Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, ON L8S 4K1, Canada.
J Appl Physiol (1985). 2010 Mar;108(3):628-36. doi: 10.1152/japplphysiol.00659.2009. Epub 2010 Jan 7.
Exercise training under conditions of reduced carbohydrate (CHO) availability has been reported to augment gains in skeletal muscle oxidative capacity; however, the underlying mechanisms are unclear. We examined the effect of manipulating CHO intake on the acute metabolic response to high-intensity interval exercise, including signaling cascades linked to mitochondrial biogenesis. Ten men performed two trials in random order separated by >or=1 wk. Each trial consisted of a morning (AM) and afternoon (PM) training session (5 x 4 min cycling at approximately 90-95% of heart rate reserve) separated by 3 h of recovery during which subjects ingested a high-CHO drink (HI-HI) or nonenergetic placebo (HI-LO) before PM exercise. Biopsies (vastus lateralis) revealed that muscle phosphocreatine and ATP content were similar after AM exercise but decreased to a greater extent during PM exercise in HI-LO vs. HI-HI. Phosphorylation of p38 mitogen-activated protein kinase (MAPK) and AMP-activated protein kinase (AMPK) increased approximately 4-fold and 2-fold, respectively, during AM exercise with no difference between conditions. After PM exercise, p38 MAPK phosphorylation was higher in HI-LO vs. HI-HI, whereas AMPK was not different between conditions. Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1 alpha) gene expression increased approximately 8-fold during recovery from AM exercise and remained elevated during PM exercise with no differences between conditions. Cytochrome oxidase subunit 4 (COXIV) mRNA was also elevated 3 h after AM exercise, with no difference between conditions. These data provide evidence that p38 MAPK is a nutrient-sensitive signaling molecule that could be involved in the altered skeletal muscle adaptive response reported after exercise training under conditions of restricted CHO intake, but further research is required to confirm this hypothesis.
在碳水化合物（CHO）供应减少的条件下进行运动训练已被报道可增强骨骼肌氧化能力的增加；然而，其潜在机制尚不清楚。我们研究了操纵 CHO 摄入量对高强度间歇运动的急性代谢反应的影响，包括与线粒体生物发生相关的信号级联。10 名男性以随机顺序进行了两次试验，间隔>或= 1 周。每个试验都包括上午（AM）和下午（PM）训练时段（5 x 4 分钟，约为心率储备的 90-95%的自行车运动），其间有 3 小时的恢复期，在此期间，受试者在 PM 运动前摄入高 CHO 饮料（HI-HI）或非能量安慰剂（HI-LO）。活检（股外侧肌）显示，上午运动后肌肉磷酸肌酸和 ATP 含量相似，但在 PM 运动中，HI-LO 比 HI-HI 下降幅度更大。p38 丝裂原活化蛋白激酶（MAPK）和 AMP 激活的蛋白激酶（AMPK）的磷酸化在 AM 运动中分别增加了约 4 倍和 2 倍，但两种情况下没有差异。在 PM 运动后，HI-LO 中的 p38 MAPK 磷酸化高于 HI-HI，而 AMPK 在两种情况下没有差异。过氧化物酶体增殖物激活受体γ共激活因子 1-α（PGC-1α）基因表达在 AM 运动后的恢复期间增加了约 8 倍，并在 PM 运动期间保持升高，两种情况下没有差异。细胞色素 c 氧化酶亚基 4（COXIV）mRNA 也在 AM 运动后 3 小时升高，两种情况下没有差异。这些数据提供了证据表明，p38 MAPK 是一种营养敏感的信号分子，可能参与了在限制 CHO 摄入条件下进行运动训练后报告的骨骼肌适应性反应的改变，但需要进一步研究来证实这一假设。
