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Patients with chronic fatigue syndrome performed worse than controls in a controlled repeated exercise study despite a normal oxidative phosphorylation capacity - Source: Journal of Translational Medicine, Oct 11, 2010

  [ 10 votes ]   [ 1 Comment ]
By Ruud CW Vermeulen, et al. • • October 11, 2010

[Note: to read the full text of this article, click HERE

Background: The aim of this study was to investigate the possibility that a decreased mitochondrial ATP synthesis causes muscular and mental fatigue and plays a role in the pathophysiology of the chronic fatigue syndrome (CFS/ME).

Methods: Female patients (n=15) and controls (n=15) performed a cardiopulmonary exercise test (CPET) by cycling at a continuously increased work rate till maximal exertion. The CPET was repeated 24 h later.

Before the tests, blood was taken for the isolation of peripheral blood mononuclear cells (PBMC), which were processed in a special way to preserve their oxidative phosphorylation, which was tested later in the presence of ADP and phosphate in permeabilized cells with glutamate, malate and malonate plus or minus the complex I inhibitor rotenone, and succinate with rotenone plus or minus the complex II inhibitor malonate in order to measure the ATP production via Complex I and II, respectively.

Plasma CK was determined as a surrogate measure of a decreased oxidative phosphorylation in muscle, since the previous finding that in a group of patients with external ophthalmoplegia the oxygen consumption by isolated muscle mitochondria correlated negatively with plasma creatine kinase, 24 h after exercise.

Results: At both exercise tests the patients reached the anaerobic threshold and the maximal exercise at a much lower oxygen consumption than the controls and this worsened in the second test.

This implies an increase of lactate, the product of anaerobic glycolysis, and a decrease of the mitochondrial ATP production in the patients. In the past this was also found in patients with defects in the mitochondrial oxidative phosphorylation.

However the oxidative phosphorylation in PBMC was similar in CFS/ME patients and controls. The plasma creatine kinase levels before and 24 h after exercise were low in patients and controls, suggesting normality of the muscular mitochondrial oxidative phosphorylation.

Conclusion: The decrease in mitochondrial ATP synthesis in the CFS/ME patients is not caused by a defect in the enzyme complexes catalyzing oxidative phosphorylation, but in another factor.

Trial registration: Clinical trials registration number: NL16031.040.07

Source: Journal of Translational Medicine, Oct 11, 2010;8:93. DOI:10.1186/1479-5876-8-93, by Vermeulen R, Kurk RM, Visser FC, Sluiter W, Scholte HR. CFS/ME and Pain Research Center Amsterdam; Departmentd of Neurology and Neuroscience, Erasmus MC University Medical Center, Rotterdam, The Netherlands. [E-mail:]

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Article Comments Post a Comment

Posted by: xxxshyguy
Oct 20, 2010
i find the discussion about atp production interesting .. i am a cfs sufferer of 30 years plus and have found that anything that was beneficial also had an atp enhancing influence . particularly anything in the asmino acid/ sports medicine line that is used to slow down catabolic effects of excercise ,, ie things like creatine ,hmb stacketc .. these suppliments are used by sports people particulalry body buildrs to slow muscle break down. i also note .. and i think this is very important that people with low atp have also low production of glutithione ,, or visa versa .. cheers cliff
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