Question Decreasing the Breathing Reflex....Possible?

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That indeed happens, all else being equal the urge will come a bit later when breathing O2. But it will be hard to notice that in real dives, already because as said, in most situations breathing patterns will not be governed by the urge. I know that e.g. I do not notice a difference between air and EAN32 for very similar profiles in my own diving.
Interesting. I'm fairly sure that my own breathing patterns while diving are governed by the urge to breathe. I'm going to go check my computer logs and see if there's any difference in my SAC rate/air consumption on nitrox vs air dives; easy to run a t-test on those numbers.
 
Poor use of oxygen is what causes breathlessness and headaches, a feeling of not getting a sufficient breath.
No, it is CO2 retention which causes these problems.
There is always plenty of oxygen when scuba diving, possibly even too much if using Nitrox at high percentage.
 
No, it is CO2 retention which causes these problems.
There is always plenty of oxygen when scuba diving, possibly even too much if using Nitrox at high percentage.
I mean how the body is able to use oxygen and clear CO2, is it not true that we inhale more than enough oxygen but some transfer oxygen better than others.
The Bohr Effect.
 
I mean how the body is able to use oxygen and clear CO2, is it not true that we inhale more than enough oxygen but some transfer oxygen better than others.
The Bohr Effect.
Although of course there is some relationship, the point is how to get rid of CO2, not to inhale oxygen.
Some breathing patterns (quick and shallow) provide you a lot of oxygen but are inefficient in evacuating CO2, and this results in headache, dumbness and narcosis.
 
Although of course there is some relationship, the point is how to get rid of CO2, not to inhale oxygen.
Some breathing patterns (quick and shallow) provide you a lot of oxygen but are inefficient in evacuating CO2, and this results in headache, dumbness and narcosis.
Thankfully I never get headaches diving, but always take nice long slow breaths. I think of it as keeping my breathing pattern easy and relaxed.
 
I mean how the body is able to use oxygen and clear CO2, is it not true that we inhale more than enough oxygen but some transfer oxygen better than others.
The Bohr Effect.


The Bohr effect describes how binding affinity for O2 to hemoglobin decreases with reduction in pH. This is most beneficial for understanding oxygen unloading in tissue where pCO2 rises and increases the efficiency of oxygen delivery.

What you are talking about is diffusion vs. perfusion limitation. And yes at 1atm both CO2 and O2 are perfusion limited. Meaning the gas exchange across the alveoli occurs more quickly than the blood flows through the length of the capillary associated with the alveoli. if you experience diffusion limitation at 1 atm odds are good you are not diving because if you have a condition that leads to this a physician will not clear you for diving. Given O2 is perfusion limited at a partial pressure of 0.21 atm it is then quite clear that at depth there will be no issue saturating the blood with oxygen. In fact, as we often discuss it is the inverse we concern ourselves with in oxygen management (ie hyperoxia).

However, CO2 is being produced at a constant rate (relatively) and must still be eliminated. But now we’ve changed the dynamics of this substantially and this is seemingly largely related to the densities of the gas. CO2 is elimination is dependent on minute ventilation. That is tidal volume x respiratory rate. At depth with increased gas density the air does not move as freely through the lungs and gas exchange is impaired. The physiology of this does not appear to be fully understood from my reading of the literature. However, suffice it to say we do not eliminate CO2 as efficiently at depth. Further, our basic compensatory mechanism of increased minute ventilation through increased respiratory rate does not appear to work well given the dynamics of gas exchange at depth. The elimination of CO2 as optimized by oxygen displacement at the level of the alveolus is explained by the Haldane effect. But this mechanism seems to be intact at depth.
 
Interesting. I'm fairly sure that my own breathing patterns while diving are governed by the urge to breathe. I'm going to go check my computer logs and see if there's any difference in my SAC rate/air consumption on nitrox vs air dives; easy to run a t-test on those numbers.

Would indeed be interesting to check! "Urge to breathe" is a bit unspecific. It can be a rather psychological urge, that would then not change with fO2. Or it can be driven by CO2 and the need to eliminate that, which is quite similar for air and nitrox. A notable difference in gas consumption (air vs. nitrox) one would only get if the component of the urge that is governed by O2 would become the dominant one. I personally do not really see that happening regularly in scuba diving. But the effect itself is without doubt there, and it surely is interesting to compare notes!
 
There is no way I am aware for oxygen to become the dominant factor in the respiratory drive. There are exclusively chemoreceptors for HCO3 driving this. Their sensitivity can be influenced by O2 but there is no direct measurement of O2 levels anywhere. CO2 is always the drive force. If it were possible for O2 to substantially affect the respiratory drive divers at depth with a pO2 of 1.4 or 1.6 would experience the most extreme version of this possible prior to oxygen toxicity. It is likely that whatever the maximal influence of oxygen on the chemoreceptors for CO2 is has already been exhausted at that point. And there are no reports I am aware of of divers feeling minimal need to breath when at that PO2. While respiratory drive is influenced by psychological factors this is more related to its influence on the sympathomimetic system not consciously driven. The point remains. CO2 is simply the driver of respiration. And affects from O2 are not a significant component. One could say there may be some theoretical influence beyond the level at which humans experience O2 toxicity. But this is a truly moot point given it is impossible to reach in vivo.
 
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