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Understanding Muscle Dysfunction in Chronic Fatigue Syndrome

Lookup NU author(s): Gina Rutherford, Dr Philip Manning, Emerita Professor Julia Newton



This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).


© 2016 Gina Rutherford et al. Introduction. Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a debilitating disorder of unknown aetiology, characterised by severe disabling fatigue in the absence of alternative diagnosis. Historically, there has been a tendency to draw psychological explanations for the origin of fatigue; however, this model is at odds with findings that fatigue and accompanying symptoms may be explained by central and peripheral pathophysiological mechanisms, including effects of the immune, oxidative, mitochondrial, and neuronal pathways. For example, patient descriptions of their fatigue regularly cite difficulty in maintaining muscle activity due to perceived lack of energy. This narrative review examined the literature for evidence of biochemical dysfunction in CFS/ME at the skeletal muscle level. Methods. Literature was examined following searches of PUB MED, MEDLINE, and Google Scholar, using key words such as CFS/ME, immune, autoimmune, mitochondria, muscle, and acidosis. Results. Studies show evidence for skeletal muscle biochemical abnormality in CFS/ME patients, particularly in relation to bioenergetic dysfunction. Discussion. Bioenergetic muscle dysfunction is evident in CFS/ME, with a tendency towards an overutilisation of the lactate dehydrogenase pathway following low-level exercise, in addition to slowed acid clearance after exercise. Potentially, these abnormalities may lead to the perception of severe fatigue in CFS/ME.

Publication metadata

Author(s): Rutherford G, Manning P, Newton JL

Publication type: Review

Publication status: Published

Journal: Journal of Aging Research

Year: 2016

Volume: 2016

Online publication date: 13/01/2016

Acceptance date: 13/01/2016

ISSN (print): 2090-2204

ISSN (electronic): 2090-2212

Publisher: Hindawi Publishing Corporation


DOI: 10.1155/2016/2497348