Moderate exercise prevents impaired Ca2+ handling in heart of CO-exposed rat: implication for sensitivity to ischemia-reperfusion.
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.
Farah
C
C
Research Laboratory EA 4278, Physiology and Physiopathology of Cardiovascular Adaptations to Exercise, Faculty of Sciences, Avignon University, Avignon, France.
Meyer
G
G
André
L
L
Boissière
J
J
Gayrard
S
S
Cazorla
O
O
Richard
S
S
Boucher
F
F
Tanguy
S
S
Obert
P
P
Reboul
C
C
D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D020013:Calcium Signaling / Q000187:drug effects*; D002248:Carbon Monoxide / Q000633:toxicity*; D002374:Catalase / Q000378:metabolism; D016923:Cell Death; D005979:Glutathione Peroxidase / Q000378:metabolism; D019570:Inhalation Exposure; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control; D015428:Myocardial Reperfusion Injury / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D010807:Physical Endurance; D051381:Rats; D017208:Rats, Wistar; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control
D000393:Air Pollutants; D000975:Antioxidants; C506948:Atp2a2 protein, rat; D002248:Carbon Monoxide; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases