Just wanted to follow up on some potential confusion from today’s altitude conversation.
First, I think Chad and Nate were ‘arguing’ the same point. What threw me off was the switch to hyperoxia - I’ll address that in a bit. But before touching on hyperoxia, I want to do a bit of dive (small dive as I’m typing) on hypoxia and perhaps live high- train low (LHTL).
What’s important first though, is to talk about oxygen transport. We typically use the Fick equation to talk about oxygen consumption VO2 = Q x CaO2-CvO2, where Q = cardiac output (stroke volume x HR) and CaO2 is content of arterial oxygen and CvO2 is content of venous oxygen. The CaO2-CvO2 term is really a measure of oxygen extraction and the Q is a measure of the pumping capacity or blood delivery. We can rearrange this equation a little to be O2 delivery = Q x CaO2 or blood delivery x oxygen content in the blood.
Now our blood is quite good at carrying oxygen when bound to hemoglobin and when we’re at sea-level. The equation looks something like 1.34 x [Hb] x % Saturation + 0.003. At sea-level we are 97% saturated and males typically have about 15 g of Hb/100ml of blood. The 0.003 is related to the amount of dissolved O2 in plasma. So, at sea-level this typically works out to about 20 ml O2/100 ml of blood or 200 ml/L. Q at rest is about 5 L/min and can go up to 40 L/min in elite athletes at maximal exercise. So, we have the capacity to deliver a lot of oxygen (however, compared to thoroughbred racehorses, we’re a joke!).
Not to go too far off base here, but you can see how blood doping or EPO use can improve O2 delivery substantially as you can increase [Hb] an therefore O2 delivery. This is also the premise behind altitude training. But there are some caveats with altitude training. However, when you go to altitude, there is a substantial drop in the % saturation as there is a lower partial pressure of oxygen at high altitude - % is the same, but lower barometric pressure (I think Chad mistakenly said less O2 concentration, I know he meant partial pressure). This means we drop O2 delivery and need an adaptation.
First, the adaptation that occurs to allow improved performance following altitude training is related to the adaptations resulting from acclimatization. There is little evidence to support the improved performance being a result of hypoxic training (I’ll explain this below, but will focus on acclimatization for now).
Typically we see decreases in Q on early exposure to altitude and then a slight improvement over a few weeks, but it typically does not go above sea-level values (this is likely related to the ventricular filling vs. heart rate component, but not really key for here). The two big benefits of acclimatization are the increased ventilation that occurs (your ability to move more air), the increase in red cell mass (Hb), and initially and improved vascular control to increase peripheral blood flow to active tissues (however, this disappears in about a week or so). Now, the ventilation and RBC adaptations lasts for a couple of weeks and are independent of training - you get them if you go to altitude whether you train or not. There is one BIG caveat here - you can’t already have lots of RBC at sea-level prior to ascent. If you do, LHTL likely won’t work for you.
Now in studies that have looked training at altitude (LHTH) haven’t really seen improvements in performance above LHTL. The suggestion is that there is a reduction in absolute load that one can undertake. This reduced absolute load means that there is a reduction in flux of oxygen along the O2 delivery cascade - atmosphere, to lung, to heart, to blood vessels, to muscle, to mitochondria. If we start with lower oxygen (lower PO2) and then increase O2 demand, we likely can’t meet the demand and therefore we actually have a reduction in flux through all of the steps in the O2 delivery cascade and therefore no stimulus for adaptation. In fact, we have a stimulus for detraining!
Some other points that are important is that living high might lead to sleep disturbance, loss of appetite and dehydration, as well as acute mountain sickness so the return to sea-level can help with this and is also the reason that 2500m seems to be the ceiling. I’ve been to 5000m for 4 weeks and it sucked and was at 4000m for 10-days this summer (had my 10-year-old daughter doing VO2max tests! will post a video after this post) and that was hard too. Regardless, the quality of recovery needs to be addressed with LHTL and LHTH camps.
Ok, think I covered the hypoxia part, but happy answer any more questions that come up… like how high (2000-4000 although 2500-2800m seems to be the sweet spot) how long do I have to stay at altitude (probably more than 12 hrs per day and for (30-50 days to achieve 95% probability of an increase in RBC mass for 2500m, less for 3000m, but still weeks), when should I compete after I come down (within 10 days for adaptations to still be optimal, 14 days things start to disappear), type of training (USE TRAINERROAD - they have excellent plans, although no LHTL plan yet maybe that’ll get me a free subscription haha)
Ok, hyperoxia… it’s a miracle, like EPO or blood doping or altitude training. But it’s only useful for acute performance improvements (this was Chad’s comment) and only up to about 40% O2 (sea-level is 21%). Studies using higher (70%), show a reduction in the Q components so O2 delivery doesn’t actually increase. You could live at altitude full time and then breathe 40% during training (I think this was Nate’s comment) - this is essentially LHTL and we’ve done some studies like this at 5000m and it’s improved physiological variables back towards sea-level values. However, when used at sea-level, and over time it doesn’t seem to improve normoxia performance (again, likely due to the slight reductions in Q and limb blood flow).
Ok, that took an hour to write and one 6.8% Category 12 Wild IPA! Happy to chat more about some of this cool physiology… really that means “drink more beer”.