A few questions... (Breathing Up Technique and diving environment)

[Johan Andersson]

The goal of underventilating is for me to induce a quicker dive response, and reduce O2 consumption.

That high CO2 triggers the diving response more/faster has been stated before here at DB, but as far as I know it does not agree with studies about the different types of stimuli that initiates or affects the diving response in humans. Low O2 is more important for the diving response than high CO2.

The influences of alveolar or arterial O2 and CO2 partial pressures on the cardiovascular responses collectively called the diving response have been investigated. It can be concluded that the diving response is triggered by respiratory arrest and is not dependent of chemoreceptor stimulation for it's initiation. However, once initated, the bradycardia is augmented by hypoxia and attenuated by hyperoxia. But the magnitude of bradycardia appears to be largely independent of changes in CO2.

Similarly, the peripheral vasoconstriction is augmented by hypoxia and attenuated by hyperoxia. Hypocapnia (low CO2) does not prevent significant peripheral vasoconstriction.

Some studies on this:
Arterial blood gas changes and the diving response... [Aust J Exp Biol Med Sci. 1971] - PubMed result
Effects of alveolar PO 2 and PCO 2 on apneic brady... [J Appl Physiol. 1973] - PubMed result
Effects of hypercapnia, hypoxia, and rebreathing o... [J Appl Physiol. 1983] - PubMed result
Effects of hypercapnia, hypoxia, and rebreathing o... [J Appl Physiol. 1983] - PubMed result
Hypoxia augments apnea-induced peripheral vasocons... [J Appl Physiol. 2001] - PubMed result

/Johan

 

[trux]

Thanks for the great details, Johan! Certainly everyone agrees that already the facial immersion and respiratory arrest start the diving reflex, and that hypoxia plays in many aspects more important role than hypercapnia, especially in regards to the bradycardia.

I see for example in the study you quoted (Effects of hypercapnia, hypoxia, and re-breathing o... [J Appl Physiol. 1983] - PubMed result) that the HR was reduced by 18% by hypoxia and only 6% by hypercapnia. So far so good, and you are perfectly right. The problem is that a freediver cannot start his performance already hypoxic for improving his time, so the hypoxia is not helpful for increasing the diving response in the initial phase of the breath hold. Hence he needs to rely on the other means, and hypercapnia (or at least avoiding hypocapnia) is a good way to accelerate the diving response (although it is less intensive than hypoxia would be).

And also, in many studies about breath-hold diving and about sleeping apnoea, I see that "hypercapnia is a well-documented source of centrally mediated vasoconstriction" (from Sleep apnea: current diagnosis and ... - Google Books, but it is a very frequent claim). The early vasoconstriction is crucial for freediver's muscles to start working in anaerobic mode, hence consuming less precious oxygen needed for the brain and heart.

So in conclusion, I would tell that you are certainly right that hypoxia is from the quantitative point of view more important, but from the qualitative and practical point of view it is the hypercapnia. Using hypoxia to the advantage of a freediver (and for increasing his performance) is simply not practical. In contrary, using hypercapnia does not cause such troubles.

 

[Johan Andersson]

I did not mean that you should use hypoxia to trigger your diving response when diving. Having as much O2 as possible in the beginning is better.

I just wanted to add what I know about the triggering of the diving response. And repetitively seeing here on DB that hypercapnia strenghtens the responses to diving in humans is not in conjunction with my understanding of physiology.

I see for example in the study you quoted (Effects of hypercapnia, hypoxia, and re-breathing o... [J Appl Physiol. 1983] - PubMed result) that the HR was reduced by 18% by hypoxia and only 6% by hypercapnia.

Unfortunately, you read the results from Lin et al slightly wrong. In that study, hypercapnia did not cause 6% of the bradycardia - it increased heart rate by 6%. That is, hypoxia reduces heart rate whereas hypercapnia increases heart rate! According to that study, hypercapnia would weaken your diving response. There are other studies showing that hypercapnia potentially strenghtens the bradycardia, but the effect is marginal at best.

That was the bradycardia. So what about the peripheral vasoconstriction?

And also, in many studies about breath-hold diving and about sleeping apnoea, I see that "hypercapnia is a well-documented source of centrally mediated vasoconstriction" (from Sleep apnea: current diagnosis and ... - Google Books, but it is a very frequent claim).

OK, it is often stated that hypercapnia causes/strenghtens peripheral vasoconstriction. However, just because it is often stated it doesn't automatically mean it's right. I have been going through my archive of studies about circulatory responses to apnea in humans and can find no support for that claim. I may be wrong and may have missed some study, but as long as I do not see a study actually showing that hypercapnia will strenghten peripheral vasoconstriction during voluntary apnea, I trust the studies I have read that show that CO2 has little or no effect on the peripheral vasoconstriction. There are a few studies supporting the latter conclusion that are in agreement with each other. But it should be noted that the relationship between apneic peripheral vasoconstriction and hypercapia is not as well "researched" as the relationship between bradycardia and hypercapnia.

Also in the reference you provide, the claim is put forward without any original reference. Therefore I suspect that the author(s) of that text are referring to information not directly pertinent to apnea diving. For instance, responses to exposure to hypercapnia while breathing, results from animal studies, and results from sleep apnea patients (that often have other pathologies as well) cannot be directly used to draw conclusions about the vasoconstrictor response to voluntary apnea in healthy humans.

I could continue, but the post is already long enough (for most people to not read it all...?). I just want to end by stating that my conclusions are that both in the beginning, middle, and end of an apnea, the effects of the changes in O2 is more important for the cardiovascular responses than the effects of the changes in CO2 (the cerebral circulation being the exception - the cerebral circulation is highly responsive to changes in CO2!).

/Johan

 

[trux]

Very interesting indeed. Thanks for the head-up on the 6% increase of HR instead of decrease - that was a small but crucial oversight! Still, the bradycardia is not so important from this point of view. At the initial phase it is triggered by the facial immersion and the respiratory arrest to a much higher degree, so if we are in normocapnia instead of hypocapnia (which would be the case after hyperventilation), it won't change a lot.

Besides it, not having the full text of those documents, I do not know whether they studied also hypocapnia, which is clearly (as you wrote yourself) the starting point of practically all breath-holds in real life. If we speak here about trying to keep the CO2 when starting a BH, we are possibly still in a lightly hypocapnic state, or in normocapnic at best.

I agree a more detailed study on the influence of CO2 on the diving response would be indeed interesting.

Regarding the vasoconstriction, it really surprises me that you claim there is no know relation between CO2 and vasoconstriction, because all searches on given topic return plenty of scientific documents. Not having access to the full text of most of them, it is difficult to find their relevance to breath-hold diving, but if there is absolutely no relation between hypercapnia and vasoconstriction, it would be a quite important new fact to most of us.

 

[trux]

I looked up the web for the relation between vasoconstriction and hypercapnia, but am quite limited by my access to the document abstracts only (in most cases). However, even in studies about breath-hold diving there are frequent quotes about hypercapnia-induced vasoconstriction, but it is true I did not find any reference to the source of such claims (and that's why I considered it an accepted consensus).

This study for example seems to speak about measuring vasoconstrictive sensibility at breath-holds induced by hypercapnia, but again I do not have the full text, so cannot tell how much relevant and reliable it is: SpringerLink - Human Physiology, Volume 32, Number 3

This test is based on the following principle: during voluntary breath holding, the blood concentration of carbon dioxide increases, stimulating the respiratory center, which responds reflexively by adrenergic vasoconstriction...

 

[Johan Andersson]

...if there is absolutely no relation between hypercapnia and vasoconstriction, it would be a quite important new fact to most of us.

Yes, and that is why I am being stubborn/persistent/obnoxious/whatever you would like to call it.

I might return with more information and pertinent references...

/Johan

 

[Johan Andersson]

However, even in studies about breath-hold diving there are frequent quotes about hypercapnia-induced vasoconstriction, but it is true I did not find any reference to the source of such claims (and that's why I considered it an accepted consensus).

Yes, that is the problem. Once someone assumed there to be such a relationship, and it has been quoted over and over again until finally it has been accepted as a fact. But try to find the original study where you can find "hard scientific evidence" supporting that notion! I have not found it yet...

/Johan

 

[trux]

On the other hand I am quite sure that there are studies demonstrating that it is the hypercapnia, and not the hypoxia that is mainly responsible for the respiratory drive (urge to breathe). I do not have the links at the hand, but I am absolutely certain I saw several of them with a rather detailed evidence. And I also saw documents explaining that the urge to breathe leads to the release of stress hormones, and among them there are several with vasoconstrictive effects. Is it all wrong too?

 

[Johan Andersson]

This study for example seems to speak about measuring vasoconstrictive sensibility at breath-holds induced by hypercapnia, but again I do not have the full text, so cannot tell how much relevant and reliable it is: SpringerLink - Human Physiology, Volume 32, Number 3

This study is according to me written by authors that have a limited understanding about apnea physiology. Do a search on PubMed on these authors' names and apnea or diving or breath-holding - I guarantee there is no studies. They may be excellent researchers (I don't know), but in this particular case they have not looked into the published literature to any great extent. It is another example of a scientific study stating that hypercapnia triggers vasoconstriction without providing a proper reference for the statement. They write (PM me if you want the full text):

This test is based on the following principle: during voluntary breath holding, the blood concentration of carbon dioxide increases, stimulating the respiratory center, which responds reflexively by adrenergic vasoconstriction.

The fact is the that vasoconstriction occurs to the same degree also without hypercapnia, so there is no basis for that statement. It is the respiratory arrest, not the increase in CO2, that initiates the adrenergic vasoconstriction.

/Johan

 

[Kars]

To see weather CO2 helps or limits vascular constriction, maybe I'll try the following.

A) short, shallow and slow 'breath-up' <Retaining CO2> - 2' Empty lungs static at -3.80m depth. This gets me in contractions and when I'm bcak at the surface I have a big bloodshift effect feeling the blood shunt back to my limbs.

B) repeat A,

C) repeat A with the addition of hyperventilation.

Well I think I need a very capable buddy for this test. Maybe ask Eric Fattah first, he may very well have done it already.

 

[trux]

Well, it is possible that they know little about breath-hold diving. But then again, when I look at the terms "respiratory drive" + vasoconstrictor - there are so many documents from all possible areas of the medicine from pneumology over neurology to anesthesiology, and with so many details and so many references, that it seems to be pretty clear that respiratory drive leads to the stimulation of vasoconstrictive nerves.

Now, in normal state the respiratory drive is controlled mainly by pH, but in case the pH chemoreceptors are dysfunctional, the PaO2 chemoreceptors take over the control of the respiratory drive. So you may be very well right that the diving response or the vasoconstriction can be triggered by the hypoxia alone too. But from my understanding, it is the "plan B", and in no way it means that hypercapnia is not the normal way to trigger it, and that it cannot be used for strengthening the diving response.

Of course, these are just my uneducated logical conclusion, with no hard scientific evidence in the specific field of breath-holding, but from what I understood, you do not have any evidence against such conclusion either, hence perhaps it may be a bit premature to exclude hypercapnia as a contributing factor to the diving response. Or am I completely wrong?

 

[Johan Andersson]

On the other hand I am quite sure that there are studies demonstrating that it is the hypercapnia, and not the hypoxia that is mainly responsible for the respiratory drive (urge to breathe). I do not have the links at the hand, but I am absolutely certain I saw several of them with a rather detailed evidence. And I also saw documents explaining that the urge to breathe leads to the release of stress hormones, and among them there are several with vasoconstrictive effects. Is it all wrong too?

No, that hypercapnia is important for the urge to breathe is right!

For instance,
Physiological and conventional breath-hold breakin... [J Appl Physiol. 1974] - PubMed result
shows that it is the arterial PCO2 that triggers the involuntary breathing movements (contractions) at the "physiological breaking point".

In one of my recent studies (discussed in another thread - the one about the brain damage marker) we discussed the relationship between the hypercapnic and hypoxic ventilatory drives. Here is a section of that discussion:

It should be noted that because of the extensive preapneic hyperventilation, PaCO2 at the end of apnea (45 Torr) was only slightly above the baseline value (39 Torr). Observations of small increases in PCO2 have been used as support for the notion that trained breath-hold divers rely on the hypoxic ventilatory drive as a cue to end apneas. In fact, the old notion that hypercapnia is the most important factor generating “air hunger” is challenged by observations that the hypoxic ventilatory drive predicts breath-hold duration and that hypoxia can generate “air hunger” equivalent to that generated by hypercapnia.

I don't recognize the connection to stress hormones (that the urge to breathe leads to the release of stress hormones). Any references?

/Johan

 

[trux]

I don't recognize the connection to stress hormones (that the urge to breathe leads to the release of stress hormones). Any references?

Not at hand right now, and I do not recall any work about it directly from the field of breath-hold diving research. Stress hormones are often quoted in studies about drowning. And also Sebastian Murat spoke about them often in his articles. However, I see now, after looking up the relation between respiratory drive and vasoconstrictors, that there is even a more direct neurological relation between the two, so the stress hormones are just another kick in plus.

 

[cdavis]

Wow, every now and then threads get supremely interesting.

Thank you Johan. I think stubborn is great. Pointing places where conventional wisdom doesn't match the science is even better. It is a large part of how we make progress.
On co2 levels,seems like the science and our "diver experience" are not in concert and I'd like to know why. Maybe we are misinterpreting what we see or maybe we are talking past each other. Anyway, here is my experience. How does that square with the science you are familiar with?

I switched to FRC diving a couple of years ago, now diving at about 55-60 % of full lung. FRC theory says taking down more co2 helps the dive reflex, especially vasoconstriction, kick in early and sure enough, my old breathup, which was definitely hyperventilation, did not work so well on FRC. As I began reducing my ventilation during breathup, my dive times got longer. I went to a very minimal ventilation rate, at present about 8/minute, less than 1 liter each. Plus I use a very large diameter snorkel, lots of dead space. I regulate the ventilation amount by reducing it until I can just barely feel an urge to breath, so I know I'm not hyperventilating. I think I'm probably hypercapnic, as my resting ventilation rate seems to be higher than this. That got me long dives, which got even longer when I added a few mild (maybe 3 liter ventilation per breath, total time maybe 10 seconds) purges at the end of the breathup. At that point, I've blown off some c02, but still am way beyond the c02 amt I would take down on full lung and I'm getting dive times close to double what I could do full lung. Anyway, it sure looks to me like high c02 levels, at least for FRC diving, work better.

Any other explanation?

On your previous question about why assume people with differing co2 trigger levels might respond differently to mild hyperventilation, I'm not really assuming anything. Its just my observation that some people are much more susceptible to B0 than others and I'd like to know why.

Thanks again for some great food for thought.

Connor

 

[Johan Andersson]

...from what I understood, you do not have any evidence against such conclusion either...

Well, I provided the references I based my conclusions on in one of my earlier posts. But here they are again, with "some" more details (I know my posts tend to be long, and this is going to be looong).

Elsner R, Gooden BA, Robinson SM. Arterial blood gas changes and the diving response in man. Aust J Exp Biol Med Sci 1971; 49(5): 435-444.
Arterial blood gas changes and the diving response... [Aust J Exp Biol Med Sci. 1971] - PubMed result

They studied the right forearm blood flow during apnea
1) with normal air in the lungs
2) with high arterial O2 tension but normal CO2 tension
3) with high arterial O2 tension and lowered CO2 tension

They write:
"If the diving response still occurred despite hyperoxia and hypocapnia, this fact would further support the concept that asphyxial blood gas changes played little or no part in the etiology of this response."

Results:
There was no significant difference between the forearm blood flow responses produced by conditions 1 and 2. Forearm blood flow was significantly reduced by both conditions (i.e., hyperoxia does not affect the peripheral vasoconstriction).

In addition, there was no significant difference between the forearm blood flow response produced by conditions 1 and 3. Forearm blood flow was significantly reduced by both conditions (i.e., hypocapnia does not affect the peripheral vasoconstriction).

Their conclusions:
"Asphyxial blood gas changes were not essential for the development of the diving response in man."
"The hypercapnia did not potentiate the cardiovascular response."


Lin YC, Shida KK, Hong SK. Effects of hypercapnia, hypoxia, and rebreathing on circulatory response to apnea. J Appl Physiol 1983; 54(1): 172-177.
Effects of hypercapnia, hypoxia, and rebreathing o... [J Appl Physiol. 1983] - PubMed result

They studied the total peripheral resistance (related to peripheral vasoconstriction) during breath-holds (BH) like this:
BH-1) Control BH, a 90-s continuous BH with air, involving a progressive hypoxia and hypercapnia as well as cessation of respiratory movements
BH-2) BH with air with rebreathing at 15-s intervals. Like BH-1, this involved a progressive hypoxia and hypercapnia but not cessation of breathing. In this and the following BH experiments with rebreathing, the effect of absent respiratory movements is abolished.
BH-3) BH with air with rebreathing through a CO2 absorber (progressive hypoxia, minimized effects of hypercapnia).
BH-4) BH with O2 with rebreathing (no hypoxia but hypercapnia).
BH-5) BH with O2 with rebreathing through a CO2 absorber (no hypoxia, minimized effects of hypercapnia).

Results:
Vasoconstriction was well established by 30 s and was maintained throughout the BH. The total peripheral resistance (vasoconstriction) during BH with reduced alveolar CO2 levels increased more than during BH with increased CO2 levels from the pre-BH levels. Thus, if anything, by looking at their results it seems as if hypercapnia during BH-2 and BH-4 prevented the peripheral vasoconstriction from developing to the same degree as during BH-3 and BH-5 (with minimized effects of hypercapnia).

Their discussion:
"The difference in TPR between high and low CO2 levels in BH with air (BH-2 vs. BH-3) and BH with O2 (BH-4 vs. BH-5) were unexpected. One expects that the secondary compensatory effect of hypercapnia is to produce stronger vasoconstriction. We observed just the opposite in both BH with air and with O2 and offer no explanation at this time."

I can't recall any other studies concerning the connection between CO2 and peripheral vasoconstriction during voluntary apnea in healthy humans right now. But the studies above supports the conclusion that hypercapnia is not important for eliciting a pronounced peripheral vasoconstriction.

Stimuli promoting a strong vasoconstrictor response:
1) Apnea itself
2) Cold-water stimulation of the face (the water should be approx 10°C colder than the ambient air for a maximal effect)
3) Hypoxia
4) ...
but not hypercapnia as far as I know.

I don't have the time to perform a study on this right now. However, I will see if I can get any student to perform a thesis project on this topic later this spring. If so, I will provide the results.

/Johan

 

[Johan Andersson]

Connor, right now it's getting too late where I am for higher brain functions to work properly. I think I have to get some sleep. But just as a final note today/tonight, the topic of FRC diving is very interesting, I think, even though I can't explain all what you describe.

Oh, just remembered one thing, so I have to continue. More than 10 years ago I did a study on the effects of different lung volumes on the diving response (Effects of lung volume and involuntary breathing m... [Eur J Appl Physiol Occup Physiol. 1998] - PubMed result). The responses to holding 60, 85, and 100% of ones vital capacity in the lungs during apnea was studied. At 60%, the diving response was most pronounced (no difference in O2 or CO2 between conditions). You dive at 55-60% lung volume, you say. Thus, according to that study, you also initiate a pronounced diving response (unrelated to high CO2). I can't say this is the only explanation, but it could contribute.

/Johan

 

[cdavis]

To add something that might bear on one of the results listed above: Often when I dive with a very minimal breathup, I will feel a transient and very small urge to breath at 20-30 seconds into BH. Its a signal that usually means the dive with be long and comfortable. I had interpreted that as meaning that hypercapnia was kicking in dive response fast and hard, with the resulting good performance.

So 60 per cent might be the magic number. I love it , thanks

Connor

 

[cdavis]

Johan, when you get back up in the morning, one more piece of info. I played with ventilation amount and during a minimal breathup, my ventilation amount gets down to about .4 liters, maybe less. I'll check that again next time I'm in the water.

 

[trux]

Very interesting! Thanks, Johan, for the quotes from the documents. Don't worry about the length of your posts - the longer the better

It is a pity the documents are not available publicly in full text. I'd love to see the details, and the quantitative results.

It is also a pity the studies are not more complete: At the first one, I miss a measurement at hypercapnia. And at the second study, if I understand it correctly, they actually did not measure values at a breath hold (except of the first control group BH1), but all four groups BH2-BH5 were rebreathing. Hence it is a question to which extent it is relevant to breath-hold diving. I understand the need for isolating individual factors (hypoxia, hypercapnia, respiratory arrest), but it would have been even better if they isolated all of them, and did all the 8 possible permutations (I mean also the missing three groups with respiratory arrest), and comparing them quantitatively all.

BTW, did they compensate in their measurements of the peripheral resistance for changes in cardiac output? I saw a study which addressed the occasional association of mild hypercapnia with vasodilatation, but found out that the dilatation was due to the increased cardiac output, and not due to direct dilatation of peripheral vessels (http://bja.oxfordjournals.org/content/96/6/708.full). If they did not count in the changes of the cardiac output (the other study you quoted, mentioned 6% increase of HR), couldn't it explain the unexpected difference in TPR between the groups? Or is the type of measurement they did already independent on the cardiac output?

Thanks again for spending your time with us here on the forum, and sharing your knowledge!

 

[Kars]

Connor, could you describe the FRC learning curve, from start to your current level?

I suspect FRC divers are training their brain and body through association to induce parts of the dive response through brainpower.
So the High CO2 helps through association, not through biochemical ways.

It would be interesting if you would have an untrained copy of yourself and see how your minimal breathing works on him, in comparison with you.

Also you could try to have a Low CO2 FRC dive, same O2 and the rest, and see how they compare.

Interesting discussion!