Muscle disuse atrophy is not accompanied by changes in skeletal muscle satellite cell content

2013 ◽  
Vol 126 (8) ◽  
pp. 557-566 ◽  
Author(s):  
Tim Snijders ◽  
Benjamin T. Wall ◽  
Marlou L. Dirks ◽  
Joan M. G. Senden ◽  
Fred Hartgens ◽  
...  

Two weeks of muscle disuse led to a loss in muscle mass and strength. The loss in muscle mass was attributed to both type I and type II muscle fibre atrophy, and was not accompanied by a decline in satellite cell content.

2021 ◽  
Vol 12 ◽  
Author(s):  
Baubak Shamim ◽  
Donny M. Camera ◽  
Jamie Whitfield

Concurrent exercise training has been suggested to create an ‘interference effect,’ attenuating resistance training-based skeletal muscle adaptations, including myofibre hypertrophy. Satellite cells support myofibre hypertrophy and are influenced by exercise mode. To determine whether satellite cells contribute to the ‘interference effect’ changes in satellite cell and myonuclear content were assessed following a period of training in 32 recreationally active males (age: 25 ± 5 year; body mass index: 24 ± 3 kg⋅m–2; mean ± SD) who undertook 12-week of either isolated (3 d⋅w–1) resistance (RES; n = 10), endurance (END; n = 10), or alternate day (6 d⋅w–1) concurrent (CET, n = 12) training. Skeletal muscle biopsies were obtained pre-intervention and after 2, 8, and 12 weeks of training to determine fibre type-specific cross-sectional area (CSA), satellite cell content (Pax7+DAPI+), and myonuclei (DAPI+) using immunofluorescence microscopy. After 12 weeks, myofibre CSA increased in all training conditions in type II (P = 0.0149) and mixed fibres (P = 0.0102), with no difference between conditions. Satellite cell content remained unchanged after training in both type I and type II fibres. Significant correlations were observed between increases in fibre type-specific myonuclear content and CSA of Type I (r = 0.63, P < 0.0001), Type II (r = 0.69, P < 0.0001), and mixed fibres (r = 0.72, P < 0.0001). Resistance, endurance, and concurrent training induce similar myofibre hypertrophy in the absence of satellite cell and myonuclear pool expansion. These findings suggest that myonuclear accretion via satellite cell fusion is positively correlated with hypertrophy after 12 weeks of concurrent training, and that individuals with more myonuclear content displayed greater myofibre hypertrophy.


2001 ◽  
Vol 189 (2) ◽  
pp. 189-196 ◽  
Author(s):  
Marie Csete ◽  
Jean Walikonis ◽  
Nicole Slawny ◽  
Yuewang Wei ◽  
Sheryl Korsnes ◽  
...  

2006 ◽  
Vol 54 (11) ◽  
pp. 1177-1191 ◽  
Author(s):  
Peter S. Zammit ◽  
Terence A. Partridge ◽  
Zipora Yablonka-Reuveni

2020 ◽  
Vol 129 (1) ◽  
pp. 5-16 ◽  
Author(s):  
Erik D. Hanson ◽  
Andrew C. Betik ◽  
Cara A. Timpani ◽  
John Tarle ◽  
Xinmei Zhang ◽  
...  

Low testosterone levels during skeletal muscle disuse did not worsen declines in muscle mass and function, although hypogonadism may attenuate recovery during subsequent reloading. Diets high in casein did not improve outcomes during immobilization or reloading. Practical strategies are needed that do not compromise caloric intake yet provide effective protein doses to augment these adverse effects.


2020 ◽  
Vol 117 (49) ◽  
pp. 30907-30917 ◽  
Author(s):  
Se-Jin Lee ◽  
Adam Lehar ◽  
Yewei Liu ◽  
Chi Hai Ly ◽  
Quynh-Mai Pham ◽  
...  

Myostatin (MSTN) is a transforming growth factor-β (TGF-β) family member that normally acts to limit muscle growth. The function of MSTN is partially redundant with that of another TGF-β family member, activin A. MSTN and activin A are capable of signaling through a complex of type II and type I receptors. Here, we investigated the roles of two type II receptors (ACVR2 and ACVR2B) and two type I receptors (ALK4 and ALK5) in the regulation of muscle mass by these ligands by genetically targeting these receptors either alone or in combination specifically in myofibers in mice. We show that targeting signaling in myofibers is sufficient to cause significant increases in muscle mass, showing that myofibers are the direct target for signaling by these ligands in the regulation of muscle growth. Moreover, we show that there is functional redundancy between the two type II receptors as well as between the two type I receptors and that all four type II/type I receptor combinations are utilized in vivo. Targeting signaling specifically in myofibers also led to reductions in overall body fat content and improved glucose metabolism in mice fed either regular chow or a high-fat diet, demonstrating that these metabolic effects are the result of enhanced muscling. We observed no effect, however, on either bone density or muscle regeneration in mice in which signaling was targeted in myofibers. The latter finding implies that MSTN likely signals to other cells, such as satellite cells, in addition to myofibers to regulate muscle homeostasis.


2009 ◽  
Vol 6 (3) ◽  
pp. 895-904 ◽  
Author(s):  
Guqi Wang ◽  
Frank J. Burczynski ◽  
Brian B. Hasinoff ◽  
Kaidong Zhang ◽  
Qilong Lu ◽  
...  

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