L-taurine is an amino sulfonic acid that has garnered scientific interest for its role in supporting mitochondrial function. Research indicates that taurine is present in high concentrations in tissues with high energy demands, such as the heart and skeletal muscle, suggesting a physiological role in cellular energy metabolism. Mechanistically, taurine is involved in stabilizing mitochondrial membranes, regulating calcium homeostasis, and modulating oxidative stress—each of which is critical for optimal mitochondrial function. Experimental studies, particularly in animal models, have demonstrated that taurine deficiency can impair mitochondrial respiratory chain activity and increase susceptibility to oxidative damage. Supplementation with taurine has been shown to restore mitochondrial function and decrease markers of oxidative stress in these models.

In human studies, evidence is more limited but promising. Some small clinical trials and observational studies suggest that taurine supplementation can improve exercise performance and muscle function, potentially through its effects on mitochondrial energetics. However, large-scale, well-controlled clinical trials are lacking, and the precise mechanisms in humans remain to be fully elucidated. Overall, while the evidence base is not yet robust enough for a higher rating, there is scientific validation—especially from preclinical research—for taurine's supportive role in mitochondrial health.