussion makes it obvious that exercise metabolism in general provides a constant acidifying influence. When the metabolic rate is raised to seven or eight times that of the resting level, the increase in C02 is proportional, but ventila- tion can usually keep pace to maintain acid-base equilibrium. However, when the work load goes beyond aerobic capacity, lactic acid becomes the end product of metabolism, instead of C02. This cannot be removed quickly by respiration as is the case with C02. It has already been pOinted out that under conditions of heavy anaerobic exercise the pH can drop as low as 6.80 (207). The combination of two different buffer systems, that is carbonic acid-bicarbonate and blood protein, absorbed the shock to prevent the sudden changes in pH. Ultimately, however, physiological changes have to be brought about to maintain the organism in lOl homeostasis over a longer period of time, and these changes mainly involve the lungs and the kidneys. Permeability of the muscle cell membrane and the ratio of blood-muscle lactate both seem to be elevated in the alkaline state. It also has been suggested that the increased concentration of HCOS ions in the blood after sodium bicarbonate injection results in an increase of buffering capacity to lactate ions which migrate from muscle cells (90). This migration of lactate is believed to post- pone fatigue and improve performance during exercise. The alkaline reserve (bicarbonate and base excess), which may be defined as the buffering capacity of blood, is influenced almost exclusively by changes in non-volatile acids. The most important of these are lactate and pyruvate. Both Figures 4.15 and 4 17indicated that the lowest values of bicarbonate and base excess were reached either at the termination of exercise or during the first five minutes of recovery. The ALB-R1 Changes were from 12.40 to 10.29 units of HCOE and from -14.63 to -17.41 units of BE. This could be explained by the fact that the maximal value of blood lactate (11.41 mML/L) was reached at five minutes of recovery (Figure 4.l9e). In agreement with the results of this study, several investigators have shown a large decrease in the alkaline reserve of the body following maximal exercise (90, 94, 170, 264, 268). It is well documented that regularly performed endurance exercise, such as long distance running, results in major bio- chemical adaptations in skeletal muscle (20, 23, 94, 125, 197, 205, 102 263). Numerous investigators have shown an increased ability to tolerate acid metabolites (mainly lactic acid) after a period of training. Thus they have proposed that this increased tolerance might be due to an increase in the buffering ability (alkaline reserve) of the blood. In addition, physical training has been found to result in increased blood volume and total hemoglobin content. Most of the increase in blood volume reflects an increase in the amount of plasma and total hemoglobin (65, 171, 234) rather than an actual rise in the red blood cell volume. The blood's hemo- globin concentration is therefore usually unchanged or slightly decreased after training. The total proteins contained in the plasma and the red blood cells are active in the buffer action and constitute a mobile reserve of amino acids. Several previous studies (Dennig, Jones, Jones and Sutton, Simmons and Hardt) furnish strong evidence for the value of alkaline salts in the improvement of performance times in subjects who were untrained or only moderately trained. However, the present study is in agreement with the results of Johnson and Black (145), Margaria (187), and Karpovich and Sinning (162) who were unable to Show improved performance times in endurance athletes following oral ingestion of alkalizing agents. It appears that highly trained athletes may be less sensitive in that they may have already improved the buffer capacity of their blood through training. The relevant literature and the present study both tend to support this view. CHAPTER V SUMMARY, CONCLUSIONS AND RECOMMENDATIONS Summary The purpose of this study was to investigate the effects of the oral ingestion of sodium bicarbonate under different dietary conditions (i.e., high carbohydrate and fat-protein) upon acid-base equilibrium and performance time in long-distance runners during an intermittent multi-stage treadmill run to exhaustion. Eight fit male distance runners, 20-40 years of age from the central Michigan area, volunteered to be subjects in this study. The subjects were stress tested and were fully informed of the aims of the study. The subjects then were tested on a treadmill under four treatment conditions, which were administered in random order, during a four-week period. Thecxnufitions included: (a) the ingestion of sodium bicarbonate following a three day high carbo- hydrate diet (SC), (b) the ingestion of sodium bicarbonate following a three-day high fat-protein diet (SFP), (c) the ingestion of a placebo following a three-day high carbohydrate diet (PC), and (d) the ingestion of a placebo following a three-day high fat-protein diet (PFP). The supplements were given orally, two hours before the treadmill tests, in capsules containing either sodium bicarbonate as an alkalizer or dextrose as a placebo and were administered in amounts of .065 and .05 gm/kg of body weight, respectively. 103 104 Each subject received a list of standard American foods con- tained in the high carbohydrate or high fat-protein diets. Prior to each exercise test a dietary recall was conducted to detennine the percentages of carbohydrate, fat, and protein that were consumed. The exercise test consisted of six progressively higher work levels at defined speeds and grades. Three-minute rest intervals were alternated with a three-minute work interval at each level. On each test after the subject ran to exhaustion the recovery was followed for fifteen minutes. Heart rate was measured during each work interval, each rest interval, and the recovery period. Respiratory rate was monitored only during the work and rest inter— vals. Energy metabolism measurements were conducted during all levels of exercise, the rest intervals, and the recovery period. The standard Douglas bag method was used. Arterialized capillary blood was sampled prior to exercise, innmdiately following each work level, and after five, ten and fifteen minutes of recovery. The blood samples were analyzed for lactic acid using the enzymatic method and for pH, P002, P02, TCOZ, HCOE, and BE using the Astrup method. A repeated measures analysis of variance (ANOVA) was employed, with diet and supplement as the independent variables, to determine if there were any significant differences among the four treatment conditions. The sign test was used in selected instances to analyze continuous curvilinear data. No statistically significant differences were observed in performance time, maximum oxygen intake, or gross oxygen debt under 105 any of the treatment conditions. The oxygen uptake results also showed no significant differences. Utilizing the sign test, the ventilation measures were higher following the fat-protein diet. The SC condition resulted in consistently higher ventilation values than did the PC condition; whereas, under the SFP treatment the ventilation values were consistently lower than under the PFP treatment. The ANOVA analysis of the heart rate data revealed a signifi- cant interaction between ten and fifteen minutes of recovery. In respiratory rate, a statistically significant sodium bicarbonate effect was evident during the first level of exercise. Significant sodium bicarbonate effects on blood pH were detected in the pre-run data (P = .09) and in the difference between the values at the end of exercise and at five minutes of recovery (ALB-R1) (P = .03). The pH values were consistently high with sodium bicarbonate supplementation under both dietary conditions (sign test, P = .01). The PCO2 analysis across treatments revealed there were decreased values following the carbohydrate diet at levels two and three of work (P = .02 and P = .09). Application of the sign test showed that the P002 values were significantly lower following a carbohydrate diet than when a fat-protein diet was used. With supplementation of sodium bicarbonate, the PC02 was significantly decreased under both dietary treatments (P = .002). The P0 measurements were consistently high following the 2 carbohydrate diet (sign test, P = .002). The P02 values were also 106 consistently higher under the condition SC than they were under the SFP condition (sign test, P = .002). The ANOVA program showed there was a significant dietary effect on total carbon dioxide (TCOZ) at level 2 of exercise. In addition, the supplement difference between the end of level 5 and five minutes of recovery (ALS-Rl) was statistically significant. Application of the sign test showed the TCO2 values to be signifi- cantly depressed under both the SC and the pooled carbohydrate diet treatments. There was a significant supplement effect on serum bicarbo- nate from the termination of exercise to the first five minutes of recovery (ALS-Rl) (P = .07). The comparison of different measures indicated that there were consistently low serum bicarbonate values following the carbohydrate diet both before and during exercise (sign test, P = .02). The base excess (BE) results showed that the only supplement effect occurred during the first five minutes of recovery (ALS-Rl) (P = .01). The BE values were consistently low during work follow- ing the carbohydrate diet (sign test, P = .09). When the sodium bicarbonate supplementation data were pooled, the BE values were significantly increased (sign test, P = .02) at the various levels of work and at 10 and 15 minutes of recovery. The ANOVA analysis of the lactate data showed that the only significant effect occurred between level 5 and fifteen minutes of recovery (ALE - R3) (P = .09). In this comparison, the lactate differences were highest under bicarbonate supp1ementation. 107 Conclusions 1. The oral ingestion of sodium bicarbonate, in the dosage of .065 gms/kg of body weight, alters the acid-base status of the blood of trained distance runners toward greater alkalinity. 2. In the absence of supplementary sodium bicarbonate intake, a high carbohydrate diet Changes the acid-base status of the blood of the trained distance runners toward greater alkalinity. 3. The oral ingestion of sodium bicarbonate two hours before work did not significantly increase the maximum performance time of trained distance runners. 4. A high carbohydrate diet did not significantly increase the maximum performance time of trained distance runners. 5. The effects of sodium bicarbonate supplementation and a high carbohydrate diet are not synergistic in trained distance runners. 6. There were no significant improvements in the maximum oxygen intake or oxygen debt under either the NaHCO3 or the carbo- hydrate diet treatments, and no interaction of two was Observed. Recommendations 1. In further studies of this nature, the dietary regimens, supplementation time, physical activities and other related factors should be controlled by feeding. 2. In further studies of this nature, an acidotic condition should be incorporated. APPENDICES 108 APPENDIX A DIETS 109 110 TABLE A-l.--High Carbohydrate Diet. DIET: HIGH CARBOHYDRATE Foods that can be consumed in any amounts: Fruit (except cranberries, plums, prunes) Vegetables (except corn and lentils) Bread Cereal Potatoes, Rice, Macaroni Margarine Sugar Skim Milk (no more than 3 servings of whole milk) Cottage Cheese Lettuce Pancakes No more than one serving of any combination of the following can be consumed each day: AN EFFORT MUST Meat E99 Fish Nuts (including peanut butter) Corn, Lentils Cranberries, Plums, Prunes Cakes and Cookies, plain Butter BE MADE TO KEEP YOUR TOTAL CALORIC INTAKE RELATIVELY CONSTANT. A BODY WEIGHT LOSS OR GAIN DURING THE CONTROLLED DIET PERIOD COULD EFFECT THE EXPERIMENTAL RESULTS. 111 TABLE A-2.--High Fat s Protein Diet. DIET: HIGH FAT - PROTEIN Foods that can be consumed in any amounts: Meat Fish Fowl Eggs Nuts Peanut Butter Bacon Butter Corn Lentils Cranberries Lettuce Margarine AT LEAST 3 SERVINGS OF ANY COMBINATION OF MEAT, FISH, AND FOWL MUST BE CONSUMED EACH DAY. No more than three servings of any combination of the following can be consumed each day: Fruit Vegetables Bread Cereal Potatoes, Rice, Macaroni Margarine Sugar Milk Cakes and Cookies, plain Pancakes AN EFFORT MUST BE MADE TO KEEP YOUR TOTAL CALORIC INTAKE RELATIVELY CONSTANT. A BODY WEIGHT LOSS OR GAIN DURING THE CONTROLLED DIET PERIOD COULD EFFECT THE EXPERIMENTAL RESULTS. 112 .COOOQOQ vac .mo—cccc .oufiu cfimda .ACOCNONE .auuunwmnm m053HOCHE 4 vcw ocfiuwvu: Coon 35am .masom oowuou .NOH ocuou .wcuam0u .Oumfiouozu .Omvcam.n=uzw .umwsm .zafiofi .Ema .%v=mu .aaouu OOH no; «vow .Ouo .muacxwaov .moxmucma .mvoow voxma «woo»; vosuwuao can .aauuou camp» odes: wo~na~u~o> van muwauw uusuo cosmos .wnfinu ”mucumuom mofipmuumu> onHom .cuuuw Ammo; mausuu usuuwu new nvOuNEOH humusnamz .uuu .suwu .umaz HHO .uOuuan uacmua .uuuuzn .Ocaummuma .mcmun voaua mwwm umounu Jaw: .w>< HouOH mufiflxwu 0:0 .aw .aaezm .Em Dee m m e P 3 e 2 .Eu oEmz .w>< awash Oaufiuwnm awn hum mwcfi>pom HO Confisz Afimbocaw :«5 Boom .u3 .uz xom Ow< \ \ .v..: Powwmsm J<:c_>_az_ z< _C mzzflvca an we mxmuca coon «0 >umEE:m11.m1< mam<9 APPENDIX B TIMING 0F SUPPLEMENTATION 113 TIMING 0F SUPPLEMENTATION It was not evident from the literature how long prior to exercise NaHCO3 ingestion would produce maximum alterations in blood acid-base balance. An oral dose of .065 gram NaHCO3 per kilogram body weight produced maximum changes in blood pH and BE after two to four hours with the pH and BE gradually decreasing after reaching its maximum value until only half of the increase was evident at twelve hours (Figure B.l). If another equal dose was given about twelve hours following the first dose a slightly greater increase in alkalinity was achieved (Figure 8.2). 114 115 0.0 8 a o._ m1 . 6 ON .0 v ( Qm ... u . 0.4 x .mmmoxm mmmm vcm :a noofim _mempL< co covpmmmcH mouzmz Page we poww5u11._.m mLsmwu .9888 “.5me no 24% NIP mezmmmmamm P256. <20 :03 555558 5 9:5 moo; 68:62 ....o zofimmoz. mmtq :5 m2: N. m w 0 _ IL, _ _ A _ _ .VN ON m__ _ _ _ _ b 31. mwfl 116 x----% tube m) '38 QNI QMI .mmmoxu mmmm new :5 voopm megmpL< co moozmz we mmmoo 03H mo OOOCCMI1.N.m mgzmwu .3838 02:. no 232 mg m_ P266 <53 :03 .950: m. .2 omemmoz. ms; 35:5 83. mmoo ozoomm 4 556358 5 9.25 $8 noozoz do 2955:. $54 :5 ms: N. w .v 0 _ _ . _ . _ QN ON 1C @— . p h ..."00:62 no _ 29.632. 5:52“. 11_ 141-1 .vN waw 1m¢~ 1¢¢N Emex Hd APPENDIX C EXERCISE STRESS TEST 117 EXERCISE STRESS TEST Certain individuals exhibit abnormalities in electro- cardiogram (ECG) and blood pressure (BP) under the stress of exercise even though these abnormalities are not evident in a resting state. By using a graded exercise stress test where the intensity of the exercise increases gradually while the ECG and BP are monitored a subject's ECG and BP response to exercise can be obtained in relative safety. Adaptations in the Bruce protocol (8l) for graded exercise stress testing were made so that the test would stress the subjects adequately to insure a valid ECG and BP response at the high intensity of the experimental exercise. Equipment and Materials l. Disposable 3M Red Dot Monitoring Electrodes, Minnesota Mining Co., 3M Center, St. Paul, Minn. 55lOl. 2. Cambridge 3030 EKG Unit, Cambridge Inst. Co., Inc., 73 Spring St., Ossining, New York 10562. Procedure Electrodes were placed on the subject in a single bipolar V5 electrocardiograph configuration (Figure 3.1), a resting BP was ll8 l19 taken, and a resting ECG was recorded. The subject then was exercised under the following conditions: 1. Level 1 - 3.5 miles/hour, 8% grade, 3 minutes duration. 2. Level 2 - 4.2 miles/hour, 12% grade, 3 minutes duration. 3. Level 3 - 6.0 miles/hour, 12% grade, 3 minutes duration. 4. Level 4 - 8.0 miles/hour, 12% grade, 1.5 minutes duration. Blood pressure was measured immediately following the exercise at each level. The electrocardiogram was monitored throughout the test, and an ECG was recorded between exercise levels. The test was continued as soon as the BP and ECG were recorded. The following criteria were used for terminating the stress test before all four levels were completed. 1. Systolic blood pressure over 220 mmHg. 2. Diastolic blood pressure over 110 mmHg. Depression over 2 mm of the ST segment of the ECG. 4300 Premature ventricular contractions (PVCs) in pairs or with increasing frequency. None of the individuals used as subjects exhibited PVCs, any ST segment depression, or abnormal blood pressures. APPENDIX D BLOOD MEASURES 120 BLOOD SAMPLING Principle It has been shown that arterialized capillary blood very closely approximates arterial blood gas composition. The finger or ear lobe must be warmed (in about 45°C water) to insure rapid flow of blood, and 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. Heparinized capillary tubes must be used to keep the blood from clotting. Procedure 1. The finger was prewarmed for about three 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 surface of the pool. 121 ACID-BASE MEASURES The 120-ul blood sample that was obtained in the heparinized capillary tube was used for direct measurement of pH, PC02 and P02 using a PHM75 MK2 Digital Acid-Base Analyzer and a BM53 MK2 blood micro system. The blood was injected directly from the sample capillary tube into the measuring well of the blood micro system. Measurements were then obtained across the membrane compo- and P0 measuring electrodes. A second capillary nents of the PC02 2 was used to measure blood pH. This sample was aspirated directly into blood pH electrode for direct measurement. The HCOQ, TCO2 and BE were determined indirectly by the Astrup Equilibration Method for acid—base variables, using the Siggaard-Andersen Alignment Nomogram (Figure D.l). l22 Code 984-203 123 SlGGAARD-ANDERSEN ALIGNMENT NOMOGRAM Total-CO; mMol/l plasma. Pco; 60 T- 37‘ C mm Hg HCO? mEq/l plasma 1 a l lallallllllaaj Base Excess MEq/l blood or plasma. U‘ 0 1 pH 8 JLL AdLLth .a U‘ 8.0 ,1.1,1.1.L1.1.1.1.l . ...1. . .. w All 0...; O N O N U" w 0 7 4 Palnonl Idonllllclhofl u U‘ '6’ d IIIIILLCJLdeaLLIaa '6‘ {71 1.I.l.111.1.1.l.1,1.1.1,1 Dale and how ..a U“ J_L_L.I_L I 6 Arlovial 7.1 Capillary Vanoua .1.1.l.1.1. V! O BLOOD ACID-BASE VALUES Actual pH O O 10 — Baaa Excess. 6 7 mEq/l blood Tolal CO». mMol/l plasma \l O 66 O O '0 O é I’ INHIIVIV'HII'IV'llllYlITYYIIYTYTIYYflIYVVIIIVlTIrYYTIT l I Y [IITIYIIITIIITITIYIVIII'IIIVIII—TITIII—rI—II T I I I I I V I I I I I Y I I I I I T OTHER VALUES -a,~‘1‘_gfis I 1 1 Home lobin. 9/100 all h— 110 _ angen aaluvalion, 'l. h 120 T Oxygen lanaion. Po», mm H9 _130 _ J; T l— 150 COPYRlGHT ; m: :57 av RADIOMETER A s - EuonuPVEJ 72 put-mo COPENHAGEN NV . DENMARK . L__- 6.». .-.. 'oa-l “‘|0 a. : I a A. a 6m. J -.--' N-3- ... 5’.»I--os' Wt.- a‘Ll J"i'!ihvr via.“ Figure 0.1 LACTATE DETERMINATIONS Principle NADH is formed when lactate is oxidized to pyruvate. _ LDH _ Lactate + NAD +.+ Pyruvate + NADH By incubating the reaction in an alkaline environment and by trap- ping pyruvate with hydrazine, lactate can be completely oxidized. The equimolar formation of NADH then is measured at 340 nanometers (nm) to determine the lactate concentration. Reagents l. Lactic dehydrogenase enzyme (LDH) stock no. 826-6. 2. Glycine buffer (contains glycine and hydrazine pH 9.2) stock no. 826-3. 3. NAD preweighed vial stock no. 260-110. 4. Lactic acid standard solution, stock no. 826-10. 5. Sigma metabolite control, product no. s-3005. The above reagents are from Sigma Chemical Company, P.D. Box l4508, St. Louis, Missouri 63178. 6. Perchloric acid, 70%. Solutions Perchloric Acid 7 m1 of 70% perchloric was diluted with 100 ml distilled water. 124 125 Lactic Acid Diluted Standard 1.0 ml of lactic acid standard solution was diluted with 5.0 ml distilled water. Specimen Collection and Preparation 1. The One hundred microliters of blood was pipetted into centrifuge tube containing 200 pl of cold perchloric acid. The mixture was centrifuged five to ten minutes at approximately 32 gs (International Chemical Centrifuge, Fisher Scientific Co.). The protein free supernatant which was ready for use in the lactate determination was stored for up to six days at 0-3°C before analysis took place. Sigma metabolite control was mixed with 5 ml distilled water. The metabolite control was treated the same as a pre-exercise sample (2.2 mM/l) and was used with each analysis batch. Test Procedures The number of NAD vials needed was determined. number of samples + 2 number of NAD vials = 4 Into each NAD vial the following was pipetted: 2.0 ml glycine buffer 4.0 ml distilled water 0.1 ml lactic dehydrogenase enzyme vials were inverted several times to dissolve the NAD. The solution from all the vials was mixed. Into each test rube 1.4 ml solution from step13was pipetted and the test tubes were labeled blank through appropriate sample number. To blank, .1 ml of perchloric acid was added. 126 To all samples taken before exercise, .1 ml of protein-free supernatant was added. To all samples taken after exercise, .05 ml of protein-free supernatant and .05 m1 of perchloric acid was added. Since the above solution is only accurate for lactate values of up to about 7 mM/L and postexercise values were expected to be over 10 mM/L,only 1/2 of the protein-free supernatant in the postexercise samples was used. The test tubes were incubated at least 45 minutes at 25°C. The absorbance was read directly at 340 nm on the Gilford Stasar II Spectrophotometer. APPENDIX E ENERGY METABOLISM DETERMINATIONS 127 ENERGY METABOLISM DETERMINATIONS Principle The volume of expired gases must be corrected to standard temperature pressure dry (STPD) conditions. This can be accomplished using the following STPD correction factor: STPD PB ' PH20 correction = factor 760 (1 + .00367 T) 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, .00367 = 1 divided by 273 (273 is the conversion factor for converting temperature in Centigrade to Kelvin). This computation can be greatly simplified by using the line chart devised by Darling (55). The correction factor is then multiplied by the VE ambient temperature pressure saturated (ATPS) in order to obtain VE (STPD). The volume of oxygen consumed can be found by obtaining the number of m1 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 (RQ) is equal to 1.00. The following formula for ture O2 corrects for this difference in the inspired and expired gas volume. 128 129 TRUE 02 = %N2 in expired air x .265 - %02 in expired air %02 in ambient air Where: .26 5 = %N2 in ambient air The same correction must be made in calculating RQ. %C02 in expired air - .03 R0 = - %O2 in ambient air %N2 in ambient air x .265 Where: .03 = solubility coefficient for CO2 in human blood %02 in ambient air .265 = %N2 in ambient air Both the above computations can be simplified by using the line chart developed at the Harvard Fatigue Laboratory (55). Procedure 1. An STPD correction factor was obtained for each gas collection bag using the nomogram developed by Darling. 2. The STPD correction factor was multiplied by the total gas volume for the apprOpriate gas collection bag. 3. True 0 and R0 were obtained from the Harvard Fatigue Laboratory line chart. 4. True 02 was multiplied by corrected V (STPD) and divided by 100 to get the volume of 02 consumed in each gas collection bag. 5. Oxygen uptake per minute (VD ) was obtained by dividing the 02 consumed by the amoung of time spent in collec- tion of gas for that bag (in fractions of a whole minute). The maximum 0 uptake (VD max) was considered to the maximum value for 0 upta e found in two last 30-second bags during the run (holding about 1 minute). 130 Oxygen uptake curves were constructed using the O consumed from each gas collection bag during exergise, rest intervals and recovery period. Gross 0 debt was considered the sum of the oxygen uptake galues for all of the recovery bags. APPENDIX F BASIC DATA 131 TABLE F.1.--Performance Time (secs), VD Oxygen Debt (liter). 132 2max (ml/kg) and Gross Treatments NaHCO3 NaHCO3 Placebo Placebo + + + + CHO Fat-Pro CHO Fat-Pro Subjects (SC) (SFP) (PC) (PFP) (a) Performance Time SF 0990 1023 0997 0967 BM 0616 0640 0639 0627 DS 0856 0858 0825 0767 BR 0814 0816 0792 0810 DA 0840 0799 0810 0805 GC 0780 0800 0787 0769 BK 0830 0788 0780 0831 GS 0764 0656 0660 0750 X 811.25 797.50 786.25 790.75 SD 104.0 119.0 110.0 95.0 (b) V02max SF 090.30 098.50 100.03 089.20 BM 075.20 074.47 075.64 078.50 05 090.47 073.42 090.38 071.54 BR 082.11 082.45 083.00 080.55 DA 080.86 076.08 074.54 075.74 60 083.71 083.15 078.98 087.09 BK 076.05 077.59 073.09 076.53 GS 066.44 068.37 061.77 067.80 X 80.64 79.25 79.68 78.37 SD 8.05 9.13 11.63 7.24 (c) Gross Oxygen Debt SF 14.64 16.53 20.58 16.62 BM 16.04 15.34 14.39 15.76 05 13.07 10.72 11.31 07.85 BR 15.82 17.16 17.28 16.51 DA 15.23 15.02 12.93 14.61 00 12.61 12.97 11.95 11.11 BK 15.55 15.53 14.95 15.59 GS 18.07 15.38 14.48 17.17 X 15.13 14.83 14.73 14.40 SD 1.73 2.06 3.01 3.26 133 50.0 50.0 50.0 00.0 ...0 NN.0 00.0 00.0 00.0 00.. 00.0 .0.0 00.0 N5.0 .0.0 N0.0 0N.. 09.. 00.0 00.0 05.0 00.0 .0.0 .. v5.0 N0.0 00.0 00.. 00.. .0.0 -- -- -- 00.0 00.0 05.0 No.0 00.0 00.. .0.. 00.0 -- -- 0N.v «0.0 00.0 00.0 05.0 00.0 0N.. 00.0 00.N -- -- 05.0 00.0 00.0 00.0 N0.0 00.0 00.. 00.. 00.0 -- -- N0.v 50.0 55.0 v0.0 «5.0 50.. «0.. 00.. 5N.v -- 00.0 00.0 00.0 00.0 00.0 00.0 05.0 05.0 00.0 50.. -- 50.N 0N.0 .0.0 50.0 05.0 N0.0 00.0 0N.. 00.. 05.0 -- -- -- 50.0 05.0 05.0 00.0 No.. ov.. 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O.N- m... um Aumv.ozu +‘monnz .owwa .omwg _cwe4 .mme; _o»o4 gum” muueaoam .Acco_m 4\:wsv mmcuxu omcm .mumo u_wcm--.m.-_ u4m

mumz >Lo>mUmm xgm>wuom ~omo4 .omw4 _wmm4 .mmw; _m”o4 xmmn m xgm>moom xgw>wuom me>wUma —omw4 .mww; .mmmd Fume; .onma xmmu muumnazm EEnEF‘IEV‘Ih‘FFrEthlI-IIn”iulkkuu”"“klul‘lhulu “Urdu“:uflfllhfiupnlufluh .. n u.” ... .rlnfiNlhquh | . Fuhnflhuflnnulni Hula nuuhhhl' .AA\_ozeV manage; mace ammum--.m_-u wgmqh REFERENCES 150 "K'.%.‘\M\.-.“sz ,_ . . REFERENCES Adler, S. “The role of pH, PC02, and bicarbonate in regulating rat diaphragm citrate content." 9, Clin. Invest. 49zl647-l655, l970. Adler, 3., B. Anderson, and L. Zemotel. "Metabolic acid-base effects on tissue citrate content and metabolism in the rat.“ Am. a. Physiol. 220:986-992, l97l. Adler, 5., A. Roy, and A. S. Relman. "Intracellular acid-base regulation. II. The interaction between C02 tension and extracellular bicarbonate in the determination of muscle cell pH." 9, Clin. Invest. 44:2l-30, l965. Adler, S., A. Roy, and A. S. Relman. "Intracellular acid- base regulation. 1. 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