Cardiovascular disease is the leading cause of death among diabetic patients, due mostly to mitochondrial dysfunction and resulting oxidative stress. Endurance exercise has been firmly established as a way to reduce diabetes and cardiovascular disease morbidity and mortality. The importance of mitochondria for both training performance and health underlies the significance of better understanding the factors that regulate exercise-induced adaptations in mitochondrial network dynamics. The effects on mitochondrial skeletal and cardiac muscle have already been well documented in the past. However, the specific impact of aerobic training on respiratory capacity in the vasculature remain to be established. Furthermore, the relationship between aerobic exercise and mitochondrial function in diabetic patients has yet to be investigated. We hypothesized that a long-term aerobic exercise intervention would enhance mitochondrial respiratory capacity in vascular smooth muscle cells. First, we investigated the effects of training in the vasculature of healthy mice (C57BL/6) and compared them to their sedentary counterparts. We found that exercise stimulates a rise in vascular mitochondrial content and respiratory capacity, especially complex I respiration (p < 0.05). However, when comparing diabetic trained mice to diabetic sedentary controls, it was found that aerobic training induced a downregulation in mitochondrial protein expression as well as a decrease in complex I respiration. In these experiments, our findings suggest that despite the demonstrated benefits of exercise, careful measures should be taken when exposing diabetic models that carry an inherently high risk of cardiovascular disease to prolonged exercise
