Literature DB >> 27389587

Exercise-induced mitochondrial dysfunction: a myth or reality?

Sergej M Ostojic1.   

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.
© 2016 The Author(s). published by Portland Press Limited on behalf of the Biochemical Society.

Entities:  

Keywords:  DNA deletion; aging; athletes; exhaustive exercise; peroxisome proliferator-activated receptor γ co-activator 1-α (PGC-1α); reactive oxygen species

Mesh:

Year:  2016        PMID: 27389587     DOI: 10.1042/CS20160200

Source DB:  PubMed          Journal:  Clin Sci (Lond)        ISSN: 0143-5221            Impact factor:   6.124


  7 in total

Review 1.  Novel Insights and Current Evidence for Mechanisms of Atherosclerosis: Mitochondrial Dynamics as a Potential Therapeutic Target.

Authors:  Dan Li; Shengjie Yang; Yanwei Xing; Limin Pan; Ran Zhao; Yixi Zhao; Longtao Liu; Min Wu
Journal:  Front Cell Dev Biol       Date:  2021-07-07

Review 2.  What do over-trained athletes and patients with neurodegenerative diseases have in common? Mitochondrial dysfunction.

Authors:  Sergej M Ostojic; Laszlo Ratgeber; Andras Olah; Jozsef Betlehem; Acs Pongras
Journal:  Exp Biol Med (Maywood)       Date:  2021-02-07

3.  Resistance Training with Co-ingestion of Anti-inflammatory Drugs Attenuates Mitochondrial Function.

Authors:  Daniele A Cardinale; Mats Lilja; Mirko Mandić; Thomas Gustafsson; Filip J Larsen; Tommy R Lundberg
Journal:  Front Physiol       Date:  2017-12-19       Impact factor: 4.566

4.  Peroxisome Proliferator-Activated Receptor-γ Coactivator-1α (PGC-1α) Regulates the Expression of B-Cell Lymphoma/Leukemia-2 (Bcl-2) and Promotes the Survival of Mesenchymal Stem Cells (MSCs) via PGC-1α/ERRα Interaction in the Absence of Serum, Hypoxia, and High Glucose Conditions.

Authors:  Min Wang; Guangxin Yang; Xiaoyan Jiang; Debin Lu; Hao Mei; Bing Chen
Journal:  Med Sci Monit       Date:  2017-07-16

5.  β-glucan Salecan Improves Exercise Performance and Displays Anti-Fatigue Effects through Regulating Energy Metabolism and Oxidative Stress in Mice.

Authors:  Xi Xu; Yijian Ding; Yunxia Yang; Yan Gao; Qi Sun; Junhao Liu; Xiao Yang; Junsong Wang; Jianfa Zhang
Journal:  Nutrients       Date:  2018-07-03       Impact factor: 5.717

Review 6.  Pathophysiology of skeletal muscle disturbances in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).

Authors:  Klaus J Wirth; Carmen Scheibenbogen
Journal:  J Transl Med       Date:  2021-04-21       Impact factor: 5.531

7.  H2O2 Signaling-Triggered PI3K Mediates Mitochondrial Protection to Participate in Early Cardioprotection by Exercise Preconditioning.

Authors:  Yang Yuan; Shan-Shan Pan; Dong-Feng Wan; Jiao Lu; Yue Huang
Journal:  Oxid Med Cell Longev       Date:  2018-07-25       Impact factor: 6.543

  7 in total

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