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Molecular Mechanisms of Muscle Fatigue

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 16272

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Division of Physiology, Pharmacology and Neuroscience, School of Life Sciences, Queen’s Medical Centre, University of Nottingham Medical School, Nottingham NG7 2UH, UK
Interests: type 2 diabetes; muscle insulin resistance; sepsis; inflammation; energy metabolism; ageing; inactivity
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Dear Colleagues,

Large parts of the global population have recently been exposed to the still unabated COVID-19 coronavirus. While the percentage of people recovering from virus exposure without significant ill-health symptoms or side effects is fortunately high, However, some survivors (10%) experience a syndrome that includes long-term debilitating extreme tiredness (fatigue), pulmonary (shortness of breath, chest pain or tightness), and mental difficulties.

The prime sites of fatigue seem to be within the muscle cell itself and, for the most part, do not implicate the central nervous system or the neuromuscular junction. The British NICE guideline scope (October 2020) defines post-COVID syndrome as signs consistent with symptoms that develop during or following an infection. This condition is well known to be positively associated with muscle wasting.

Muscle atrophy can also occur after long periods of inactivity in association with poor nutrition. When muscle wasting occurs, muscles become less bulky and floppier. Each muscle fibre is just as strong, but there are not so many of them so, collectively, they do not contract as effectively. This easily leads to exhaustion when one tries to do things that would have been easier when the muscles were fit. Fortunately, with regular controlled exercise regimes, pharmacological intervention, and sensible dieting, the condition is reversible even with increasing age, albeit to a lower degree than for younger generations.

By validating the recognized inflammation/infection-related molecular mechanisms underlying muscle fatigue/waste, one could then apply sensible pharmacological, physiological (e.g., targeted exercise regimen) or nutritional interventions aimed at increasing muscle mass and regaining of muscle strength. This special issue welcomes both original research articles and comprehensive reviews (4000+ words) related to the topic.

Dr. Dumitru Constantin-Teodosiu
Guest Editor

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Keywords

  • infection
  • inflammation
  • protein catabolism
  • muscle wasting
  • energy metabolism
  • muscle mass
  • muscle signalling pathway
  • muscle hypertrophy interventions

Published Papers (1 paper)

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Review

16 pages, 1036 KiB  
Review
Molecular Mechanisms of Muscle Fatigue
by Dumitru Constantin-Teodosiu and Despina Constantin
Int. J. Mol. Sci. 2021, 22(21), 11587; https://doi.org/10.3390/ijms222111587 - 27 Oct 2021
Cited by 22 | Viewed by 15428
Abstract
Muscle fatigue (MF) declines the capacity of muscles to complete a task over time at a constant load. MF is usually short-lasting, reversible, and is experienced as a feeling of tiredness or lack of energy. The leading causes of short-lasting fatigue are related [...] Read more.
Muscle fatigue (MF) declines the capacity of muscles to complete a task over time at a constant load. MF is usually short-lasting, reversible, and is experienced as a feeling of tiredness or lack of energy. The leading causes of short-lasting fatigue are related to overtraining, undertraining/deconditioning, or physical injury. Conversely, MF can be persistent and more serious when associated with pathological states or following chronic exposure to certain medication or toxic composites. In conjunction with chronic fatigue, the muscle feels floppy, and the force generated by muscles is always low, causing the individual to feel frail constantly. The leading cause underpinning the development of chronic fatigue is related to muscle wasting mediated by aging, immobilization, insulin resistance (through high-fat dietary intake or pharmacologically mediated Peroxisome Proliferator-Activated Receptor (PPAR) agonism), diseases associated with systemic inflammation (arthritis, sepsis, infections, trauma, cardiovascular and respiratory disorders (heart failure, chronic obstructive pulmonary disease (COPD))), chronic kidney failure, muscle dystrophies, muscle myopathies, multiple sclerosis, and, more recently, coronavirus disease 2019 (COVID-19). The primary outcome of displaying chronic muscle fatigue is a poor quality of life. This type of fatigue represents a significant daily challenge for those affected and for the national health authorities through the financial burden attached to patient support. Although the origin of chronic fatigue is multifactorial, the MF in illness conditions is intrinsically linked to the occurrence of muscle loss. The sequence of events leading to chronic fatigue can be schematically denoted as: trigger (genetic or pathological) -> molecular outcome within the muscle cell -> muscle wasting -> loss of muscle function -> occurrence of chronic muscle fatigue. The present review will only highlight and discuss current knowledge on the molecular mechanisms that contribute to the upregulation of muscle wasting, thereby helping us understand how we could prevent or treat this debilitating condition. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Muscle Fatigue)
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