Skeletalmuscleatrophieswithdisusewhilewithincreaseduseandincreasedloadskeletalmuscleexhibitshypertrophy,withanincreaseinthesizeofexistingmusclefibers.OnesignalingpathwayinvolvedinregulatingskeletalmuscleatrophyandhypertrophyistheAKT/mTORpathway(seemTORpathway).ThemTORpathwayactivityincreasesinresponsetomuscleactivityduringhypertrophyanddecreasesinactivityduringatrophy.BlockingthispathwaygeneticallyorwiththemTORinhibitorrapamycinblockshypertrophyandgeneticactivationofthepathwayinduceshypertrophy.OneagentthatpromotesmusclehypertrophyisthegrowthfactorIGF-1.IGF-1activatesAKT,GSK-3betaandmTORtopromotehypertrophy.Incontrast,thecalcineurinpathwayisnotinvolvedinhypertrophyandisdown-regulatedbyagentssuchasIGF-1thatpromotehypertrophy.Calcineurinmaymodulateotheraspectsofmusclefunctionsuchasthedevelopmentofslowmusclefibersthroughtranscriptionalregulation.Thesepathwaysleadtoregulationofproteintranslation,withincreasedtranslationapparentlyactingasakeyregulatorypointinskeletalmusclehypertrophy.AgentssuchasIGF-1thatstimulateskeletalmusclehypertrophymayprovidetreatmentsformuscleatrophyandwasting.

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