Five male subjects performed exercise at 33, 66, and 95% of their maximum power output on three occasions in random order. Each study was preceded by a 3-h period in which capsules were taken by mouth, containing either CaCO3 (control, NH4Cl (acidosis), or NaHCO3 (alkalosis) in a dose of 0.3 g/kg body wt; preexercise blood pH was 7.38 +/- 0.015, 7.21 +/- 0.033, and 7.43 +/- 0.029, respectively. Exercise was continuous and maintained for 20 min at the two lower power outputs and for as long as possible at the highest. Compared with control (270 +/- 13 s), endurance time at the highest power output was reduced in acidosis (160 +/- 22 s) and increased in alkalosis (438 +/- 120 s). No differences were observed for central cardiovascular changes in exercise (cardiac output, frequency, or stroke volume). The respiratory changes expected from changes in blood pH were observed, with a higher alveolar ventilation in acidosis. At all power outputs arterialized venous lactate was lowest in acidosis and highest in alkalosis. Plasma glycerol and free fatty acids were lowest in acidosis. Changes in blood [HCO3-] and pH were shown to have major effects on metabolism in exercise which presumably were responsible for impaired endurance.

The effects of the menstrual cycle on cardiorespiratory variables, blood lactate, and performance were studied in exercising females. Nine healthy subjects, 20--24 yr of age, were investigated in midfollicular and midluteal phases of the menstrual cycle at 33, 66, and 90% of maximum power output (light, heavy, and exhaustive exercise). Occurrence of ovulation was confirmed in all subjects by measurement of progesterone, which increased from 0.6 +/- 0.1 (mean +/- SE) in the follicular to 8.9 +/- 2.2 ng/ml in the luteal phase. There was no difference in heart rate (HR), ventilation, O2 uptake, or CO2 output between the two phases during light and heavy exercise, and there was no difference in HR at exhaustion. Cardiac output measured midway through light and heavy exercise periods was not affected by the phase of testing. Time for which exhaustive exercise could be maintained increased from 1.57 +/- 0.32 in the follicular to 2.97 +/- 0.63 min in the luteal phase (P less than 0.02). Blood lactate was higher in the follicular phase after heavy exercise (6.62 +/- 0.8 vs. 4.92 +/- 0.5 mmol/l) (P less than 0.05) and at exhaustion (8.12 +/- 0.9 vs. 6.76 +/- 0.6 mmol/L) (P less than 0.01). A further study showed no effect of cycle phase on lactate disappearance during exercise. We conclude that while aerobic performance and the cardiorespiratory adaptations to exercise are not influenced by the phase of the menstrual cycle, performance of high-intensity exercise is improved, and lactate production appears to be decreased in the luteal phase when estradiol and progesterone levels are elevated.

1. Five males were studied on three occasions, after oral administration of CaCO3 (control), NH4Cl (acidosis) and NaHCO3 (alkalosis), in a dose of 0.3 g/kg, taken over a 3 h period at rest. The subjects then exercised on a cycle ergometer for 20 min at 33% maximal oxygen uptake (VO2 max.), followed by 20 min at 66% and at 95% VO2 max. until exhaustion. 2. Endurance at 95% VO2 max. was longest with alkalosis (5.44 +/- 1.05 min), shortest with acidosis (3.13 +/- 0.97 min) and intermediate in the control study (4.56 +/- 1.31 min); venous blood pH at exhaustion was 7.33 +/- 0.02 (mean +/- 1 SEM), 7.13 +/- 0.02 and 7.26 +/- 0.02 respectively. 3. Concentrations of plasma lactate at exhaustion were 7.10 +/- 0.8 mmol/1 4.0 +/- 0.5 and 7.9 +/- 0.9 mmol/l in the control, acidosis and alkalosis studies respectively. 4. Muscle lactate increased most from rest to exhaustion with alkalosis to 17.1 +/- 2.5 mumol/g and least with acidosis to 12.2 +/- 1.4 mumol/g. Muscle glycogen depletion was comparable in control and alkalosis studies. 5. The lower plasma lactate concentration during exercise in acidosis compared with control and alkalosis appears to be due to an inhibition of muscle glycolysis combined with a reduction in lactate efflux from muscle.

This study was designed to examine the influence of exercise on purine metabolism in man. In 15 men, the plasma uric acid concentration increased from 6.9 to 8.5 mg/dl following a 5000-m race and from 6.2 to 7.9 mg/dl in 11 men following a 42-km marathon. During a progressive exercise test on a cycle ergometer, the plasma uric acid ocnentration did not change significantly in 11 subjects. However, the plasma oxypurines increased from 19 micrM at rest to 50 microM at exhaustion and the urinary excretion of oxypurines increased from 140 to 400 mumol/g creatinine. Intracellular ATP decreased from 5.17 to 2.91 mumol/g and ADP and AMP increased from 0.85 to 1.29 and from 0.12 to 0.15 mumol/g wet weight, respectively. These observations suggest that there is an accelerated degradation of purine nucleotides to the precursors of uric acid in skeletal muscle during vigorous exercise.