Effects of Different Exercise Interventions on Cardiac Function in Rats With Myocardial Infarction

Abstract

High-intensity interval training (HIIT) and aerobic training (AT) both improve cardiac function; however, their effects on cardiac function after myocardial infarction (MI) and the molecular mechanisms are unclear. In this study, HIIT, AT and sedentary (SED) interventions were performed for 4 weeks to compare the effects on cardiac function after MI and explore a more suitable approach for clinical application and the potential mechanisms. Twenty-four (24) male rats were randomly divided into a control group (CON), MI-sedentary group (MI-SED), MI-aerobic training group (MI-AT), and MI-high-intensity interval training group (MI-HIIT). After 4 weeks of intervention the exercise capacity, heart rate (HR), left ventricular end-diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), left ventricular ejection fraction (LVEF), AMP-activated protein kinase α1 (AMPKα1), cardiomyocyte morphology, and cardiac mitochondria were assessed. After intervention: 1) exercise capacity in the MI-AT (49.08±3.141 m; p<0.001) and MI-HIIT (51.70±7.572m; p<0.001) groups was significantly more increased than the MI-SED group; there was no significant difference between the MI-AT and MI-HIIT group (p=0.33). 2) LVEDD and LVESD in the MI-SED (p<0.01) and MI-HIIT (p<0.01) groups was significantly more increased than the CON group; the MI-AT group showed no significant difference in LVEDD and LVESD compared with the CON group; LVEF in the MI-AT (53.47±7.913%; p=0.03) and MI-HIIT (56.20±7.224%; p=0.006) groups was significantly more increased than the MI-SED group, and there was no statistical difference between the MI-AT and MI-HIIT groups. 3) AMPKα1 expression was significantly increased in the MI-AT (1.15±0.264; p=0.001) and MI-HIIT (1.04±0.238; p=0.003) groups and decreased in the MI-SED group (0.71±0.257; p<0.001) when compared with the CON group. 4) The MI-SED group exhibited sarcoplasmic dissolution and fibrous hyperplasia in the myocardium, cardiac mitochondrial damage and reduced mitochondrial numbers; the MI-HIIT group displayed swollen and vacuolated cardiac mitochondria with disrupted cristae; the MI-AT and MI-HIIT groups had significantly increased cardiac mitochondrial numbers than the MI-SED group; there was no statistical difference between the MI-AT and MI-HIIT groups. Aerobic training and HIIT for 4 weeks had similar cardioprotection and were superior to SED intervention. Both AT and HIIT improved cardiac function and exercise capacity by upregulating AMPKα1 expression. However, 4 weeks of intervention resulted in left ventricular dilation and cardiac myocardial mitochondrial injury in the MI-HIIT group.