The previous page showed how, under anaerobic conditions, the cell could produce ATP via glycolysis. Also, how the cell prevents the buildup of pyruvate, and recycles NAD+, by converting the pyruvate to lactic acid. This is how the cell is designed to produce ATP via glycolysis under anaerobic conditions. And, according to australian researchers, this process appears to be operating as designed in the person with CFIDS.
However, as you can see on this page, in the person with fibromyalgia if the cell must produce ATP anaerobically, there appears to be a breakdown in the process that converts pyruvate to lactic acid. This process is important because it dissociates NAD+ from NADH and makes it available for reuse in other glycolysis processes. As a result of this failed operation, NAD+ may eventually become unavailable as it is all binded up as NADH. (The NADH is unable to enter the mitochondria to deliver the H+ because there is no oxygen.) This could further contribute to impairing glycolysis within the cell such that even under anaerobic conditions ATP production is impaired.
This difference in the way that the cell handles pyruvate may be where CFIDS and FMS diverge in the type of symptoms unique to each condition. The build up of pyruvate, acidifying the cell, may be responsible for the all over the body pain experienced by people with fibromyalgia. The low energy, associated with both conditions, may be the result of the low levels of ATP being generated by the cell. The root cause (at the cell level) for both conditions may be due to a lack of oxygen at the mitochondria. Lack of oxygen at the mitochondria prevents the production of ATP via the aerobic pathways, the Kreb Cycle and the Electron Transport Chain.
We could focus on trying to find out why NADH is not binding with pyruvate under anaerobic conditions. The related article points out that there is a possible decrease in the enzyme that performs this operation. (Don't forget, this seems to be working as designed in CFIDS, so fixing this deficiency in FMS would probably only upgrade the condition from FMS to CFIDS; Probably not a very desirable exchange.) However, if the cell had sufficient oxygen in the first place the reduced quantity of this enzyme would probably not be an issue.
Why is the cell in an anaerobic state to begin with? Why is the cell not being supplied sufficient oxygen to meet demands for ATP production? This is the issue that needs to be addressed and corrected.
Side Note: Some suggest that supplementing NADH might prove beneficial. While there may be some benefit to taking NADH in capsules, my thinking is this: The cell evidently has sufficient NAD+ otherwise glycolysis would be unable to manufacture pyruvate in the first place. Since researchers have found pyruvate to be elevated in the cell, NAD+ is apparently not lacking and may be tied up as NADH. If the hypothesis being presented is correct then there is likely a buildup of NADH in the cell already. This NADH is unable to be processed due to lack of oxygen. Assuming that NADH taken orally even gets to the cell, which I tend to doubt because digestive processes would break it down into more simple elements for absorption. It would still not be able to generate ATP because the required oxygen would be missing. (assuming that our hypothesis is correct.) I suspect that the benefit that people report by taking NADH supplements is coming as a result of the electrons that the substance is providing.
(I want to remind you that I am not a medical researcher. My background is engineering. But, the information I am using for this hypothesis is based on research done by those trained in medical research. Based on what I have studied on the subject this makes sense. Remember, this is all theoretical.)