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more evidence of mitochondrial dysfunction in excercise intolerant patients

Discussion in 'Latest ME/CFS Research' started by Gerwyn, Feb 14, 2010.

  1. Gerwyn

    Gerwyn Guest

    These patients excercising abiliity was measured objectively

    IDIOPATHIC CHRONIC FATIGUE, MICROSCOPIC AND ENZYMATIC
    MITOCHONDRIAL STUDY
    Poca-Dias V1, Ojanguren Sabn I2, Pereira dos Santos C3, Snchez-Vizcano E4, Ariza
    Fernndez A2, Garca-Fructuoso F1
    1 Rheumatology Department, CIMA Clinic, Barcelona, Spain
    2 Department of Pathological Anatomy, Hospital Universitari Germans Trias i Pujol,
    Badalona, Barcelona, Spain
    3 Biological Anthropology Unit, Autonomous University of Barcelona, Bellaterra,
    Barcelona, Spain
    4 Laboratorio Dr. Echevarne, CIMA Clinic, Barcelona, Spain
    INTRODUCTION
    The role of mitochondria in human illness has recently become one of the most
    developed medical fields. Mitochondrial respiratory chain malfunction is apparent from
    a very wide range of symptoms, and abnormal tiredness and intolerance to exercise
    are common symptoms in mitochondrial disorders, chronic fatigue syndrome (CFS)
    and idiopathic chronic fatigue (ICF). Mitochondrial respiratory chain dysfunction can
    result in a wide range of symptoms which include serious fatigue and intolerance to
    exercise, even in patients without specific phenotypical expression.
    OBJECTIVE
    The objective of our study was to evaluate signs of mitochondrial dysfunction in ICF
    patients.
    MATERIAL AND METHODS

    Each patient exercised on a treadmill using Bruce protocol to establish their MET value
    and theoretical maximum cardiac frequency according to AMA guidelines. An open
    deltoid muscle biopsy was then performed and the sample analyzed under an optical
    microscope with Gomori tint to identify ragged red fibers. Structural mitochondrial
    changes (e.g. number, size and location, presence and accumulation of glycogen,
    lipofuscin or lipids) were evaluated with an electronic microscope.
    Mitochondrial function was studied by assessing 5 enzymatic complexes in
    mitochondria and homogenate. Their oxidation activity was also studied.
    RESULT
    ________________________________________
    Page 2
    When viewed under the optical microscope, not one patient presented ragged red
    fibers with Gomori tint. Using the electronic microscope, we observed an increase in
    the number of mitochondria in 60% of patients, with a tendency to subsarcolemmal
    (see Image 1).
    Glycogen and lipofuscin accumulation increased in 87% and 53% of patients,
    respectively.
    There was an alteration of the mitochondrial function in mitochondria and homogenate
    in 60% and 40% of patients, respectively. Oxidation activity was different in 40% of
    patients.
    CONCLUSION
    The study detected an increased number of mitochondria, glycogen and lipid
    accumulation, and a change in mitochondrial enzymatic activity. There was a
    correlation between the presence of lipofuscin accumulation and the presence of lipid
    accumulation, patients ages and MET values. The main correlation was the presence
    in 33% of patients of a greater alteration of mitochondrial function, mitochondrial
    pleomorphism, cephalalgia in their mothers, and hearing loss in the patients.

    Table -1
    N=15
    Average
    Median
    Standard deviation
    Age
    49.3
    51
    12.5
    Height
    161.3
    158
    7.3
     

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