oxidative phosphorylation (OXPHOS)

<p><a href="https://translational-medicine.biomedcentral.com/articles/10.1186/1479-5876-8-93https://translational-medicine.biomedcentral.com/articles/10.1186/1479-5876-8-93">https://translational-medicine.biomedcentral.com/articles/10.1186/1479-5876-8-93https://translational-medicine.biomedcentral.com/articles/10.1186/1479-5876-8-93</a></p>

<p class="Para">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.</p>

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<h3 class="Heading">Conclusion</h3>

<p class="Para">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.</p>

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