In ovo feeding of IGF-1 to ducks influences neonatal skeletal muscle hypertrophy and muscle mass growth upon satellite cell activation

2012 ◽  
Vol 227 (4) ◽  
pp. 1465-1475 ◽  
Author(s):  
He-He Liu ◽  
Ji-Wen Wang ◽  
Rong-Ping Zhang ◽  
Xi Chen ◽  
Hai-Yue Yu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Muscle Mass ◽  
Muscle Hypertrophy ◽  
Cell Activation ◽  
In Ovo ◽  
Mass Growth ◽  
Skeletal Muscle Hypertrophy ◽  
Satellite Cell Activation ◽  
In Ovo Feeding

scholarly journals Akt1 deficiency diminishes skeletal muscle hypertrophy by reducing satellite cell proliferation

2018 ◽  
Vol 314 (5) ◽  
pp. R741-R751 ◽  
Author(s):  
Nobuki Moriya ◽  
Mitsunori Miyazaki
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Protein Synthesis ◽  
Satellite Cell ◽  
Muscle Mass ◽  
Satellite Cells ◽  
Muscle Hypertrophy ◽  
Mtor Signaling ◽  
Skeletal Muscle Hypertrophy ◽  
Satellite Cell Proliferation

Skeletal muscle mass is determined by the net dynamic balance between protein synthesis and degradation. Although the Akt/mechanistic target of rapamycin (mTOR)-dependent pathway plays an important role in promoting protein synthesis and subsequent skeletal muscle hypertrophy, the precise molecular regulation of mTOR activity by the upstream protein kinase Akt is largely unknown. In addition, the activation of satellite cells has been indicated as a key regulator of muscle mass. However, the requirement of satellite cells for load-induced skeletal muscle hypertrophy is still under intense debate. In this study, female germline Akt1 knockout (KO) mice were used to examine whether Akt1 deficiency attenuates load-induced skeletal muscle hypertrophy through suppressing mTOR-dependent signaling and satellite cell proliferation. Akt1 KO mice showed a blunted hypertrophic response of skeletal muscle, with a diminished rate of satellite cell proliferation following mechanical overload. In contrast, Akt1 deficiency did not affect the load-induced activation of mTOR signaling and the subsequent enhanced rate of protein synthesis in skeletal muscle. These observations suggest that the load-induced activation of mTOR signaling occurs independently of Akt1 regulation and that Akt1 plays a critical role in regulating satellite cell proliferation during load-induced muscle hypertrophy.

scholarly journals Inducible Activation of Akt Increases Skeletal Muscle Mass and Force Without Satellite Cell Activation

2010 ◽  
Vol 98 (3) ◽  
pp. 153a ◽  
Author(s):  
Bert Blaauw ◽  
Canato Marta ◽  
Lisa Agatea ◽  
Luana Toniolo ◽  
Cristina Mammucari ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Cell Activation ◽  
Satellite Cell Activation ◽  
Inducible Activation

Inducible activation of Akt increases skeletal muscle mass and force without satellite cell activation

2009 ◽  
Vol 23 (11) ◽  
pp. 3896-3905 ◽  
Author(s):  
Bert Blaauw ◽  
Marta Canato ◽  
Lisa Agatea ◽  
Luana Toniolo ◽  
Cristina Mammucari ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Cell Activation ◽  
Satellite Cell Activation ◽  
Inducible Activation

scholarly journals Castration induces satellite cell activation that contributes to skeletal muscle maintenance

2018 ◽  
Vol 1 (1) ◽  
pp. 1-16 ◽  
Author(s):  
Alanna Klose ◽  
Wenxuan Liu ◽  
Nicole D. Paris ◽  
Sophie Forman ◽  
John J. Krolewski ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Cell Activation ◽  
Satellite Cell Activation

scholarly journals Satellite cell activation and apoptosis in skeletal muscle from severely burned children

2016 ◽  
Vol 594 (18) ◽  
pp. 5223-5236 ◽  
Author(s):  
Christopher S. Fry ◽  
Craig Porter ◽  
Labros S. Sidossis ◽  
Christopher Nieten ◽  
Paul T. Reidy ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Cell Activation ◽  
Satellite Cell Activation

Protein Intake for Skeletal Muscle Hypertrophy with Resistance Training in Seniors

2006 ◽  
Vol 16 (4) ◽  
pp. 362-372 ◽  
Author(s):  
Ryan D. Andrews ◽  
David A. MacLean ◽  
Steven E. Riechman
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Lean Mass ◽  
Protein Intake ◽  
Muscle Hypertrophy ◽  
Protein Supplementation ◽  
Protein Supplement ◽  
Resistance Exercise Training ◽  
Post Exercise ◽  
Skeletal Muscle Hypertrophy

Variability in protein consumption may influence muscle mass changes induced by resistance exercise training (RET). We sought to administer a post-exercise protein supplement and determine if daily protein intake variability affected variability in muscle mass gains. Men (N = 22) and women (N = 30) ranging in age from 60 to 69 y participated in a 12-wk RET program. At each RET session, participants consumed a post-exercise drink (0.4 g/kg lean mass protein). RET resulted in significant increases in lean mass (1.1 ±1.5 kg), similar between sexes (P > 0.05). Variability in mean daily protein intake was not associated with change in lean mass (r < 0.10, P > 0.05). The group with the highest protein intake (1.35 g · kg−1 · d−1, n = 8) had similar (P > 0.05) changes in lean mass as the group with the lowest daily protein intake (0.72 g · kg−1 · d−1, n = 9). These data suggest that variability in total daily protein intake does not affect variability in lean mass gains with RET in the context of post-exercise protein supplementation.

scholarly journals p21-Activated Kinase 1 Is Permissive for the Skeletal Muscle Hypertrophy Induced by Myostatin Inhibition

2021 ◽  
Vol 12 ◽  
Author(s):  
Caroline Barbé ◽  
Audrey Loumaye ◽  
Pascale Lause ◽  
Olli Ritvos ◽  
Jean-Paul Thissen
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Muscle Hypertrophy ◽  
Molecular Mechanisms ◽  
Muscle Development ◽  
The Body ◽  
Negative Regulator ◽  
Skeletal Muscle Hypertrophy ◽  
Myostatin Inhibition

Skeletal muscle, the most abundant tissue in the body, plays vital roles in locomotion and metabolism. Understanding the cellular processes that govern regulation of muscle mass and function represents an essential step in the development of therapeutic strategies for muscular disorders. Myostatin, a member of the TGF-β family, has been identified as a negative regulator of muscle development. Indeed, its inhibition induces an extensive skeletal muscle hypertrophy requiring the activation of Smad 1/5/8 and the Insulin/IGF-I signaling pathway, but whether other molecular mechanisms are involved in this process remains to be determined. Using transcriptomic data from various Myostatin inhibition models, we identified Pak1 as a potential mediator of Myostatin action on skeletal muscle mass. Our results show that muscle PAK1 levels are systematically increased in response to Myostatin inhibition, parallel to skeletal muscle mass, regardless of the Myostatin inhibition model. Using Pak1 knockout mice, we investigated the role of Pak1 in the skeletal muscle hypertrophy induced by different approaches of Myostatin inhibition. Our findings show that Pak1 deletion does not impede the skeletal muscle hypertrophy magnitude in response to Myostatin inhibition. Therefore, Pak1 is permissive for the skeletal muscle mass increase caused by Myostatin inhibition.

Signaling satellite-cell activation in skeletal muscle: Markers, models, stretch, and potential alternate pathways

2005 ◽  
Vol 31 (3) ◽  
pp. 283-300 ◽  
Author(s):  
Ashley C. Wozniak ◽  
Jiming Kong ◽  
Erika Bock ◽  
Orest Pilipowicz ◽  
Judy E. Anderson
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Cell Activation ◽  
Satellite Cell Activation
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