this study may be confirming that a population of T cells is inappropriately activated - rather than there being some bodywide OXPHOS dysfunction that is also occurring in other cells like muscle, liver, etc (although deranged cytokine signaling from the activated T cells can potentially cause mitochondrial dysfunction in those other cells).
I wanted to say this as well. It's very tempting to look at results like this, and go "Look, this proves we can't produce ATP as well as healthy people! This is why we're tired!", but the key thing a lot of people looking at studies like that are forgetting is cell types. The human body is made of a multitude of different types and suptypes of cells, that do very different things, express different proteins, and have many other differing properties. And yes, the energy metabolizm of most cells consists of the same molecular machinery - glycolysis, pyruvate decarboxylation, beta-oxidation, krebs cycle, electron transport chain. But the regulation of those processes differs from cell to cell. Every time you hear about a discovered intracellular dysfunction, you have to ask the question "okay, what cells exactly?"
A lot of those studies, even Ron's work, use PBMCs. Peripheral Blood Mononuclear Cells are a middle layer of blood, separated by centrifugation. It contains T-cells, B-cells, NK cells, monocytes, and sometimes trace basophils. In other words, immune system cells. Our PBMCs having its energy metabolism impaired doesn't directly explain us feeling fatigue, or not being able to tolerate exercise. Such findings in muscle cells could maybe, kinda explain it (I don't think fully though). Interestingly enough, Fluge and Mella did, in fact, perform those same Seahorse measurements in cultured muscle cells exposed to ME/CFS serum. And the results were the opposite - oxygen consumption was actually increased, not decreased. So I would be careful with assuming that those results here, or any similar studies, can be extrapolated to the whole body. Those results are indicative of an *immune* alteration, if anything. It can be a dysfuntion of the immune cells, a different cell type ratio than the controls, or just immune activation. We don't know.
It's nice the UK is coming around to doing actual research in ME/CFS. But this doesn't really tell us anything new about the illness mechanism, in my opinion.
What I would like to see more of, is actual cell sorting in those studies. If the measurements of those things varied a lot across PBMC types, it could tell us more about what the immune system is doing, and if they didn't, that would actually be indicative of a body-wide cellular metabolism impairment.
This is also why I was excited when Ron said he wanted to use pluripotent stem cells, because that way you can test all the cell types you want (with limitations, but still).