Fujita Satoshi, Abe Takashi, Drummond Micah J, Cadenas Jerson G, Dreyer Hans C, Sato Yoshiaki, Volpi Elena, Rasmussen Blake B
Department of Internal Medicine, University of Texas Medical Branch, Galveston, Texas, USA.
J Appl Physiol (1985). 2007 Sep;103(3):903-10. doi: 10.1152/japplphysiol.00195.2007. Epub 2007 Jun 14.
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.
低强度抗阻运动训练结合血流限制（REFR）与高负荷传统抗阻运动一样能增加肌肉大小和力量。然而，REFR诱导肥大和力量增加的细胞机制尚不清楚。我们最近发现，在人体进行一次急性高强度抗阻运动后，雷帕霉素哺乳动物靶蛋白（mTOR）信号通路和肌肉蛋白合成（MPS）均受到刺激。因此，我们假设一次急性REFR会增强mTOR信号并刺激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。受试者在血流限制期间（REFR，双侧腿部伸展运动，负荷为1次重复最大值的20%，同时在双侧大腿近端放置压力袖带并充气至200 mmHg）接受了一次研究，第二次使用相同的运动方案，但不使用压力袖带[对照组（Ctrl）]。使用稳定同位素技术测量股外侧肌中的MPS，并通过免疫印迹法测定信号蛋白的磷酸化状态。与Ctrl组相比，REFR后血乳酸、皮质醇和生长激素水平更高（P < 0.05）。mTOR的下游靶点核糖体S6激酶1（S6K1）磷酸化增加，同时真核翻译延伸因子2（eEF2）磷酸化减少，REFR后MPS增加46%（P < 0.05）。运动后Ctrl组的MPS和S6K1磷酸化没有变化。我们得出结论，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期间肌肉蛋白合成增强的原因。
