[No authors listed]
AIMS:Myocardial infarction (MI) is accompanied with skeletal muscle abnormalities. The aims are to explore an optimal exercise mode to improve cardiac function and prevent skeletal muscle atrophy, and detect the possible mechanisms of exercise-induced inhibition of muscle atrophy. MAIN METHODS:Rats were subjected to four weeks of different types of exercise after MI surgery (resistance training, RT; moderated-intensity continuous aerobic exercise, MCE and high-intensity intermittent aerobic exercise, HIA). Cardiac function, histological changes of heart and skeletal muscle, oxidative stress, antioxidant capacity and the expression of muscle atrophy-related factors were detected in skeletal muscle. KEY FINDINGS:The three types of exercise improved heart function, reduced cardiac fibrosis and increased muscle weight and cross-section area (CSA) of muscle fibers in different degrees. The survival rates of MI rats intervened by RT and MCE were higher than HIA. Exercise down-regulated the mRNA levels of murf1 and atrogin-1, decreased reactive oxygen species level, increased antioxidant capacity, regulated the expression of insulin-like growth factor 1 (IGF1), mechano growth factor (MGF), Neuregulin1 (NRG1) and Myostatin (MSTN), and activated Akt and Erk1/2 signalings in soleus muscle. Furthermore, CSA of muscle fibers and the expression of IGF1, MGF, NRG1 in skeletal muscle had correlations with cardiac function. SIGNIFICANCE:RT and MCE are the first two choices for the early exercise rehabilitation following MI. All types of exercise can effectively inhibit skeletal muscle atrophy through increasing the antioxidant capacity, reducing oxidative stress and protein degradation, and regulating the growth factors expression in skeletal muscle.
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