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Figure 2. Purported mechanisms by which L-CIT improves exercise performance alone and combined with exercise training. De novo synthesis of L-ARG (1) from circulating L-CIT increases nNOS (nNOSμ) activity in the skeletal muscle (2). NO produced by nNOSμ stimulates expression of PGC-1α (3), a regulator of mitochondrial respiration. Improved peripheral NO-mediated vasodilation and subsequent muscle oxygen utilization in active skeletal muscles contribute to enhance exercise performance (4). An enhanced mitochondrial respiratory capacity from the combined effect of PGC-1α expression and O2 availability from vasodilation contributes to improve exercise performance (5). Moreover, L-CIT directly promotes muscle protein synthesis by stimulation of the mTORC1 pathway, which involves increased phosphorylation of S6K1 and 4E-BP1 (6). This effect of L-CIT on protein synthesis may improve muscle mass or strength when combined with exercise training in obese older adults (7 and 8). Enhanced mitochondrial metabolism and skeletal muscle function may contribute to improve exercise performance. *NO produced by nNOS may contribute to vasodilation after L-CIT supplementation.