Carnosine (β-alanyl-L-histidine) plays an important role in exercise performance and skeletal muscle homeostasis. Dietary supplementation with the rate-limiting precursor β-alanine leads to an increase in skeletal muscle carnosine content, which further potentiates its effects. There is significant interest in carnosine and β-alanine across athletic and clinical populations. Traditionally, attention has been given to performance outcomes with less focus on the underlying mechanism(s). Putative physiological roles in human skeletal muscle include acting as an intracellular pH buffer, modulating energy metabolism, regulating Ca2+ handling and myofilament sensitivity, and scavenging of reactive species. Emerging evidence shows that carnosine could also act as a cytoplasmic Ca2+–H+ exchanger and form stable conjugates with exercise-induced reactive aldehydes. The enigmatic nature of carnosine means there is still much to learn regarding its actions and applications in exercise, health, and disease. In this review, we examine the research relating to each physiological role attributed to carnosine, and its precursor β-alanine, in exercising human skeletal muscle.
1Sport, Health and Performance Enhancement (SHAPE) Research Centre, Musculoskeletal Physiology Research Group, School of Science and Technology, Nottingham Trent University, Nottingham, UNITED KINGDOM
2Research Centre for Life and Sport Sciences (CLaSS), School of Health and Life Sciences, Department of Sport and Exercise, Birmingham City University, Birmingham, UNITED KINGDOM
3Applied Physiology and Nutrition Research Group, Rheumatology Division, Faculdade de Medicina FMUSP, Universidade de São Paulo, BRAZIL
4Centre for Diabetes, Chronic Diseases, and Ageing, School of Science and Technology, Nottingham Trent University, Nottingham, UNITED KINGDOM
Address for correspondence: Craig Sale, Ph.D., Nottingham Trent University, Erasmus Darwin Building, Clifton Lane, Nottingham, NG11 8NS, United Kingdom; E-mail: email@example.com.
Submitted for publication March 2019.
Accepted for publication April 2019.
Online date: May 10, 2019