Background
I am a 50 something sportive rider. Tried competing in my youth and discovered my genetic gifts lay elsewhere. Been vegetarian most of my life LCHF for the last four years. Went there for reasons unrelated to performance. TR two years.
Issue
I have a pretty thorough annual physical with work. It includes spirometer test. Recently the doc mentioned offhandedly that my lung function was lower than average. Just another genetic gift keeping me off the Champs Elysee. This got me thinking on O2 uptake. Can’t find a lot out there on it. Given fat burning uses far more O2 than dear old glycogen, wondering what the impact of being fat adapted with ventilation inhibitors might be. Nothing on Google. Any references, opinions or wry comments?
Just curious. You mentioned being vegetarian for most of your life and then going LCHF. Does that mean you went to eating meat? I’m new to vegetarian and have not yet heard of people going the opposite direction. Don’t mean to hijack the thread. Just curious.
I could be wrong, but I do believe “lung function” is different than oxygen utilisation function. That’s to say, the size/power of your lungs are not related to how much oxygen actually gets into your blood stream. You’d probably have to do a VO2max gas exchange test to know for sure.
As well, how do you know you are truly fat adapted? That would also require a lab test, I think.
I guess it would bump up your breathing rate and thus your RPE but as @d_diston said you mostly aren’t limited by lung size. Some elite athletes can be limited mostly due to the speed their blood is pumping through the lungs reduces the time oxygen has to associate with haemoglobin. Fat adaptation will increase the intensity at which you can keep predominantly burning fat but at the higher intensities you’re going increasingly anaerobic anyway.
Fair comment. The reality is I can’t be sure but given I track food intake routinely and seldom hit 50 grms. Routinely ride +4hrs unfueled and have had the health outcomes I was gunning for with it (and a few bonus ones) I would not be too afraid to bet on it.
Not really concerned with the performance limitations that may be implied by it but rather the dietary issues it raised. I did experiment with adding carbs back in to fuel hard effort on long rides but that experiment ended badly: GI distress came back. Just wondering what factors might have a bearing on that issue.
I am interested in exploring this. Since I think that position is predicated on the fact that even at full whack your exhalations still have in excess of 16% O2, implying O2 uptake is not limiting. On the other hand the reason we breath harder is driven by the need to dump CO2. That gas exchange does seem to be size limited.
[Edit] I should add that if CO2 clearance is limited then O2 uptake will be too as all you can do is store the excess CO2 in the blood displacing O2. Or is there another mechanism?
If you stop ingesting carbs your body loses all the gut goodies required to process carbs. So basically you are shocking your system with those hard effort carb bombs and distress is the result.
Another reason to do endurance rides on fat and the intensity rides on carbs.
If you are HFLC for health reasons then some sacrifice of performance might just be part of the package.
A spirometry test has nothing to do with your O2 uptake or utilization. It’s just a measure of lung volume and how forcefully you can expel air. The test is done at rest. You should be in a largely fat burning state, and well below your vo2 capabilities so it won’t come into play at all for this functional lung test.
I’m not sure, CO2 is more soluble in blood than O2, so doesn’t need haemoglobin to be transported (although some will move this way). Because it’s transported in the blood itself, it should cross into the lungs more quickly than O2. Secondly, as its only present in the atmosphere in very low quantities there’s a strong concentration gradient driving it towards clearance.
The other thing is CO2 is produced in the Krebs cycle so a different reaction to O2 use. An increase in O2 with fats use won’t necessarily mean an increase in CO2 production. Someone might correct me on that though.
Yeah way back in the day I did a bit of work of sorts on this. Or at least I gained some knowledge of hemoglobin, specifically Carboxyhemoglobin. Not relevant in this case. I do recall though that only 20% or so of CO2 was transported back to the lungs that way the rest as you say in other solutions. I just wonder if the bottle neck is the lung volume or more specifically the surface area what the impact is on O2 uptake. It seems to me that it would be a factor since marginal clearing of the CO2 would be hampered. At least from my perspective gas exchange from saturated liquids is fairly quick. Is the same true of HbCO2?
I’d need to dig out my notes as well. Think CO2 binds at a different site to O2 on haemoglobin but can’t remember if the binding is higher or lower affinity. I’m a bit on the rusty side as well. I think that its pretty much always surface area. More dependent on capillarisation. There’s a pressure gradient within the lungs that favours the upper or lower part of the lungs. It means one area can facilitate exchange more than the other. Can’t remember which though, that might be affected by lung size alright.
Nah! Dairy is pretty much there on its own if you steer clear of “Low fat” products. I’d be completely blown away by a Vegan HFLC. That takes serious work.
A few months ago I was sniffing around as how to ahieve this…I couldn’t really come up with anything sustainable. Would be interesting to know if anyone actually does this long term.
Fun fact: at hyberbaric pressures, oxygen will dissolve directly in blood without needing to bind to hemoglobin. If you could fit a trainer in the chamber, I bet that would be an amazing place to do an ftp test.
