The time course of myonuclear accretion during hypertrophy in young adult and older rat plantaris muscle

Meer, Sander F.T. van der; Jaspers, Richard T.; Jones, David A.; Degens, Hans

doi:10.1016/j.aanat.2010.08.004

Cited by 31 publications

(34 citation statements)

References 54 publications

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“…We recently showed that normal myofiber hypertrophy and force generation, in the absence of myonuclear accretion, occurred in response to compensatory overload of the plantaris muscle in tamoxifen-treated Pax7-DTA mice, resulting in a significantly larger myonuclear domain (15). It is possible that myonuclear accretion through satellite cell fusion and myofiber hypertrophy are not temporally coordinated (28) such that deficits in muscle growth may occur at later time points; however, taken together these studies show that the ratio between myonuclei and cytoplasmic volume is altered during muscle adaptation, allowing for large increases in domain size with overload (15) and considerable decreases with hindlimb unloading. Thus, the myonuclear domain appears to be remarkably flexible depending on physiological conditions, and therefore processes involved in protein turnover may be more important than the regulation of satellite cells.…”

Section: Discussionmentioning

confidence: 97%

“…The role of satellite cells in muscle regeneration is well defined, and recent studies using genetic models convincingly demonstrated that with satellite cell depletion, muscle regeneration is severely attenuated (14,19,24). Furthermore, muscle hypertrophy has been shown to involve myonuclear accretion (15,28), although effective myofiber growth occurs without satellite cell-dependent myonuclear addition (15).…”

Section: Discussionmentioning

confidence: 98%

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Satellite cell depletion does not inhibit adult skeletal muscle regrowth following unloading-induced atrophy

Jackson

Mula

Kirby

et al. 2012

American Journal of Physiology-Cell Physiology

132

115

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Resident muscle stem cells, known as satellite cells, are thought to be the main mediators of skeletal muscle plasticity. Satellite cells are activated, replicate, and fuse into existing muscle fibers in response to both muscle injury and mechanical load. It is generally well-accepted that satellite cells participate in postnatal growth, hypertrophy, and muscle regeneration following injury; however, their role in muscle regrowth following an atrophic stimulus remains equivocal. The current study employed a genetic mouse model (Pax7-DTA) that allowed for the effective depletion of >90% of satellite cells in adult muscle upon the administration of tamoxifen. Vehicle and tamoxifen-treated young adult female mice were either hindlimb suspended for 14 days to induce muscle atrophy or hindlimb suspended for 14 days followed by 14 days of reloading to allow regrowth, or they remained ambulatory for the duration of the experimental protocol. Additionally, 5-bromo-2'-deoxyuridine (BrdU) was added to the drinking water to track cell proliferation. Soleus muscle atrophy, as measured by whole muscle wet weight, fiber cross-sectional area, and single-fiber width, occurred in response to suspension and did not differ between satellite cell-depleted and control muscles. Furthermore, the depletion of satellite cells did not attenuate muscle mass or force recovery during the 14-day reloading period, suggesting that satellite cells are not required for muscle regrowth. Myonuclear number was not altered during either the suspension or the reloading period in soleus muscle fibers from vehicle-treated or satellite cell-depleted animals. Thus, myonuclear domain size was reduced following suspension due to decreased cytoplasmic volume and was completely restored following reloading, independent of the presence of satellite cells. These results provide convincing evidence that satellite cells are not required for muscle regrowth following atrophy and that, instead, the myonuclear domain size changes as myofibers adapt.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 98%

Satellite cell depletion does not inhibit adult skeletal muscle regrowth following unloading-induced atrophy

Jackson

Mula

Kirby

et al. 2012

American Journal of Physiology-Cell Physiology

132

115

View full text Add to dashboard Cite

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“…For example, there is evidence that at least some degree of hypertrophy can occur without the prerequisite to activate satellite cells to add new nuclei (McCarthy et al, 2011; van der Meer et al, 2011a; Jackson et al, 2012); however, larger fibers in old muscles appear to add more nuclei than smaller fibers in young animals to maintain a relatively constant nuclear domain size (van der Meer et al, 2011b), and more nuclei improve the potential for greater transcriptional control to presumably sustain their new larger muscle fiber size (Carson and Alway, 1996; Alway et al, 2003; van der Meer et al, 2011a). In addition, the extent of hypertrophy is suppressed in models where satellite cells are absent (Fry et al, 2014).…”

Section: Satellite Cell Function In Agingmentioning

confidence: 99%

Regulation of Satellite Cell Function in Sarcopenia

Alway

Myers

Mohamed

2014

Front. Aging Neurosci.

120

105

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The mechanisms contributing to sarcopenia include reduced satellite cell (myogenic stem cell) function that is impacted by the environment (niche) of these cells. Satellite cell function is affected by oxidative stress, which is elevated in aged muscles, and this along with changes in largely unknown systemic factors, likely contribute to the manner in which satellite cells respond to stressors such as exercise, disuse, or rehabilitation in sarcopenic muscles. Nutritional intervention provides one therapeutic strategy to improve the satellite cell niche and systemic factors, with the goal of improving satellite cell function in aging muscles. Although many elderly persons consume various nutraceuticals with the hope of improving health, most of these compounds have not been thoroughly tested, and the impacts that they might have on sarcopenia and satellite cell function are not clear. This review discusses data pertaining to the satellite cell responses and function in aging skeletal muscle, and the impact that three compounds: resveratrol, green tea catechins, and β-Hydroxy-β-methylbutyrate have on regulating satellite cell function and therefore contributing to reducing sarcopenia or improving muscle mass after disuse in aging. The data suggest that these nutraceutical compounds improve satellite cell function during rehabilitative loading in animal models of aging after disuse (i.e., muscle regeneration). While these compounds have not been rigorously tested in humans, the data from animal models of aging provide a strong basis for conducting additional focused work to determine if these or other nutraceuticals can offset the muscle losses, or improve regeneration in sarcopenic muscles of older humans via improving satellite cell function.

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“…3). Under conditions of muscle growth, hypertrophy or overload, there is an increase in myonuclear number as the muscle fibre increases in size (van der Meer et al, 2011). The responses of both myonuclear number and domain size with muscle atrophy are less well understood, although loss of myonuclei from existing fibres has been reported during skeletal muscle disuse (Allen et al, …”

Section: Apoptotic Processes During Muscle Disuse Atrophymentioning

confidence: 99%

Prevention of muscle wasting and osteoporosis: the value of examining novel animal models

Reilly

Franklin

2016

Journal of Experimental Biology

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Bone mass and skeletal muscle mass are controlled by factors such as genetics, diet and nutrition, growth factors and mechanical stimuli. Whereas increased mechanical loading of the musculoskeletal system stimulates an increase in the mass and strength of skeletal muscle and bone, reduced mechanical loading and disuse rapidly promote a decrease in musculoskeletal mass, strength and ultimately performance (i.e. muscle atrophy and osteoporosis). In stark contrast to artificially immobilised laboratory mammals, animals that experience natural, prolonged bouts of disuse and reduced mechanical loading, such as hibernating mammals and aestivating frogs, consistently exhibit limited or no change in musculoskeletal performance. What factors modulate skeletal muscle and bone mass, and what physiological and molecular mechanisms protect against losses of muscle and bone during dormancy and following arousal? Understanding the events that occur in different organisms that undergo natural periods of prolonged disuse and suffer negligible musculoskeletal deterioration could not only reveal novel regulatory factors but also might lead to new therapeutic options. Here, we review recent work from a diverse array of species that has revealed novel information regarding physiological and molecular mechanisms that dormant animals may use to conserve musculoskeletal mass despite prolonged inactivity. By highlighting some of the differences and similarities in musculoskeletal biology between vertebrates that experience disparate modes of dormancy, it is hoped that this Review will stimulate new insights and ideas for future studies regarding the regulation of atrophy and osteoporosis in both natural and clinical models of muscle and bone disuse.

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The time course of myonuclear accretion during hypertrophy in young adult and older rat plantaris muscle

Cited by 31 publications

References 54 publications

Satellite cell depletion does not inhibit adult skeletal muscle regrowth following unloading-induced atrophy

Satellite cell depletion does not inhibit adult skeletal muscle regrowth following unloading-induced atrophy

Regulation of Satellite Cell Function in Sarcopenia

Prevention of muscle wasting and osteoporosis: the value of examining novel animal models

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