PURPOSE: The purpose of this study was to investigate whether aerobic exercise can improve cardiac and mitochondrial functions of heart failure induced by pressure overload in rats. We explored the mechanism of adaptational changes at the post-transcriptional level with the experimental model. METHODS: The rat model of heart failure was accomplished by abdominal aorta constriction (AC). Eight weeks after the operation, the animals were divided into 4 groups: sham control (SC), sham plus training (ST), AC without training, and AC plus training (AT). Training was performed on treadmill at 25m/min, 0° grade for 60 min per day and last for 8 weeks. Heart structural and functional parameters were measured with echocardiography. Mitochondrial respiratory functions were measured with high-resolution respirometry. The miRNAs expression profiles were investigated by Affymetrix® Microarray. RT-PCR was used to validate the expression levels of miRNAs. RESULTS: Compared with AC, the cardiac structure index LVID were significantly decreased, while the cardiac functional indexes ejection factor (EF) and fractional shortening (FS) were significantly increased in AT hearts. Mitochondrial state 3 respiration and respiratory control ratio (RCR) decreased significantly in AC vs. SC, whereas the reductions were restored by AT to SC level. Mitochondrial complex I activity in AC was significantly lower than that in SC, but such reduction was not observed in AT. MiR-10a-5p and miR-542-5p levels in AT hearts were significantly higher than those in AC, and some target mRNA of these two miRNAs were related to mitochondrial function and dynamic. For example, Coa 7 and Creb1 were affected by miR-10a-5p, and Tfrc by miR-542-5p. CONCLUSION: Aerobic exercise can ameliorate the pathogenesis of heart failure and improve heart function in experimental animals. This effect is largely achieved by improvement of mitochondrial function, especially complex I function in electron transfer chain. miR-10a-5p and miR-542-5p may be involved in this process through regulating key components of mitochondrial dynamic. This work was supported by 973 Program(2013CB531200)and Tianjin Research Program of Application Foundation and Advanced Technology (13JCYBJC39200).