In skeletal muscle, carnitine is essential for the translocation of long-chain fatty-acids into the mitochondrial matrix for subsequent β-oxidation, and in the regulation of the mitochondrial acetyl coenzyme A/ free coenzyme A ratio by buffering excess acetyl groups. Based on the concept that increased carnitine availability is beneficial to skeletal muscle metabolic process, a large amount of research was directed towards investigating the effects of carnitine supplementation on exercise performance. However, it has been debated about contribution of carnitine for energy metabolism in skeletal muscle and whether carnitine supplementation can improve physical performance in healthy subjects. Recently, in order to resolve the issues, attention has been focused on the carnitine transport mechanism across the skeletal muscle plasma membrane. Due to lack of endogenous synthesis of carnitine in myocytes, skeletal muscles need to import this molecule from blood, suggesting that muscle carnitine uptake is most likely the limiting factor to muscle carnitine availability. It has been established that the specific carnitine transporter, OCTN2, is expressed in skeletal muscles and is assumed to transport carnitine into myocytes. Carnitine uptake capacity via the OCTN2, therefore, has been assumed to be one of the important factors to the skeletal muscle energy metabolism. The purpose of the review is to summarize the role of carnitine in skeletal muscle metabolism, and the current knowledge regarding the effect of carnitine supplementation of exercise performance. Furthermore, we summarize recent observations related to the carnitine transport mechanism in skeletal muscles including contribution of OCTN2 during muscle contraction.