Document Detail


Oxygen consumption and usage during physical exercise: the balance between oxidative stress and ROS-dependent adaptive signaling.
MedLine Citation:
PMID:  22978553     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The complexity of human DNA has been affected by aerobic metabolism, including endurance exercise and oxygen toxicity. Aerobic endurance exercise could play an important role in the evolution of Homo sapiens, and oxygen was not important just for survival, but it was crucial to redox-mediated adaptation. The metabolic challenge during physical exercise results in an elevated generation of reactive oxygen species (ROS) that are important modulators of muscle contraction, antioxidant protection, and oxidative damage repair, which at moderate levels generate physiological responses. Several factors of mitochondrial biogenesis, such as peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), mitogen-activated protein kinase, and SIRT1, are modulated by exercise-associated changes in the redox milieu. PGC-1α activation could result in decreased oxidative challenge, either by upregulation of antioxidant enzymes and/or by an increased number of mitochondria that allows lower levels of respiratory activity for the same degree of ATP generation. Endogenous thiol antioxidants glutathione and thioredoxin are modulated with high oxygen consumption and ROS generation during physical exercise, controlling cellular function through redox-sensitive signaling and protein-protein interactions. Endurance exercise-related angiogenesis, up to a significant degree, is regulated by ROS-mediated activation of hypoxia-inducible factor 1α. Moreover, the exercise-associated ROS production could be important to DNA methylation and post-translation modifications of histone residues, which create heritable adaptive conditions based on epigenetic features of chromosomes. Accumulating data indicate that exercise with moderate intensity has systemic and complex health-promoting effects, which undoubtedly involve regulation of redox homeostasis and signaling.
Authors:
Zsolt Radak; Zhongfu Zhao; Erika Koltai; Hideki Ohno; Mustafa Atalay
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2012-11-16
Journal Detail:
Title:  Antioxidants & redox signaling     Volume:  18     ISSN:  1557-7716     ISO Abbreviation:  Antioxid. Redox Signal.     Publication Date:  2013 Apr 
Date Detail:
Created Date:  2013-02-15     Completed Date:  2013-08-20     Revised Date:  2014-04-01    
Medline Journal Info:
Nlm Unique ID:  100888899     Medline TA:  Antioxid Redox Signal     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1208-46     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Exercise / physiology*
Humans
Oxidative Stress / physiology
Oxygen Consumption / physiology*
Reactive Oxygen Species / metabolism*
Signal Transduction / physiology
Chemical
Reg. No./Substance:
0/Reactive Oxygen Species
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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