Background: Diabetic cardiomyopathy (DC) is a hallmark complication of long-standing hyperglycemia t caused by various metabolic and mitochondrial disturbances. Physical activities such as exercise do not only enhance conditions in healthy individuals but could also improve the state of those afflicted with diseases. However, the beneficial effects of resistance exercise in the prevention of DC and cardiac mitochondrial dysfunction are still uncertain. In this study, we investigated whether RE attenuates DC through improving mitochondrial function.
Method: We utilized an in vivo rat model of diabetes. Fourteen Otsuka Long–Evans Tokushima Fatty rats were assigned to sedentary control (SC, n=7) and RE (n=7) groups at 28 weeks of age. Long–Evans Tokushima Otsuka rats were used as the non-diabetic control. RE were trained by 20 repetitions of climbing a ladder 5 days per week. 
Results
RE showed higher glucose uptake and lower lipid profiles, indicating enhancing energy metabolism. RE significantly increased ejection fraction and fractional shortening compared to SC. RE showed increase in cardiac mitochondria numbers which increased mitochondrial biogenesis by higher expression of PGC-1α and TFAM. RE reduced proton leak and reactive oxygen species production with increased membrane potentials. These results were accompanied by higher SOD2 and lower UCP2 and UCP3 levels in RE.
Discussion: These data suggested that resistance exercise is effective in ameliorating DC by improving mitochondrial function, which may contribute to the maintenance of diabetic cardiac contractility.

Resistance exercise ameliorates diabetic cardiomyopathy