Blood flow restriction during low-intensity resistance exercise increases S6K1 phosphorylation and muscle protein synthesis
Blood flow restriction during low-intensity resistance exercise increases S6K1 phosphorylation and muscle protein synthesis
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DOI：
10.1152/japplphysiol.00195.2007
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发表时间：
2007-09-01
影响因子：
3.3
通讯作者：
Rasmussen, Blake B.
中科院分区：
文献类型：
--
作者：
Fujita, Satoshi;Abe, Takashi;Rasmussen, Blake B.
低强度阻力运动训练与血流限制 (REFR) 相结合，可以像高负荷的传统阻力运动一样增加肌肉大小和力量。然而，REFR 引起的肥大和力量增加背后的细胞机制尚不清楚。我们最近发现，在人类进行剧烈的高强度抗阻运动后，哺乳动物雷帕霉素靶点（mTOR）信号通路和肌肉蛋白合成（MPS）都会受到刺激。因此，我们假设 REFR 的急性发作会增强 mTOR 信号传导并刺激 MPS。我们测量了 6 名年轻男性受试者的 MPS 和 mTOR 相关信号蛋白的磷酸化状态。在血流限制期间对受试者进行一次研究（REFR，以 1 次最大重复次数的 20% 进行双侧腿部伸展运动，同时将压力袖带放置在双大腿近端并充气至 200 mmHg），并使用相同的运动方案但不使用压力袖带进行第二次研究 [对照 (Ctrl)]。采用稳定同位素技术测量股外侧肌的 MPS，并通过免疫印迹法测定信号蛋白的磷酸化状态。与 Ctrl 相比，REFR 后的血乳酸、皮质醇和生长激素较高（P < 0.05）。 REFR 后，核糖体 S6 激酶 1 (S6K1) 磷酸化（mTOR 的下游靶标）增加，同时真核翻译延伸因子 2 (eEF2) 磷酸化减少，MPS 增加 46%（P < 0.05）。 Ctrl 组运动后 MPS 和 S6K1 磷酸化没有变化。我们得出的结论是，mTOR 信号通路的激活似乎是一种重要的细胞机制，可能有助于解释 REFR 期间肌肉蛋白合成的增强。
Low-intensity resistance exercise training combined with blood flow restriction (REFR) increases muscle size and strength as much as conventional resistance exercise with high loads. However, the cellular mechanism(s) underlying the hypertrophy and strength gains induced by REFR are unknown. We have recently shown that both the mammalian target of rapamycin (mTOR) signaling pathway and muscle protein synthesis (MPS) were stimulated after an acute bout of high-intensity resistance exercise in humans. Therefore, we hypothesized that an acute bout of REFR would enhance mTOR signaling and stimulate MPS. We measured MPS and phosphorylation status of mTOR-associated signaling proteins in six young male subjects. Subjects were studied once during blood flow restriction (REFR, bilateral leg extension exercise at 20% of 1 repetition maximum while a pressure cuff was placed on the proximal end of both thighs and inflated at 200 mmHg) and a second time using the same exercise protocol but without the pressure cuff [control (Ctrl)]. MPS in the vastus lateralis muscle was measured by using stable isotope techniques, and the phosphorylation status of signaling proteins was determined by immunoblotting. Blood lactate, cortisol, and growth hormone were higher following REFR compared with Ctrl (P < 0.05). Ribosomal S6 kinase 1 (S6K1) phosphorylation, a downstream target of mTOR, increased concurrently with a decreased eukaryotic translation elongation factor 2 (eEF2) phosphorylation and a 46% increase in MPS following REFR (P < 0.05). MPS and S6K1 phosphorylation were unchanged in the Ctrl group postexercise. We conclude that the activation of the mTOR signaling pathway appears to be an important cellular mechanism that may help explain the enhanced muscle protein synthesis during REFR.