This is an older study (2013) but I haven't seen this result mentioned before. This extract is taken from the text of the study:
Two groups of men were studied over 15 days, including a baseline period (the week preceding the treatment period.) In the subsequent treatment period (days 1–8) they received either daily low‐dose (25 mg) sildenafil (N = 5) or placebo (N = 6) in a randomized, double‐blinded fashion The men were healthy, based on their history and screening results, represented a wide age range, and the majority (4/6 placebo, 4/5 sildenafil) were overweight based on their BMI. Subjects were instructed to continue regular activities of daily living and maintain their usual diet during the study.
In this study we found that short‐term treatment with the phosphodiesterase 5 inhibitor sildenafil reduces skeletal muscle fatigue and stimulates skeletal muscle protein synthesis while altering muscle protein expression and nitrosylation. Our findings thus provide evidence that sildenafil remodels human skeletal muscle in a functionally adaptive manner.
The differences between treatment groups in protein abundance and S‐nitrosylation observed in this study suggest that changes in myofibrillar function and actin dynamics may have contributed to an increase in muscle quality, manifested as increased fatigue resistance, in individuals receiving sildenafil. Notably, the approximate doubling of skeletal muscle protein synthesis observed in response to sildenafil is of similar magnitude to that observed in response to 100–200 mg/week testosterone injection.
Whether the short‐term responses of protein synthesis and expression eventually manifest as a change in muscle mass or simply reflect an adaptive qualitative change in muscle protein composition will be important to determine in future longer‐term studies.
Two groups of men were studied over 15 days, including a baseline period (the week preceding the treatment period.) In the subsequent treatment period (days 1–8) they received either daily low‐dose (25 mg) sildenafil (N = 5) or placebo (N = 6) in a randomized, double‐blinded fashion The men were healthy, based on their history and screening results, represented a wide age range, and the majority (4/6 placebo, 4/5 sildenafil) were overweight based on their BMI. Subjects were instructed to continue regular activities of daily living and maintain their usual diet during the study.
In this study we found that short‐term treatment with the phosphodiesterase 5 inhibitor sildenafil reduces skeletal muscle fatigue and stimulates skeletal muscle protein synthesis while altering muscle protein expression and nitrosylation. Our findings thus provide evidence that sildenafil remodels human skeletal muscle in a functionally adaptive manner.
The differences between treatment groups in protein abundance and S‐nitrosylation observed in this study suggest that changes in myofibrillar function and actin dynamics may have contributed to an increase in muscle quality, manifested as increased fatigue resistance, in individuals receiving sildenafil. Notably, the approximate doubling of skeletal muscle protein synthesis observed in response to sildenafil is of similar magnitude to that observed in response to 100–200 mg/week testosterone injection.
Whether the short‐term responses of protein synthesis and expression eventually manifest as a change in muscle mass or simply reflect an adaptive qualitative change in muscle protein composition will be important to determine in future longer‐term studies.