Objective To investigate the effects of moderate aerobic exercise and high intensity intermittent exercise on myocardial mitophagy in mice with nonalcoholic fatty liver disease and its possible mechanism. Methods Forty 3-week-old male C57BL/6J mice were randomly divided into a normal feeding group (Chow group, n=10) and high fat-fed group (HFD group, n=30). At week 18, mice in the HFD group with a body weight exceeding 20%~30% of the ordinary diet group were considered obese mice (n=26). Two mice were randomly selected for liver oil red O staining to confirm successful establishment of the NAFLD mouse model. Sixteen NAFLD mice were randomly selected and divided into a moderate intensity aerobic exercise group (MICT group) and high intensity intermittent aerobic exercise group (HIIT group) with eight mice in each group. The two groups were subjected to exercise training for 8 weeks, and samples were weighed after treatment. Masson staining was used to observe myocardial fibrosis. The ultrastructure of myocardial cells was observed by transmission electron microscopy. Mitophagy and mitochondrial biogenesis were assessed by Western blot. Results Compared with the Control group, the body weight and heart index in the Model group were significantly increased and decreased, respectively. Compared with the Model group, the body weight of MICT and HIIT groups was increased significantly, and the heart index of the MICT group was increased. Masson staining showed that, compared with the Control group, collagen fiber content in the myocardium in the Model group was significantly increased, and the myocardial fibers were disorganized and broken in electron microscopy. The myocardial morphology was disorganized, mitochondria were swollen, cristae were broken and blurred, and lipid droplets were observed. Compared with the Model group, the myocardial collagen fiber content in MICT and HIIT groups was significantly reduced, the myocardial fiber arrangement had slightly recovered in transmission electron microscopy, the z-line was clearly visible, the degree of mitochondrial degeneration was slightly improved, and lipid droplets were slightly reduced. The improvement in the cardiac tissue structure in the MICT group was better than that in the HIIT group. Western blot showed that, compared with the Control group, PINK1 and Beclin1 expression levels in myocardial tissue of the Model group underwent no significant changes, while Parkin, LAMP1, and PGC-1α expression was significantly decreased (P<0. 01). p62 protein expression and the LC3-Ⅱ/ LC3-Ⅰ ratio were significantly increased (P<0. 05, P<0. 01). Compared with the Model group, PINK1 and Beclin1 expression levels in MICT and HIIT groups were not significantly changed, while PGC-1α expression was upregulated, and Parkin and LAMP1 expression in the MICT group was significantly increased (P<0. 05). p62 protein expression and the LC3-Ⅱ/ LC3-Ⅰ ratio were significantly decreased (P<0. 05, P<0. 01), Parkin and LAMP1 expression levels were upregulated, and the LC3-Ⅱ/ LC3-Ⅰ ratio and p62 protein expression were significantly decreased in the HIIT group (P<0. 05, P<0. 01). Conclusions Different forms of aerobic exercise effectively ameliorate myocardial structural and functional injury in NAFLD mice, which may be mediated through stimulating autophagy flux of mitochondria in cardiomyocytes, activating autophagy, and restoring the normal autophagy function of cells to ameliorate myocardial cell damage, and moderate continuous aerobic exercise has a better improving effect.