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In acute myocardial infarction (AMI), reactive oxygen species may cause irreversible damage to the heart tissue. Physical training is capable of enhancing antioxidant capacity, acting as a cardioprotective factor. We assessed the preventive effects of physical training on the antioxidant and functional responses of the heart of Wistar Kyoto rats after AMI. Wistar Kyoto rats (n = 12) were allocated to sedentary (SED) or trained (EXE—aerobic training on a treadmill) groups. Echocardiographic exams were performed 48 hr before and 48 hr after the induction of AMI. Superoxide dismutase (SOD) and catalase (CAT) activities, and total glutathione (GSH) were measured in vitro in the heart tissue. After AMI, the EXE group showed higher left ventricular shortening fraction (29%; p = .004), higher cardiac output (37%; p = .032) and reduced myocardial infarction size (16%; p = .007) than SED. The EXE group showed a higher nonenzymatic antioxidant capacity (GSH, 23%; p = .004), but the SOD and CAT activities were higher in SED (23% SOD; p = .021 and 20% CAT; p = .016). In addition, the SOD activity was positively correlated with myocardial infarction size and inversely correlated with cardiac output. Physical training partially preserved cardiac function and increased intracellular antioxidant response in cardiac tissue of animals after AMI.
Schaun, Lehnen, Irigoyen, and Markoski are with the Laboratory of Cellular and Molecular Cardiology and Laboratory of Animal Experimentation, Institute of Cardiology/University Foundation of Cardiology, ICFUC-Porto Alegre, Brazil. Motta and Klamt are with the Laboratory of Cell Biochemistry, Dept. of Biochemistry, Institute of Basic Sciences and Health, Federal University of Rio Grande do Sul, UFRGS-Porto Alegre, Brazil. Teixeira and Rossato are with the Methodist University Center IPA, Porto Alegre, Brazil.