Open AccessSildenafil Increases Muscle Protein Synthesis and Reduces Muscle Fatigue
Author(s) -
SheffieldMoore Melinda,
Wiktorowicz John E.,
Soman Kizhake V.,
Danesi Christopher P.,
Kinsky Michael P.,
Dillon Edgar L.,
Randolph Kathleen M.,
Casperson Shan L.,
Gore Dennis C.,
Horstman Astrid M.,
Lynch James P.,
Doucet Barbara M.,
Mettler Joni A.,
Ryder Jeffrey W.,
PloutzSnyder Lori L.,
Hsu Jean W.,
Jahoor Farook,
Jennings Kristofer,
White Gregory R.,
McCammon Susan D.,
Durham William J.
Publication year - 2013
Publication title -
clinical and translational science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.303
H-Index - 44
eISSN - 1752-8062
pISSN - 1752-8054
DOI - 10.1111/cts.12121
Subject(s) - skeletal muscle , sildenafil , medicine , nitric oxide , cyclic guanosine monophosphate , endocrinology , cgmp specific phosphodiesterase type 5 , myofibril , muscle contraction , muscular dystrophy , phosphodiesterase , chemistry , pharmacology , biochemistry , enzyme
Reductions in skeletal muscle function occur during the course of healthy aging as well as with bed rest or diverse diseases such as cancer, muscular dystrophy, and heart failure. However, there are no accepted pharmacologic therapies to improve impaired skeletal muscle function. Nitric oxide may influence skeletal muscle function through effects on excitation‐contraction coupling, myofibrillar function, perfusion, and metabolism. 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. These findings suggest that phosphodiesterase 5 inhibitors represent viable pharmacologic interventions to improve muscle function.