Hindlimb skeletal muscle function in myostatin-deficient mice

Abstract

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 Mstnr -/- 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 Mstnr-/- mice did not parallel the increased muscle weight or CSA. Male Mstnr-/- 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. © 2010 Wiley Periodicals, Inc.