Gibala M J, Lozej M, Tarnopolsky M A, McLean C, Graham T E
Departments of Kinesiology and Medicine, McMaster University, Hamilton, Ontario L8S 4K1.
J Appl Physiol (1985). 1999 Nov;87(5):1662-7. doi: 10.1152/jappl.1999.87.5.1662.
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 approximately 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 ( approximately 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 approximately 0.05 at rest to approximately 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.
在糖原可用性较低的情况下,提高支链氨基酸(BCAA)氧化速率,会通过在2-氧代戊二酸水平给三羧酸循环设置一个碳“消耗”,从而降低肌肉三羧酸循环中间体(TCAI)的水平。六名男性在两种条件下以约最大摄氧量的70%进行15分钟的骑行:1)运动前肌肉糖原水平低(安慰剂组)和2)糖原水平低并摄入BCAA。我们之前已经表明,与单独糖原水平低相比,摄入BCAA会增加支链氧代酸脱氢酶的活性,该酶是肌肉中BCAA氧化的限速酶[M. L. 杰克曼、M. J. 吉巴拉、E. 胡尔特曼和T. E. 格雷厄姆。《美国生理学杂志》272(内分泌与代谢35):E233 - E238,1997]。安慰剂组和补充BCAA组试验中,静息时肌肉糖原浓度分别为185±22和206±22 mmol/kg干重,运动后分别降至109±18和96±10 mmol/kg干重。运动期间六种测得的TCAI总浓度(约占TCAI池的95%)的净增加在两组试验之间无差异(安慰剂组和BCAA组试验分别为3.97±0.34和3.88±0.34 mmol/kg干重)。在两项试验中,运动后肌肉2-氧代戊二酸浓度均从静息时的约0.05降至约0.03 mmol/kg干重。两项试验中TCAI池扩张的幅度与之前正常混合饮食后进行相同运动的受试者中观察到的幅度相似[M. J. 吉巴拉、M. A. 塔尔诺波尔斯基和T. E. 格雷厄姆。《美国生理学杂志》272(内分泌与代谢35):E239 - E244,1997]。这些数据表明,在人类糖原水平低的运动过程中,提高BCAA氧化速率对肌肉TCAI没有可测量的影响。此外,似乎静息糖原水平低本身并不会损害中等强度运动期间TCAI的增加。