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.
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Cover ImageGABAB receptor-mediated hypertension via hyperpolarization of solitary tract nucleus neurons that receive and integrate baroreceptor afferent inputs. See pp. 1417-1434 for further details. Image kindly provided by Omar LogueClose Modal
Review Article| July 07 2016
Exercise-induced mitochondrial dysfunction: a myth or reality?
Sergej M. Ostojic
*Faculty of Sport and Physical Education, University of Novi Sad, Novi Sad 21000, Serbia
†School of Medicine, University of Belgrade, Belgrade 11000, Serbia
Correspondence: Sergej M. Ostojic (email email@example.com).
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Clin Sci (Lond) (2016) 130 (16): 1407–1416.
March 12 2016
May 03 2016
May 10 2016
Sergej M. Ostojic; Exercise-induced mitochondrial dysfunction: a myth or reality?. Clin Sci (Lond) 1 August 2016; 130 (16): 1407–1416. doi: https://doi.org/10.1042/CS20160200
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