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The rationale for measurement of the latter was previous work from us21 and others22, 23, 24 demonstrating an important role for S‐nitrosylation in muscle physiology, as well as emerging evidence for modulation of NO synthase activity via cGMP‐mediated signaling mechanisms.25, 26, 27 Changes in both muscle mass and muscle qualities, such as protein complement, metabolic state, and neural activation strategies, can contribute to these impairments. Here we show that augmentation of nitric oxide‐cyclic guanosine monophosphate signaling by short‐term daily administration of the phosphodiesterase 5 inhibitor sildenafil increases protein synthesis, alters protein expression and nitrosylation, and reduces fatigue in human skeletal muscle. The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments. 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