That Triathlon Show | EP#169 - FTP, VO2max and VLaMax

Let us all take a deep breath (pun intended :hugs:), it is clearly not a very scientific video. As @empiricalcycling wrote, from a black box perspective what is not wrong, O2 goes in, and a significant amount of O2 comes out. If there was nothing to improve in that box, we’d have no peripheral VO2max adaptations. What is unfortunate, he concentrates on them, as if there was no or only little room for central adaptations.

Let us make each other faster!

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Except that a significant amount of O2 doesn’t come out of the legs at VO2max, even in an untrained person. This is a fundamental misunderstanding on Weber’s part. It is the sort of error in thinking that leads to people, e.g., wasting time doing one-legged pedaling drills to try to get faster.

What I don’t understand is, If Weber has got it so wrong how is it that Jumbo Visma, who utilise INSCYD and, I believe, use Weber as a consultant, seem to be getting it so right?

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It’s Bora I think, not Jumbo Visma…

It was Bora and maybe still is, if not it may account in some way for Sagans lack of form but it’s now Jumbo Visma

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I don’t know. Maybe talent? Drugs? Luck? They don’t actually pay any attention to Weber? Who the heck knows.

What can be said is that he is dead-wrong about something that anybody who has ever taken an undergrad ex fizz class should understand. That makes me question every assertion he has ever made.

Obviously talent - you can’t make a silk purse out of a sow’s ear but Drugs and/or Luck?

Just pointing out that there are multiple alternative explanations for what you offered as “evidence”.

Maybe because the method works, but his idea of why it works is wrong.


I won’t be splitting hairs on what the term significant means for you and what not. I appreciate the post, though :hugs:

No need to split hairs, the data are clear: at VO2max, roughly 90% of the oxygen in arterial blood has been extracted by the exercising muscles, i.e., only about 10% remains.

Here is an example from 11 healthy, moderately-fit young men studied in hypoxia, normoxia, and hyperoxia. As highlighted, oxygen extraction is around 90% under all three conditions.

Please feel free to transfer insignificant 10% of your salary to me :money_mouth_face:

All $1200 is yours. Where should I send it?

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Help me reconcile that with what I posted above:


@empiricalcycling already alluded to this. The arteriovenous O2 difference is greater when measured across the exercising limbs compared to that measured across the whole body. That’s because even during maximal exercise, some blood is being sent to tissues (e.g., kidneys, skin) that don’t extract nearly as much O2 as the exercising muscles themselves.

IOW, venous O2 content is higher when measured in the pulmonary artery versus, e.g., the femoral vein because the former is “contaminated” with relatively O2-rich blood.

ETA: Here is the figure from McArdle, Katch, and Katch corresponding to one you found online.


:joy: I love this forum!

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:leg: = :poultry_leg:

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.


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This isn’t what’s happening here. I’d love to admit that it were but if we take this mistake as true, then it has training implications that will not be borne out as effective. Oh right, and are not borne out by even the most basic understanding of the literature.