Nine healthy subjects were studied under control conditions and following 5 mo of heavy resistance training and 5 wk of immobilization in elbow casts. Needle biopsies were taken from triceps brachii and analyzed for adenosine triphosphate (ATP), adenosine diphosphate (ADP), creatine (C), creatine phosphate (CP, and glycogen concentrations. Training resulted in an 11% increase in arm circumference and a 28% increase in maximal elbow extension strength. Immobilization resulted in decreases in arm circumference and elbow extension strength of 5% and 35%, respectively. Training also resulted in significant increases in resting concentrations of muscle creatine (by 39%), CP (by 22%), ATP (by 18%), and glycogen (by 66%). Conversely, immobilization significantly reduced CP concentration by 25% and glycogen concentration by 40%. It was concluded that heavy-resistance training results in increases in muscle energy reserves which may be reversed by a period of immobilization-induced disuse.

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.

Six subjects exercised to exhaustion on a cycle ergometer at intensities corresponding to approximately 140% of their maximal aerobic power. Subjects attempted to pedal for 1-min intervals with 3-min rest periods between, and continued until 30 s of exercise could no longer be maintained. Venous blood was sampled for lactate and glucose analysis. Muscle biopsies were extracted from the quadriceps before and immediately after exercise and at 2-, 5-, 12-, and 24-h intervals thereafter for total glycogen analysis. Three subjects consumed a mixed controlled diet (approx. 3,100 kcal) during the 24 h after exercise, and three consumed the same diet plus an additional 2,500/kcal carbohydrate. Following exercise, glycogen concentration had dropped to a mean value of approximately 28% of its preexercise value. After 2 h, it had recovered to 39%, at 5 h to 53%, at 12 h to 67%, and at 24 h to 102% of its preexercise value, with no difference in resynthesis rate between the two groups. It was concluded that, following glycogen depletion through intense intermittent exercise, complete recovery to preexercise values may be accomplished within 24 h; and that within this time period, the rate of resynthesis cannot be accelerated by a higher than normal carbohydrate intake.

1. The activity of pyruvate dehydrogenase in its active and inactive forms was measured in biopsy samples obtained from the vastus lateralis muscle of healthy subjects before and after exercise. 2. At rest, 40 +/- 4% (mean +/- SEM) of the enzyme was in the active form. 3. After progressive aerobic exercise to exhaustion (n = 5), 88 +/- 2.3% was in the active form. 4. After intermittent supramaximal short-term exercise (1 min exercise, 3 min rest) to exhaustion (n = 6), 60 +/- 2.2% was in the active form. 5. After isometric maximal exercise of 65 +/- 3.6 s duration (n = 3), only 39 +/- 1% of the enzyme was in the active form. 6. Muscle glycogen depletion was greatest with intermittent exercise and least with isometric maximal exercise; in contrast, the increase in muscle lactate was least with progressive exercise (1.3 to 9.4 mumol/g), intermediate in intermittent maximal exercise (1.2 to 13.1 mumol/g) and greatest after isometric exercise (1.8 to 17.6 mumol/g). There were no significant differences between the three studies in the changes in lactate/pyruvate ratios. 7. In three subjects who exercised with one leg, activation of the enzyme was twice as great in the exercise as in the inactive leg. 8. The ratio of active to total enzyme in biopsies of resting muscle was greater in four well-trained athletes than in four untrained control subjects (70% compared with 41% respectively). 9. The activation of pyruvate dehydrogenase appears to play an important part in regulating the use of glycogen and glucose during exercise in man.