不同运动方式和强度对中年小鼠骨骼肌长寿蛋白的影响。

IF 2.2 4区 医学 Q3 PHYSIOLOGY Physiology international Pub Date : 2023-06-12 DOI:10.1556/2060.2023.00152
Shota Inoue, Kyohei Matsuura, Daisuke Eguchi, Masahiro Wakayama, Kosuke Ono, Hanlin Jiang, Hideki Moriyama
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引用次数: 0

摘要

体育锻炼是抗衰老最有效的方法之一。本研究的目的是验证不同运动模式和强度对中年骨骼肌中长寿蛋白的影响。采用有氧或阻力运动训练中年小鼠8周,采用western blotting检测骨骼肌中sirtuin 1 (SIRT1)、腺苷单磷酸活化激酶(AMPK)和哺乳动物雷帕霉素靶蛋白(mTOR)通路的变化。长期运动对骨骼肌SIRT1丰度没有影响,而高强度有氧运动增加了AMPK磷酸化和过氧化物酶体增殖体激活受体-γ共激活因子-1α (PGC-1α)。低强度阻力运动促进了Akt/mTOR/p70核糖体蛋白激酶S6 (p70S6K)信号传导,但不诱导肌肉肥大。相反,高强度的阻力运动刺激肌肉肥大,而不磷酸化mTOR信号相关蛋白。这些结果提示了确定运动方式和强度对中年抗衰老的重要性。
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Effects of different modes and intensities of exercise on longevity proteins in middle-aged mouse skeletal muscle.

Physical exercise represents one of the most effective approaches to anti-aging. The goal of this study was to verify the effects of different modes and intensities of exercise on longevity proteins in the skeletal muscle in midlife. Middle-aged mice were trained in aerobic or resistance exercise for 8 weeks, and the changes in sirtuin 1 (SIRT1), adenosine monophosphate-activated kinase (AMPK), and mammalian target of rapamycin (mTOR) pathways in the skeletal muscle were evaluated by western blotting. Long-term exercise had no effects on skeletal muscle SIRT1 abundance, whereas high-intensity aerobic exercise increased AMPK phosphorylation and peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α). Low-intensity resistance exercise facilitated Akt/mTOR/p70 ribosomal protein kinase S6 (p70S6K) signaling but did not induce muscle hypertrophy. Conversely, high-intensity resistance exercise stimulated muscle hypertrophy without phosphorylation of mTOR signaling-related proteins. These results suggest the importance of setting exercise modes and intensities for anti-aging in midlife.

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来源期刊
Physiology international
Physiology international Medicine-Physiology (medical)
CiteScore
3.40
自引率
0.00%
发文量
37
期刊介绍: The journal provides a forum for important new research papers written by eminent scientists on experimental medical sciences. Papers reporting on both original work and review articles in the fields of basic and clinical physiology, pathophysiology (from the subcellular organization level up to the oranizmic one), as well as related disciplines, including history of physiological sciences, are accepted.
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