Characterization and Regulation of Mechanical Loading-Induced Compensatory Muscle Hypertrophy

2012 ◽  
Author(s):  
Gregory R. Adams ◽  
Marcas M. Bamman
Keyword(s):  
Mechanical Loading ◽  
Muscle Hypertrophy ◽  
Compensatory Muscle Hypertrophy

No effect of sex steroids on compensatory muscle hypertrophy

1984 ◽  
Vol 56 (6) ◽  
pp. 1589-1593 ◽  
Author(s):  
S. R. Max ◽  
N. E. Rance
Keyword(s):  
Androgen Receptor ◽  
Sex Steroids ◽  
Muscle Hypertrophy ◽  
Specific Activity ◽  
Oxidative Capacity ◽  
Muscle Weight ◽  
Hormone Status ◽  
14Co2 Production ◽  
Synergistic Muscles ◽  
Compensatory Muscle Hypertrophy

We studied the effects of sex steroids on muscle weight and oxidative capacity of rat plantaris muscles subjected to functional overload by removal of synergistic muscles. Eight weeks after bilateral synergist removal, plantaris muscles were strikingly hypertrophic compared with unoperated controls. After this period, there were selective alterations in the ability of the muscles to oxidize three substrates of oxidative metabolism. Thus 14CO2 production from [6-14C]glucose and [2-14C]pyruvate was significantly reduced, whereas there was no alteration in 14CO2 production from beta-[3-14C]hydroxybutyrate. Succinate dehydrogenase specific activity was decreased in overloaded muscle. There was no effect of sex hormone status on any of these parameters. Finally, 30 days of functional overload did not influence cytosolic androgen receptor binding. These results are not consistent with the idea that sex steroids and functional overload act synergistically.

Mechanical loading induces the expression of a Pol I regulon at the onset of skeletal muscle hypertrophy

2012 ◽  
Vol 302 (10) ◽  
pp. C1523-C1530 ◽  
Author(s):  
Ferdinand von Walden ◽  
Vandre Casagrande ◽  
Ann-Kristin Östlund Farrants ◽  
Gustavo A. Nader
Keyword(s):  
Skeletal Muscle ◽  
Mechanical Loading ◽  
Muscle Hypertrophy ◽  
Rrna Synthesis ◽  
Rdna Transcription ◽  
Hypertrophic Response ◽  
Skeletal Muscle Hypertrophy ◽  
Pol I ◽  
Upstream Binding Factor ◽  
Polymerase I

The main goal of the present study was to investigate the regulation of ribosomal DNA (rDNA) gene transcription at the onset of skeletal muscle hypertrophy. Mice were subjected to functional overload of the plantaris by bilateral removal of the synergist muscles. Mechanical loading resulted in muscle hypertrophy with an increase in rRNA content. rDNA transcription, as determined by 45S pre-rRNA abundance, paralleled the increase in rRNA content and was consistent with the onset of the hypertrophic response. Increased transcription and protein expression of c-Myc and its downstream polymerase I (Pol I) regulon (POL1RB, TIF-1A, PAF53, TTF1, TAF1C) was also consistent with the increase in rRNA. Similarly, factors involved in rDNA transcription, such as the upstream binding factor and the Williams syndrome transcription factor, were induced by mechanical loading in a corresponding temporal fashion. Chromatin immunoprecipitation revealed that these factors, together with Pol I, were enriched at the rDNA promoter. This, in addition to an increase in histone H3 lysine 9 acetylation, demonstrates that mechanical loading regulates rRNA synthesis by inducing a gene expression program consisting of a Pol I regulon, together with accessory factors involved in transcription and chromatin remodeling at the rDNA promoter. Altogether, these data indicate that transcriptional and epigenetic mechanisms take place in the regulation of ribosome production at the onset of muscle hypertrophy.

The fate of newly formed satellite cells during compensatory muscle hypertrophy

1976 ◽  
Vol 21 (1) ◽  
pp. 113-118
Author(s):  
S. Schiaffino ◽  
S. Pierobon Bormioli ◽  
M. Aloisi
Keyword(s):  
Satellite Cells ◽  
Muscle Hypertrophy ◽  
Compensatory Muscle Hypertrophy

scholarly journals Loss of nNOS inhibits compensatory muscle hypertrophy and exacerbates inflammation and eccentric contraction-induced damage in mdx mice

2014 ◽  
Vol 24 (2) ◽  
pp. 492-505 ◽  
Author(s):  
S. C. Froehner ◽  
S. M. Reed ◽  
K. N. Anderson ◽  
P. L. Huang ◽  
J. M. Percival
Keyword(s):  
Muscle Hypertrophy ◽  
Eccentric Contraction ◽  
Mdx Mice ◽  
Compensatory Muscle Hypertrophy

scholarly journals Cellular mechanisms regulating protein synthesis and skeletal muscle hypertrophy in animals

2009 ◽  
Vol 106 (4) ◽  
pp. 1367-1373 ◽  
Author(s):  
Mitsunori Miyazaki ◽  
Karyn A. Esser
Keyword(s):  
Skeletal Muscle ◽  
Cell Culture ◽  
Protein Synthesis ◽  
Mechanical Loading ◽  
Muscle Hypertrophy ◽  
Mammalian Target Of Rapamycin ◽  
Cellular Mechanisms ◽  
Skeletal Muscle Hypertrophy

Growth and maintenance of skeletal muscle mass is critical for long-term health and quality of life. Skeletal muscle is a highly adaptable tissue with well-known sensitivities to environmental cues such as growth factors, cytokines, nutrients, and mechanical loading. All of these factors act at the level of the cell and signal through pathways that lead to changes in phenotype through multiple mechanisms. In this review, we discuss the animal and cell culture models used and the signaling mechanisms identified in understanding regulation of protein synthesis in response to mechanical loading/resistance exercise. Particular emphasis has been placed on 1) alterations in mechanical loading and regulation of protein synthesis in both in vivo animal studies and in vitro cell culture studies and 2) upstream mediators regulating mammalian target of rapamycin signaling and protein synthesis during skeletal muscle hypertrophy.

Urokinase-type plasminogen activator and macrophages are required for skeletal muscle hypertrophy in mice

2007 ◽  
Vol 293 (4) ◽  
pp. C1278-C1285 ◽  
Author(s):  
Dana M. DiPasquale ◽  
Ming Cheng ◽  
William Billich ◽  
Sharon A. Huang ◽  
Nico van Rooijen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Plasminogen Activator ◽  
Mechanical Loading ◽  
Muscle Hypertrophy ◽  
Compensatory Hypertrophy ◽  
Wild Type ◽  
Adult Skeletal Muscle ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Macrophage Accumulation

Adult skeletal muscle possesses remarkable potential for growth in response to mechanical loading; however, many of the cellular and molecular mechanisms involved remain undefined. The hypothesis of this study was that the extracellular serine protease, urokinase-type plasminogen activator (uPA), is required for muscle hypertrophy, in part by promoting macrophage accumulation in muscle subjected to increased mechanical loading. Compensatory muscle hypertrophy was induced in mouse plantaris (PLT) muscles by surgical ablation of synergist muscles. Following synergist ablation, PLT muscles in wild-type mice demonstrated edema and infiltration of neutrophils and macrophages but an absence of overt muscle fiber damage. Sham procedures resulted in no edema or accumulation of inflammatory cells. In addition, synergist ablation was associated with a large increase in activity of uPA in the PLT muscle. uPA-null mice demonstrated complete abrogation of compensatory hypertrophy associated with reduced macrophage accumulation, indicating that uPA is required for hypertrophy. Macrophages isolated from wild-type PLT muscle during compensatory hypertrophy expressed uPA and IGF-I, both of which may contribute to hypertrophy. To determine whether macrophages are required for muscle hypertrophy, clodronate liposomes were administered to deplete macrophages in wild-type mice; this resulted in reduced muscle hypertrophy. Decreased macrophage accumulation was associated with reduced cell proliferation but did not alter signaling through the mammalian target of rapamycin pathway. These data indicate that uPA and macrophages are required for muscle hypertrophy following synergist ablation.

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