Cara Tomas and colleagues from Newcastle University have recently published a report on mitochondrial function in ME/CFS, and this study is related to research on muscle fatigue they are currently pursuing with support from ME Research UK.
The mitochondria are considered the power plants of the body, generating the energy needed to support life, and substantial evidence suggests that mitochondrial function is abnormal in people with ME/CFS. But what part of the energy production pathway is faulty?
In this study, Cara and her team looked at the activity of protein complexes within the mitochondria. Electrons are transferred between these complexes, and this movement generates a molecule called ATP, which is used to transport energy within the cell.
The function of these complexes was tested in white blood cells and skeletal muscle cells, which were sampled from patients with ME/CFS and healthy control subjects, and examined using a cutting-edge technique called extracellular flux analysis.
The team found no differences in mitochondrial complex activity or respiratory activity between cells from patients and those from controls, and this was true in both white blood cells and skeletal muscle cells.
These results suggest that the abnormality in energy production in ME/CFS lies upstream of the mitochondrial respiratory chain, and this agrees with previous findings from other research groups.