PREVENTION OF DISUSE MUSCLE ATROPHY BY MEANS OF ELECTRICAL STIMULATION: MAINTENANCE OF PROTEIN SYNTHESIS

The Lancet ◽  
1988 ◽  
Vol 332 (8614) ◽  
pp. 767-770 ◽  
Author(s):  
J.N.A. Gibson ◽  
K. Smith ◽  
M.J. Rennie
Keyword(s):  
Protein Synthesis ◽  
Electrical Stimulation ◽  
Muscle Atrophy ◽  
Disuse Muscle Atrophy

scholarly journals Low-frequency Electrical Stimulation Alleviates Immobilization-evoked Disuse Muscle Atrophy via Repressing Autophagy in Skeletal Muscle of Rabbits

2021 ◽  
Author(s):  
A-Ying Liu ◽  
Quan-Bing Zhang ◽  
Hua-Long Zhu ◽  
Yong-Wei Xiong ◽  
Feng Wang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Knee Joint ◽  
Muscle Atrophy ◽  
Rabbit Model ◽  
Low Frequency ◽  
Cross Sectional ◽  
Disuse Muscle Atrophy ◽  
Joint Range ◽  
Time Point

Abstract Objective: The present study was to investigate the effect of low-frequency electrical stimulation on disuse muscle atrophy and its mechanism in a rabbit model of extending knee joint contracture.Methods: This study designed two experiments. In the time-point experiment, 24 rabbits were randomly divided into Control 1(Ctrl1), immobilization for 2 weeks (I-2), I-4, and I-6 groups. In the intervention experiment, 24 rabbits were also randomly divided into Control 2 (Ctrl2), electrical stimulation (ES), natural recovery (NR) and electrical stimulation treatment (EST) groups. All intervention effects were assessed by evaluating the knee joint range of motion (ROM), cross-sectional area (CSA) of muscle and the expression of autophagy-related proteins.Results: Time-point experiment showed that immobilization reduced knee ROM, muscle CSA, and activated autophagy in skeletal muscle. Levels of four autophagic proteins including p-mTOR, Atg7, p62 and LC3B-II, were significantly elevated in the skeletal muscle of I-4 group. The intervention experiment further presented that LFES significantly improved the immobilization-induced ROM and CSA reduction. Additionally, LFES significantly reversed autophagy activation of skeletal muscle caused by immobilization.Conclusions: Low-frequency electrical stimulation alleviates immobilization-evoked disuse muscle atrophy maybe via inhibiting autophagy in skeletal muscle of rabbits.

scholarly journals Deptor Knockdown Enhances mTOR Activity and Protein Synthesis in Myocytes and Ameliorates Disuse Muscle Atrophy

2011 ◽  
Vol 17 (9-10) ◽  
pp. 925-936 ◽  
Author(s):  
Abid A. Kazi ◽  
Ly Hong-Brown ◽  
Susan M. Lang ◽  
Charles H. Lang
Keyword(s):  
Protein Synthesis ◽  
Muscle Atrophy ◽  
Disuse Muscle Atrophy ◽  
Mtor Activity

scholarly journals Random errors in protein synthesis activate an age-dependent program of muscle atrophy in mice

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
James Moore ◽  
Rashid Akbergenov ◽  
Martina Nigri ◽  
Patricia Isnard-Petit ◽  
Amandine Grimm ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Muscle Atrophy ◽  
Strength Analysis ◽  
Dependent Manner ◽  
Random Errors ◽  
Age Related ◽  
Related Phenotype ◽  
Age Dependent ◽  
Translation Accuracy ◽  
Transcriptomic Changes

AbstractRandom errors in protein synthesis are prevalent and ubiquitous, yet their effect on organismal health has remained enigmatic for over five decades. Here, we studied whether mice carrying the ribosomal ambiguity (ram) mutation Rps2-A226Y, recently shown to increase the inborn error rate of mammalian translation, if at all viable, present any specific, possibly aging-related, phenotype. We introduced Rps2-A226Y using a Cre/loxP strategy. Resulting transgenic mice were mosaic and showed a muscle-related phenotype with reduced grip strength. Analysis of gene expression in skeletal muscle using RNA-Seq revealed transcriptomic changes occurring in an age-dependent manner, involving an interplay of PGC1α, FOXO3, mTOR, and glucocorticoids as key signaling pathways, and finally resulting in activation of a muscle atrophy program. Our results highlight the relevance of translation accuracy, and show how disturbances thereof may contribute to age-related pathologies.

Aerobic exercise and resistance exercise alleviate skeletal muscle atrophy through IGF-1/IGF-1R-PI3K/Akt pathway in mice with myocardial infarction

2021 ◽  
Author(s):  
Feng Li-Li ◽  
Li Bo-Wen ◽  
Xi Yue ◽  
Tian Zhen-Jun ◽  
Cai Meng-Xin
Keyword(s):  
Myocardial Infarction ◽  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Resistance Exercise ◽  
Aerobic Exercise ◽  
Muscle Atrophy ◽  
Cell Apoptosis ◽  
Exercise Group ◽  
Skeletal Muscle Atrophy ◽  
Akt Pathway

Objectives: Myocardial infarction (MI)-induced heart failure (HF) is commonly accompanied with profound effects on skeletal muscle. With the process of MI-induced HF, perturbations in skeletal muscle contribute to muscle atrophy. Exercise is viewed as a feasible strategy to prevent muscle atrophy. The aims of this study were to investigate whether exercise could alleviate MI-induced skeletal muscle atrophy via insulin-like growth factor 1 (IGF-1) pathway in mice. Materials and Methods: Male C57/BL6 mice were used to establish the MI model and divided into three groups: sedentary MI group, MI with aerobic exercise group and MI with resistance exercise group, sham-operated group was used as control. Exercise-trained animals were subjected to four-weeks of aerobic exercise (AE) or resistance exercise (RE). Cardiac function, muscle weight, myofiber size, levels of IGF-1 signaling and proteins related to myogenesis, protein synthesis and degradation and cell apoptosis in gastrocnemius muscle were detected. And H2O2-treated C2C12 cells were intervened with recombinant human IGF-1, IGF-1R inhibitor NVP-AEW541 and PI3K inhibitor LY294002 to explore the mechanism. Results：Exercises up-regulated the IGF-1/IGF-1R-phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling, increased the expressions of Pax7, myogenic regulatory factors (MRFs) and protein synthesis, reduced protein degradation and cell apoptosis in MI-mice. In vitro, IGF-1 up-regulated the levels of Pax7 and MRFs, mTOR and P70S6K, reduced MuRF1, MAFbx and inhibited cell apoptosis via IGF-1R-PI3K/Akt pathway. Conclusion: AE and RE, safely and effectively, alleviate skeletal muscle atrophy by regulating the levels of myogenesis, protein degradation and cells apoptosis in mice with MI via activating IGF-1/IGF-1R-PI3K/Akt pathway.

Glutamine prevents downregulation of myosin heavy chain synthesis and muscle atrophy from glucocorticoids

1995 ◽  
Vol 268 (4) ◽  
pp. E730-E734 ◽  
Author(s):  
R. C. Hickson ◽  
S. M. Czerwinski ◽  
L. E. Wegrzyn
Keyword(s):  
Protein Synthesis ◽  
Myosin Heavy Chain ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Heavy Chain ◽  
Total Protein ◽  
Female Rats ◽  
Glucocorticoid Treatment ◽  
Precursor Pool ◽  
Chain Synthesis

The aims of this study were to determine whether glutamine infusion prevents the decline in protein synthesis and muscle wasting associated with repeated glucocorticoid treatment. Hormone (cortisol acetate, 100 mg.kg body wt-1.day-1) and vehicle (carboxymethyl cellulose)-treated female rats were infused with either saline or glutamine (240 mM, 0.75 ml/h) for a 7-day period. Glutamine infusion attenuated the decline of plantaris muscle glutamine concentration (3.0 +/- 0.2 vs. 2.3 +/- 0.2 mumol/g) and prevented > 70% of the total muscle mass losses due to the glucocorticoid injections. Fractional synthesis rates of myosin heavy chain (MHC) and total protein were determined after constant [3H]leucine infusion from the leucyl-tRNA precursor pool, which was similar in all groups (range 4.8 +/- 0.5 to 6.3 +/- 0.4 disintegrations.min-1.pmol-1). MHC synthesis rates (%/day) in plantaris muscles were reduced to approximately 40% of controls (4.2/9.4). Although glutamine had no effect on MHC synthesis in vehicle-treated animals (10.1/9.4), it prevented 50% (7.6/4.2) of the hormone-induced decline in MHC synthesis rates. The same results were obtained with total protein synthesis measurements. Changes in muscle mass did not appear related to estimates of protein breakdown. In conclusion, these data show that glutamine infusion is effective therapy in counteracting glucocorticoid-induced muscle atrophy. Atrophy attenuation appears related to maintaining muscle glutamine levels, which in turn may limit the glucocorticoid-mediated downregulation of MHC synthesis.

Alterations In Macronutrient ­Metabolism In Starvation And Disease

2018 ◽  
Author(s):  
L John Hoffer
Keyword(s):  
Weight Loss ◽  
Muscle Atrophy ◽  
Systemic Inflammation ◽  
Protein Energy Malnutrition ◽  
Metabolic Adaptation ◽  
Clinical Approach ◽  
Protein Energy ◽  
Key Words Adaptation ◽  
Disuse Muscle Atrophy ◽  
Involuntary Weight Loss

This review explains starvation as both a physiologic process and a disease. It includes a detailed explanation of the modifying effects of metabolic adaptation and systemic inflammation, as interpreted in a clinical context. It navigates the reader through the difficult shoals of vague and conflicting terminology that burden this topic and provides current definitions and nuanced explanations of the important but frequently misunderstood terms related to starvation and its modifiers and consequences. It provides a succinct explanation of the physiology of total fasting and its clinical correlates. Finally, it explains the interactions among starvation, sarcopenia, frailty, involuntary weight loss, systemic inflammation, cachexia, and disuse muscle atrophy. The multiple and interacting causes of generalized muscle atrophy are pointed out. Inadequate appreciation of these interactions can result in failure to diagnose and treat starvation-induced diseases. A clinical approach to involuntary weight loss is outlined.   This review contains 6 figures, 2 tables and 56 references Key words: adaptation, cachexia, frailty, hypoalbuminemia, inflammation, ketosis, kwashiorkor, malnutrition, marasmus, muscle atrophy, protein-energy malnutrition, sarcopenia, starvation, systemic inflammation, weight loss

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