Mitochondria are often referred to as the power plants of the body because they are responsible for generating nearly all the energy needed to support life.

These kidney bean-shaped structures are found in most cells and are made up of different compartments, each with a specific role related to the metabolism of the cell they inhabit.

One of these roles is the generation of adenosine triphosphate (ATP), a molecule that is used to transport energy within a cell and thereby enable it to function properly (for example, allowing a muscle fibre to contract).

It is not surprising, therefore, that scientists have considered whether abnormalities in the mitochondria might be involved in ME/CFS, an illness characterised by a loss of muscle power following exertion, which may be due to insufficient energy within the muscle cells.

We have reported on several such studies over the last few years (from the Netherlands, Spain and the UK), but the overall picture is still not clear. Some studies have shown reduced concentrations of ATP in ME/CFS patients, while others have not.

Adding to this story (but not yet making it much clearer) is new research published in the Journal of Nature and Science. US researchers at Stanford and Columbia took blood samples from 42 ME/CFS patients and 42 healthy people in five different clinics, including the Levine Clinic and Sierra Internal Medicine. Their main aim was to look for defects in the structure or function of the mitochondria that might explain some of the symptoms of ME/CFS.

Overall, the researchers found no difference in the density, size or shape of mitochondria in patients, nor in several other aspects of their structure and function, although the cristae (protrusions of the membranes inside the mitochondria) were more condensed than usual.

They did find that ATP levels were higher than normal in the blood samples from ME/CFS patients. Further testing showed that the mitochondrial production of ATP was actually relatively normal, suggesting that the extra ATP was being generated elsewhere.

The main conclusion of the study, however, was that there were no major abnormalities in the mitochondria of ME/CFS patients: the important parts of this structure were all intact and functioning, and ATP production was normal.

It is important to note that these measurements were made in mitochondria from blood cells, and it is possible that the situation in muscle cells is quite different. But at least one study that did look at muscle mitochondria has also reported normal ATP production.

If the muscle fatigue in ME/CFS is not a result of a lack of mitochondrial ATP, then what is the cause? We still don’t know, but the intriguing hypothesis suggested by these researchers is that there is some pathological process occurring by which extra ATP is being produced somewhere else. And the scientists’ next step is to identify where and why this is happening.