The Effect of Changing the Contraction Mode During Resistance Training on mTORC1 Signaling and Muscle Protein Synthesis
The Effect of Changing the Contraction Mode During Resistance Training on mTORC1 Signaling and Muscle Protein Synthesis
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DOI：
10.3389/fphys.2019.00406
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发表时间：
2019-04-18
影响因子：
4
通讯作者：
Ogasawara, Riki
中科院分区：
文献类型：
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作者：
Ato, Satoru;Tsushima, Daisuke;Ogasawara, Riki
急性耐力运动(RE)通过激活雷帕霉素复合体的机械靶点(MTORC)增加肌肉蛋白质合成(MPS)，而慢性耐力运动(RT)可导致骨骼肌肥大。尽管在RT过程中，MPS对RE的反应随着时间的推移而变得迟钝，但还没有确定有效的恢复策略。由于离心性肌肉收缩(EC)具有强烈刺激mTORC1激活和MPS的潜力，将肌肉收缩模式改变为EC可能维持慢性RT时MPS对RE的反应。雄性大鼠随机分为RE组(1次RE)和RT组(13次RE)。此外，每组又分为等长收缩(IC)组和EC亚组。RE组采用IC或EC行急性单侧RE。RT组应用IC进行12次单侧RE。在第13回合，RT-IC亚组进行了进一步的IC回合，而RT-EC亚组改为EC。所有肌肉收缩均由经皮电刺激引起。各组均于运动后6h取肌肉标本。1RE后，EC组p70S6K Thr389的磷酸化水平显著高于IC组。然而，其他mTORC1相关蛋白(4E-BP1和核糖体蛋白S6)的磷酸化和MPS反应在不同的收缩模式下没有差异。与第1次RE相比，第13次RE后mTORC1的激活和MPS反应明显减弱。从IC改变为EC并没有改善这些反应。综上所述，将收缩模式改变为EC并不能恢复慢性RT中钝化的mTORC1激活和MPS对RE的反应。
Acute resistance exercise (RE) increases muscle protein synthesis (MPS) via activation of mechanistic target of rapamycin complex (mTORC), and chronic resistance exercise training (RT) results in skeletal muscle hypertrophy. Although MPS in response to RE is blunted over time during RT, no effective restorative strategy has been identified. Since eccentric muscle contraction (EC) has the potential to strongly stimulate mTORC1 activation and MPS, changing the muscle contraction mode to EC might maintain the MPS response to RE during chronic RT. Male rats were randomly divided into RE (1 bout of RE) and RT (13 bouts of RE) groups. Additionally, each group was subdivided into isometric contraction (IC) and EC subgroups. The RE groups performed acute, unilateral RE using IC or EC. The RT groups performed 12 bouts of unilateral RE using IC. For bout 13, the RT-IC subgroup performed a further IC bout, while the RT-EC subgroup changed to EC. All muscle contractions were induced by percutaneous electrical stimulation. Muscle samples were obtained at 6 h post exercise in all groups. After the 1st RE bout, the EC group showed significantly higher p70S6K Thr389 phosphorylation than the IC group. However, the phosphorylation of other mTORC1-associated proteins (4E-BP1 and ribosomal protein S6) and the MPS response did not differ between the contraction modes. After the 13th bout of RE, mTORC1 activation and the MPS response were significantly blunted as compared with the 1st bout of RE. Changing from IC to EC did not improve these responses. In conclusion, changing the contraction mode to EC does not reinvigorate the blunted mTORC1 activation and MPS in response to RE during chronic RT.