Taurine (2-aminoethanesulfonic acid) is a sulfur-containing β-amino acid present in high concentrations in most tissues, including skeletal muscle, liver, blood, and brain. Taurine has been suggested to have positive effects on some of the physiologic functions considered to be a cause of fatigue during exercise: Ca2+ handling in excitation–contraction coupling, regulation of ion channels, oxidative stress, and the inflammatory response. However, how and where taurine affects these processes have not been elucidated fully. Some in vitro studies have suggested that taurine treatment improves the contractile properties of skeletal muscle. Several studies have suggested that taurine is involved in regulation of energy metabolism. In contrast, whole-body taurine transporter knockout mice exhibit severe intolerance to exercise. Based on these observations, whether taurine treatment may prevent/attenuate fatigue during exercise and then improve exercise performance in humans and experimental animals has been studied. Some recent studies have investigated the effects of taurine administration on post-exercise recovery. Our group investigated the effects of taurine treatment on fatigue induced by endurance exercise. We found that post-exercise taurine administration enhanced the recovery of skeletal muscle glycogen, which is the major determinant for exercise performance. In this review, we introduce studies investigating the effects of taurine administration on exercise-induced fatigue and post-exercise recovery.
Cumulative studies showed that taurine (2-aminoethanesulfonic acid) contributes to a variety of physiological events. Transport study suggested the cellular taurine transport in an Na+- and Cl−-dependent manner, and the several members of SLC6A family have been shown as taurine transporter. At the inner blood–retinal barrier (BRB), taurine transporter (TauT/SLC6A) is involved in the transport of taurine to the retina from the circulating blood. The involvement of TauT is also suggested in γ-aminobutyric acid (GABA) transport at the inner BRB, and its role is assumed in the elimination of GABA from the retinal interstitial fluid. In the retina, taurine is thought to be a major organic osmolyte, and its influx and efflux through TauT and volume-sensitive organic osmolyte and anion channel (VSOAC) in Müller cells regulate the osmolarity in the retinal microenvironment to maintain a healthy retina. In the liver, hepatocytes take up taurine via GABA transporter 2 (GAT2/SLC6A13, the orthologue of mouse GAT3) expressed at the sinusoidal membrane of periportal hepatocytes, contributing to the metabolism of bile acid. Site-directed mutagenesis study suggests amino acid residues that are crucial in the recognition of substrates by GATs and TauT. The evidence suggests the physiological impact of taurine transporters in tissues.
Taurine has important physiological roles as well as a wide range of pharmacological effects. Studies have suggested that taurine ameliorates diabetes, hypertension, oxidative stress, and inflammatory diseases. However, its mechanisms of action are still unclear. It has been reported that N-acyl taurine activates transient receptor potential vanilloid-1 (TRPV1), which is related to the pathogenesis of many inflammatory diseases. In this study, we hypothesized that taurine has a regulatory effect on TRPV1 activation via N-acyl taurine. To evaluate this hypothesis, we assessed the calcium influx activated by a TRPV1 agonist in human keratinocyte (HaCaT) cells and paraquat-induced oxidative stress in Caenorhabditis elegans. Our results indicate that taurine inhibits TRPV-dependent activity to overcome oxidative stress in cultured cell lines and in C. elegans.