Starring or Supporting Role? Satellite Cells and Skeletal Muscle Fiber Size Regulation

Abstract

Recent loss-of-function studies show that satellite cell depletion does not promote sarcopenia or unloading-induced atrophy, and does not prevent regrowth. Although overload-induced muscle fiber hypertrophy is normally associated with satellite cell-mediated myonuclear accretion, hypertrophic adaptation proceeds in the absence of satellite cells in fully grown adult mice, but not in young growing mice. Emerging evidence also indicates that satellite cells play an important role in remodeling the extracellular matrix during hypertrophy.

Copyright © 2018 Int. Union Physiol. Sci./Am. Physiol. Soc.

Figures

FIGURE 1.

Theoretical model of fiber type-specific satellite cell dependence during hypertrophy In the presence of satellite cells (SC), oxidative myosin heavy chain (MyHC) type 1 and glycolytic MyHC type 2 muscle fibers respond to a hypertrophic stimulus via satellite cell proliferation and myonuclear accretion. In the absence of satellite cells, resident myonuclei of aerobic fibers may lack the transcriptional capacity to sustain hypertrophy due to the biosynthetic demands of oxidative metabolism combined with growth processes, whereas glycolytic fibers may possess a more flexible myonuclear domain that still permits muscle fiber growth.

FIGURE 2.

Dynamic continuum of satellite cell contribution to hypertrophy across the lifespan Young growing mice (4 mo) do not. However, aged anabolic-resistant mice (24 mo old) do not grow, regardless of the presence of satellite cells.

FIGURE 3.

Satellite cells regulate fibrosis during hypertrophy SC proliferation in response to a hypertrophic stimulus mediates proper extracellular matrix (ECM) remodeling by preventing fibrosis, which appears to allow for continued muscle fiber hypertrophy. Absence of satellite cells results in blunted hypertrophy in response to long-term mechanical overload.