Contractions in cold water.

[MarcinB]

If it's an ad hoc hypothesis overall, or if they know part of it; that co2 build-up faster in alveoli, and if so if they know it has an effect on the arterial CO2 tension.

In this study maximal breath hold duration on full lungs was 150s and it decreased to 90s when lungs were filled to 60% of the vital capacity. However, even though apnea duration was much shorter at 60% VC, the amount of CO2 in the end tidal air (which is considered to have the same composition as the alveolar air) was the same as after breath hold on full lungs (actually it was even higher but the difference was not statistically significant). pCO2 in the alveolar air and in the arterial blood is virtually the same (please don't ask me if it's only my assumption, it's basic physiology). Therefore, the conclusion is that CO2 level in the arterial blood rises much more quickly when the volume of air in the lungs during apnea is low.

the reason it dosen't makes sense is, that it is not explained why faster build-up of CO2 in the alveoli at the small lung volume, will lead to a more rapidly rising arterial CO2 tension

This is because normally CO2 diffusion in lungs is complete and partial pressure of CO2 in the alveolar air and in the blood flowing through the alveolar capillaries equilibrates. So if pCO2 in the alveoli increases it must increase also in the arterial blood.

"So while the full lungs contain around half of the O2, they can only buffer a tiny fraction of the total CO2. It means that when you decrease the lung/blood ratio by exhaling, the buffering capacity does not change much O2 storage and CO2 storage."/Trux

This is true if you consider total body CO2 content. The amount of CO2 in lungs is very small compared to the amount in blood. However, blood also contains only a small fraction of total body CO2 content, much more CO2 is dissolved in tissues. Nevertheless, although lungs do not contribute much to total body CO2 content, the level of CO2 in lungs is of the greatest importance. This is because it determines the level of CO2 in the arterial blood. And this is what is really important in terms of initiation of contractions and diving reflex. This is because both central and peripheral chemoreceptors "sense" CO2 level in the arterial blood. CO2 is the most important factor responsible for the urge to breath, this is because chemoreceptors are much more sensitive to a rise in CO2 level than drop in O2 (it has to fall below ~60 mmHg).
I'm not sure what was the context of the quoted statements by Trux and Eric Fattah. Maybe they were discussing FRC diving. I'm talking about static breath hold. I can't find any reason why arterial CO2 level during static breath hold on empty lungs would rise at a lower rate than on full lungs.

Another thing: Do we really know where the body measure co2-levels in relation to DR?

Yes we do. CO2 level is detected by arterial chemoreceptors (found in the carotid arteries and aorta) and by central chemoreceptors (in the brain stem). Both are important for initiation of the diving reflex. There is also some data indicating that diaphragm may be able to detect changes in blood CO2 level as well. However, it is not well proven.

 

[baiyoke]

I had a feeling you would come back strong I'll read it in depth later today or tomorrow...

 

[baiyoke]

Ok, now I've read it, and it doesn't change much for me I must say...

But first: I forgot a link from the thread where Efattah and Trux answered my questions... It is a bit confusing and sometimes wrong in the beginning though https://forums.deeperblue.com/threads/whats-going-on-exhale-frc-bo-co2-safety.96075/

I'm not sure what was the context of the quoted statements by Trux and Eric Fattah. Maybe they were discussing FRC diving. I'm talking about static breath hold. I can't find any reason why arterial CO2 level during static breath hold on empty lungs would rise at a lower rate than on full lungs.

Efattah is specifically talking about STATIC exhale breathhold (it's quoted) and Trux is talking about exhale in general... The reasons for lower co2 is explained in both the quotes...

In this study maximal breath hold duration on full lungs was 150s and it decreased to 90s when lungs were filled to 60% of the vital capacity. However, even though apnea duration was much shorter at 60% VC, the amount of CO2 in the end tidal air (which is considered to have the same composition as the alveolar air) was the same as after breath hold on full lungs (actually it was even higher but the difference was not statistically significant). pCO2 in the alveolar air and in the arterial blood is virtually the same (please don't ask me if it's only my assumption, it's basic physiology). Therefore, the conclusion is that CO2 level in the arterial blood rises much more quickly when the volume of air in the lungs during apnea is low.

This still does not make sense. If the lungs as a storage is quickly filled up because it is only a very, very small part of the co2 buffer, the arterial blood co2 will app. be the same as just before the blood reached the lungs. So the lungs are not doing anything here... How will you explain the rise in blood co2 from the size of lungs that don't do much??? Where would it come from? If people lay still, and metabolism has its way, how would the extra co2 be made? Is that adressed in the study, it's an important part, if there's a claim of higher exhale co2 level...

It is very difficult to judge a study I don't have access to, but on the other hand it's not going to hold me back either: That 17 year old study seems to be made with non-freedivers (from the short breathhold times). I take it that when you write "maximal breat hold duration" it's an average if it's to make sense at all. Since I can't see where the co2 should come from, and since the lungs don't seem to play much if any part in that, I have to be creative and make assumptions too: Could it be that the relative rise in co2 is due to people tensing up significantly form the uncomfortable feeling of having less than full air? There are many possibilities of this being wrong/distorted...

This is because normally CO2 diffusion in lungs is complete and partial pressure of CO2 in the alveolar air and in the blood flowing through the alveolar capillaries equilibrates. So if pCO2 in the alveoli increases it must increase also in the arterial blood.

Yes, but this is turning things upside-down. co2 in lungs is a reflection of co2 in the body. Not the other way around. And since lungs don't create co2, the co2 in arterial blood is a result of the general level of co2 in the body. High alveolar level don't CREATE anything. So the level there is not important in that respect - that is a misinterpretation of a too close focus.

Nevertheless, although lungs do not contribute much to total body CO2 content, the level of CO2 in lungs is of the greatest importance. This is because it determines the level of CO2 in the arterial blood. And this is what is really important in terms of initiation of contractions and diving reflex. This is because both central and peripheral chemoreceptors "sense" CO2 level in the arterial blood.

Like i said above you misinterpret the "lung -> arterial blood" proces and turn things upside-down. Thereby painting a picture where lung-levels is causing high arterial levels. No, during breathold high bloodlevels of co2 in general is what is causing high arterial co2...

Yes we do. CO2 level is detected by arterial chemoreceptors (found in the carotid arteries and aorta) and by central chemoreceptors (in the brain stem). Both are important for initiation of the diving reflex. There is also some data indicating that diaphragm may be able to detect changes in blood CO2 level as well. However, it is not well proven

Yes we know about some receptors, but do we really know how the body/mind use that information, if it's the only receptors, and how that information might be linked and/or conditioned by lots of other factors? I don't think so.
And what about the fact that so called warm-up, or repeated breathholds considerably delays contractions, how is that explained by a co2-only theory.
Things just don't add up to that the way I see it.

 

[MarcinB]

Efattah is specifically talking about STATIC exhale breathhold (it's quoted) and Trux is talking about exhale in general... The reasons for lower co2 is explained in both the quotes...

I've read this thread and I think I understand what they mean. However, in my opinion during the easy going phase of static apnea on low lung volume blood pCO2 will increase at a higher rate compared to full lungs.

Yes, but this is turning things upside-down. co2 in lungs is a reflection of co2 in the body. Not the other way around. And since lungs don't create co2, the co2 in arterial blood is a result of the general level of co2 in the body. High alveolar level don't CREATE anything.

I agree that what I wrote previously on gas exchange in lungs during apnea was oversimplification and a mental shortcut. Let me put it another way. Although most of the CO2 produced during apnea is stored in blood/tissues not lungs, they still buffer some CO2 and this effect is smaller when the volume of air in the lungs is low. It seems that on full lungs this buffering effect is not that small after all. In all the studies I saw pCO2 in the alveolar air increased during apnea, sometimes by as much as 30 mm Hg. I’ve browsed the literature I have at hand and on the average the volume of CO2 in lungs increases during maximal apnea by ~200ml (however this value varies from ~100 to ~300ml in different studies). This is roughly the volume of CO2 produced by the body during 80s (under relaxed conditions and assuming standard RQ of 0.8) which corresponds very well to a decrease in the duration of the easygoing phase I experience during static on empty lungs compared to full ones.

At the beginning of apnea pCO2 in the alveolar air is lower than in the venous blood so CO2 diffusion occurs normally. According to one study CO2 diffusion into the alveoli takes place for the first ~30s (inhale of 85% of VC). After that time alveolar pCO2 gets very close to pCO2 in the venous blood and CO2 diffusion becomes negligible. In another study (inhale of 80% of VC) the vast majority of CO2 diffused before the end of the easy going phase (280ml) and diffusion during the struggle phase was very small (~20ml). So some CO2 is definitely able to diffuse into the lungs during the first phase of apnea which should reduce the rate of increase in the arterial pCO2 compared to situation when lungs do nothing at all. Simply because some CO2 that would otherwise remain in blood diffuses to lungs. The greater the volume of air in lungs the greater their buffering effect. Moreover, pCO2 at the beginning of apnea on full lungs will be much lower compared to apnea on low lung volume. This is because large volume of inhaled air dilutes CO2 in the alveoli. This also contributes to the greater buffering effect of lungs when they are full with air. However, when the easygoing phase is over things likely look different.

During an easygoing phase of 2min. (dry static on full lungs) the body would produce ~400ml of CO2. DR is not activated yet, blood is still more than 90% saturated with O2 so cellular respiration should be close to normal. If only 100ml of CO2 diffused to lungs during this time the volume of CO2 added to blood would be 25% lower compared to the situation where lungs did nothing at all.

It is very difficult to judge a study I don't have access to

I can send you a copy if you want.

Could it be that the relative rise in co2 is due to people tensing up significantly from the uncomfortable feeling of having less than full air?

It think it would rather be the opposite. A person that is not used to breath hold on full lungs usually feels much more comfortable on lower lung volume. Inhale of 60% of VC that was performed in this study is still much greater than during quiet breathing.

Yes we know about some receptors, but do we really know how the body/mind use that information, if it's the only receptors, and how that information might be linked and/or conditioned by lots of other factors? I don't think so.

Peripheral and central chemoreceptors were discovered more than 50 years ago. As far as I know since that time the existence of other receptors detecting blood CO2/O2 level that would activate reflexes regulating the function of respiratory and/or circulatory system has not been proved. There is some information that diaphragm may also sense blood CO2 and/or O2 but there is some controversy on this matter in the literature. Thousands of papers investigating chemoreceptor properties and reflexes initiated by them were published so far. So they are quite well studied, but of course under normal conditions not breath hold. Nevertheless large part of this information applies also to breath hold. Of course there is still much to discover, especially in terms of DR but it is not so mysterious and obscure as you suggest.

And what about the fact that so called warm-up, or repeated breathholds considerably delays contractions, how is that explained by a co2-only theory.

It was found that the easygoing phase (but not struggle phase) duration is not increased by warmup breath holds in people lacking spleen. So this organ seems to play the key role in this phenomenon. When the DR kicks in, spleen contracts and ejects large number of erythrocytes to the circulation. Repetitive apneas induce cumulative effect that persists for a few minutes after the breath hold. Due to this effect blood Hb concentration and hematocrit may increase by up to 6% (in subjects lacking spleen these values remain stable). So prolongation of the easygoing phase after warmup seems to be related to elevated erythrocyte number. In my opinion this effect may be (at least in part) related to CO2. Some CO2 found in blood (5-22% different values are given in different sources) is bound to hemoglobin. My hypothesis is that elevated Hb level increases the buffering capacity of blood for CO2. But this is only a speculation.

I don’t claim that CO2 is the only factor that counts in freediving physiology but in my opinion it is important.

 

[baiyoke]

Not sure what to reply to the above, except that it is of course interesting with the different papers and every small piece to the bigger puzzle. You got some interesting pieces, but for me right now things don't yet add up overall.

I respect you for what you know, and for your orientation towards scientific reasearch and that you want to hook your view on frediving processes up on that knowledge. But the way I see it, we also have to be hesitant making conclussions on a too hastely pace, and keep an open mind towards the blind spots. It seems your insight into physiological processes and papers ankers your focos there. For me the possibility and likelyhood of a very complex proces (DR) seems to dominate, one that involves processes that is not easy to describe i simple ways, and one where some physiological aspect are dependent on others and the mental aspect also.

One thing that is still puzzling me on a more practical level:
-It must be really easy to test the hypothesis that cold water facial immersion can change the time of contraction onset (head in an icebucket). This must have been done many times I would assume (I'll do that also when I get the time just out of interest)
- It must also be fairly easy (in a doctors physiological research) to measure blood co2 levels on a full versus empty lung, and this must also have been done many times I would assume.

I'd like to see some trustworthy data adressing these to simple aspects. But not sure if it exists. More than often - like in this thread - the papers adresses some slightly different aspects only related to things of interest.

The study from 1998 is puzzling I agree on that. But I'm not sure how to interpret that. Not until co2 production on emptylung is specifically adressed in a research setup.

- Also the differnce between contraction onset time before and after warmup for me is probably around the +70% increased time (or 170% of the no-warmup time). That is a rather huge difference despite the causes.
- The difference between contraction onset time on empty lung and full lung hold is probably +150% (or 250% of the empty-time). Also a rather huge difference.

However I'll aknowledge (true to my perspective) that the difference can be explained by processes that don't nescesarrily show the same ratio on a simle basis. And that co2 of course plays a role.

One thing that also still have me puzzled, is the short addition from @trux that "Strong DR is not depending on the CO2. According to studies, CO2 does not seem to be a major DR contributor...."

 

[MarcinB]

Not sure what to reply to the above

At least you didn't say it doesn't make sense at all

One thing that also still have me puzzled, is the short addition from @trux that "Strong DR is not depending on the CO2. According to studies, CO2 does not seem to be a major DR contributor...."

Why then hyperventilation delays the onset of the DR considerably?

 

[growingupninja]

The cold water facial immersion test is extremely easy to replicate but in general population results will vary wildly, just as we know that dive response shows a great deal of variance among individuals, and also in my own experience contraction/struggle phase began sooner (even though lung O2 was high) which in untrained individuals would probably cause them to abort. Also after one minute or so I couldn't even find a radial pulse anymore because vasoconstriction was so strong although my fingertip meter had no problems.

 

[MarcinB]

Which pulse oxymeter do you use?

 

[growingupninja]

I think I have posted a link in the past so you may be able to find it. It was USD $70, is water resistant, rated to 50% SaO2 and I think 30bpm. It is nothing too special but probably something you would need to find online instead of buy at a drugstore. I would definitely try to find one with a pulse graph--for training it is great because you will see the pattern flatten out as vasoconstriction kicks in.

 

[MarcinB]

I've tried one cheap fingertip pulseoxymeter. It worked fine under normal conditions but as soon as the DR was activated it simply hung until I started breathing again. But it was much cheaper than yours. What is the brand this device? I was not able to find the link you mentioned.

 

[growingupninja]

Sorry, i searched and could not find it either. It was I think a rather generic brand called ultranebs, made in china. They seem to spit out a lot of models and mine has not even a model or brand stamp number on it. It is rubber coated and water resistant, intended more for athletes and altitude use as opposed to infants or hospital settings. I feel like i got very good results with it but may have stumbled onto a good model by sheer luck.

 

[MarcinB]

I found an interesting study related to the subject of the thread: Argacha et al. Facial cooling and peripheral chemoreflex mechanisms in humans. Acta Physiol 2008, 194: 161-170

According to this study facial cooling enchances the response of peripheral chemoreceptors to hypoxia. Unfortunately, their sensitivity to hypercapnia was not studied.

 

[MarcinB]

I've done several breath holds (lungs 80-90% full, wearing only nose clip) until the first contraction with face immersed in 36C and 14C water. I did not found any clear difference in the time to first contraction. Sometimes it was 10s shorter for cold water vs. the warm one and sometimes 10s longer. I'll try to repeat this experiment with 10C water to see if it makes any difference.

Ninja, did you perform your experiments on full lungs too?

 

[growingupninja]

Yes, I mostly tested full lung and I will redo them as soon as i get time with more strict metering, etc. For me if the water is cold I got very strong and fast response even on full lung. Vasoconstriction also starts sooner than bradycardia in my case.

When I was doing it I was mostly testing to see if I was prone to ascent tachycardia using water temps that I typically spear in with eye towards swb safety--I would wait until strong DR was established then start mild/medium exertion to see if my pulse would rise significantly (it didn't once DR was fully locked in).

I think the cold water test is going to be highly variable among individuals. There is likely a big genetic component. Unfortunately in my case it was impossible to separate any conditioning effects since I was already trained and accustomed to diving in cold water on a regular basis.

 

[growingupninja]

36C by the way would do nothing at all for me unless it was flowing water perhaps. 14C would do something.

I dive year round in water that is usually 10C to 12C at depth; my cold water induced dive response is strongest at those ranges or colder. Again, I don't know if I came out of the box wired that way or if it is conditioning. I get a quickish response full lung in warmer water but it has to be flowing and I usually need to be relaxed/extremely low exertion (basically freefalling in ocean or little more than a fin twitch when doing DYN).

And of course wearing a mask mutes the response significantly...