Glycogen availability does not affect the TCA cycle or TAN pools during prolonged, fatiguing exercise

Baldwin, Jacinta, Snow, Rod, Gibala, Martin J., Garnham, Andrew, Howarth, Krista and Febbraio, Mark A. 2003, Glycogen availability does not affect the TCA cycle or TAN pools during prolonged, fatiguing exercise, Journal of applied physiology, vol. 94, pp. 2181-2187.

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Title Glycogen availability does not affect the TCA cycle or TAN pools during prolonged, fatiguing exercise
Author(s) Baldwin, Jacinta
Snow, Rod
Gibala, Martin J.
Garnham, Andrew
Howarth, Krista
Febbraio, Mark A.
Journal name Journal of applied physiology
Volume number 94
Start page 2181
End page 2187
Publisher American Physiological Society
Place of publication Bethesda, Md.
Publication date 2003-06
ISSN 8750-7587
Keyword(s) citric acid cycle
metabolic stress
hypoxanthine
Summary The hypothesis that fatigue during prolonged exercise arises from insufficient intramuscular glycogen, which limits tricarboxylic acid cycle (TCA) activity due to reduced TCA cycle intermediates (TCAI), was tested in this experiment. Seven endurance-trained men cycled at approximately 70% of peak O(2) uptake (Vo(2 peak)) until exhaustion with low (LG) or high (HG) preexercise intramuscular glycogen content. Muscle glycogen content was lower (P < 0.05) at fatigue than at 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 was similar after 103 +/- 15 min of exercise (2.62 +/- 0.31 and 2.59 +/- 0.28 mmol/kg dry wt for LG and HG, respectively), 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 the size of the TCAI pool. Neither the total adenine nucleotide pool (TAN = ATP + ADP + AMP) nor IMP was altered compared with rest in either trial, whereas creatine phosphate levels were not different when values measured at fatigue were compared 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 or creatine phosphate 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.
Language eng
Field of Research 111601 Cell Physiology
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2003, American Physiological Society
Persistent URL http://hdl.handle.net/10536/DRO/DU:30006458

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