The behaviour of satellite cells in response to exercise: what have we learned from human studies?

Abstract

Understanding the complex role played by satellite cells in the adaptive response to exercise in human skeletal muscle has just begun. The development of reliable markers for the identification of satellite cell status (quiescence/activation/proliferation) is an important step towards the understanding of satellite cell behaviour in exercised human muscles. It is hypothesised currently that exercise in humans can induce (1) the activation of satellite cells without proliferation, (2) proliferation and withdrawal from differentiation, (3) proliferation and differentiation to provide myonuclei and (4) proliferation and differentiation to generate new muscle fibres or to repair segmental fibre injuries. In humans, the satellite cell pool can increase as early as 4 days following a single bout of exercise and is maintained at higher level following several weeks of training. Cessation of training is associated with a gradual reduction of the previously enhanced satellite cell pool. In the elderly, training counteracts the normal decline in satellite cell number seen with ageing. When the transcriptional activity of existing myonuclei reaches its maximum, daughter cells generated by satellite cell proliferation are involved in protein synthesis by enhancing the number of nuclear domains. Clearly, delineating the events and the mechanisms behind the activation of satellite cells both under physiological and pathological conditions in human skeletal muscles remains an important challenge.

Hesr1 and Hesr3 are essential to generate undifferentiated quiescent satellite cells and to maintain satellite cell numbers

“…2G). Upon activation, the organelles and volume of cytoplasm in satellite cells increase and the cells become mitotically active as they transit from the G0 to G1 cell cycle phase (Kadi et al, 2005;Fukada et al, 2007). These results suggest that the satellite cells in dKO mice were not in a quiescent state, but in a more differentiated and/or activated state.…”

Cellular Degradation Machineries in Age-Related Loss of Muscle Mass (Sarcopenia)

“…According to morphometric analysis the ratio myofiber volume to a myonucleus remains fairly constant suggesting an optimal size of the www.intechopen.com domain supported by the machinery of one myonucleus. The impressive increase in muscle mass during late fetal and postnatal development but also in conditions of repair in adult muscle across life-span is dependent on recruitment of myogenic progenitors from the resident satellite cells (SC) in the stem cell niche (Kadi et al, 2005). SCs remain quiescent until activation through trophic stimuli e.g.…”

Effects of aging and gender on the spatial organization of nuclei in single human skeletal muscle cells

“…As each nucleus determines the transcription in its cytoplasmic neighbourhood (Pavlath et al, 1989), the myonuclear domain (MND) is defined as the volume unit in which the transcriptional activity is controlled by a single myonucleus. It is generally accepted that muscle hypertrophy is related to an increased myonuclear number through activation of satellite cells (Kadi et al, 2005;Mackey et al, 2007), while muscular atrophy is related to an apoptotic decrease in myonuclear number (Allen et al, 1997a,b;Alway & Siu, 2008). However, there are several reports demonstrating a less stringent relationship between myonuclear number and fibre size, i.e., there are reports of muscle fibre hypertrophy without satellite cell activation (McCarthy & Esser, 2007) as well as atrophy accompanied by either an increased, decreased or unaltered number of myonuclei (Allen et al, 1995(Allen et al, , 1996(Allen et al, , 1997aKasper & Xun, 1996;Gundersen & Bruusgaard, 2008).…”