Split thread That's a really great and very helpful document @JaimeS. I appreciate we probably can't have the document itself in our library, but could we include it as a linked reference in our Library thread (rather than just this library discussion thread)? And a question. In your document ... ... the authors state in their conclusion ... Could you give some insight what this is saying please to a non-medic, especially the second sentence. Sounds very significant, though I suppose it depends on how well peer reviewed the paper is.
Sure, it can be included in the references. Yes, it's significant. It's saying the heart and the lungs are working well, but that oxygen uptake by muscles is poor. You can see this in differences between PO2 and VO2. The former shows uptake by lungs and ability of the heart to pump it around the body (just literally, how much oxygen is in the blood). The latter shows how much oxygen is being utilized. Using myself as an example, my PO2 was 117% of normal, but my VO2 was only 66% of normal on a single-day CPET. That means I'm taking in air as fast as I can: my lungs are working hard to draw in air, and my heart is working hard to pump oxygenated blood throughout my body; but my cells aren't taking up that oxygen well at all. These percentages are by age (and gender, as I recall) so they are not absolute. As I recall, my doc at the time told me they were appropriate for an 80-year-old. Since Vermeulen et al compared ME/CFS patients to sedentary folk (and the ME/CFS patients were still significantly worse off) this can't be a matter of deconditioning. Moreover, they were measuring cardiac output and seeing that the heart is pumping / working well, which is NOT the case in deconditioning: From www.sciencedirect.com Surely if you're on bedrest you would note decreases in cardiac output, because the patient is ALSO deconditioned. But for people with ME who are up and walking around -- at least, enough to perform a single exercise test -- they are not deconditioned. The argument that they were was made here, but they're referring to people who are bedbound or severely limited in their movements. Proving that those people are deconditioned is like proving someone in a wheelchair has weaker leg muscles: duh.
Thanks for that @JaimeS . What you say sounds like a closed loop, where the controller output, PO2, is artificially high as it attempts in vain to raise the process variable, VO2, which for whatever reason cannot respond (no doubt in reality any control loop will be very complex). Whether that is really the case I don't know, but that's the impression I get. Like a battery charger ramping the volts higher than it would normally need to, as it strives to push energy into a broken battery that cannot hold a full charge. Feels like the deconditioning theory is akin to saying the battery is fine albeit only part-charged, and simply needs a few recharge cycles to get it back to full health again. Ignoring the possibility the battery might simply be screwed, and is part-charged because it cannot hold more, and all the charging in the world cannot make it better. And yes, proving that people too ill to do any exercise are deconditioned, really doesn't sound like the most insightful of observations does it!
Good metaphor! And yes, I think the answer is going to be less simple than we might like to say. Maybe the mitochondria aren't able to process the oxygen as fast as they ought? Okay -- if so, why? No, no... I'm sure more exercise will work, @Barry ... you just have to BELIEVE. Yes; the issue here is that everyone with ME/CFS isn't even deconditioned. It's just those who are so severely affected that they can't move around. Those of us well enough to be active are trying to keep active in tiny, tiny doses, not lying around on our fainting couches. So.
When my blood gases were analyzed at the hospital some months ago, before and after exertion (up and down a large flight of stairs) my venous oxygen saturation was quite low. I don't recall what it might mean, but my oxygen saturation on my pulse oximeter is always 98-99% (unless laying in the wrong position, or crashed).
Yes. Didn't come across in my post, but previously on PR I've noted that I don't think my wife is deconditioned significantly if at all. In fact I strongly suspect the average couch potato is far more likely to be deconditioned than my wife, who perseveres very determinedly, but very sensibly, within her "performance envelope".
?!?!?! Ditto, I have a finger oxometer (oxymeter?) and it's usually 98%, unless I'm beginning to have trouble breathing. Then it drops a bit (not very significantly). This is a plummet. I don't understand. Have you gotten this double-checked, I'd be disinclined to believe it could be so low!
Well, it was tested twice, 12 minutes apart, and both results were low This was at a very good hospital as well, with up-to-date equipment.
Coming late to this discussion, I'm not sure what's being measured here, but surely venous oxygen would be significantly lower than arterial oxygen, which I assume is what the pulse oximeter is measuring. If I read it correctly, your venous oxygen seems to go up after the exercise?? I'm probably talking rubbish.
Normal is 70-80%. Basically there are up to 4 oxygen molecules per red blood cell, from what I recall, and they should be losing one after blood fully circulates. So it's at 100% in arterial blood, then 75% in venous blood. And if there's a problem, it's most likely to end up very close to 25% or 50% (versus something in between, like 40% or 65%) since there's 1 or 2 molecules out of the possible 4. My oxygen (both saturation and PO2) did go up after exercise, due to breathing more heavily. But the low PO2 values also support the measured O2 saturation not being a fluke or error. Edited to add: Apparently pulse oximeters can only detect arterial blood, due to needing to detect a pulse to get a reading. It sounds like veins and capillaries don't have a pulse due to pressure differences, so anything picked up by a pulse oximeter will be arterial flow. Accordingly, values should stay near 100%.
No, it was at the mitochondrial disease clinic, and from the blood gas analysis the doctor was solely interested in the lactate levels. They really don't give a damn unless the problem is conclusively due to known genetic defects, and he didn't even have any suggestions on what I should do next with all my other funky results from the clinic.
Does this mean your body is extracting far more arterial oxygen per blood circuit than it would normally do for a healthy person, because your body is desperately trying to manufacture more ATP from scratch, given most of it has gone down the drain as it was converted to ATP->ADP->AMP?
Maybe I don't remember what the other explanations might be. Slow circulation or low blood volume might be possible as well.
That's something I can confirm subjectively. My muscles burn very fast, even with the slightest usage (e.g. brushing hair). When I was ok and doing my training, of course I had muscle burning. You want to get into this area regularly in order to improve your capacity. For this a certain amount of regeneration has to be taken into account. But what I experience now is quite different. When I experienced the early burning for the first times I deduced it might be due to too less muscle oxygen. Why I couldn't and can't tell. Today, I still hold the burning (I am "used to it"), but the muscles weaken very fast so that I need to rest very fast. And there is not the slightest improvement, quite the contrary. That's not the case with a healthy person. Depending on how far above the aerobic threshold one is and training status you can go on for 30s to 2h until glycogen in the muscles are emptied. (If glycogen is emptied you really cannot go above the aerobic threshold again, no way, rest doesn't help. You need to refill muscle glycogen by calory intake.) After that you still can perform in the aerobic area for quite a while (although it feels shitty). The body can switch between aerobic and anaerobic metabolism and it's good to train that so that switching happens faster.
