CO2 compartment hypothesis

[efattah]

Suddenly, it dawned upon me. I'd like to introduce a concept for breath-holding which really isn't new, but should explain a lot of weird mysteries many of us have noticed while doing apnea.

Let's start with some physiology review:
- O2 has almost no solubility in water
- CO2 is very soluble in water
Because of that,
- Most of your oxygen must be stored in hemoglobin and myoglobin, and lungs
- CO2 can be dissolved in the blood plasma (i.e. blood water), as well as the rest of the water in the body

The 'bohr' effect states that the hemoglobin will only release oxygen in the presence of adequate acidity.
When CO2 dissolves in water, it creates carbonic acid, and thus acidity.
[this is all old news, just bear with me]

Thus, when you overbreathe, your CO2 level goes down, and your blood becomes very alkaline, preventing hemoglobin from releasing O2.
Further, low CO2 causes blood vessels to vasoconstrict. Vasoconstriction prevents blood flow, and thus prevents oxygen flow to vasoconstricted areas. The result is tingling fingers, fading vision, and finally hypocapnic blackout.

However, all of those effects are caused primarily by the acidity (or alkalinity) of the blood itself. By rapidly hyperventilating, you will rapidly change the acid-base balance of your blood. However, in the short term, the remaining 50kg of water in your body will not be affected. This is a huge point.

Let's divide your body water into two compartments:
- Water in the blood (i.e. blood plasma) = about 5L
- Water in the rest of the body (body water) = about 50L

As you hyperventilate, your blood water rapidly becomes alkaline, and can cause a hypocapnic blackout. This could occur even if your BODY WATER were still very acidic, and laced with CO2.

For example, suppose you finished a CO2 table and were laced with CO2. Now, you hyperventilate until your vision fades. You conclude that you have blown off all the CO2 from the CO2 table -- incorrect. Your blood is now alkaline, but your body water is still very acidic, because it takes a long time for acidity to 'diffuse' from your body water into your blood, and vice-versa.

The same effect can be seen by watching your exhaled CO2% during a CO2 table. If you do a pattern of 1'30" hold, one breath, 1'30" hold, one breath, etc., and you measure your expired CO2% on each exhale, it will quickly rise to around 7.5%, and remain there for many cycles. You assume that you are in a steady state, blowing off the same amount of CO2 that you are accumulating. In fact, the CO2 is diffusing into the body water. If you keep it up for at least 10 minutes, then, still doing the same pattern, suddenly your expired CO2 will soar to 8.0%, 8.5%, 9.0%, and 9.5% and 10% -- because now your body water is saturated with CO2 and there is no where else for the CO2 to go.

For a long time I did the following static pattern [note; hyperventilation in this context means fire breathing]
- two breaths, then inhale+pack, 3'30" static
- short recovery
- two breaths, then inhale+pack, 5'00" static
- 2'00" of hyperventilating
- Full exhale, 2'00" static
- 2'00" of hyperventilating
- Full exhale, 2'00" static
- 2'00" hyperventilating
- Full pack, 6'00" static
- 2'00" hyperventilating
- Full pack, max static, 6'30"+

The contractions would come the latest on the last breath-hold. I would feel heavily depleted from the exhale statics, and too many statics in general. However, for a reason which I didn't understand, I needed this long pattern in order to delay the contractions long enough to hit a huge time. I could only hyperventilate for 2 minutes -- no more -- otherwise I would black out during packing (not to mention feel awful).

I assumed that 2 minutes of hyperventilation would 'blow off' all my CO2 (since I would get all light-headed). If that were so, then it seems that a 2-minute hyperventilation on only the 2nd or 3rd breath-hold should do it, and delay the contractions as much as I needed -- but it wouldn't work. Why did I need so many cycles?

In fact, if you look at the above pattern, there is a total of 8 minutes of hyperventilation. The exhale statics are so short they don't result in CO2 accumulation. Even the 6'00" inhale static did not accumulate much CO2, as evidenced by my CO2 monitor upon exhaling.

What was really happening was that I needed 8 minutes of hyperventilation to 'blow off' the CO2 stored in my body water. Because of slow diffusion, it is impossible to blow off the body water CO2 in only 2 minutes of hyperventilation, even though those same 2 minutes caused me to nearly black out from hypocapnia.

So, this would explain why some people have great success by doing 8-minute breathe-ups, doing relatively slow, deep breathing. The breathing rate is not enough to over-alkalinize the blood (i.e. no hypocapnia blackout), but, by maintaining the blood generally alkaline, it allows a gradual blow off of the CO2 stored in the giant 50L body water supply.

So, if my hypothesis is correct, then a slow, 8 or 10 minute breathe-up, should delay the contractions far more than 2 or 3 minutes of hyperventilation to the point of dizziness.

So, to summarize:
________________________
"CO2 Compartment Hypothesis":
- Rapid hyperventilation changes the blood acidity rapidly, and does not allow the body water to equalize with the blood. Rapid hyperventilation will cause light-headedness and hypocapnia symptoms long before the body water is alkaline. In order to alkalinize the body water, the blood must be kept alkaline for a long time (10 minutes+). In order to acidify the body water, the blood must be kept acidic for a long time (10min+). Using this methodology, the athlete can choose to begin his apnea in any one of four configurations:
1. Acidic blood, alkaline body water
2. Acidic blood, acidic body water
3. Alkaline blood, alkaline body water
4. Alkaline blood, acidic body water

Each state would be reached by approximately the following pattern:

1. Acidic blood/alkaline body water = 10 minutes of slow deep breathing, followed by a 5-minute CO2 table
2. Acidic blood/acidic body water = 20-minute CO2 table
3. Alkaline blood, alkaline body water = 10 minutes of slow deep breathing
4. Alkaline blood, acidic body water = 20-minute CO2 table followed by 2 minutes of rapid hyperventilation
____________________________

Application to the Real World

Given that blacking out from packing, and all hypocapnic blackouts are caused by alkaline blood, then in theory the diver could reach a very low state of total CO2 without suffering from hypocapnic problems by choosing state #1 = acidic blood, alkaline body water. In fact, the blood would not need to be acidic, just neutral. So, 10 minutes of slow deep breathing, followed by a 2 minute breath-hold, should allow the diver to inhale and pack to the max without hypocapnic symptoms. At the same time, the alkalinity of the body water would be so high that the diver would have a huge CO2 buffering capacity.

Eric Fattah
BC, Canada

[Pezman]

That's sounds like a really promising insight. Since the urge to breathe is triggered primarily by changes in blood pH etc (as opposed to absolute levels), your idea seems like it could actually cause the urge to breathe to decline for a long time into the hold because receptors would be subject to a constant or slowly falling pH level.

It also helps explain why sudden hypering seems to make breath-holds initially very comfortable and then you suddenly hit a wall in a relatively short time (at least I do).

In fact, it explains a lot ... I'm going to try putting this idea into practice (sans 6:30 statics ).

[Memo]

very nice theory and it sounds logical. I really appriciate reading it.

[ADR]

EF,

Great thinking and I'm sure you've just discovered something significant here, thanks for sharing it with us. The challenge now will be how to test and verify your thinking. I have a couple of related questions.

1. Is partial pressure differences the primary mechanisim for moving CO2 from body water->blood->lungs. With the PH of the blood simply providing a favourable/unfavourable enviroment for this transfer?

2. Does the level of O2 in the blood bonded or dissolved(I'll come back to this point) have any impact on the bodies ability to move the CO2 from body water->blood->lungs

3. In moving to a slow 10min breathe up what type of breathing pattern do you think would be optimal

FROM MY POST ABOVE - O2 in the blood bonded or dissolved
From my tech diving days we did some long deco on 50% O2 at 18m to open the "oxygen window" which allowed a secondary pathway for off gassing nitrogen. This mechanism assumed dissolved blood oxygen as well as bonded oxygen. Is a similar situation possibly relevant here. I recognise that we aren't breathing the benefits of 50% O2 but neither are we facing the nitrogen saturation levels of tech divers. .....just some thoughts

[Jeff06]

very interesting Eric!
And I am pretty sure you can extend your thoughts to dynamic apnea sessions....

Regards,
Jeff

[Ben Gowland]

Excellent thinking as always Eric.

A few points:

1) CO2 is not just dissolved in blood but is also bonded to the Haemoglobin. It bonds to the outside of each of the four protein molecules in the Haemoglobin. This means that the blood store of CO2 is greater than just the plasm and cytoplasm content. I don't think this impacts your thinking much, but it means the difference between blood and body CO2 carrying capacity is not quite as big as first thought.

2) I disagree that you should be able to get the acid blood/alkaline body scenario. I agree with the other 3. With the 10 mins of deep breathing, you would of course get rid of lots of CO2, but in your mini-CO2 table, the CO2 would build up in the 'bodywater' just as much as it would in the blood. Then you would breathe off some blood CO2, gain a bit of O2 and do your breathold. This means you would end up with slightly alkaline blood and 'bodywater'.

Anyway - great stuff as always. I am sure you are on to something here. In some ways it is looking full circle - i.e. we are back to the 'breathe deeply' prep that was the done thing 10 years ago. I will defintely be thinking of how to apply this thought to my diving. I may even do a dreaded static or two......

Ben

[ruppst]

Sounds very scientific. But in practicality I can relate. When spearfishing I am in the water for sometimes 2 hours. As soon as I enter the water my breathing pattern changes from normal. I relax and conciously take slow deep breaths then 3 or 4 hyperventilations before the dive. I hold this breathing pattern thru-out the dive session. This feels natural and it seems as the dive progresses my bottom time keeps improving until of course fatigue sets in.
Ray

[SThompson]

This is the kind of post that I love to see on the board. Reasoning behind a proposed theory, and the possible practical application of said theory. Bravo!

One thing I would note: it seems to me that the time to resaturate the body tissues back to their normal "resting state" CO2 levels would be much shorter than the initial breathing required to lower it. The circulation of the blood through the body combined with the atmospheric partial pressures of surrounding CO2 provides a really good diffusion rate to force the CO2 back into the tissues. The 5 minute CO2 tables may be too much. You may need to cut back to 3 minutes to get the optimal. This is only a thought, but I am wary to think that the time to release the CO2 is at a 1:1 ratio with the time to reabsorb it into body tissues.

I think of it this way. The removing of CO2 from the tissues through deep breathing techniques is like doing work to move a rock uphill. You are adding enough energy to the system to not only move the rock, but to overcome gravity. However, moving the rock to the bottom of the hill much less energy/time is required as gravity is adding to the movement.

Ok that is a really bad analogy, but hopefully you get the gist of it.

Maybe a better analogy would be in nitrogen saturation at depth on scuba. It doesn't take long to saturate the tissues, but it takes a looooonnnggggg time even at the surface to release it again.

My 2 cents,

[Jersey Jim]

What a great article! I can hardly wait to put it to the test in the spring. Who would've considered, what seemingly was "ruining a good breathup" with a 2 minute static before a dive. Especially after investing 10 minutes preparation. Curiousity has me wondering if different individuals transfer acidity/alkalinity from one "compartment" to the other, at varying rates. I would also think a slower transfer would be desirable. That would lend itself to fewer dives of greater duration. At the end of the day it would be interesting to see if an equal bottom time had accumulated on the computer, opposed to prior to applying this technique.

Again, a great article. One for the personal archives.

Jim U.

[efattah]

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

[Jersey Jim]

Eric:

Interesting you mentioned the diet to replace the carbonic acid with another form for your "acid system of diving". On the 25 minute ride home from work last night I began back on the 1-breath static pracice that I mentioned in the spring training thread. I usually forget about all statics for the 3 months between Nov. & January. What was surprising, was that I didn't get around to eating my afternoon pink grapefruit until shortly before leaving work. I was worried it would negatively affect the static. The pattern of 1:30, 1-breath, 1:30, etc., was noticably easier than last year. I feel I can progress this year to 1:35-1:40. I wonder if the ascorbic acid from the grapefruit had an impact in the manner you mentioned? As I always peel away the secondary skin & pectin, there was very little "bulk" that would require blood diversion for digestion. Although I did, and always do take vitamin E with my grapefruit, in the form of almonds. This also probably resulted in very little fiber bulk to divert blood. I found this to be surprising because my best static practices occur on an empty stomach, and this one was pretty comfortable.

Just .02 more cents for the puzzle. Maybe someday some one will piece it all together. Sorry I don't have an answer to your question, but enjoyed considering the possibilities.

Jim U.

[fpernett]

This Eric theory make a lot of sense to me.
I decide to listen my brother, on how to make the beath-up for a max static, this is the pattern:
6 min breath-up
Doing some packs every minute or 30 secs (for me 6-10)
Stop packing for the last 2 min of breath-up
Maximal performance (without packing) no special numbers, just until you can't hold it anymore.
8 min breathe-up (without packing)
Final attempt after full packing
With this method I could get my PB in the first attempt and improve it in the final.
I think this is related not only with pH but also with O2 stores.
In the CO2 movement we have to take into account that after a extreme breath-hold the venous CO2 is very low, the build-up during the apnea remain local (cell), after some minutes it start to be released to the circulation. If we remember and old study in AMA divers, the etCO2 was very low inmediatly after the dive.
I think we are still far to found "the key" but I love to see people like Eric, that is always looking for answers.

[Ben Gowland]

CO2 binds to haemoglobin irrespective of O2 as the sites are remote from each other, however, I do seem to remember that this is one of the mechanisms by which the bhor shift occurs. Thus the bound CO2 affects the binding site of the O2 and reduces the bond strength.

Frank's post stirred up some thoughts in my head about the time it takes to get CO2 from the body to the lungs. If memory serves (which it may not ) then it takes 5-10 minutes for a red blood cell to make a return trip from the lungs to the legs and back when at rest. This figure is more like 1 minute to the brain and back. This means that any build up of CO2 in the body would still take 2.5-5 mins to get from the legs to the lungs and once the lungs are resisting the offload of CO2 from the blood, the CO2 in the arterial blood will increase and trigger the chemoreceptors in the aorta, carotid sinuses and the medulla. I think that some simple modelling of blood flow and chemistry would go nicely here - although I don't have the time at the moment. I will certainly give it a go soon.

The thing that has been bugging me for some time about all our theories of blood acidity and O2 saturation etc is that we seem to be relying on qualitative concepts i.e. acidic blood offloads O2 better (and is worse at picking it up, don't forget). The problem with that is that it isn't refernced to the actual figures that the effect curve gives and relating these to the figures that is seen in the blood during a breathold. I know Eric and others have done some great stuff with a lot of instruments (oximeters etc) and gained some proper data. I think we could use that data more effectively if we feed it into some model.

I think this idea of Eric's is great, but I'm still not convinced that we are applying the concept correctly to human physiology. A spot of modelling might go nicely here. I don't have time to do it at present, but may well do so in a week or two. I think we could have much to gain.

Eric - I'll email you to discuss models etc.

[bevan dewar]

hi. the 4 configurations eric describes seem to make sense, but i dont know what take from it. it will help with formulating hypothises and designing experiments which could be carried out in water, but there in lies the problem for me. i wouldnt want to change my breathup routine for reasons purely academic, so i would want some empiracle evidence that one of these configurations works better for me than another. but as i see it the only way to decide this would be to try all four breathups decribed before attempting dives to progressively deeper depths, until i had reached a depth where three of the breathups had resulted in a samba. only then would i have a winner.(c.w i'm talking about). difficult to do in practice because you cant have 3 sambas in a row and expect the fourth dive to be a true reflection of anything. and if you do one of these configuration dives per day you have the problem of unknown variables entering the experiment from one day to the next. also, i think my instincts of self preservation would object to two minutes of hyperventilation before a very deep dive. do these experiments need to be done? and like this? what do you all think? short of sifting through 5000 posts of anecdotal evidance i dont see any other way. i'm thinking as i write, so i hope this makes some sence. cheers
bevan

[Pezman]

Wouldn't gentle movement while breathing up assist in the rate at which CO2 is transported out of peripheral parts of the body (legs etc.) by increasing blood flow, both on a macro scale and a micro scale. I realize that it would also increase the rate of CO2 production, but I wonder what the net effect would be ...

Also, I've wondered from time to time about the effect of Lactic acid on the urge to breathe. Does it stimulate demand just as CO2 would, does it compete for the receptors, but not stimulate the demand to breathe (i.e. act as an agonist) or does it have no effect?