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Mesterolone is a synthetic oral anabolic androgenic steroid used to treat hypogonadism. Limited information is available about how this drug exerts its effects on skeletal muscle. Satellite cells (SCs) are mononuclear myogenic stem cells that contribute to postnatal skeletal muscle growth and maintenance. As SCs' activation and subsequent differentiation to new myonuclei is a major event during skeletal muscle hypertrophy, this study investigated the influence of Mesterolone on SC distribution within type I oxidative fibers of the adult avian skeletal muscle. Immunocytochemical techniques and morphometric analyses were used to calculate the fiber size, and numbers of SCs and myonuclei within the anterior latissimus dorsi (ALD) muscle of the chicken. The ALD is a slow (tonic) contracting muscle that is made up exclusively of slow‐twitch type I oxidative red fibers. The number of SCs was significantly (P<0.01) increased by very high doses (12 and 16 mg/kg) of Mesterolone administration. Similarly, the number of myonuclei was increased by administering the high doses of Mesterolone. However, this increase did not reach significant levels except at the Mesterolone dose of 12 mg/kg as the number of myonuclei increased significantly (P<0.05) by 32% compared to the number of myonuclei in the control birds. In addition, no significant (P>0.05) differences were detected in the fiber area and the myonuclear domain size between control and Mesterolone‐treated birds. This study indicates that Mesterolone treatment can increase the numbers of SCs and myonuclei without inducing hypertrophy in type I fibers of the adult avian skeletal muscle. This is because SCs in type I fibers are, most probably, required for fiber maintenance rather than hypertrophy since these fibers have a higher rate of protein breakdown because they are the ones that mostly used in daily routine activities.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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