CFS-ME & MITOCHONDRIAL DYSFUNCTION

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

Ruud CW Vermeulen^1*, Ruud M Kurk¹, Frans C Visser¹, Wim Sluiter² and Hans R Scholte³

FULL Version of the study can be found at: http://www.translational-medicine.com/content/8/1/93

Published:

11 October 2010

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).

Conclusions of the above study:

The decrease in mitochondrial ATP production at increasing work rate, detected by the CPET tests in the present well-characterized though small group of CFS/ME patients, is a secondary phenomenon. This was shown by the normality of the oxidative phosphorylation in peripheral blood mononuclear cells. The chain of mechanisms that couple (external) pulmonary to (internal) cellular respiration showed no abnormal differences in this study between CFS patients and healthy controls at the pulmonary, cardiac and circulatory level. Two possible explanations for the insufficient energy production in CFS remained: a lower transport capacity of oxygen as in anemia or a mitochondrial insufficiency. We showed that the mitochondrial ATP production shows no defect. Then the conclusion must be that the transport capacity of oxygen is limited in CFS patients.