Efeitos do treinamento resistido de intensidade moderada na prevenção de anormalidades cardiovasculares de ratos com infarto agudo do miocárdio

Abstract

Introduction: Acute myocardial infarction (MI) is a cardiovascular disease that affects approximately 300 thousand Brazilians annually, of which 30% die. Many factors influence the onset of MI, with emphasis on a sedentary lifestyle and poor diet. The practice of aerobic exercise is highly recommended for preventing cardiovascular diseases. However, the cardioprotective mechanism of resistance exercise still needs to be further clarified. Objective: To evaluate the effects of resistance training (RT) in preventing cardiac abnormalities in animals with isoproterenol-induced acute myocardial infarction. Methods: The animals were divided into 4 groups: 1) SED (sedentary): animals subjected to electrical stimulation and administration of saline solution (0.9%, i.p.), 2) RT (trained): animals subjected to RT and administration of saline solution, 3) MI: animals subjected to electrical stimulation and administration of isoproterenol (ISO, 100 mg/kg, i.p.) and 4) RT+MI: animals subjected to RT and administration of ISO. RT was performed with moderate intensity (60%) of the one repetition maximum test, 3x per week, for 4 weeks. Anthropometric and morphological changes, infarction area, biochemical markers of tissue injury, electrocardiogram, autonomic modulation, ventricular contractility, oxidative stress and expression of apoptotic pathway proteins were evaluated. Results: The results showed that animals in the RT and RT+MI groups had lower body mass and greater strength gains when compared to animals in the SED and MI groups. ISO increased heart size in animals in the MI and RT+MI groups. The area of myocardial injury and extravasation of lactate dehydrogenase (LDH), total creatine phosphokinase (CPK-Total) and creatine phosphokinase MB fraction (CK-MB) increased in the MI group and were significantly reduced with RT. Furthermore, RT reduced the incidence of ST elevation (40%), heart rate (12%) and QTc interval prolongation (17%). Infarction induction increased the autonomic modulation of the sympathetic nervous system that was prevented in response to RT. RT (31.6 ± 4.8 mmHg) also prevented the contractile dysfunction observed in infarcted animals (9.6 ± 2.6 mmHg). The results also revealed that RT prevented the increase in lipid peroxidation, promoted an increase in the activity of superoxide dismutase (SOD) by 40% and glutathione peroxidase (GPx) by 120% when compared to the MI group. The activity of catalase enzymes (CAT) was reduced in the MI group, but RT did not prevent this reduction. The production of reactive oxygen species (ROS), assessed by the intensity of DHE fluorescence, was elevated in the MI group (1.25 ± 0.01 a.u) compared to the SED and TR groups, being restored in response to TR ( 0.9 ± 0.02 a.u.). In the presence of apocynin, an inhibitor of NADPH oxidase (NOX), there was no increase in ROS production between the experimental groups. The results revealed a decrease in the expression of Bax (0.7 ± 0.2) and caspase 3 (0.7 ± 0.1) in animals in the EXE+IM group in relation to the MI group (Bax: 1.6 ± 0. 2 and caspase 3: 1.5 ± 0.2). Conclusion: Given this, our results indicate that RT has a cardioprotective effect in a MI model, preventing the loss of myocardial contractility and electrocardiographic changes (QTc prolongation, ST elevation and increased heart rate). Furthermore, TR reduced sympathetic autonomic modulation associated with decreased oxidative stress and inhibition of the apoptotic pathway.