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      Muscle fatigue: general understanding and treatment

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          Abstract

          Muscle fatigue is a common complaint in clinical practice. In humans, muscle fatigue can be defined as exercise-induced decrease in the ability to produce force. Here, to provide a general understanding and describe potential therapies for muscle fatigue, we summarize studies on muscle fatigue, including topics such as the sequence of events observed during force production, in vivo fatigue-site evaluation techniques, diagnostic markers and non-specific but effective treatments.

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          Most cited references126

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          Neural Contributions to Muscle Fatigue: From the Brain to the Muscle and Back Again.

          During exercise, there is a progressive reduction in the ability to produce muscle forces. Processes within the nervous system, as well as within the muscles contribute to this fatigue. In addition to impaired function of the motor system, sensations associated with fatigue, and impairment of homeostasis can contribute to impairment of performance during exercise. This review discusses some of the neural changes that accompany exercise and the development of fatigue. The role of brain monoaminergic neurotransmitter systems in whole-body endurance performance is discussed, particularly with regard to exercise in hot environments. Next, fatigue-related alterations in the neuromuscular pathway are discussed in terms of changes in motor unit firing, motoneuron excitability and motor cortical excitability. These changes have mostly been investigated during single-limb isometric contractions. Finally, the small-diameter muscle afferents that increase firing with exercise and fatigue are discussed. These afferents have roles in cardiovascular and respiratory responses to exercise, and in impairment of exercise performance through interaction with the motor pathway, as well as providing sensations of muscle discomfort. Thus, changes at all levels of the nervous system including the brain, spinal cord, motor output, sensory input and autonomic function occur during exercise and fatigue. The mix of influences and the importance of their contribution varies with the type of exercise being performed.
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            The Role of Exercise-Induced Myokines in Muscle Homeostasis and the Defense against Chronic Diseases

            Chronic inflammation is involved in the pathogenesis of insulin resistance, atherosclerosis, neurodegeneration, and tumour growth. Regular exercise offers protection against type 2 diabetes, cardiovascular diseases, colon cancer, breast cancer, and dementia. Evidence suggests that the protective effect of exercise may to some extent be ascribed to the antiinflammatory effect of regular exercise. Here we suggest that exercise may exert its anti-inflammatory effect via a reduction in visceral fat mass and/or by induction of an anti-inflammatory environment with each bout of exercise. According to our theory, such effects may in part be mediated via muscle-derived peptides, so-called “myokines”. Contracting skeletal muscles release myokines with endocrine effects, mediating direct anti-inflammatory effects, and/or specific effects on visceral fat. Other myokines work locally within the muscle and exert their effects on signalling pathways involved in fat oxidation and glucose uptake. By mediating anti-inflammatory effects in the muscle itself, myokines may also counteract TNF-driven insulin resistance. In conclusion, exercise-induced myokines appear to be involved in mediating both systemic as well as local anti-inflammatory effects.
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              Vitamin and mineral status: effects on physical performance.

              Public health recommendations encourage the selection of a balanced diet and increasing physical activity to foster health and well-being. Whereas the adverse effects of restricted intakes of protein, fat, and carbohydrate on physical performance are well known, there is limited information about the impact of low intakes of vitamins and minerals on the exercise capacity and performance of humans. Physically active people generally consume amounts of vitamins and minerals consistent with the recommendations for the general public. However, when intakes are less than recommendations, some noticeable functional impairments occur. Acute or short-term marginal deficiencies, identified by blood biochemical measures of vitamin B status, had no impacts on performance measures. Severe deprivation of folate and vitamin B12 result in anemia and reduce endurance work performance. Evidence of vitamin A and E deficiencies in athletic individuals is lacking apparently because body storage is appreciable. In contrast to vitamins, marginal mineral deficiencies impair performance. Iron deficiency, with or without anemia, impairs muscle function and limits work capacity. Magnesium deprivation increases oxygen requirements to complete submaximal exercise and reduces endurance performance. Use of vitamin and mineral supplements does not improve measures of performance in people consuming adequate diets. Young girls and individuals participating in activities with weight classifications or aesthetic components are prone to nutrient deficiencies because they restrict food intake and specific micronutrient-rich foods. This information will be useful to professionals who counsel physically active people and scientific groups who make dietary recommendations to improve health and optimize genetic potential.
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                Author and article information

                Journal
                Exp Mol Med
                Exp. Mol. Med
                Experimental & Molecular Medicine
                Nature Publishing Group
                1226-3613
                2092-6413
                October 2017
                06 October 2017
                1 October 2017
                : 49
                : 10
                : e384
                Affiliations
                [1 ]Department of Pharmacology, School of Pharmacy, Second Military Medical University , Shanghai, China
                Author notes
                [* ]Department of Pharmacology, School of Pharmacy, Second Military Medical University , 325 Guohe Road,Yangpu District, Shanghai 200433, China. E-mail: lxflying@ 123456aliyun.com or dawnysun@ 123456126.com
                [2]

                These authors contributed equally to this work.

                Article
                emm2017194
                10.1038/emm.2017.194
                5668469
                28983090
                2ca8dc96-a1e7-4d79-b2f8-835d1ad5c312
                Copyright © 2017 The Author(s)

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                : 19 February 2017
                : 20 May 2017
                : 23 May 2017
                Categories
                Review

                Molecular medicine
                Molecular medicine

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