@Progecitor
I find it difficult to follow your posts. Sorry about that!
Your latest post here consists of lots of quotes of scientific text using specialised medical terms that I think very few people would understand unless they have a very specialised medical background. Perhaps you yourself have a specialised medical background?
Your post seems to have a theme of the condition hypoxia. That's one term that I could guess the meaning of 
I have a feeling that you might be making an interesting point but it's hidden amongst all the medical jargon. Are you able to summarise how you think pois might be connected with hypoxia in one short sentence of let's say about 20 words, readable to those of us on the forum who do not have a science/medical background?
If I could tell you in one sentence I would have done so, but you have to see the whole process to understand how it all comes together. I am not exactly sure how much hypoxia is involved, but ROS is a certain culprit and there is clearly a glycolytic shift in our metabolism partly due to mitochondrial dysfunction. Mitochondrial dysfunction itself may come about due to a variety of reasons (e.g. sepsis, senescence, autoimmunity, etc). If we consider the treatments that we, ME/CFS and long covid patients have used with some degree of success, then it is easy to see that HIF-1a regulation is majorly involved in disease control. It is especially interesting to see that post-exertional malaise (PEM) in long covid patients last for about a week, similarly to a POIS episode, when there is a back shift towards oxidative phosphorylation. However the tricarboxylic acid (TCA) cycle remains impaired with somewhat elevated glycolytic metabolites even at baseline. This is quite relevant from my point of view as I have POIS/CFS and this exactly could explain the difference between my acute (dominated by POIS) and chronic phases (dominated by CFS).