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First published online on March 8, 2002.
 Copyright © 2002 by The Physiological Society
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2001.012983v1
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Received July 11, 2001
Accepted after revision January 16, 2002

Exercise with low muscle glycogen augments TCA cycle anaplerosis but impairs oxidative energy provision in humans

M. J. Gibala1*, Nick Peirce2, Dimitru Constantin-Teodosiu2, and Paul L. Greenhaff2

1 Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, ON L8S 4K1, Canada
2 School of Biomedical Sciences, Queen's Medical Centre, University of Nottingham, Nottingham, UK

* To whom correspondence should be addressed. E-mail: gibalam{at}mcmaster.ca.

We tested the hypotheses that: (i) exercise with low muscle glycogen would reduce pyruvate flux through the alanine aminotransferase (AAT) reaction and attenuate the increase in tricarboxylic acid cycle (TCA) cycle intermediates, and (ii) attenuation of tricarboxylic acid cycle intermediate (TCAI) expansion would limit TCA cycle flux, thereby accelerating phosphocreatine (PCr) degradation. Eight men cycled for 10 min at 70 % of their O2,max on two occasions: (i) following their normal diet (CON) and (ii) after cycling to exhaustion and consuming a low carbohydrate diet for ~2 days (LG). Biopsies (m. vastus lateralis) confirmed that [glycogen] was lower in LG vs. CON at rest (257 ± 18 vs. 611 ± 54 mmol (kg dry mass)-1; P <= 0.05); however, net glycogenolysis was not different after 1 or 10 min of exercise. PCr degradation from rest to 1 min was ~26 % higher in LG vs. CON (38 ± 4 vs. 28 ± 4 mmol (kg dry mass)-1; P <= 0.05). The sum of five measured TCAIs (~90 % of total pool) was not different between trials at rest and after 1 min, but was higher after 10 min in LG vs. CON (5.51 ± 0.43 vs. 4.45 ± 0.49 mmol (kg dry mass)-1; P <= 0.05. Pyruvate dehydrogenase complex (PDC) activity was lower during exercise in LG vs. CON (2.2 ± 0.2 vs. 1.4 ± 0.2 mmol min-1 (kg wet weight)-1 after 10 min; P <= 0.05), and acetylcarnitine was ~threefold less, implying increased pyruvate availability for flux through AAT. Resting muscle [glutamate] was higher in LG vs. CON (16.1 ± 0.8 vs. 11.8 ± 0.4 mmol (kg dry mass)-1; P <= 0.05) and the net decrease in [glutamate] during exercise was ~30 % greater in LG vs. CON. These findings suggest that: (i) contrary to our hypotheses, LG increased anaplerosis by decreasing PDC flux and/or increasing the conversion of glutamate carbon to TCAI, and (ii) accelerating the rate of muscle TCAI expansion did not affect oxidative energy provision during the initial phase of contraction, since changes in [TCAI] were not temporally related to PCr degradation.




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