Exercising heart failure patients: cardiac protection through preservation of mitochondrial function and substrate utilization?

Current heart failure (HF) therapy remains unable to substantially improve exercise capacity. Studies have shown that exercise training has beneficial effects on the heart in both health and disease. How mitochondria respond to exercise in this setting has, however, received less attention in literature. These beneficial effects may include protective changes in mitochondrial function and adaptations in substrate utilization. This review describes exercise-induced changes in cardiac metabolism, including changes in mitochondrial function and substrate utilization and their effects on cardiac function. We conclude that exercising HF patients can improve mitochondrial function and optimize substrate utilization, eventually improving or restoring cardiac function. This suggests that exercise itself should be incorporated in the HF treatment plan, to improve cardiac function and in term exercise capacity. Extending knowledge on mechanisms by which exercise exerts protective effects could potentially lead to development of therapies directed at improving mitochondrial function and substrate utilization in HF.