Exercise and Biochemical Nutrition Laboratory, Department of Health, Human Performance, and Recreation, Baylor University, Waco, TX 76706, USA.
Department of Exercise Science, Arnold School of Public Health, University of South Carolina, Columbia, SC 29208, USA.
Nutrients. 2020 Oct 15;12(10):3145. doi: 10.3390/nu12103145.
Research has suggested that nutrient, exercise, and metabolism-related proteins interact to regulate mammalian target of rapamycin complex one (mTOR) post-exercise and their interactions needs clarification. In a double-blind, cross-over, repeated measures design, ten participants completed four sets to failure at 70% of 1-repitition maximum (1-RM) with 45 s rest on angled leg press with or without pre-exercise maltodextrin (2 g/kg) after a 3 h fast. Vastus lateralis biopsies were collected at baseline before supplementation and 1 h post-exercise to analyze Focal Adhesion Kinase (FAK), ribosomal protein S6 kinase beta-1 (p70S6K), insulin receptor substrate 1 (IRS-1), phosphatidylinositol 3-kinase (PI3K), and 5' AMP-activated protein kinase (AMPK) activation. FAK and IRS-1 activity were only elevated 1 h post-exercise with carbohydrate ingestion ( < 0.05). PI3K and p70S6K activation were both elevated after exercise in both conditions ( < 0.05). However, AMPK activity did not change from baseline in both conditions ( > 0.05). We conclude that FAK does not induce mTOR activation through PI3K crosstalk in response to exercise alone. In addition, FAK may not be regulated by AMPK catalytic activity, but this needs further research. Interestingly, carbohydrate-induced insulin signaling appears to activate FAK at the level of IRS-1 but did not enhance mTOR activity 1 h post-exercise greater than the placebo condition. Future research should investigate these interactions under different conditions and within different time frames to clearly understand the interactions between these signaling molecules.
研究表明，营养、运动和代谢相关蛋白相互作用以调节哺乳动物雷帕霉素靶蛋白复合物 1（mTOR）运动后，它们的相互作用需要阐明。在一项双盲、交叉、重复测量设计中，10 名参与者在禁食 3 小时后，以 70%的 1 重复最大（1-RM）进行 4 组至力竭，每组间隔 45 秒，在斜腿按压机上进行，或在运动前补充麦芽糊精（2 g/kg）后进行。在补充前和运动后 1 小时收集股外侧肌活检，以分析粘着斑激酶（FAK）、核糖体蛋白 S6 激酶β-1（p70S6K）、胰岛素受体底物 1（IRS-1）、磷酸肌醇 3-激酶（PI3K）和 5' AMP 激活蛋白激酶（AMPK）的激活。只有在碳水化合物摄入后 1 小时，FAK 和 IRS-1 的活性才会升高（<0.05）。在两种情况下，运动后 PI3K 和 p70S6K 的活性都升高（<0.05）。然而，在两种情况下，AMPK 活性均未从基线发生变化（>0.05）。我们得出结论，FAK 不会通过 PI3K 串扰在单独运动时诱导 mTOR 激活。此外，FAK 可能不受 AMPK 催化活性的调节，但这需要进一步研究。有趣的是，碳水化合物诱导的胰岛素信号似乎在 IRS-1 水平上激活 FAK，但在运动后 1 小时，与安慰剂条件相比，它并没有增强 mTOR 活性。未来的研究应在不同条件下和不同时间框架内研究这些相互作用，以清楚了解这些信号分子之间的相互作用。
