Ben,
Some points:
I neglected the bonding of CO2 to hemoglobin. If I'm not mistaken, only deoxygenated hemoglobin can bind CO2? Correct me if I'm wrong. Anyway, I think the total CO2 binding capacity of the hemoglobin is small compared to the body water.
Second, I'm certain that it is possible to reach acidic blood and alkaline body water. Keep in mind that when I do the 1'30"/one-breath/1'30" style CO2 table, my etCO2 is level around 7.5% for 15 minutes, before suddenly soaring to over 10% in the next five minutes -- why would it take so long? I'm getting contractions from the first few holds -- my O2 is still high, so the contractions are caused by acidic blood (and not low O2) -- yet, although my blood is acidic enough to cause contractions even at the start, it takes 15 minutes of steady state acidic to cause my etCO2 to soar.
I think it is true that the rates of diffusion differ: CO2 in the body water can only be removed by diffusion into the blood and then removal by the lungs. However, CO2 accumulates 'on-site' in the tissues/water itself. However, as long as the blood is pumping, the blood wipes away the CO2 which is produced in the tissue/water. If the blood did not pump, or if the lungs are empty, then the CO2 in the body water would accumulate extremely rapidly. However, inhale apnea causes CO2 accumulation in the body water only very slowly, because the lungs and blood can store significant CO2 (combined), and the constant flow of blood prevents accumulation of CO2 in the tissues, unless the blood itself is acidic.
This is why I think that during inhale apnea, CO2 accumulation in the body water is slow. So, if we alkaline all the fluids by 10-minutes of breathing, then do one apnea to contractions, I strongly doubt that in those 3 minutes the entire body water has been saturated with CO2. This means that the blood must be acidic while the body water is (relatively) alkaline.
Once again, the main idea is that it takes a 20-min+ CO2 table to cause etCO2 to soar.
Here is a question for the geniuses:
- We know that hyperventilating increases the total O2 store by increasing the hemoglobin oxygen saturation of VENOUS blood (i.e. from 60% to 80%) while the arterial O2 saturation remains > 98% (i.e. see Lindholm's thesis)
- The disadvantage is hypocapnia (or so we thought)
So, would it then be possible to make the body water acidic, then do rapid hyperventilation in order to increase the O2 store? If so, then the acidity of the body water would prevent hypocapnia in the later stages of the breath-hold, thus giving you the 'best of both worlds' : good CO2 level to ensure O2 release, and high O2 to start the breath-hold.
This method mimics what I currently use for deep diving; something I call the 'acidic system of diving.' The idea is to use an acid other than carbonic acid (CO2) to supply the acidity to release oxygen from the blood. By eating a diet high in acid forming foods (mainly meat / protein), the body becomes acidic (mostly from uric acid I think). In this acidic state, I can hyperventilate for a long time, pack without dizziness, and thus start with high O2, but not suffer over-alkaline blood, because even with the lack of CO2 for acid, the uric acid takes its place, keeping the blood pH in the useful zone to retain consciousness at the end of the dive. This has worked wonders in constant weight, but it sucks for static (at least for me).
Eric Fattah
BC, Canada
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