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Myocardial infarction (MI) is the leading course of sudden cardiac death, especially the accompanied arrhythmia induced by the autonomic nervous system (ANS) imbalance. Exercise can improve cardiac function after MI, however, the benefit of exercise still keeps controversial because of its proarrhythmic effect. In this study we investigated how exercise affects the incidence of arrhythmic events and the ANS in MI model mice.
Wild-type male mice which underwent sham-operation or MI-made operation were divided into one control group and two MI groups: sedentary group and exercise training group (MI-Ex). MI-Ex group underwent treadmill training from 7 days after MI for 7-8 weeks. Cardiac function and structural changes were assessed by echocardiography and histology. Based on telemetry recording, autonomic nervous function was evaluated by pharmacological blockades test and heart rate variability (HRV). The incidence of spontaneous ventricular arrhythmia was calculated through telemetry electrocardiography. Gene expressions in left ventricular tissues were investigated by real-time PCR and Western blotting.
There were no significant differences in echocardiographic findings and survival rate between two MI groups. Also there was no obvious difference in the ratio of fibrotic area. Comparing with sedentary group, MI-Ex group showed lower incidence of spontaneous ventricular arrhythmia and increased parasympathetic tone index. The real-time PCR indicated changes in Ca2＋handling-related gene expressions (higher SERCA2a, lower phospholamban) in MI-Ex group.
Chronic exercise training modulated the ANS imbalance without increasing the incidence of spontaneous arrhythmia in MI mice mainly through the normalization of Ca2＋dynamics.