Lack of myostatin results in excessive muscle growth but impaired force generation
2007
Amthor, Helge | Macharia, Raymond | Navarrete, Roberto | Schuelke, Markus | Brown, Susan C. | Otto, Anthony | Voit, Thomas | Muntoni, Francesco | Vrbová, Gerta | Partridge, Terence | Zammit, Peter | Bünger, L (Lutz) | Patel, Ketan
The lack of myostatin promotes growth of skeletal muscle, and blockade of its activity has been proposed as a treatment for various muscle-wasting disorders. Here, we have examined two independent mouse lines that harbor mutations in the myostatin gene, constitutive null (Mstn⁻/⁻) and compact (Berlin High Line, BEHc/c). We report that, despite a larger muscle mass relative to age-matched wild types, there was no increase in maximum tetanic force generation, but that when expressed as a function of muscle size (specific force), muscles of myostatin-deficient mice were weaker than wild-type muscles. In addition, Mstn⁻/⁻ muscle contracted and relaxed faster during a single twitch and had a marked increase in the number of type IIb fibers relative to wild-type controls. This change was also accompanied by a significant increase in type IIB fibers containing tubular aggregates. Moreover, the ratio of mitochondrial DNA to nuclear DNA and mitochondria number were decreased in myostatin-deficient muscle, suggesting a mitochondrial depletion. Overall, our results suggest that lack of myostatin compromises force production in association with loss of oxidative characteristics of skeletal muscle.
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