Apró William, Moberg Marcus, Hamilton D Lee, Ekblom Björn, van Hall Gerrit, Holmberg Hans-Christer, Blomstrand Eva
Åstrand Laboratory, Swedish School of Sport and Health Sciences, Stockholm, Sweden; Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden;
Åstrand Laboratory, Swedish School of Sport and Health Sciences, Stockholm, Sweden;
Am J Physiol Endocrinol Metab. 2015 Mar 15;308(6):E470-81. doi: 10.1152/ajpendo.00486.2014. Epub 2015 Jan 20.
Combining endurance and strength training in the same session has been reported to reduce the anabolic response to the latter form of exercise. The underlying mechanism, based primarily on results from rodent muscle, is proposed to involve AMPK-dependent inhibition of mTORC1 signaling. This hypothesis was tested in eight trained male subjects who in randomized order performed either resistance exercise only (R) or interval cycling followed by resistance exercise (ER). Biopsies taken from the vastus lateralis before and after endurance exercise and repeatedly after resistance exercise were assessed for glycogen content, kinase activity, protein phosphorylation, and gene expression. Mixed muscle fractional synthetic rate was measured at rest and during 3 h of recovery using the stable isotope technique. In ER, AMPK activity was elevated immediately after both endurance and resistance exercise (∼90%, P < 0.05) but was unchanged in R. Thr(389) phosphorylation of S6K1 was increased severalfold immediately after exercise (P < 0.05) in both trials and increased further throughout recovery. After 90 and 180 min recovery, S6K1 activity was elevated (∼55 and ∼110%, respectively, P < 0.05) and eukaryotic elongation factor 2 phosphorylation was reduced (∼55%, P < 0.05) with no difference between trials. In contrast, markers for protein catabolism were differently influenced by the two modes of exercise; ER induced a significant increase in gene and protein expression of MuRF1 (P < 0.05), which was not observed following R exercise only. In conclusion, cycling-induced elevation in AMPK activity does not inhibit mTOR complex 1 signaling after subsequent resistance exercise but may instead interfere with the hypertrophic response by influencing key components in protein breakdown.
据报道，在同一会话中结合耐力训练和力量训练会降低对后一种运动形式的合成代谢反应。基于主要来自啮齿动物肌肉的结果，其潜在机制被认为涉及AMPK依赖性对mTORC1信号传导的抑制。在八名受过训练的男性受试者中对这一假设进行了测试，他们以随机顺序分别进行仅阻力运动（R）或间歇骑行后进行阻力运动（ER）。在耐力运动前后以及阻力运动后反复从股外侧肌采集活检样本，评估糖原含量、激酶活性、蛋白质磷酸化和基因表达。使用稳定同位素技术在静息状态和恢复3小时期间测量混合肌肉分数合成率。在ER组中，耐力运动和阻力运动后AMPK活性立即升高（约90%，P<0.05），但在R组中无变化。在两项试验中，运动后S6K1的Thr(389)磷酸化立即增加数倍（P<0.05），并在整个恢复过程中进一步增加。恢复90分钟和180分钟后S6K1活性升高（分别约为55%和110%，P<0.05），真核生物延伸因子2磷酸化降低（约55%，P<0.05），两组试验之间无差异。相比之下，两种运动模式对蛋白质分解标记物的影响不同；ER组诱导MuRF1基因和蛋白质表达显著增加（P<0.05），仅进行R运动时未观察到这种情况。总之，骑行诱导的AMPK活性升高在随后的阻力运动后不会抑制mTOR复合物1信号传导，反而可能通过影响蛋白质分解中的关键成分来干扰肥大反应。
