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more evidence of mitochondrial dysfunction in excercise intolerant patients

G

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
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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