Endothelial dysfunction and ME/CFS

[Weltverloren]

I referred to normal perfusion in general, on the basis that we do not have any clinical evidence of either general or local hypoxia. General tissue hypoxia would show as cyanosis or breathlessness. That is what you get with a poor output state (cardiac failure). Local ischaemia in muscle may not have been studied experimentally specifically on standing but I was really referring to clinical information. If proximal leg muscles were ischaemic we would expect there to be a claudicating history - the person can do the activity for a certain repeatable length of time and then would get pain and weakness. If ME/CFS was associated with muscle claudication I think that would have been documented long ago.

But the clinical presentation you're describing here sounds exactly like what I (and other patients in the patient groups I'm in) are describing.
And it's not just orthostatic intolerance, because it happens irrespective of posture and the muscle doing the effort.

I can walk, even run down the road for a little bit, but I'll get burning (claudication-type) pain within a minute.
I can do squats, but the same thing happens and if I push it, my muscles get weak to the point of trembling.
Similarly, I can do push-ups just fine, but after a couple, my arm muscles will show those same symptoms.
If I get stranded somewhere and have to walk, ignoring those symptoms, the claudication-type pain lasts for weeks and my baseline deteriorates.
Furthermore, in a ramp test in the lab, the point my legs gave in was not associated with high lactate (so must have had a different cause) - rather, peak lactate occurred 15min post effort, which isn't necessarily an indication for microvascular issues, but fits that puzzle.

So, as a patient (read layman, not a scientist), I'm kind of confused as to why you'd say the clinical presentation doesn't fit microvascular dysfunction?