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[bimg=Prof Julia Newton of Newcastle University|no-lightbox]http://www.newcastle-hospitals.org.uk/_assets/media/people/Julia_Newton.jpg[/bimg] Prof Julia Newton of Newcastle University has conducted a review of the research literature on muscle dysfunction in ME/CFS, it has been published in the Journal of Ageing Research.
Understanding muscle dysfunction in ME/CFS: Literature Review in Journal of Ageing Research
Prof Newton is probably the UK's leading biomedical expert on ME/CFS and the project received funding from Action for ME and the government National institute for Health Research (NIHR)
[article=http://downloads.hindawi.com/journals/jar/aip/328971.pdf]Abstract
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.
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 biochemical
abnormalities may lead to the perception of severe muscular fatigue in CFS/ME
Key words
Chronic fatigue syndrome/Myalgic encephalomyelitis
Muscle dysfunction
Biochemical abnormality
2
Exercise [/article]
Understanding muscle dysfunction in ME/CFS: Literature Review in Journal of Ageing Research
Prof Newton is probably the UK's leading biomedical expert on ME/CFS and the project received funding from Action for ME and the government National institute for Health Research (NIHR)
[article=http://downloads.hindawi.com/journals/jar/aip/328971.pdf]Abstract
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.
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 biochemical
abnormalities may lead to the perception of severe muscular fatigue in CFS/ME
Key words
Chronic fatigue syndrome/Myalgic encephalomyelitis
Muscle dysfunction
Biochemical abnormality
2
Exercise [/article]
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