Richvank made some comments a few years back that would have a bearing on this subject.
http://forums.phoenixrising.me/inde...o-my-cells-brain-body.7501/page-2#post-147858
[I would like to contribute my views on what is going on with oxygen, CO2, and breathing in ME/CFS.
As I see it, the fundamental issue here is that the mitochondria in cells particularly of the tissues that are most depleted in glutathione are dysfunctional. A major fraction of the total cell mass is in the skeletal muscles, and they are glutathione-depleted. One result is that these tissues do not utilize oxygen at as high as normal a rate, and they also do not produce carbon dioxide at as high as normal a rate.
The blood, of course, circulates to all the tissues, including those with serious mito dysfunction and those that are still operating more normally. The latter include the vital organs, which have complete transsulfuration pathways, and are thus able to make cysteine from methionine, while cells such as those in the skeletal muscles cannot. So when cysteine is in short supply, the vital organs are able to make cysteine to replenish their glutathione and continue to function to preserve life, while the skeletal muscles and some other types of tissues become dysfunctional.
Here's the key point: The respiratory center in the brainstem controls the rate and depth of breathing by sending signals to the muscles involved in breathing. The respiratory center performs this regulation by monitoring the level of CO2 and the pH in the blood it receives. It pays attention to oxygen only when it becomes very low, and hits a trip point, which produces gasping. The CO2 level and pH of the blood represents an average of the effects of the mitochondria throughout the body, but they are dominated by the effects of the skeletal muscles, because of their large fraction of total cellular mass. So the respiratory center sees a low CO2 level in the averaged blood it receives, and it therefore slows and shallows the breathing, trying to raise the CO2 level. However, because the mitochondria are dysfunctional and can't produce CO2 very well, this doesn't work as well as normal, and that's why the rate and depth of breathing remain low.
Unfortunately, other tissues that still have a normal oxygen demand, and which must share the same blood supply, may find that they are not able to get enough oxygen, because the shallowing and slowing of the breathing will also mean that the oxygen intake by the lungs into the blood will be lower than normal. This gives rise to the feeling of "air hunger" or "shortness of breath." In response, people take conscious control of their breathing and raise its rate and depth.
When a person in this condition falls asleep, their normal ability to take conscious control of their breathing ("remind themself to breathe") is not present. Therefore, they can develop sleep apnea (not obstructive sleep apnea, but a central version, due to this confused signal getting to the respiratory center) and can awaken gasping periodically, as their oxygen level repeatedly drops down to the emergency trip point. This is just one more thing contributing to sleep problems in this disorder, added to things like abnormalities in cortisol, blood sugar level, melatonin, and others (all of which also stem from the same root vicious circle mechanism, in my view).
Dr. Cheney's observation that the oxygen saturatioin level of the blood in ME/CFS does not drop as rapidly as normal on breath holding is a consequence of a lower rate of whole-body oxygen utilization because of the mito dysfunction in muscle cells and some other types of cells.
His observation of oxygen toxicity is a consequence of the fact that if more oxygen is supplied to mitochondria that are dysfunctional, more of it is converted to superoxide ions, rather than to water molecules, as is normal. This exacerbates the state of oxidative stress that is already present, and that's why it feels "toxic."
There have been at least four studies reporting hypocapnia (low carbon dioxide partial pressure in exhaled gas) in ME/CFS. This has been attributed (I believe wrongly) to hyperventilation. In fact, it is due to mito dysfunction, and PWMEs/PWCs in fact mostly have HYPOventilation. The one study that actually measured ventilation rate in ME/CFS did not find hyperventilation.
I believe that all of this fits together, and it all comes back down to the vicious circle mechanism described by the GD-MCB hypothesis. This vicious circle mechanism is responsible for the mito dysfunction, and that's what brings on all the rest of what I have discussed here. This vicious circle also explains the other abnormalities in ME/CFS in straightforward detail, taking account of known biochemistry and physiology.
Best regards,
Rich
richvank,
May 17, 2011]
It really has been and is, a huge ongoing commitment.
