The Åstrand Laboratory of Work Physiology, GIH, The Swedish School of Sport and Health Sciences, Box 5626, 114 86 Stockholm, Sweden.
J Appl Physiol (1985). 2011 Nov;111(5):1335-44. doi: 10.1152/japplphysiol.00086.2011. Epub 2011 Aug 11.
Combining endurance and strength training (concurrent training) may change the adaptation compared with single mode training. However, the site of interaction and the mechanisms are unclear. We have investigated the hypothesis that molecular signaling of mitochondrial biogenesis after endurance exercise is impaired by resistance exercise. Ten healthy subjects performed either only endurance exercise (E; 1-h cycling at ∼65% of maximal oxygen uptake), or endurance exercise followed by resistance exercise (ER; 1-h cycling + 6 sets of leg press at 70-80% of 1 repetition maximum) in a randomized cross-over design. Muscle biopsies were obtained before and after exercise (1 and 3 h postcycling). The mRNA of genes related to mitochondrial biogenesis [(peroxisome proliferator-activated receptor-γ coactivator-1 (PGC-1)α, PGC-1-related coactivator (PRC)] related coactivator) and substrate regulation (pyruvate dehydrogenase kinase-4) increased after both E and ER, but the mRNA levels were about twofold higher after ER (P < 0.01). Phosphorylation of proteins involved in the signaling cascade of protein synthesis [mammalian target of rapamycin (mTOR), ribosomal S6 kinase 1, and eukaryotic elongation factor 2] was altered after ER but not after E. Moreover, ER induced a larger increase in mRNA of genes associated with positive mTOR signaling (cMyc and Rheb). Phosphorylation of AMP-activated protein kinase, acetyl-CoA carboxylase, and Akt increased similarly at 1 h postcycling (P < 0.01) after both types of exercise. Contrary to our hypothesis, the results demonstrate that ER, performed after E, amplifies the adaptive signaling response of mitochondrial biogenesis compared with single-mode endurance exercise. The mechanism may relate to a cross talk between signaling pathways mediated by mTOR. The results suggest that concurrent training may be beneficial for the adaptation of muscle oxidative capacity.
将耐力和力量训练（协同训练）相结合可能会改变与单一模式训练相比的适应情况。然而，相互作用的部位和机制尚不清楚。我们已经提出了一个假设，即耐力运动后线粒体生物发生的分子信号会被抗阻运动所损害。10 名健康受试者以随机交叉设计的方式分别进行仅耐力运动（E；以最大摄氧量的 65%进行 1 小时的自行车运动）或耐力运动后紧接着进行抗阻运动（ER；1 小时的自行车运动+70-80%1 次最大重复的腿推 6 组）。在运动前后（运动后 1 小时和 3 小时）采集肌肉活检。与线粒体生物发生相关的基因（过氧化物酶体增殖物激活受体-γ共激活因子-1（PGC-1）α、PGC-1 相关共激活因子（PRC））和底物调节（丙酮酸脱氢酶激酶-4）的 mRNA 在 E 和 ER 后均增加，但 ER 后的 mRNA 水平高约 2 倍（P < 0.01）。参与蛋白质合成信号级联的蛋白质（雷帕霉素靶蛋白（mTOR）、核糖体 S6 激酶 1 和真核伸长因子 2）的磷酸化在 ER 后而不是在 E 后发生改变。此外，ER 诱导与正向 mTOR 信号相关的基因（cMyc 和 Rheb）的 mRNA 增加更大。两种运动后 1 小时，AMP 激活的蛋白激酶、乙酰辅酶 A 羧化酶和 Akt 的磷酸化均相似地增加（P < 0.01）。与我们的假设相反，结果表明 ER 在 E 之后进行，与单一模式的耐力运动相比，放大了线粒体生物发生的适应性信号反应。其机制可能与 mTOR 介导的信号通路之间的串扰有关。结果表明，协同训练可能有益于肌肉氧化能力的适应。
