Document Detail


Moderate exercise prevents impaired Ca2+ handling in heart of CO-exposed rat: implication for sensitivity to ischemia-reperfusion.
MedLine Citation:
PMID:  20889839     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Sustained urban carbon monoxide (CO) exposure exacerbates heart vulnerability to ischemia-reperfusion via deleterious effects on the antioxidant status and Ca(2+) homeostasis of cardiomyocytes. The aim of this work was to evaluate whether moderate exercise training prevents these effects. Wistar rats were randomly assigned to a control group and to CO groups, living during 4 wk in simulated urban CO pollution (30-100 parts/million, 12 h/day) with (CO-Ex) or sedentary without exercise (CO-Sed). The exercise procedure began 4 wk before CO exposure and was maintained twice a week in standard filtered air during CO exposure. On one set of rats, myocardial ischemia (30 min) and reperfusion (120 min) were performed on isolated perfused rat hearts. On another set of rats, myocardial antioxidant status and Ca(2+) handling were evaluated following environmental exposure. As a result, exercise training prevented CO-induced myocardial phenotypical changes. Indeed, exercise induced myocardial antioxidant status recovery in CO-exposed rats, which is accompanied by a normalization of sarco(endo)plasmic reticulum Ca(2+)-ATPase 2a expression and then of Ca(2+) handling. Importantly, in CO-exposed rats, the normalization of cardiomyocyte phenotype with moderate exercise was associated with a restored sensitivity of the myocardium to ischemia-reperfusion. Indeed, CO-Ex rats presented a lower infarct size and a significant decrease of reperfusion arrhythmias compared with their sedentary counterparts. To conclude, moderate exercise, by preventing CO-induced Ca(2+) handling and myocardial antioxidant status alterations, reduces heart vulnerability to ischemia-reperfusion.
Authors:
C Farah; G Meyer; L André; J Boissière; S Gayrard; O Cazorla; S Richard; F Boucher; S Tanguy; P Obert; C Reboul
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-10-01
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  299     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-12-03     Completed Date:  2011-01-13     Revised Date:  2012-02-06    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H2076-81     Citation Subset:  IM    
Affiliation:
Research Laboratory EA 4278, Physiology and Physiopathology of Cardiovascular Adaptations to Exercise, Faculty of Sciences, Avignon University, Avignon, France.
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MeSH Terms
Descriptor/Qualifier:
Air Pollutants / toxicity*
Animals
Antioxidants / metabolism
Calcium Signaling / drug effects*
Carbon Monoxide / toxicity*
Catalase / metabolism
Cell Death
Glutathione Peroxidase / metabolism
Inhalation Exposure
Male
Myocardial Contraction / drug effects
Myocardial Infarction / chemically induced,  metabolism,  prevention & control
Myocardial Reperfusion Injury / chemically induced,  metabolism,  physiopathology,  prevention & control*
Myocytes, Cardiac / drug effects*,  metabolism,  pathology
Physical Endurance*
Rats
Rats, Wistar
Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism
Superoxide Dismutase / metabolism
Time Factors
Ventricular Fibrillation / chemically induced,  metabolism,  prevention & control
Chemical
Reg. No./Substance:
0/Air Pollutants; 0/Antioxidants; 630-08-0/Carbon Monoxide; EC 1.11.1.6/Catalase; EC 1.11.1.9/Glutathione Peroxidase; EC 1.15.1.1/Superoxide Dismutase; EC 3.6.3.8/Atp2a2 protein, rat; EC 3.6.3.8/Sarcoplasmic Reticulum Calcium-Transporting ATPases

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