Background: Physical exercise has been considered an important non-pharmacological therapy for the prevention and treatment of cardiovascular diseases. However, its effects on minor cardiac remodeling are not clear. Objective: To evaluate the influence of aerobic exercise on the functional capacity, cardiac structure, left ventricular (LV) function, and gene expression of NADPH oxidase subunits in rats with small-sized myocardial infarction (MI). Methods: Three months after MI induction, Wistar rats were divided into three groups: Sham; sedentary MI (MI-SED); and aerobic [...] Abstract Background: Physical exercise has been considered an important non-pharmacological therapy for the prevention and treatment of cardiovascular diseases. However, its effects on minor cardiac remodeling are not clear. Objective: To evaluate the influence of aerobic exercise on the functional capacity, cardiac structure, left ventricular (LV) function, and gene expression of NADPH oxidase subunits in rats with small-sized myocardial infarction (MI). Methods: Three months after MI induction, Wistar rats were divided into three groups: Sham; sedentary MI (MI-SED); and aerobic

Introduction: Exercise is an important therapeutic strategy for preventing and treating myocardial infarction (MI)-induced cardiac remodeling and heart failure. However, the myocardial effects of resistance exercise on infarcted hearts are not completely established. In this study, we investigated the effects of resistance exercise on structural, functional, and molecular cardiac alterations in infarcted rats. Methods: Three months after MI induction or simulated surgery, Wistar rats were assigned into three groups: Sham (n = 14); MI (n = 9); and exercised MI (MI-Ex, n = 13). Exercised rats performed, 3 times a week for 12 weeks, four climbs on a ladder with progressive loads. Cardiac structure and left ventricle (LV) function were analyzed by echocardiogram. Myocyte diameters were evaluated in hematoxylin- and eosin-stained histological sections as the smallest distance between borders drawn across the nucleus. Myocardial energy metabolism, lipid hydroperoxide, malondialdehyde, protein carbonylation, and antioxidant enzyme activities were evaluated by spectrophotometry. Gene expressions of NADPH oxidase subunits were evaluated by RT-PCR. Statistical analyses were performed using ANOVA and Tukey or Kruskal–Wallis and Dunn’s test. Results: Mortality did not differ between the MI-Ex and MI groups. MI had dilated left atrium and LV, with LV systolic dysfunction. Exercise increased the maximum load-carrying capacity, with no changes in cardiac structure or LV function. Myocyte diameters were lower in MI than in Sham and MI-Ex. Lactate dehydrogenase and creatine kinase activity were lower in MI than in Sham. Citrate synthase and catalase activity were lower in MI and MI-Ex than in Sham. Lipid hydroperoxide concentration was lower in MI-Ex than in MI. Nox2 and p22phox gene expressions were higher in MI-Ex than in Sham. Gene expression of Nox4 was higher in MI and MI-Ex than in Sham, and p47phox was lower in MI than in Sham. Conclusion: Late resistance exercise was safe in infarcted rats. Resistance exercise improved maximum load-carrying capacity, reduced myocardial oxidative stress, and preserved myocardial metabolism, with no changes in cardiac structure or left ventricle function in infarcted rats.

Introduction: High-intensity interval training (HIIT) has been recommended in post-myocardial infarction (MI) cardiac rehabilitation; however, its effects on MI-induced cardiac remodeling and skeletal muscle remain unclear. This study evaluated the effects of HIIT on functional capacity, cardiac remodeling, and the soleus skeletal muscle in rats after long-term MI. Methods: Three months after MI induction, Wistar rats were assigned to Sham, MI, and MI subjected to HIIT (MI-HIIT) groups. HIIT was performed three times per week for three months on a treadmill. Cardiac function and functional capacity were assessed before and after training. Oxidative stress markers, energy metabolism enzyme activities, and trophism were analyzed in the soleus. The statistical analysis included ANOVA and Bonferroni or Kruskal–Wallis and Dunn tests. Results: HIIT improved functional capacity compared to the Sham and MI groups. The infarcted groups had left ventricular dilation, hypertrophy, and systolic dysfunction, which were not modulated by HIIT. Soleus fiber cross-sectional areas did not differ between the groups. Catalase activity was lower in the MI and MI-HIIT groups than in the Sham group, while other oxidative stress markers were unchanged. HIIT increased citrate synthase activity compared to the Sham and MI groups, and phosphofructokinase and carnitine palmitoyltransferase-1 activities compared to the MI group. Conclusions: High-intensity interval training improves functional capacity despite unchanged cardiac remodeling in long-term infarcted rats. Enhanced physical capacity is associated with the increased activity of the enzymes involved in the energy metabolism of the soleus muscle.