mTOR signaling response to resistance exercise is altered by chronic resistance training and detraining in skeletal muscle
mTOR signaling response to resistance exercise is altered by chronic resistance training and detraining in skeletal muscle
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DOI：
10.1152/japplphysiol.01161.2012
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发表时间：
2013-04-01
影响因子：
3.3
通讯作者：
Ishii, Naokata
中科院分区：
文献类型：
--
作者：
Ogasawara, Riki;Kobayashi, Koji;Ishii, Naokata
mTOR 信号对抗阻运动的反应会因骨骼肌的长期抗阻训练和去训练而改变。 J Appl Physiol 114: 934-940, 2013。首次发表于 2013 年 1 月 31 日； doi: 10.1152/japplphyol.01161.2012.-阻力训练引起的肌肉合成代谢和随后的肥大在训练的早期阶段发生得最快，并随着时间的推移逐渐变慢。目前，人们对肌肉对训练刺激敏感性变化的细胞内信号传导机制知之甚少。我们研究了长期抗阻训练和随后的停止训练期间运动诱导的肥大信号蛋白磷酸化的变化。雄性大鼠被分为四组：1 回合（1B）、12 回合（12B）、18 回合（18B）和停止训练（DT）。 DT组大鼠进行12次运动，停训12天，再进行1次运动，然后处死。等长训练包括最大等长收缩，这是通过每隔一天经皮电刺激腓肠肌产生的。最后一次锻炼后 24 小时去除肌肉。测量了 p70S6K、4E-BP1、rpS6 和 p90RSK 的总水平和磷酸化水平，急性抗阻运动后，与对照肌肉 (CON) 相比，1B 组的 p70S6K、rpS6 和 p90RSK 磷酸化水平升高，而反复运动则抑制了 12B 和 18B 组的磷酸化。有趣的是，DT 组停止训练 12 天后，这些磷酸化水平恢复了。相反，4E-BP1 的磷酸化并没有随着长期训练和训练中断而改变，这表明，通过长期阻力训练，合成代谢信号对阻力运动刺激变得不那么敏感，但在短暂的训练中断后又恢复了。
mTOR signaling response to resistance exercise is altered by chronic resistance training and detraining in skeletal muscle. J Appl Physiol 114: 934-940, 2013. First published January 31, 2013; doi: 10.1152/japplphysiol.01161.2012.-Resistance training-induced muscle anabolism and subsequent hypertrophy occur most rapidly during the early phase of training and become progressively slower over time. Currently, little is known about the intracellular signaling mechanisms underlying changes in the sensitivity of muscles to training stimuli. We investigated the changes in the exercise-induced phosphorylation of hypertrophic signaling proteins during chronic resistance training and subsequent detraining. Male rats were divided into four groups: 1 bout (1B), 12 bouts (12B), 18 bouts (18B), and detraining (DT). In the DT group, rats were subjected to 12 exercise sessions, detrained for 12 days, and then were subjected to 1 exercise session before being killed. Isometric training consisted of maximum isometric contraction, which was produced by percutaneous electrical stimulation of the gastrocnemius muscle every other day. Muscles were removed 24 h after the final exercise session. Levels of total and phosphorylated p70S6K, 4E-BP1, rpS6, and p90RSK levels were measured, and phosphorylation of p70S6K, rpS6, and p90RSK was elevated in the 1B group compared with control muscle (CON) after acute resistance exercise, whereas repeated bouts of exercise suppressed those phosphorylation in both 12B and 18B groups. Interestingly, these phosphorylation levels were restored after 12 days of detraining in the DT group. On the contrary, phosphorylation of 4E-BP1 was not altered with chronic training and detraining, indicating that, with chronic resistance training, anabolic signaling becomes less sensitive to resistance exercise stimuli but is restored after a short detraining period.