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Myostatin knockout mice have larger muscle fibres with normal function and morphology

Degens, H., Patel, K. and Matsakas, A. (2025) Myostatin knockout mice have larger muscle fibres with normal function and morphology. Muscle & Nerve. ISSN 1097-4598 (In Press)

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Abstract/Summary

Aim: We assessed whether muscle fibres in Myostatin knockout (MSTN-/-) mice are just larger, or also exhibit morphological, metabolic and functional differences from MSTN+/+ mice. Methods: We compared single fibre contractile properties and histological fibre properties in muscles from MSTN-/- and MSTN+/+ mice. Results: Even though in permeabilised muscle fibres from the extensor digitorum longus and soleus muscle maximal force was higher (P < 0.001) there were no significant differences in specific power (power per unit volume), specific tension (force per cross-sectional area), maximal shortening velocity, or curvature of the force-velocity relationship between MSTN-/- and MSTN+/+ mice. In histological sections of the soleus muscle, fibres were larger (P < 0.001), but the succinate dehydrogenase staining intensity and capillary density did not differ significantly between MSTN-/- and MSTN+/+ mice, which was explicable by the larger number of capillaries around a fibre (P < 0.001). A model showed no significant differences in soleus muscle oxygenation. Discussion: In conclusion, the larger force generating capacity of fibres from MSTN-/- mice is explicable by the larger fibre cross-sectional area. Combined with the similar fibre oxidative capacity, and the relationship between capillary supply and the size of a fibre in the soleus muscle, this indicates that muscle fibres from MSTN-/- mice are quantitatively, but not qualitatively different from muscle fibres from MSTN+/+ mice. This suggests that myostatin inhibition may help increase muscle mass in conditions accompanied by muscle weakness without detrimental impact on muscle quality, but systemic side effects need to be considered.

Item Type:Article
Refereed:Yes
Divisions:Life Sciences > School of Biological Sciences > Biomedical Sciences
ID Code:121205
Publisher:Wiley-Blackwell

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