Effects of Beta-Alanine Supplementation on Cardiac Function and Health

Cardiac muscle, like skeletal muscle, is rich in histidine containing dipeptides, such as carnosine, despite the marked differences in energy metabolism between the two types of muscle. Cardiomyocytes are dependent upon oxidative metabolism to match their energy demands and, under normal physiological conditions, there is limited H+ accumulation in cardiomyocytes. The presence of histidine containing dipeptides in cardiac muscle cells, in spite of a virtual absence of acidosis, suggests that their role in the heart is not related to pH regulation. On the other hand, the importance of tightly regulated cardiomyocyte contractile function suggests that Ca2+ transients and sensitivity might be the primary role of HCDs in cardiac muscle. In isolated rat hearts, carnosine can potentiate cardiac contractility, with the suggestion that carnosine may be an effective cardioprotective agent, regulating calcium flux and cardiac contractility. Carnosine might also provide a protective mechanism to the cardiac tissue through its proposed physiological role against exercise-induced production of reactive species. The aim of the proposed programme of work will be to examine a potential physiological role for carnosine in the cardiomyocyte and to determine the effects of beta-alanine supplementation upon cardiac function in humans.