Muscle research and ME/CFS

NOTE:  A new research study adds further support to the view that muscle tissue abnormalities play a role in the pathogenesis of ME/CFS – see abstract below.

The MEA is currently funding research into muscle function in ME/CFS at the University of Newcastle – see report in the May issue of ME Essential magazine.

More information on other research into muscle abnormalities in ME/CFS can be found in section 5:3 of ME/CFS/PVFS – An Exploration of the Key Clinical Issues – booklet available from the MEA on the pdf website ORDER FORM

RESEARCH ABSTRACT

Functional characterization of muscle fibres from patients with chronic fatigue syndrome: case-control study.

‘Functional characterization of muscle fibres from patients with chronic fatigue syndrome: case-control study.’

Pietrangelo T, Toniolo L, Paoli A, Fulle S, Puglielli C, Fan X00f2 G, Reggiani C.

Int J Immunopathol Pharmacol. 2009 April-June;22(2):427-436.

PMID: 19505395 [PubMed – as supplied by publisher]

http://www.ncbi.nlm.nih.gov/pubmed/19505395

Chronic fatigue syndrome (CFS) is a disabling condition characterized by unexplained chronic fatigue that impairs normal activities. Although immunological and psychological aspects are present, symptoms related to

skeletal muscles, such as muscle soreness, fatigability and increased lactate accumulation, are prominent in CFS patients. In this case-control study, the phenotype of the same biopsy samples was analyzed by determining

i) fibre-type proportion using myosin isoforms as fibre type molecular marker and gel electrophoresis as a tool to separate and quantify myosin isoforms, and

ii) contractile properties of manually dissected, chemically made permeable and calcium-activated single muscle fibres. The results showed that fibre-type proportion was significantly altered in CSF samples, which showed a shift from the slow- to the fast-twitch phenotype. Cross sectional area, force, maximum shortening velocity and calcium sensitivity were not significantly changed in single muscle fibres from CSF samples. Thus, the contractile properties of muscle fibres were preserved but their proportion was changed, with an increase in the more fatigue-prone, energetically expensive fast fibre type. Taken together, these results support the view that muscle tissue is directly involved in the pathogenesis of CSF and it might contribute to the early onset of fatigue typical of the skeletal muscles of CFS patients.

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