Effect of infusing branched-chain amino acid during incremental exercise with reduced muscle glycogen content

1994 ◽  
Vol 69 (1) ◽  
pp. 26-31 ◽  
Author(s):  
Maurizio Varnier ◽  
Patrizio Sarto ◽  
Diego Martines ◽  
Liliana Lora ◽  
Francesco Carmignoto ◽  
...  
Keyword(s):  
Amino Acid ◽  
Muscle Glycogen ◽  
Glycogen Content ◽  
Incremental Exercise ◽  
Muscle Glycogen Content ◽  
Branched Chain Amino Acid ◽  
Branched Chain

Nutritional status affects branched-chain oxoacid dehydrogenase activity during exercise in humans

1997 ◽  
Vol 272 (2) ◽  
pp. E233-E238 ◽  
Author(s):  
M. L. Jackman ◽  
M. J. Gibala ◽  
E. Hultman ◽  
T. E. Graham
Keyword(s):  
Amino Acid ◽  
Oxygen Uptake ◽  
Muscle Glycogen ◽  
Random Order ◽  
Submaximal Exercise ◽  
The Other ◽  
Branched Chain Amino Acid ◽  
Low Carbohydrate ◽  
Branched Chain ◽  
Exercise In Humans

We examined the effect of glycogen availability and branched-chain amino acid (BCAA) supplementation on branched-chain oxoacid dehydrogenase (BCOAD) activity during exercise. Six subjects cycled at approximately 75% of their maximal oxygen uptake to exhaustion on three occasions under different preexercise conditions: 1) low muscle glycogen (LOW), 2) low muscle glycogen plus BCAA supplementation (LOW+BCAA), and 3) high muscle glycogen (CON). The LOW trial was performed first, followed by the other two conditions in random order, and biopsies for all trials were obtained at rest, after 15 min of exercise (15 min), and at the point of exhaustion during the LOW trial (49 min). BCOAD activity was not different among the three conditions at rest; however, at 15 min BCOAD activity was higher (P < or = 0.05) for the LOW (31 +/- 5%) and LOW+BCAA (43 +/- 11%) conditions compared with CON (12 +/- 1%). BCOAD activity at 49 min was not different from respective values at 15 min for any condition. These data indicate that BCOAD is rapidly activated during submaximal exercise under conditions associated with low carbohydrate availability. However, there was no relationship between BCOAD activity and glycogen concentration or net glycogenolysis, which suggests that factors other than glycogen availability are important for BCOAD regulation during exercise in humans.

Effect of chronic supplementation with branched-chain amino acids on the performance and hepatic and muscle glycogen content in trained rats

Life Sciences ◽  
2006 ◽  
Vol 79 (14) ◽  
pp. 1343-1348 ◽  
Author(s):  
Jonas A. de Araujo ◽  
Gina Falavigna ◽  
Marcelo M. Rogero ◽  
Ivanir S.O. Pires ◽  
Rogerio G. Pedrosa ◽  
...  
Keyword(s):  
Amino Acids ◽  
Muscle Glycogen ◽  
Glycogen Content ◽  
Branched Chain Amino Acids ◽  
Muscle Glycogen Content ◽  
Branched Chain

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

1999 ◽  
Vol 87 (5) ◽  
pp. 1662-1667 ◽  
Author(s):  
Martin J. Gibala ◽  
Marco Lozej ◽  
Mark A. Tarnopolsky ◽  
Cyndy McLean ◽  
Terry E. Graham
Keyword(s):  
Amino Acid ◽  
Muscle Glycogen ◽  
Tricarboxylic Acid Cycle ◽  
Total Concentration ◽  
Exercise Bout ◽  
Branched Chain Amino Acid ◽  
Branched Chain ◽  
Tricarboxylic Acid Cycle Intermediates ◽  
Rate Limiting ◽  
Exercise In Humans

We examined the hypothesis that increasing the rate of branched-chain amino acid (BCAA) oxidation, during conditions of low glycogen availability, reduces the level of muscle tricarboxylic acid cycle intermediates (TCAI) by placing a carbon “drain” on the cycle at the level of 2-oxoglutarate. Six men cycled at ∼70% of maximal oxygen uptake for 15 min under two conditions: 1) low preexercise muscle glycogen (placebo) and 2) low glycogen combined with BCAA ingestion. We have previously shown that BCAA ingestion increased the activity of branched-chain oxoacid dehydrogenase, the rate-limiting enzyme for BCAA oxidation in muscle, compared with low glycogen alone [M. L. Jackman, M. J. Gibala, E. Hultman, and T. E. Graham. Am. J. Physiol. 272 ( Endocrinol. Metab. 35): E233–E238, 1997]. Muscle glycogen concentration was 185 ± 22 and 206 ± 22 mmol/kg dry wt at rest for the placebo and BCAA-supplemented trials, respectively, and decreased to 109 ± 18 and 96 ± 10 mmol/kg dry wt after exercise. The net increase in the total concentration of six measured TCAI (∼95% of TCAI pool) during 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 ∼0.05 at rest 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 subjects 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 ( Endocrinol. Metab. 35): E239–E244, 1997]. These data suggest that increasing the rate of BCAA oxidation has no measurable effect on muscle TCAI during exercise with low glycogen in humans. Moreover, it appears that low resting glycogen per se does not impair the increase in TCAI during moderate exercise.

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