Institute of Biomedical Problems, Russian Academy of Sciences, Moscow, 123007, Russia.
Lomonosov Moscow State University, Faculty of Fundamental Medicine, Moscow, 119991, Russia.
Biochemistry (Mosc). 2018 Jun;83(6):613-628. doi: 10.1134/S0006297918060019.
A large body of experimental data have shown that aerobic exercise of different duration, intensity, and pattern affect molecular mechanisms regulating mitochondrial biogenesis in skeletal muscles. This review focuses on the effects of exercise duration and intensity on the molecular mechanisms of mitochondrial biogenesis regulation in skeletal muscles, namely PGC-1α-dependent signaling. Studies of the effects of acute exercise and exercise training showed that an increase in the duration of aerobic exercise from 30 to 90 min does not provide additional stimuli to activate signaling pathways regulating post-translational modification of peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) and expression of the PGC-1α gene (PPARGC1A). Conversely, exercise intensity substantially affects mitochondrial biogenesis due to the increase in the recruitment of type II muscle fibers with accompanying pronounced metabolic shift leading to the activation of signaling cascades and expression of genes regulating mitochondrial biogenesis. Therefore, intermittent exercise, which recruits type II muscle fibers, is more efficient in the activation of mitochondrial biogenesis than work-matched continuous exercise. In skeletal muscle adapted to aerobic training, intensity-dependent activation of mitochondrial biogenesis after acute exercise is associated primarily with the AMP-activated protein kinase/PGC-1α pathway, expression of PGC-1α-regulated genes, and expression of PPARGC1A from the alternative (distal) inducible promoter regulated by the cAMP response element-binding protein 1-related transcription factors and their coactivators. Elucidation of the effects of duration and intensity of aerobic exercise on the PGC-1α-dependent and -independent mechanisms of mitochondrial biogenesis is important for treatment of patients with various metabolic disorders, as well as for optimization of training in athletes.
大量实验数据表明，不同持续时间、强度和模式的有氧运动都会影响调节骨骼肌线粒体生物发生的分子机制。本综述重点讨论了运动持续时间和强度对调节骨骼肌线粒体生物发生的分子机制（即 PGC-1α 依赖性信号通路）的影响。急性运动和运动训练的研究表明，从 30 分钟增加到 90 分钟的有氧运动持续时间不会提供额外的刺激来激活调节过氧化物酶体增殖物激活受体 γ 共激活因子 1α（PGC-1α）的翻译后修饰和 PGC-1α 基因（PPARGC1A）表达的信号通路。相反，运动强度会由于募集具有伴随明显代谢转变的 II 型肌肉纤维而显著影响线粒体生物发生，从而激活信号级联和调节线粒体生物发生的基因表达。因此，募集 II 型肌肉纤维的间歇运动比工作匹配的连续运动更有效地激活线粒体生物发生。在适应有氧运动的骨骼肌中，急性运动后依赖强度的线粒体生物发生的激活主要与 AMP 激活的蛋白激酶/PGC-1α 通路、PGC-1α 调节基因的表达以及由 cAMP 反应元件结合蛋白 1 相关转录因子及其共激活因子调节的替代（远端）诱导启动子调节的 PPARGC1A 表达有关。阐明有氧运动的持续时间和强度对 PGC-1α 依赖性和非依赖性线粒体生物发生机制的影响，对于治疗各种代谢紊乱患者以及优化运动员的训练都非常重要。
