scholarly journals Starting blocks: The biochemical basis of contraction-induced signal transduction in skeletal muscle

2012 ◽  
Vol 34 (3) ◽  
pp. 12-19
Author(s):  
Brendan Egan ◽  
Philip Newsholme
Keyword(s):  
Skeletal Muscle ◽  
Physical Inactivity ◽  
Regular Exercise ◽  
Muscular Force ◽  
Intense Exercise ◽  
Biochemical Basis ◽  
Disease States ◽  
Skeletal Muscle Insulin Resistance ◽  
And Function ◽  
Induced Signal

How does skeletal muscle adapt to regular exercise? This question has puzzled and enthused exercise physiologists for the best part of half a century since seminal work by John Holloszy demonstrated the remarkable plasticity of skeletal muscle in response to intense exercise training1. This phenomenon is overtly illustrated by the remodelling of muscle structure and function, with respect to muscular force, endurance and contractile velocity as a result of alterations in functional demand elicited by regular exercise2, or the ability of regular exercise to prevent or ameliorate pathophysiological disease states to which physical inactivity and skeletal muscle insulin resistance contribute3.

scholarly journals Adiponectin is expressed by skeletal muscle fibers and influences muscle phenotype and function

2008 ◽  
Vol 295 (1) ◽  
pp. C203-C212 ◽  
Author(s):  
Matthew P. Krause ◽  
Ying Liu ◽  
Vivian Vu ◽  
Lawrence Chan ◽  
Aimin Xu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fiber Type ◽  
Muscle Fibers ◽  
Low Frequency ◽  
Disease States ◽  
L6 Myotubes ◽  
Type Composition ◽  
Low Frequency Fatigue ◽  
And Function

Adiponectin (Ad) is linked to various disease states and mediates antidiabetic and anti-inflammatory effects. While it was originally thought that Ad expression was limited to adipocytes, we demonstrate here that Ad is expressed in mouse skeletal muscles and within differentiated L6 myotubes, as assessed by RT-PCR, Western blot, and immunohistochemical analyses. Serial muscle sections stained for fiber type, lipid content, and Ad revealed that muscle fibers with elevated intramyocellular Ad expression were consistently type IIA and IID fibers with detectably higher intramyocellular lipid (IMCL) content. To determine the effect of Ad on muscle phenotype and function, we used an Ad-null [knockout (KO)] mouse model. Body mass increased significantly in 24-wk-old KO mice [+5.5 ± 3% relative to wild-type mice (WT)], with no change in muscle mass observed. IMCL content was significantly increased (+75.1 ± 25%), whereas epididymal fat mass, although elevated, was not different in the KO mice compared with WT (+35.1 ± 23%; P = 0.16). Fiber-type composition was unaltered, although type IIB fiber area was increased in KO mice (+25.5 ± 6%). In situ muscle stimulation revealed lower peak tetanic forces in KO mice relative to WT (−47.5 ± 6%), with no change in low-frequency fatigue rates. These data demonstrate that the absence of Ad expression causes contractile dysfunction and phenotypical changes in skeletal muscle. Furthermore, we demonstrate that Ad is expressed in skeletal muscle and that its intramyocellular localization is associated with elevated IMCL, particularly in type IIA/D fibers.

scholarly journals The biochemical basis of the health effects of exercise: an integrative view

2004 ◽  
Vol 63 (2) ◽  
pp. 199-203 ◽  
Author(s):  
Frank W. Booth ◽  
R. Andrew Shanely
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Physical Inactivity ◽  
Biological Significance ◽  
Skeletal Muscle Cell ◽  
Gene Interactions ◽  
Amp Kinase ◽  
Biochemical Basis ◽  
Phenotypic Changes ◽  
Integrative View

Physical inactivity–gene interactions result in changes in gene expression, leading to phenotypic changes in the skeletal muscle cell. A subpopulation of those genes that show changes in expression during physical inactivity are candidates for the environment–gene interactions that cross a threshold of biological significance such that overt clinical disease occurs. AMP kinase, GLUT4 and myosin heavy chain IIx are proposed as candidates for physical inactivity-modulated genes that have an altered function that may trigger a crossing of a threshold to disease. Future experiments will be needed to test the validity of the ideas presented.

scholarly journals PAI-1, the Plasminogen System, and Skeletal Muscle

2020 ◽  
Vol 21 (19) ◽  
pp. 7066 ◽  
Author(s):  
Fasih Ahmad Rahman ◽  
Matthew Paul Krause
Keyword(s):  
Skeletal Muscle ◽  
Cell Fate ◽  
Plasminogen Activator Inhibitor ◽  
Cell Types ◽  
Plasminogen Activator Inhibitor 1 ◽  
Disease States ◽  
Muscle Health ◽  
And Function ◽  
Pai 1

The plasminogen system is a critical proteolytic system responsible for the remodeling of the extracellular matrix (ECM). The master regulator of the plasminogen system, plasminogen activator inhibitor-1 (PAI-1), has been implicated for its role in exacerbating various disease states not only through the accumulation of ECM (i.e., fibrosis) but also its role in altering cell fate/behaviour. Examination of PAI-1 has extended through various tissues and cell-types with recent investigations showing its presence in skeletal muscle. In skeletal muscle, the role of this protein has been implicated throughout the regeneration process, and in skeletal muscle pathologies (muscular dystrophy, diabetes, and aging-driven pathology). Needless to say, the complete function of this protein in skeletal muscle has yet to be fully elucidated. Given the importance of skeletal muscle in maintaining overall health and quality of life, it is critical to understand the alterations—particularly in PAI-1—that occur to negatively impact this organ. Thus, we provide a comprehensive review of the importance of PAI-1 in skeletal muscle health and function. We aim to shed light on the relevance of this protein in skeletal muscle and propose potential therapeutic approaches to aid in the maintenance of skeletal muscle health.

scholarly journals Attenuation of Adverse Effects of Aging on Skeletal Muscle by Regular Exercise and Nutritional Support

2016 ◽  
Vol 11 (1) ◽  
pp. 4-16 ◽  
Author(s):  
Arthur S. Leon
Keyword(s):  
Skeletal Muscle ◽  
Adverse Effects ◽  
Nutritional Support ◽  
Biological Process ◽  
Regular Exercise ◽  
Muscle Loss ◽  
Progressive Reduction ◽  
Effects Of Aging ◽  
And Function ◽  
Loss Of Strength

Beginning early in midlife, natural/primary aging is inevitably associated with a progressive reduction in muscle mass and function. This process can progress with aging to a substantial loss of strength, particularly in the lower extremities, reducing mobility. This condition, commonly referred to as sarcopenia, can result in frailty, reducing one’s ability to live independently. This article reviews the underlying biological process contributing to the development of sarcopenia and the roles of regular exercise and nutritional support for attenuating aging-associated muscle loss as well as risk and management of sarcopenia and associated frailty.

scholarly journals Essential Role of Septin 7 in Skeletal Muscle Structure and Function

2020 ◽  
Vol 118 (3) ◽  
pp. 258a
Author(s):  
Laszlo Csernoch ◽  
Mónika Gönczi ◽  
Zsolt Ráduly ◽  
László Szabó ◽  
Nóra Dobrosi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Essential Role ◽  
Structure And Function ◽  
Muscle Structure ◽  
And Function

scholarly journals Mapping of the contraction-induced phosphoproteome identifies TRIM28 as a significant regulator of skeletal muscle size and function

Cell Reports ◽  
2021 ◽  
Vol 34 (9) ◽  
pp. 108796
Author(s):  
Nathaniel D. Steinert ◽  
Gregory K. Potts ◽  
Gary M. Wilson ◽  
Amelia M. Klamen ◽  
Kuan-Hung Lin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Size ◽  
And Function

scholarly journals Alterations in intestinal microbiota diversity, composition, and function in patients with sarcopenia

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lin Kang ◽  
Pengtao Li ◽  
Danyang Wang ◽  
Taihao Wang ◽  
Dong Hao ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
16S Rrna ◽  
Intestinal Microbiota ◽  
Muscle Growth ◽  
Growth Function ◽  
16S Rrna Sequencing ◽  
Fecal Samples ◽  
Lipopolysaccharide Biosynthesis ◽  
Rrna Sequencing ◽  
And Function

Abstract16S rRNA sequencing of human fecal samples has been tremendously successful in identifying microbiome changes associated with both aging and disease. A number of studies have described microbial alterations corresponding to physical frailty and nursing home residence among aging individuals. A gut-muscle axis through which the microbiome influences skeletal muscle growth/function has been hypothesized. However, the microbiome has yet to be examined in sarcopenia. Here, we collected fecal samples of 60 healthy controls (CON) and 27 sarcopenic (Case)/possibly sarcopenic (preCase) individuals and analyzed the intestinal microbiota using 16S rRNA sequencing. We observed an overall reduction in microbial diversity in Case and preCase samples. The genera Lachnospira, Fusicantenibacter, Roseburia, Eubacterium, and Lachnoclostridium—known butyrate producers—were significantly less abundant in Case and preCase subjects while Lactobacillus was more abundant. Functional pathways underrepresented in Case subjects included numerous transporters and phenylalanine, tyrosine, and tryptophan biosynthesis suggesting that protein processing and nutrient transport may be impaired. In contrast, lipopolysaccharide biosynthesis was overrepresented in Case and PreCase subjects suggesting that sarcopenia is associated with a pro-inflammatory metagenome. These analyses demonstrate structural and functional alterations in the intestinal microbiota that may contribute to loss of skeletal muscle mass and function in sarcopenia.

PROLONGED INTRAVENOUS INFUSION OF LABELLED IODOCOMPOUNDS IN THE RAT: [125I]IODIDE METABOLISM AND EFFECTS OF MODERATE DIETARY IODINE DEFICIENCY

1979 ◽  
Vol 82 (2) ◽  
pp. 227-234 ◽  
Author(s):  
VIPA BOONNAMSIRI ◽  
J. C. KERMODE ◽  
B. D. THOMPSON
Keyword(s):  
Skeletal Muscle ◽  
Iodine Deficiency ◽  
Intravenous Infusion ◽  
Structure And Function ◽  
Continuous Intravenous Infusion ◽  
Close Approximation ◽  
Faecal Excretion ◽  
And Function ◽  
Layer Chromatography ◽  
Secretion Rates

SUMMARY Radio-iodide was administered by prolonged continuous intravenous infusion to rats maintained under iodine-replete conditions and in moderate iodine deficiency. A close approximation to equilibrium labelling was thereby achieved. Labelled iodocompounds extracted from various tissues were analysed by thin-layer chromatography. Moderate iodine deficiency resulted in a slight increase in the ratio of mono-iodotyrosine to di-iodotyrosine in the thyroid. No change in the ratio of tri-iodothyronine (T3) to thyroxine (T4) was found in thyroid, plasma or skeletal muscle. Faecal excretion of T3 declined appreciably relative to that of T4. Under iodine-replete conditions the ratio of thyroidal secretion rates of T3 and T4 was estimated to be more than three times higher than the ratio of these iodocompounds within the thyroid. Heterogeneity of thyroglobulin structure and function may explain these observations.

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