Sorry, seeing this a bit late, but interesting conversation. Hope I can still contribute.
Very general suggested explanation: that’s where most of the metabolic activity is occurring, ie. the greatest disruption to metabolic milieu, and subsequently the greatest signals back to your brain that “something is wrong down there” =
I haven’t seen much investigation into why or when someone might feel leg-limited vs breathing-limited. Would be interested if anyone else has. But I was surprised to see how much variability TR users were reporting in that other thread a while ago.
This adds to the greater point about local vs systemic a-vO2 differences. The microvasculature closest to/within the tissues where O2 is being utilized will obviously have greater O2 extraction and greater a-vO2 diff than tissues further away. If femoral vein a-vO2 diff is ~90%, I would guess that approaches 100% within the microvasculature, before ‘contamination’ from other less metabolically active tissues being drained into the femoral vein. eg. blood volume coming from skin and fat tissue, which is mostly still oxygenated.
I’m with you here. VLamax is a very convenient tool that appears to quantify phenotype well. But I’m skeptical how literally true or at least relevant the VLa measurement is to anything.
It’s up to us though to build on the VLamax model and/or make something that works better in the lab and on the road. Not just tear it down and walk away, IMO.