Understanding muscle dysfunction in CFS: Prof Julia Newton

Seanko

Well-Known Member
[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]
 
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Seanko

Well-Known Member
[article]Conclusion
CFS/ME patient perceptions of the nature of their condition frequently cite ‘peripheral’ as
opposed to a central origin, with many descriptions of their fatigue regularly referring to
difficulty in maintaining muscle activity due to perceived lack of energy, or through muscle
fatigue [15,17]. There is increasing evidence to suggest muscular bio-chemical abnormality
may play a major role in CFS/ME associated fatigue. The literature suggests patients to
exhibit profound intramuscular dysfunction regarding acid generation and clearance, with a
tendency towards an over-utilisation of the lactate dehydrogenase pathway following
relatively low-level activity. However, the precise mechanisms underlying the dysfunction
are yet to be fully elucidated. There is a real need for adequately powered studies to examine
PDC function in vitro, to determine the mechanisms responsible for bio-energetic dysfunction
and peripheral fatigue.
[/article]
 

Seanko

Well-Known Member
Prof Newton made a video for the Dutch ME/CFS on tthe subject in 2014.
>Short & watchable.

 

Seanko

Well-Known Member
Prof Jo Nijs also covered muscle dysfunction in his rather good talk for the CMRC 2015 conference on ME/CFS held in October 2015.
He is based in Brussels with his work partly funded by the British ME Assocation & he is a major collaborator with Prof Newton's team.

 

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