Introduction: Chronic fatigue syndrome/ Myalgic Encephalomyelitis (CFS/ME) is a debilitating disorder of unknown aetiology and is characterised by severe disabling fatigue in the absence of an 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 examines the literature for evidence of biochemical dysfunction in CFS/ME at the skeletal muscle level.
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Methods: This narrative review examines literature following searches of PUB MED, MEDLINE and Google scholar, using key words such as (e.g. CFS,ME, Immune, autoimmune, mitochondria, muscle, acidosis).
Results: Studies show evidence for skeletal muscle bio-chemical abnormality in CFS/ME patients. Following a low-level repeat exercise protocol CFS/ME patients exhibited a significantly greater muscular acidosis in addition to a slowed time to recovery from acidosis. There is also evidence for impaired AMPK activation following electrical pulse stimulation in CFS/ME patient myotube samples.
Discussion: Bio-energetic peripheral muscle dysfunction is evident in CFS/ME, with a tendency towards an over-utilisation of the lactate dehydrogenase pathway during low-level exercise, in addition to delayed acid clearance post-exercise. AMPK activation is impaired in CFS/ME myotube samples following electrical pulse stimulation. Potentially, these bio-chemical abnormalities may lead to the perception of severe muscular fatigue in CFS/ME.
Source: Gina Rutherford MSc, Philip Manning PhD, Julia L Newton MD, PhD. Understanding muscle dysfunction in Chronic Fatigue Syndrome. Journal of Aging Research. Received 1 September 2015; Revised 12 December 2015; Accepted 13 January 2016