Intermittent aerobic exercise training can reverse the reduced expression of mitofusin 2 (MFN2) and optic atrophy 1 (OPA1) and inhibit the increased expression of dynamin-related protein 1 (DRP1) caused by myocardial infarction [89], which suggests that exercise training can promote mitochondrial membrane fusion of cardiomyocytes, improve mitochondrial energy metabolism, increase resistance capacity to oxidative stress of cardiomyocyte postmyocardial infarction [89]. This evidence concerns the gene MFN2 and myocardial infarction.