Although it is well known that carnosine plays an important role in exercise performance and skeletal muscle homeostasis, its definitive role is still not established. Carnosine functions as a high-energy phosphate system comparable to the creatine/phosphocreatine system. In their experiments, Severin et al. demonstrated that carnosine plays a role in contractile function of skeletal muscle. In nerve-muscle preparation of frogs, it has been shown that the offset of the fatigue could occur during rhythmic nerve-stimulated muscle contractions if 10 mM of carnosine was added to the surrounding medium. This is also true for anserine[1].
Carnosine is a dipeptide synthesized in the body from β-alanine and L-histidine. It is found in high concentrations in the brain, muscle, and gastrointestinal tissues of humans and is present in all vertebrates. Carnosine has a number of beneficial antioxidant properties. For example, carnosine scavenges reactive oxygen species (ROS) as well as alpha-beta unsaturated aldehydes created by peroxidation of fatty acid cell membranes during oxidative stress. Carnosine can oppose glycation, and it can chelate divalent metal ions. Carnosine alleviates diabetic nephropathy by protecting podocyte and mesangial cells, and can slow down aging[1].
Evidence from animal studies showed that carnosine supplementation may reduce body weight, blood pressure level, serum lipid levels, and atherosclerotic plaque instability, thus inhibiting the development and/or progression of hypertension and atherosclerosis. However, well controlled human clinical trials investigating the role of carnosine in preserving and improving cardiovascular health are still scarce. A randomized placebo-controlled trial reported that 4-month treatment with a dietary supplement containing cinnamon, chromium, and carnosine (1.2 g/day) decreased fasting blood glucose and increased fat-free mass in overweight or obese pre-diabetic subjects. Furthermore, other randomized controlled trial demonstrated that L-carnosine (500 mg/d), added to conventional therapy for six months, significantly improved cardiopulmonary exercise test and the 6-min walking test, but not left-ventricular ejection fraction in patients with chronic heart failure[1].