Journal
MUSCLE & NERVE
Volume 43, Issue 1, Pages 49-57Publisher
WILEY
DOI: 10.1002/mus.21796
Keywords
muscle weakness; muscle weight; myostatin deficiency; peak tetanic force; sex differences
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Funding
- NCRR NIH HHS [T32 RR007004] Funding Source: Medline
- NICHD NIH HHS [HD058834, R21 HD058834, R21 HD058834-02] Funding Source: Medline
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R21HD058834] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [T32RR007004] Funding Source: NIH RePORTER
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Absence of functional myostatin (MSTN) during fetal development results in adult skeletal muscle hypertrophy and hyperplasia. To more fully characterize MSTN loss in hind-limb 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 43: 49-57, 2011
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