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Exercise-induced mitochondrial dysfunction: a myth or reality?
Ostojic SM1.
Author information
1Faculty of Sport and Physical Education, University of Novi Sad, Novi Sad 21000, Serbia School of Medicine, University of Belgrade, Belgrade 11000, Serbia).
Clin Sci (Lond). 2016 Aug 1;130(16):1407-16. doi: 10.1042/CS20160200.
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.
KEYWORDS: DNA deletion; aging; athletes; exhaustive exercise; peroxisome proliferator-activated receptor γ co-activator 1-α (PGC-1α); reactive oxygen species
DOI: 10.1042/CS20160200
http://www.ncbi.nlm.nih.gov/pubmed/27389587
Ostojic SM1.
Author information
1Faculty of Sport and Physical Education, University of Novi Sad, Novi Sad 21000, Serbia School of Medicine, University of Belgrade, Belgrade 11000, Serbia).
Clin Sci (Lond). 2016 Aug 1;130(16):1407-16. doi: 10.1042/CS20160200.
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.
KEYWORDS: DNA deletion; aging; athletes; exhaustive exercise; peroxisome proliferator-activated receptor γ co-activator 1-α (PGC-1α); reactive oxygen species
DOI: 10.1042/CS20160200
http://www.ncbi.nlm.nih.gov/pubmed/27389587