Specific force generation and injury susceptibility of permeabilized single skeletal muscle fibers from myostatin‐deficient mice

Abstract

Myostatin is a negative regulator of skeletal muscle mass. Compared with wild‐type (WT) mice, the extensor digitorum longus (EDL) muscles of myostatin‐deficient (KO) mice have greater mass; produce greater maximum isometric force (Fo); exhibit decreased specific force (sFo), defined as Fo normalized by muscle cross‐sectional area (CSA); and sustain greater losses in force following an injury‐inducing lengthening contraction. Our working hypothesis is that the reduced sFo and increased susceptibility to injury observed in whole EDL muscles from KO mice arise from corresponding differences in the constituent fibers. We tested the hypotheses that, compared with WT mice, individual fibers from KO mice have: 1) a reduced sFo and 2) increased susceptibility to contraction‐induced injury. The hypotheses were tested using permeabilized single fibers obtained from EDL muscles. While KO mice had a 21% increase in CSA, the Fo of fibers from WT and KO mice was not different and the sFo of fibers from KO mice was reduced by 18%. There was no difference in force deficits following injury. We conclude that a reduction in the sFo of individual fibers in KO mice contribute to the reduction in sFo at the whole muscle level. Our hypothesis that fibers from KO mice are more susceptible to injury was not supported.