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Contraction mode itself does not determine the level of mTORC1 activity in rat skeletal muscle

机译:收缩模式本身并不能决定大鼠骨骼肌中mTORC1的活性水平

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摘要

Resistance training with eccentric contraction has been shown to augment muscle hypertrophy more than other contraction modes do (i.e., concentric and isometric contraction). However, the molecular mechanisms involved remain unclear. The purpose of this study was to investigate the effect of muscle contraction mode on mammalian target of rapamycin complex 1 (mTORC1) signaling using a standardized force‐time integral (load (weight) × contraction time). Male Sprague–Dawley rats were randomly assigned to three groups: eccentric contraction, concentric contraction, and isometric contraction. The right gastrocnemius muscle was exercised via percutaneous electrical stimulation‐induced maximal contraction. In experiment 1, different modes of muscle contraction were exerted using the same number of reps in all groups, while in experiment 2, muscle contractions were exerted using a standardized force‐time integral. Muscle samples were obtained immediately and 3 h after exercise. Phosphorylation of molecules associated with mTORC1 activity was assessed using western blot analysis. In experiment 1, the force‐time integral was significantly different among contraction modes with a higher force‐time integral for eccentric contraction compared to that for other contraction modes (P < 0.05). In addition, the force‐time integral was higher for concentric contraction compared to that for isometric contraction (P < 0.05). Similarly, p70S6K phosphorylation level was higher for eccentric contraction than for other modes of contraction (P < 0.05), and concentric contraction was higher than isometric contraction (P < 0.05) 3 h after exercise. In experiment 2, under the same force‐time integral, p70S6K (Thr389) and 4E‐BP1 phosphorylation levels were similar among contraction modes 3 h after exercise. Our results suggest that mTORC1 activity is not determined by differences in muscle contraction mode itself. Instead, mTORC1 activity is determined by differences in the force‐time integral during muscle contraction.
机译:偏心收缩的阻力训练已显示出比其他收缩方式(即同心收缩和等距收缩)更能增强肌肉肥大。但是,涉及的分子机制仍不清楚。这项研究的目的是使用标准化的力-时间积分(负荷(重量)×收缩时间)研究肌肉收缩模式对雷帕霉素复合物1(mTORC1)信号转导的哺乳动物目标的影响。将雄性Sprague–Dawley大鼠随机分为三组:离心收缩,同心收缩和等距收缩。右腓肠肌通过经皮电刺激引起的最大收缩来锻炼。在实验1中,在所有组中使用相同的次数重复执行不同的肌肉收缩模式,而在实验2中,使用标准的力时积分进行肌肉收缩。立即和运动后3小时获得肌肉样本。使用蛋白质印迹分析评估与mTORC1活性相关的分子的磷酸化。在实验1中,各收缩模式之间的力时积分存在显着差异,与其他收缩模式相比,偏心收缩的力时积分更高(P <0.05)。此外,同心收缩的力-时间积分要比等距收缩的力-时间积分要高(P <0.05)。同样,运动后3小时,离心收缩的p70S6K磷酸化水平高于其他收缩模式(P <0.05),同心收缩高于等轴收缩(P <0.05)。在实验2中,在相同的力时积分下,运动后3小时的收缩模式中的p70S6K(Thr389)和4E-BP1磷酸化水平相似。我们的结果表明,mTORC1活性不是由肌肉收缩模式本身的差异决定的。取而代之的是,mTORC1的活性取决于肌肉收缩过程中力-时间积分的差异。

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