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运动诱导的线粒体功能障碍:是虚构还是事实?

Exercise-induced mitochondrial dysfunction: a myth or reality?

作者信息

Ostojic Sergej M

机构信息

Faculty of Sport and Physical Education, University of Novi Sad, Novi Sad 21000, Serbia School of Medicine, University of Belgrade, Belgrade 11000, Serbia

出版信息

Clin Sci (Lond). 2016 Aug 1;130(16):1407-16. doi: 10.1042/CS20160200.

DOI:10.1042/CS20160200
PMID:27389587
Abstract

Beneficial effects of physical activity on mitochondrial health are well substantiated in the scientific literature, with regular exercise improving mitochondrial quality and quantity in normal healthy population, and in cardiometabolic and neurodegenerative disorders and aging. However, several recent studies questioned this paradigm, suggesting that extremely heavy or exhaustive exercise fosters mitochondrial disturbances that could permanently damage its function in health and disease. Exercise-induced mitochondrial dysfunction (EIMD) might be a key proxy for negative outcomes of exhaustive exercise, being a pathophysiological substrate of heart abnormalities, chronic fatigue syndrome (CFS) or muscle degeneration. Here, we overview possible factors that mediate negative effects of exhaustive exercise on mitochondrial function and structure, and put forward alternative solutions for the management of EIMD.

摘要

体育活动对线粒体健康的有益影响在科学文献中得到了充分证实,规律运动可改善正常健康人群、心脏代谢和神经退行性疾病患者以及老年人的线粒体质量和数量。然而,最近的几项研究对这一模式提出了质疑,表明极重度或力竭性运动可引发线粒体紊乱,这可能会在健康和疾病状态下永久性损害其功能。运动诱导的线粒体功能障碍(EIMD)可能是力竭性运动负面结果的关键指标,是心脏异常、慢性疲劳综合征(CFS)或肌肉退化的病理生理基础。在此,我们概述了介导力竭性运动对线粒体功能和结构产生负面影响的可能因素,并提出了管理EIMD的替代解决方案。

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