Low glycogen and branched-chain amino acid ingestion do not impair anaplerosis during exercise in humans

Citation
Mj. Gibala et al., Low glycogen and branched-chain amino acid ingestion do not impair anaplerosis during exercise in humans, J APP PHYSL, 87(5), 1999, pp. 1662-1667
Citations number
26
Categorie Soggetti
Physiology
Journal title
JOURNAL OF APPLIED PHYSIOLOGY
ISSN journal
87507587 → ACNP
Volume
87
Issue
5
Year of publication
1999
Pages
1662 - 1667
Database
ISI
SICI code
8750-7587(199911)87:5<1662:LGABAA>2.0.ZU;2-M
Abstract
Gibala, Martin J., Marco Lozej, Mark A. Tarnopolsky, Cyndy McLean, and Terr y E. Graham. Low glycogen and branched-chain amino acid ingestion do not im pair anaplerosis during exercise in humans. J. Appl. Physiol. 87(5): 1662-1 667, 1999. -We examined the hypothesis that increasing the rate of branched -chain amino acid (BCAA) oxidation, during conditions of low glycogen avail ability, reduces the level of muscle tricarboxylic acid cycle intermediates (TCAI) by placing a carbon "drain" on the cycle at the level of 2-oxogluta rate. Six men cycled at similar to 70% of maximal oxygen uptake for 15 min under two conditions: 1) low preexercise muscle glycogen (placebo) and 2) l ow glycogen combined with BCAA ingestion. We have previously shown that BCA A ingestion increased the activity of branched-chain oxoacid dehydrogenase, the rate-limiting enzyme for BCAA oxidation in muscle, compared with low g lycogen alone [M. L. Jackman, M. J. Gibala, E. Hultman, and T. E. Graham. A m. J. Physiol. 272 (Endocrinol. Metab. 35): E233-E238, 1997]. Muscle glycog en concentration was 185 +/- 22 and 206 +/- 22 mmol/kg dry wt at rest for t he placebo and BCAA-supplemented trials, respectively, and decreased to 109 +/- 18 and 96 +/- 10 mmol/kg dry wt after exercise. The net increase in th e total concentration of six measured TCAI (similar to 95% of TCAI pool) du ring exercise was not different between trials (3.97 +/- 0.34 vs. 3.88 +/- 0.34 mmol/kg dry wt for the placebo and BCAA trials, respectively). Muscle 2-oxoglutarate concentration decreased from similar to 0.05 at rest to simi lar to 0.03 mmol/kg dry wt after exercise in both trials. The magnitude of TCAI pool expansion in both trials was similar to that seen previously in s ubjects who performed an identical exercise bout after a normal mixed diet [M. J. Gibala, M. A. Tarnopolsky, and T. E. Graham. Am. J. Physiol. 272 (En docrinol. Metab. 35): E239-E244, 1997]. These data suggest that increasing the rate of BCAA oxidation has no measurable effect on muscle TCAI during e xercise with low glycogen in humans. Moreover, it appears that low resting glycogen per se does not impair the increase in TCAI during moderate exerci se.