Myostatin deficiency increased maximum tetanic force in EDL and soleus muscles, but decreased specific force and increased susceptibility to contraction-induced injury in EDL muscles.
Does myostatin deficiency alter the contractile properties and susceptibility to injury in EDL and soleus muscles of mice?
Myostatin deficiency increases absolute muscle force but impairs specific force and increases injury susceptibility in fast-twitch muscles, highlighting its role in muscle contractility and extracellular matrix composition.
Myostatin is a negative regulator of muscle mass. The impact of myostatin deficiency on the contractile properties of healthy muscles has not been determined. We hypothesized that myostatin deficiency would increase the maximum tetanic force (P(o)), but decrease the specific P(o) (sP(o)) of muscles and increase the susceptibility to contraction-induced injury. The in vitro contractile properties of extensor digitorum longus (EDL) and soleus muscles from wild-type (MSTN(+/+)), heterozygous-null (MSTN(+/-)), and homozygous-null (MSTN(-/-)) adult male mice were determined. For EDL muscles, the P(o) of both MSTN(+/-) and MSTN(-/-) mice were greater than the P(o) of MSTN(+/+) mice. For soleus muscles, the P(o) of MSTN(-/-) mice was greater than that of MSTN(+/+) mice. The sP(o) of EDL muscles of MSTN(-/-) mice was less than that of MSTN(+/+) mice. For soleus muscles, however, no difference in sP(o) was observed. Following two lengthening contractions, EDL muscles from MSTN(-/-) mice had a greater force deficit than that of MSTN(+/+) or MSTN(+/-) mice, whereas no differences were observed for the force deficits of soleus muscles. Myostatin-deficient EDL muscles had less hydroxyproline, and myostatin directly increased type I collagen mRNA expression and protein content. The difference in the response of EDL and soleus muscles to myostatin may arise from differences in the levels of a myostatin receptor, activin type IIB. Compared with the soleus, the amount of activin type IIB receptor was approximately twofold greater in EDL muscles. The results support a significant role for myostatin not only in the mass of muscles but also in the contractility and the composition of the extracellular matrix of muscles.
Mendias et al. (Fri,) conducted a other in Myostatin deficiency. Myostatin deficiency vs. Wild-type (MSTN+/+) was evaluated on Maximum tetanic force (P(o)) and specific P(o) (sP(o)). Myostatin deficiency increased maximum tetanic force in EDL and soleus muscles, but decreased specific force and increased susceptibility to contraction-induced injury in EDL muscles.