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Hindlimb skeletal muscle function in myostatin‐deficient mice
Author(s) -
Gentry Bettina A.,
Ferreira J. Andries,
Phillips Charlotte L.,
Brown Marybeth
Publication year - 2011
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.21796
Subject(s) - myostatin , hindlimb , endocrinology , medicine , muscle hypertrophy , skeletal muscle , biology , muscle atrophy , gastrocnemius muscle , plantaris muscle , soleus muscle , anatomy
Absence of functional myostatin (MSTN) during fetal development results in adult skeletal muscle hypertrophy and hyperplasia. To more fully characterize MSTN loss in hindlimb muscles, the morphology and contractile function of the soleus, plantaris, gastrocnemius, tibialis anterior, and quadriceps muscles in male and female null ( Mstn −/− ), heterozygous ( Mstn +/− ), and wild‐type ( Mstn +/+ ) mice were investigated. Muscle weights of Mstn −/− mice were greater than those of Mstn +/+ and Mstn +/− mice. Fiber cross‐sectional area (CSA) was increased in female Mstn −/− soleus and gastrocnemius muscles and in the quadriceps of male Mstn −/− mice; peak tetanic force in Mstn −/− mice did not parallel the increased muscle weight or CSA. Male Mstn −/− muscle exhibited moderate degeneration. Visible pathology in male mice and decreased contractile strength relative to increased muscle weight suggest MSTN loss results in muscle impairment, which is dose‐, sex‐, and muscle‐dependent. Muscle Nerve, 2011