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The Molecular Adaptive Responses of Skeletal Muscle to High-Intensity Exercise/Training and Hypoxia.
Antioxidants ( IF 6.0 ) Pub Date : 2020-07-24 , DOI: 10.3390/antiox9080656
Jia Li 1, 2 , Yanchun Li 3 , Muhammed M Atakan 2, 4 , Jujiao Kuang 2 , Yang Hu 3 , David J Bishop 2 , Xu Yan 2, 5
Affiliation  

High-intensity exercise/training, especially interval exercise/training, has gained popularity in recent years. Hypoxic training was introduced to elite athletes half a century ago and has recently been adopted by the general public. In the current review, we have summarised the molecular adaptive responses of skeletal muscle to high-intensity exercise/training, focusing on mitochondrial biogenesis, angiogenesis, and muscle fibre composition. The literature suggests that (peroxisome proliferator-activated receptor gamma coactivator 1-alpha) PGC-1α, vascular endothelial growth factor (VEGF), and hypoxia-inducible factor 1-alpha (HIF1-α) might be the main mediators of skeletal muscle adaptations to high-intensity exercises in hypoxia. Exercise is known to be anti-inflammatory, while the effects of hypoxia on inflammatory signalling are more complex. The anti-inflammatory effects of a single session of exercise might result from the release of anti-inflammatory myokines and other cytokines, as well as the downregulation of Toll-like receptor signalling, while training-induced anti-inflammatory effects may be due to reductions in abdominal and visceral fat (which are main sources of pro-inflammatory cytokines). Hypoxia can lead to inflammation, and inflammation can result in tissue hypoxia. However, the hypoxic factor HIF1-α is essential for preventing excessive inflammation. Disease-induced hypoxia is related to an upregulation of inflammatory signalling, but the effects of exercise-induced hypoxia on inflammation are less conclusive. The effects of high-intensity exercise under hypoxia on skeletal muscle molecular adaptations and inflammatory signalling have not been fully explored and are worth investigating in future studies. Understanding these effects will lead to a more comprehensive scientific basis for maximising the benefits of high-intensity exercise.

中文翻译:

骨骼肌对高强度运动/训练和缺氧的分子适应性反应。

高强度运动/训练,尤其是间歇运动/训练,近年来越来越受欢迎。半个世纪前,低氧训练被引入精英运动员,最近已被普通大众采用。在当前的综述中,我们总结了骨骼肌对高强度运动/训练的分子适应性反应,重点关注线粒体生物发生、血管生成和肌纤维组成。文献表明,(过氧化物酶体增殖物激活受体γ共激活剂1-α)PGC-1α、血管内皮生长因子(VEGF)和缺氧诱导因子1-α(HIF1-α)可能是骨骼肌适应的主要介质缺氧时进行高强度运动。众所周知,运动具有抗炎作用,而缺氧对炎症信号传导的影响则更为复杂。单次运动的抗炎作用可能是由于抗炎肌因子和其他细胞因子的释放以及 Toll 样受体信号传导的下调所致,而训练引起的抗炎作用可能是由于抗炎肌因子和其他细胞因子的减少所致腹部和内脏脂肪(促炎细胞因子的主要来源)。缺氧会导致炎症,炎症又会导致组织缺氧。然而,缺氧因子 HIF1-α 对于防止过度炎症至关重要。疾病引起的缺氧与炎症信号的上调有关,但运动引起的缺氧对炎症的影响尚不明确。缺氧下高强度运动对骨骼肌分子适应和炎症信号传导的影响尚未得到充分探索,值得在未来的研究中进行研究。了解这些影响将为最大限度地提高高强度运动的益处提供更全面的科学依据。
更新日期:2020-07-24
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