Exercise training increases branched-chain oxoacid dehydrogenase kinase content in human skeletal muscle
Exercise training increases branched-chain oxoacid dehydrogenase kinase content in human skeletal muscle
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DOI：
10.1152/ajpregu.00115.2007
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发表时间：
2007-09-01
影响因子：
2.8
通讯作者：
Gibala, Martin J.
中科院分区：
文献类型：
--
作者：
Howarth, Krista R.;Burgomaster, Kirsten A.;Gibala, Martin J.
支链含氧酸脱氢酶复合物（BCOAD）是骨骼肌中支链氨基酸（BCAAs）氧化的速率决定因子。运动训练减弱人骨骼肌中急性运动诱导的BCOAD（BCOAD a）活化（McKenzie S，菲利普斯SM，Carter SL，洛瑟S，Gibala MJ，Tarnopolsky MA. Am J Physiol Endocrinol Metab 278：E580 - E587，2000）;然而，其机制尚不清楚。我们假设训练会增加肌肉中BCOAD激酶的蛋白含量，BCOAD激酶是一种负责磷酸化使BCOAD失活的酶。20名受试者[ 23 +/-1岁;峰值摄氧量（V. O-2 peak）= 41 +/-2ml中心点kg（-1）中心点min（-1）]在自行车测力计上进行6周的高强度间歇或连续中等强度训练（n = 10/组）.在训练前后，受试者进行60分钟的自行车在65%的训练前V. O-2峰值，针活检样本（股外侧肌）之前和之后立即获得运动。训练的效果表现为运动期间V. O2峰值增加、柠檬酸合成酶最大活性增加和肌糖原分解减少，组间无差异（主效应，P < 0.05）。训练后BCOAD a降低（主效应，P < 0.05），这与BCOAD激酶蛋白含量增加30%（主效应，P < 0.05）有关。我们认为，运动训练后骨骼肌BCOAD激酶蛋白质含量的增加可能参与了BCOAD a降低的机制。这些数据还突出了用于研究骨骼肌BCAA代谢调节的模型的差异，因为先前报道运动训练可增加大鼠运动期间的BCOAD a并降低BCOAD激酶含量。
The branched- chain oxoacid dehydrogenase complex ( BCOAD) is rate determining for the oxidation of branched- chain amino acids ( BCAAs) in skeletal muscle. Exercise training blunts the acute exercise- induced activation of BCOAD ( BCOADa) in human skeletal muscle ( McKenzie S, Phillips SM, Carter SL, Lowther S, Gibala MJ, Tarnopolsky MA. Am J Physiol Endocrinol Metab 278: E580 - E587, 2000); however, the mechanism is unknown. We hypothesized that training would increase the muscle protein content of BCOAD kinase, the enzyme responsible for inactivation of BCOAD by phosphorylation. Twenty subjects [ 23 +/- 1 yr; peak oxygen uptake ( V. O-2peak) = 41 +/- 2 ml center dot kg(-1) center dot min(-1)] performed 6 wk of either high- intensity interval or continuous moderate- intensity training on a cycle ergometer ( n = 10/ group). Before and after training, subjects performed 60 min of cycling at 65% of pretraining V. O-2peak, and needle biopsy samples ( vastus lateralis) were obtained before and immediately after exercise. The effect of training was demonstrated by an increased V. O2peak, increased citrate synthase maximal activity, and reduced muscle glycogenolysis during exercise, with no difference between groups ( main effects, P < 0.05). BCOADa was lower after training ( main effect, P < 0.05), and this was associated with a similar to 30% increase in BCOAD kinase protein content ( main effect, P < 0.05). We conclude that the increased protein content of BCOAD kinase may be involved in the mechanism for reduced BCOADa after exercise training in human skeletal muscle. These data also highlight differences in models used to study the regulation of skeletal muscle BCAA metabolism, since exercise training was previously reported to increase BCOADa during exercise and decrease BCOAD kinase content in rats.