Informatics Inference of Exercise-Induced Modulation of Brain Pathways Based on Cerebrospinal Fluid Micro-RNAs in ME/CFS, 2020, Narayan et al

I still don't know what you are referring to. It is impossible to know if a cardiopulmonary effort will be maximal (in terms of VO2) a-priori and it is also difficult to know in hindsight too, without repeated replication of the performance. So it makes little sense to select patients on this basis.

If the aim is to induce PEM, then I'd argue it doesn't matter as PEM will result even if it is a strong, but submaximal effort.

One key point I'd like to make, due to the mention of Cara Tomas who focuses on biochemistry, rather than physiology, is that VO2 max is limited by the cardiopulmonary system, not the mitochondria in cells. VO2Max still occurs far below the threshold of all motor units being recruited, hence there is always excess oxidative capacity, unless someone suffers from a severe genetic mitochondrial disease.

The limiting factor is either in the lungs, or the heart. For most people the limitation is the amount of oxygen that the heart can pump to the muscles. But the lungs can be a the limiting factor for people with COPD or prior lung damage, or athletes with very high VO2Max who have reached the maximum that they can train/condition their heart to pump out. Obviously the latter (lung disease or highly trained athletes) should not be participants in such studies.

 

Just the ones on TRPM3 and TRPM2 already discussed here on the forum.