Affiliation:
1. Department of Physiology, The University of Melbourne, Parkville 3052;
2. Department of Human Movement, Recreation, and Performance, and
3. Department of Human Movement Studies, The University of Queensland, Brisbane 4072, Australia
4. Exercise Metabolism Unit, Department of Chemistry and Biology, Centre for Rehabilitation, Exercise, and Sport Science, Victoria University of Technology, Footscray 3011; and
Abstract
Six men were studied during four 30-s “all-out” exercise bouts on an air-braked cycle ergometer. The first three exercise bouts were separated by 4 min of passive recovery; after the third bout, subjects rested for 4 min, exercised for 30 min at 30–35% peak O2 consumption, and rested for a further 60 min before completing the fourth exercise bout. Peak power and total work were reduced ( P < 0.05) during bout 3 [765 ± 60 (SE) W; 15.8 ± 1.0 kJ] compared with bout 1 (1,168 ± 55 W, 23.8 ± 1.2 kJ), but no difference in exercise performance was observed between bouts 1 and 4 (1,094 ± 64 W, 23.2 ± 1.4 kJ). Before bout 3, muscle ATP, creatine phosphate (CP), glycogen, pH, and sarcoplasmic reticulum (SR) Ca2+ uptake were reduced, while muscle lactate and inosine 5′-monophosphate were increased. Muscle ATP and glycogen before bout 4 remained lower than values before bout 1( P < 0.05), but there were no differences in muscle inosine 5′-monophosphate, lactate, pH, and SR Ca2+ uptake. Muscle CP levels before bout 4 had increased above resting levels. Consistent with the decline in muscle ATP were increases in hypoxanthine and inosine before bouts 3 and 4. The decline in exercise performance does not appear to be related to a reduction in muscle glycogen. Instead, it may be caused by reduced CP availability, increased H+ concentration, impairment in SR function, or some other fatigue-inducing agent.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology
Cited by
118 articles.
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