Document Detail


Exercise induces a cardiac mitochondrial phenotype that resists apoptotic stimuli.
MedLine Citation:
PMID:  18083894     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ischemia-reperfusion-induced calcium overload and production of reactive oxygen species can trigger apoptosis by promoting the release of proapoptotic factors via the mitochondrial permeability transition pore. While it is clear that endurance exercise provides cardioprotection against ischemia-reperfusion-induced injury, it is unknown if exercise training directly alters mitochondria phenotype and confers protection against apoptotic stimuli in both subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria. We hypothesized that exercise training increases expression of endogenous antioxidant enzymes and other antiapoptotic proteins, resulting in a SS and IMF mitochondrial phenotype that resists apoptotic stimuli. Mitochondria isolated from hearts of sedentary (n = 8) and exercised-trained (n = 8) adult male rats were studied. Endurance exercise increased the protein levels of primary antioxidant enzymes in both SS and IMF mitochondria. Furthermore, exercise increased the levels of antiapoptotic proteins in the heart, including the apoptosis repressor with a caspase recruitment domain and inducible heat shock protein 70. Importantly, our findings reveal that endurance exercise training attenuates reactive oxygen species-induced cytochrome c release from heart mitochondria. These changes are accompanied by a lower maximal rate of mitochondrial permeability transition pore opening (V(max)) and prolonged time to V(max) in both SS and IMF cardiac mitochondria. These novel findings reveal that endurance exercise promotes biochemical alterations in cardiac SS and IMF mitochondria, resulting in a phenotype that resists apoptotic stimuli. Furthermore, these results are consistent with the concept that exercise-induced mitochondrial adaptations contribute to exercise-induced cardioprotection.
Authors:
Andreas N Kavazis; Joseph M McClung; David A Hood; Scott K Powers
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2007-12-14
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  294     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2008 Feb 
Date Detail:
Created Date:  2008-02-12     Completed Date:  2008-03-31     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H928-35     Citation Subset:  IM    
Affiliation:
Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL 32611, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antioxidants / metabolism
Apoptosis / physiology*
Blotting, Western
Cytochromes c / metabolism
Dose-Response Relationship, Drug
Male
Microscopy, Electron
Mitochondria, Heart / enzymology,  metabolism,  physiology*
Myofibrils / physiology
Phenotype
Physical Conditioning, Animal / physiology*
Physical Endurance / physiology
Rats
Rats, Sprague-Dawley
Reactive Oxygen Species / metabolism
Sarcolemma / physiology
Grant Support
ID/Acronym/Agency:
R01HL067855/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Reactive Oxygen Species; 9007-43-6/Cytochromes c

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


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