Resistance exercise with whey protein ingestion affects mTOR signaling pathway and myostatin in men
Resistance exercise with whey protein ingestion affects mTOR signaling pathway and myostatin in men
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DOI：
10.1152/japplphysiol.00087.2009
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发表时间：
2009-05-01
影响因子：
3.3
通讯作者：
Mero, Antti A.
中科院分区：
文献类型：
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作者：
Hulmi, Juha J.;Tannerstedt, Jorgen;Mero, Antti A.
Hulmi JJ、Tannerstedt J、Selanne H、Kainulainen H、Kovanen V、Mero AA。摄入乳清蛋白的抗阻运动会影响男性的 mTOR 信号通路和肌肉生长抑制素。 J Appl Physiol 106: 1720-1729, 2009。首次发表于 2009 年 3 月 19 日； doi:10.1152/japplphyol.00087.2009.-信号通路感知局部和全身信号并调节肌肉肥大。乳清蛋白摄入对抗阻运动的急性和长期信号反应的影响尚不清楚。以前未经训练的年轻男性被随机分为蛋白质组 (n = 9)、安慰剂组 (n = 9) 和对照组 (n = 11)。股外侧肌 (VL) 肌肉活检在 5 X 10 次重复腿举[阻力运动 (RE)] 之前、之后 1 小时和 48 小时以及阻力训练 (RT) 21 周（每周 2 次）之后进行。在单次 RE 回合以及整个 RT 期间的每次 RE 锻炼之前和之后摄入蛋白质（15 克乳清）或非能量安慰剂。蛋白质组在第 10.5 周时其体重和 VL 肌肉厚度（通过超声检查测量）已增加（P < 0.05）。第 21 周时，蛋白质组和安慰剂组的肌纤维尺寸也有类似的增加。在未锻炼的对照中没有观察到变化。然而，通过蛋白质印迹测量，p70（S6K）和核糖体蛋白S6（rpS6）的磷酸化在RE后1小时增加，其中前者随着蛋白质摄入而增加。哺乳动物雷帕霉素靶点 (mTOR) 磷酸化在 RE 回合和 RT 后仅在蛋白质组中增加，而蛋白质摄入阻止了 RE 后磷酸化真核起始因子 4E 结合蛋白 1 (p-4E-BP1) 的减少。 RT 后 Akt 磷酸化下降，而磷酸化真核延伸因子 2 未观察到变化。RE 后肌肉肌生长抑制素蛋白减少仅发生在安慰剂组中。结果表明，抗阻运动会迅速增加 mTOR 信号传导，并可能降低肌肉中肌生长抑制素蛋白的表达，而乳清蛋白会增加并延长 mTOR 信号传导反应。
Hulmi JJ, Tannerstedt J, Selanne H, Kainulainen H, Kovanen V, Mero AA. Resistance exercise with whey protein ingestion affects mTOR signaling pathway and myostatin in men. J Appl Physiol 106: 1720-1729, 2009. First published March 19, 2009; doi:10.1152/japplphysiol.00087.2009.-Signaling pathways sense local and systemic signals and regulate muscle hypertrophy. The effects of whey protein ingestion on acute and long-term signaling responses of resistance exercise are not well known. Previously untrained young men were randomized into protein (n = 9), placebo (n = 9), and control (n = 11) groups. Vastus lateralis (VL) muscle biopsies were taken before and 1 h and 48 h after a leg press of 5 X 10 repetitions [resistance exercise (RE)] and after 21 wk (2 times per week) of resistance training (RT). Protein (15 g of whey) or nonenergetic placebo was ingested before and after a single RE bout and each RE workout throughout the RT. The protein group increased its body mass and VL muscle thickness (measured by ultrasonography) already at week 10.5 (P < 0.05). At week 21, the protein and placebo groups had similarly increased their myofiber size. No changes were observed in the nonexercised controls. However, the phosphorylation of p70(S6K) and ribosomal protein S6 (rpS6) were increased at 1 h post-RE measured by Western blotting, the former being the greatest with protein ingestion. Mammalian target of rapamycin (mTOR) phosphorylation was increased after the RE bout and RT only in the protein group, whereas the protein ingestion prevented the post-RE decrease in phosphorylated eukaryotic initiation factor 4E binding protein 1 (p-4E-BP1). Akt phosphorylation decreased after RT, whereas no change was observed in phosphorylated eukaryotic elongation factor 2. A post-RE decrease in muscle myostatin protein occurred only in the placebo group. The results indicate that resistance exercise rapidly increases mTOR signaling and may decrease myostatin protein expression in muscle and that whey protein increases and prolongs the mTOR signaling response.