Role of aerobic exercise training on myocardial infarction-induced cardiac dysfunction, dysautonomia, and oxidative stress in female ob/ob mice.

Abstract

We investigated the effects of aerobic exercise training (ET) on cardiac function, autonomic modulation, and inflammatory and oxidative stress markers in an experimental model of diabetes and obesity following myocardial infarction (MI). Female ob/ob mice were randomized into sham sedentary (S), MI sedentary (MIS), and MI + ET (MIT) groups. MI was induced by coronary artery occlusion. Cardiac function was evaluated in the beginning and at the end of the protocol. Aerobic exercise training was performed on treadmill for 4 weeks. RR interval was recorded in awake animals at the end of the protocol. Cardiac autonomic modulation was evaluated by linear and nonlinear analysis of heart rate variability. Oxidative stress and inflammatory markers were assessed. As expected, in the beginning of the protocol, the MI and MIT had a reduced ejection fraction (MIS: -44%; MIT: -33% vs. S), stroke volume (SV) (MIS: -46%; MIT: -52% vs. S), and cardiac output (CO) (MIS: -55%; MIT: -55% vs. S). At the end of the protocol, the MIS group presented lower vagal modulation, higher cardiac lipoperoxidation and protein oxidation, and lower catalase activity in the heart. On the other hand, the animals submitted to ET showed higher exercise capacity, parasympathetic modulation (RMSSD index and SD1), cardiac IL-10 and catalase activity, and lower lipoperoxidation and protein oxidation in the heart, as well as higher SV (MIT: 90% vs. Initial) and CO (MIT: 90% vs. Initial). Altogether, the results showed that myocardial infarction led to a reduction in vagal modulation and cardiac function, which was accompanied by an increased oxidative stress, while aerobic exercise training prevented/attenuated these impairments in female ob/ob mice.