Journal of Applied Physiology AJP: Lung Cellular and Molecular Physiology
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J Appl Physiol 84: 1687-1691, 1998;
8750-7587/98 $5.00
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Vol. 84, Issue 5, 1687-1691, May 1998

Muscle metabolites and performance during high-intensity, intermittent exercise

Mark Hargreaves1, Michael J. McKenna2, David G. Jenkins4, Stuart A. Warmington1, Jia L. Li2, Rodney J. Snow3, and Mark A. Febbraio1

1 Department of Physiology, The University of Melbourne, Parkville 3052; 2 Department of Human Movement, Recreation, and Performance, and 3 Exercise Metabolism Unit, Department of Chemistry and Biology, Centre for Rehabilitation, Exercise, and Sport Science, Victoria University of Technology, Footscray 3011; and 4 Department of Human Movement Studies, The University of Queensland, Brisbane 4072, Australia

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.

muscle fatigue; metabolism; glycogen; creatine phosphate; hydrogen ion


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