Monday, October 11, 2010

Patients with chronic fatigue syndrome performed worse than controls in a contro

 
The (provisional) full text is available for free at:
http://bit.ly/aIKH8k   i.e.
http://www.translational-medicine.com/content/pdf/1479-5876-8-93.pdf   

Final full text will be linked from:
http://www.translational-medicine.com/content/8/1/93/abstract  

Patients with chronic fatigue syndrome performed worse than controls in a controlled repeated exercise study despite a normal oxidative phosphorylation capacity

Author: Ruud Vermeulen, Ruud Kurk,Frans Visser,Wim Sluiter,Hans Scholte

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

Credits/Source: Journal of Translational Medicine 2010, 8:93


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