Myostatin-Deficient Mice:Contractile Properties of EDL and Soleus Muscles

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J Appl Physiol. 2006 May 18

Contractile Properties of EDL and Soleus Muscles of Myostatin-

Deficient Mice.

Mendias CL, Marcin JE, Calderon DR, Faulkner JA.

Molecular and Integrative Physiology, University of Michigan, Ann

Arbor, Michigan, United States.

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 (Po), but decrease the

specific Po (sPo) of muscles and increase the susceptibility to

contraction-induced injury.

The in vitro contractile properties of EDL and soleus muscles from

wild type (MSTN(+/+)), heterozygous-null (MSTN(+/-)) and homozygous-

null (MSTN(-/-)) adult male mice were determined. For EDL muscles,

the Po of both MSTN(+/-) and MSTN(-/-) mice were greater than the Po

of MSTN(+/+) mice. For soleus muscles, the Po of MSTN(-/-) mice was

greater than that of MSTN(+/+) mice. The sPo of EDL muscles of MSTN(-

/-) mice was less than MSTN(+/+) mice.

For soleus muscles, however, no difference in sPo was observed.

Following two lengthening contractions, EDL muscles from MSTN(-/-)

mice had a greater force deficit than 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, ActRIIB.

Compared with the soleus, the amount of ActRIIB was approximately two-

fold 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 ECM of muscles.