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Articles in PresS, published online ahead of print November 27, 2002
J Appl Physiol, 10.1152/jap.00866.2002
Submitted on September 20, 2002
Accepted on November 24, 2002
1 Department of Physiology, The University of Melbourne, Parkville, Victoria, Australia
2 School of Health Sciences, Deakin University, Burwood, Victoria, Australia
3 Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada
4 Department of Physiology, The University of Melbourne, Parkville, Victoria, Australia; Skeletal Muscle Research Laboratory, School of Medical Sciences, RMIT University, Bundoora, Victoria, Australia
* To whom correspondence should be addressed. E-mail: mark.febbraio{at}rmit.edu.au.
The hypothesis that fatigue during prolonged exercise arises from insufficient intramuscular glycogen that limits the tricarboxylic acid cycle (TCA) activity due to reduced TCA cycle intermediates (TCAI) was tested in this experiment. Seven endurance trained men cycled at ~70% VO2peak until exhaustion with either low (LG) or high (HG) pre-exercise intramuscular glycogen content. Muscle glycogen content was lower (P<0.05) at fatigue compared with rest in both trials. However, the increase in the sum of four-measured TCAI (>70% of the total TCAI pool) from rest to 15 min of exercise was not different between trials and TCAI content were similar after 103 ± 15 min of exercise (LG: 2.62 ± 0.31 v HG: 2.59 ± 0.28 mmol.kg-1 dw), which was the point of volitional fatigue during LG. Subjects cycled for an additional 52 ± 9 min during HG, and although glycogen was markedly reduced (P<0.05) during this period, no further change in the TCAI pool was observed, thus demonstrating a clear dissociation between exercise duration and size of the TCAI pool. Neither the total adenine nucleotide pool (TAN = ATP + ADP + AMP) nor inosine monophosphate (IMP), were altered compared with rest in either trial, while creatine phosphate (CP) levels were not different when comparing values measured at fatigue with those measured after 15 min of exercise. These data demonstrate that altered glycogen availability neither compromises TCAI pool expansion, nor affects the TAN pool, CP or IMP content during prolonged exercise to fatigue. Therefore, our data do not support the concept that a decrease in muscle TCAI during prolonged exercise in humans compromises aerobic energy provision or is the cause of fatigue.
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