Reactive hyperemia is not responsible for stimulating muscle protein synthesis following blood flow restriction exercise
Reactive hyperemia is not responsible for stimulating muscle protein synthesis following blood flow restriction exercise
复制标题
DOI：
10.1152/japplphysiol.01267.2011
复制
发表时间：
2012-05-01
影响因子：
3.3
通讯作者：
Rasmussen, Blake B.
中科院分区：
文献类型：
--
作者：
Gundermann, David M.;Fry, Christopher S.;Rasmussen, Blake B.
Gundermann DM，Fry CS，Dickinson JM，步行者DK，Timmerman KL，Drummond MJ，Volpi E，Rasmussen BB.反应性充血并不是血流限制运动后刺激肌肉蛋白质合成的原因。J Appl Physiol 112：1520-1528，2012.首次发表于2012年2月23日; doi：10.1152/japplphysiol.01267.2011.-在低强度阻力运动训练期间，对收缩骨骼肌的血流限制（BFR）增加了人类的肌肉力量和大小。然而，这些影响的机制在很大程度上是未知的。我们以前已经表明，哺乳动物雷帕霉素复合物1（mTORC 1）信号转导和肌肉蛋白合成（MPS）刺激后，急性回合的BFR运动。本研究的目的是检验反应性充血是BFR运动后刺激mTORC 1信号传导和MPS的机制这一假设。6名年轻男性（24 +/- 2岁）被用于一项随机交叉研究，包括两项运动试验：低强度抗阻运动与BFR（BFR试验）和低强度抗阻运动与硝普钠（SNP），一种药理学血管扩张剂输注到股动脉后立即运动，以模拟反应性充血反应后BFR运动（SNP试验）。运动后股外侧肌混合肌合成率在BFR试验中增加了49%（P < 0.05），而在SNP试验中没有变化（P > 0.05）。BFR运动增加了mTOR、S6激酶1、核糖体蛋白S6、ERK 1/2和Mnk 1相互作用激酶1的磷酸化（P < 0.05），而SNP试验中mTORC 1信号通路没有变化（P > 0.05）。我们得出结论，反应性充血不是BFR运动诱导mTORC 1信号传导和MPS的主要机制。需要进一步研究以阐明急性和慢性BFR运动后mTOR信号传导、MPS和肥大增加的细胞机制。
Gundermann DM, Fry CS, Dickinson JM, Walker DK, Timmerman KL, Drummond MJ, Volpi E, Rasmussen BB. Reactive hyperemia is not responsible for stimulating muscle protein synthesis following blood flow restriction exercise. J Appl Physiol 112: 1520-1528, 2012. First published February 23, 2012; doi:10.1152/japplphysiol.01267.2011.-Blood flow restriction (BFR) to contracting skeletal muscle during low-intensity resistance exercise training increases muscle strength and size in humans. However, the mechanism(s) underlying these effects are largely unknown. We have previously shown that mammalian target of rapamycin complex 1 (mTORC1) signaling and muscle protein synthesis (MPS) are stimulated following an acute bout of BFR exercise. The purpose of this study was to test the hypothesis that reactive hyperemia is the mechanism responsible for stimulating mTORC1 signaling and MPS following BFR exercise. Six young men (24 +/- 2 yr) were used in a randomized crossover study consisting of two exercise trials: low-intensity resistance exercise with BFR (BFR trial) and low-intensity resistance exercise with sodium nitroprusside (SNP), a pharmacological vasodilator infusion into the femoral artery immediately after exercise to simulate the reactive hyperemia response after BFR exercise (SNP trial). Postexercise mixed-muscle fractional synthetic rate from the vastus lateralis increased by 49% in the BFR trial (P < 0.05) with no change in the SNP trial (P > 0.05). BFR exercise increased the phosphorylation of mTOR, S6 kinase 1, ribosomal protein S6, ERK1/2, and Mnk1-interacting kinase 1 (P < 0.05) with no changes in mTORC1 signaling in the SNP trial (P > 0.05). We conclude that reactive hyperemia is not a primary mechanism for BFR exercise-induced mTORC1 signaling and MPS. Further research is necessary to elucidate the cellular mechanism(s) responsible for the increase in mTOR signaling, MPS, and hypertrophy following acute and chronic BFR exercise.