Introduction:<\/strong> Chronic fatigue syndrome\/ Myalgic Encephalomyelitis (CFS\/ME) is a Historically, there has been a tendency to draw\u00a0psychological explanations for the origin of fatigue, however this model is at odds with\u00a0findings that fatigue and accompanying symptoms may be explained by central and\u00a0peripheral pathophysiological mechanisms, including effects of the immune, oxidative,\u00a0mitochondrial and neuronal pathways. For example, patient descriptions of their fatigue\u00a0regularly cite difficulty in maintaining muscle activity due to perceived lack of energy.<\/p>\n This\u00a0narrative review examines the literature for evidence of biochemical dysfunction in CFS\/ME\u00a0at the skeletal muscle level.<\/p>\n Methods:<\/strong> This narrative review examines literature following searches of PUB MED, Results:<\/strong> Studies show evidence for skeletal muscle bio-chemical abnormality in CFS\/ME Discussion<\/strong>: Bio-energetic peripheral muscle dysfunction is evident in CFS\/ME, with a Understanding muscle dysfunction in Chronic Fatigue Syndrome<\/a>, by Gina Rutherford, Philip Manning, and Julia L Newton in<\/span> Journal of aging research, <\/em>13 January 2016<\/p>\n <\/p>\n <\/p>\n","protected":false},"excerpt":{"rendered":" Review article abstract: Introduction: Chronic fatigue syndrome\/ Myalgic Encephalomyelitis (CFS\/ME) is a debilitating disorder of unknown aetiology and is characterised by severe disabling fatigue in\u00a0 the absence of an alternative diagnosis. Historically, there has been a tendency to draw\u00a0psychological explanations … Continue reading
\ndebilitating disorder of unknown aetiology and is characterised by severe disabling fatigue in\u00a0 the absence of an alternative diagnosis.<\/p>\n
\nMEDLINE and Google scholar, using key words such as (e.g. CFS,ME, Immune,
\nautoimmune, mitochondria, muscle, acidosis).<\/p>\n
\npatients. Following a low-level repeat exercise protocol CFS\/ME patients exhibited a
\nsignificantly greater muscular acidosis<\/a> in addition to a slowed time to recovery from acidosis.\u00a0There is also evidence for impaired AMPK activation <\/a>following electrical pulse stimulation\u00a0in CFS\/ME patient myotube<\/a> samples.<\/p>\n
\ntendency towards an over-utilisation of the lactate dehydrogenase pathway during low-level\u00a0exercise, in addition to delayed acid clearance post-exercise. AMPK activation is impaired in\u00a0CFS\/ME myotube samples following electrical pulse stimulation. Potentially, these biochemical abnormalities may lead to the perception of severe muscular fatigue in CFS\/ME.<\/p>\n