Effects of myostatin depletion on muscle contractile properties in middle-aged mice
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Myostatin is a growth factor that is known to regulate muscle content, where a decrease in myostatin expression causes an increase in muscle mass. The effects of myostatin deficiency on the contractile properties of post-developmental myostatin deletion in adult mice have not yet been studied. We measured contractile properties in the fast-type extensor digitorum longus (EDL) and slow-type soleus muscles in 12 - 18 month old inducible myostatin knockout compared to control mice. Myostatin was deleted by tamoxifen administration when mice were 4 months old. We hypothesized that muscle mass and maximum tetanic force output (Po) would be significantly increased in myostatin null mice, but that specific force (sPo) would be decreased. Myostatin deletion was also hypothesized to increase in muscle injury following eccentric contractions. Po force output was increased by myostatin deletion in the EDL, but was unexpectedly in decreased soleus muscle. Myostatin deletion decreased sPo in both EDL and soleus muscles, as previously reported. Following five eccentric lengthening contractions, the EDL muscle of myostatin deficit mice showed significantly more damage. Damage to the soleus muscle was similar across genotypes, implying that the EDL is more susceptible to damage following myostatin deletion. These results indicate that myostatin depletion in middle aged mice influences muscle mass and its contractibility, and supports the possible use of anti-myostatin therapy in various conditions associated with muscle atrophy.