Effect of exercise on improving myocardial mitochondrial function in decreasing diabetic cardiomyopathy

What is the topic of this review? The mechanism of exercise decrease diabetic cardiomyopathy by improving the mitochondrial homeostasis of the myocardium, and new insights for the treatment of diabetic cardiomyopathy with exercise. What advances does it highlight? Mitochondrial dysfunction induced by a high-glucose environment is one of the main causes of diabetic cardiomyopathy. The mitochondrial mechanism is mainly mitochondrial metabolic substrate disorder, mitochondrial dynamics change, mitochondrial Ca2+ regulation imbalance, and so on. Exercise can improve the function of myocardial mitochondria in multiple ways, so as to achieve the effect of decreasing diabetic cardiomyopathy.Diabetic cardiomyopathy (DCM) is a significant cause of heart failure in patients with diabetes, and its pathogenesis is closely related to myocardial mitochondrial injury and functional disability. Studies have shown that the development of diabetic cardiomyopathy is related to disorders in mitochondrial metabolic substrates, changes in mitochondrial dynamics, an imbalance in mitochondrial Ca2+ regulation, defects in the regulation of microRNAs, and mitochondrial oxidative stress. Physical activity may play a role in resistance to the development of diabetic cardiomyopathy by improving myocardial mitochondrial biogenesis, the level of autophagy and dynamic changes in fusion and division; enhancing the ability to cope with oxidative stress; and optimising the metabolic substrates of the myocardium. This paper puts forward a new idea for further understanding the specific mitochondrial mechanism of the occurrence and development of diabetic cardiomyopathy and clarifying the role of exercise-mediated myocardial mitochondrial changes in the prevention and treatment of diabetic cardiomyopathy. This is expected to provide a new theoretical basis for exercise to reduce diabetic cardiomyopathy symptoms.