Exhaling at depth puts you in the same situation as an FRC ascent. Anyway the exhale at 25m was experimentally confirmed as advantageous by doing long hangs at 25m, then performing the ascent with or without an exhale first. Exhaling before ascending resulted in prolonging of the total dive time to BO, which to most was very counter-intuitive. I only discovered it because I knew that I could ascend from 25m on an FRC dive with vision 'gone' from hypoxia and still make a clean exit, whereas the same state at 25m on a packing dive would be a subsurface BO. So the obvious action was to convert the packing dive into an FRC dive; I don't think the lung O2 store has much relevance in the latter part of the ascent, the main gain by exhaling is preventing the expanding lungs from applying pressure to the heart and arteries and reversing the blood shift. If you watch my 104m dive video on youtube you can see the massive exhale at 25m (in fact I exhale twice, once at 25m and again a few meters later). Immediately after the exhale I apply exhale pressure on the abdomen, forcing blood into my head, which prolongs consciousness if the lungs are empty but causes a BO if the lungs are full.
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DCI and freediving
- Thread startersebastien murat
- Start date
Thread Status: Hello
, There was no answer in this thread for more than 60 days.
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It can take a long time to get an up-to-date response or contact with relevant users.
Exhaling at depth puts you in the same situation as an FRC ascent. Anyway the exhale at 25m was experimentally confirmed as advantageous by doing long hangs at 25m, then performing the ascent with or without an exhale first. Exhaling before ascending resulted in prolonging of the total dive time to BO, which to most was very counter-intuitive. I only discovered it because I knew that I could ascend from 25m on an FRC dive with vision 'gone' from hypoxia and still make a clean exit, whereas the same state at 25m on a packing dive would be a subsurface BO. So the obvious action was to convert the packing dive into an FRC dive; I don't think the lung O2 store has much relevance in the latter part of the ascent, the main gain by exhaling is preventing the expanding lungs from applying pressure to the heart and arteries and reversing the blood shift. If you watch my 104m dive video on youtube you can see the massive exhale at 25m (in fact I exhale twice, once at 25m and again a few meters later). Immediately after the exhale I apply exhale pressure on the abdomen, forcing blood into my head, which prolongs consciousness if the lungs are empty but causes a BO if the lungs are full.
FRC is a pretty loose term when diving. Take the example of passively exhaling at the surface and then maintaining a patent airway. Gas will continuously exit until you get to RV (and less actually), with no effort on your part. So, if you exhale forcibly at 25m you are not exhaling to FRC but more likely RV, unless you try to `feel´ for what FRC (surface) might be.
Besides the problem of O2 loss mentioned earlier...and we differ greatly here....there is another salient issue. If you exhale you also lose CO2, rendered all the more significant by the low cardiac output; you should have a low cardiac output because you now have a hypoxia-driven DR. This means that the `slow´ blood-flow passing through your lungs now experiences a sudden, albeit relative hypocapnia. If you exhale forcibly, this hypocapnia could develop, let's say, explosively. It may reduce your urge to breathe perhaps (fools paradise) and could potentially reverse the DR, since hypercpnia under apnea is an importnat contributor to the development of the DR. There is a more sinister side too: hypocapnia reduces hypoxia tolerance. Reduced hypoxia tolerance means: low duration tolerance to O2 deprivation at any level of O2 deprivation
All in all, in mind at least, these are all `catch your tail´ strategies that require lots of trade-offs and a very high level of physiologic knowledge, expertise, and experience....hardly commensurate with the vast number of divers out there.
My final opinion on this (just my opinion of course): Its not rocket-science but it can be if you rely on a number of exotic/esoteric strategies to get you through. In short keep it clean by keeping it simple. There is no fixed recipe for diving. Exhale dives have their place but the trick is in knowing (intuitively) when to use what strategy where and when.
Besides the problem of O2 loss mentioned earlier...and we differ greatly here....there is another salient issue. If you exhale you also lose CO2, rendered all the more significant by the low cardiac output; you should have a low cardiac output because you now have a hypoxia-driven DR. This means that the `slow´ blood-flow passing through your lungs now experiences a sudden, albeit relative hypocapnia. If you exhale forcibly, this hypocapnia could develop, let's say, explosively. It may reduce your urge to breathe perhaps (fools paradise) and could potentially reverse the DR, since hypercpnia under apnea is an importnat contributor to the development of the DR. There is a more sinister side too: hypocapnia reduces hypoxia tolerance. Reduced hypoxia tolerance means: low duration tolerance to O2 deprivation at any level of O2 deprivation
All in all, in mind at least, these are all `catch your tail´ strategies that require lots of trade-offs and a very high level of physiologic knowledge, expertise, and experience....hardly commensurate with the vast number of divers out there.
My final opinion on this (just my opinion of course): Its not rocket-science but it can be if you rely on a number of exotic/esoteric strategies to get you through. In short keep it clean by keeping it simple. There is no fixed recipe for diving. Exhale dives have their place but the trick is in knowing (intuitively) when to use what strategy where and when.
Yes, Seb, in absolute terms you are right, but those are not really important. It is the ppCO2 that is important, and it does not change with the exhale at depth with any meaningfull difference. And besides it, the CO2 is mostly stored in the blood (dissolved in plasma, stored as bicarbonate, and bound to hemoglobin). It does not difuse much into lungs after reaching cetain PP level relatively soon into the breath-hold. It means if you exhale it will have practically no impact on the CO2 in the blood, the pH, and hence the DR, or the hypoxic resistance (Bohr curve shift)
As pointed out already in another thread about the freediving DCS, one reason the bend and mend method is of a higher risk is the vasodilation of cerebral vessels during apnea, due to the high CO2 level. Once you surface, and start breathing, the vessels contract, and can so easily entrap the bubbles. If you then do your deco with O2, the cerebral vasoconstriction may even get worse due to hyperventilation. This does not really happen on scuba, hence the reference to scuba is not well suitable.
Hi Trux,
I respectfully disagree.
The purpose of the lungs is to effectively unload CO2 (and upload O2). It is an extremely fast acting buffering system; it needs to be and that is one of its major purposes.
What is important here is the CO2 in the red blood cells (RBCs), not in the plasma. Only small amounts of CO2 are dissolved in plasma and, moreover, the carbonic anhydrase located within the RBCs, one of the fastest catalytic enzymes known, quickly converts carbonic acid to CO2. This reaction proceeds extremely quickly, so that even subtle changes in ventilation result in changes in blood pH and pCO2, to say nothing of major changes in ventilation, like forcibly exhaling. You can probably find graphs of this in most texts on respiratory physiology.
If you an elevated ppCO2 and you then exhale you create a difference in the fractional concentration between alveolar and pulmonary capillary CO2. This in itself results in a direct partial pressure difference.
It would be ok if this blown off CO2 was adequately displaced with lung O2 but the fact remains lung O2 stores are low, for two reasons: you simply run out of it because of the O2-consuming act of breath-holding and you're also exhaling it, along with the CO2.
What I'm talking about is this `new´ relatively hypocapnic blood that has suddenly been expose to this major ventilatory maneuver and that will shortly (maybe only 6 seconds) travel from the pulmonary capillaries to the brain. You have to think of the blood in term so segments.
I've been diving for a while now and cannot for the life of me look anyone in the eye and tell them that sport freediving, as it stands, is a safe and healthy activity to get into. There's a lot of sugar-coating of its problems with numerous purported counter-defensive strategies, but from where I stand it is still maladaptive. The fact remains: risking SWB, narcosis, and DCI are maladaptive behaviors, no matter how you sugar coat it. If you then knowingly engage in maladaptive behavior then you are pathological, and this is the problem.
My aim, if you could call it that, is not to `sell´ anyone on exhale as the be all and end all strategy. Rather, I wish to bring to your attention that freediving, in its current form, is unsustainable in the long-term. Its going to be brought out for what it is, if not by me, surely by someone else. No use burying one's head in the sand and hoping it will all go away...it never does
I respectfully disagree.
The purpose of the lungs is to effectively unload CO2 (and upload O2). It is an extremely fast acting buffering system; it needs to be and that is one of its major purposes.
What is important here is the CO2 in the red blood cells (RBCs), not in the plasma. Only small amounts of CO2 are dissolved in plasma and, moreover, the carbonic anhydrase located within the RBCs, one of the fastest catalytic enzymes known, quickly converts carbonic acid to CO2. This reaction proceeds extremely quickly, so that even subtle changes in ventilation result in changes in blood pH and pCO2, to say nothing of major changes in ventilation, like forcibly exhaling. You can probably find graphs of this in most texts on respiratory physiology.
If you an elevated ppCO2 and you then exhale you create a difference in the fractional concentration between alveolar and pulmonary capillary CO2. This in itself results in a direct partial pressure difference.
It would be ok if this blown off CO2 was adequately displaced with lung O2 but the fact remains lung O2 stores are low, for two reasons: you simply run out of it because of the O2-consuming act of breath-holding and you're also exhaling it, along with the CO2.
What I'm talking about is this `new´ relatively hypocapnic blood that has suddenly been expose to this major ventilatory maneuver and that will shortly (maybe only 6 seconds) travel from the pulmonary capillaries to the brain. You have to think of the blood in term so segments.
I've been diving for a while now and cannot for the life of me look anyone in the eye and tell them that sport freediving, as it stands, is a safe and healthy activity to get into. There's a lot of sugar-coating of its problems with numerous purported counter-defensive strategies, but from where I stand it is still maladaptive. The fact remains: risking SWB, narcosis, and DCI are maladaptive behaviors, no matter how you sugar coat it. If you then knowingly engage in maladaptive behavior then you are pathological, and this is the problem.
My aim, if you could call it that, is not to `sell´ anyone on exhale as the be all and end all strategy. Rather, I wish to bring to your attention that freediving, in its current form, is unsustainable in the long-term. Its going to be brought out for what it is, if not by me, surely by someone else. No use burying one's head in the sand and hoping it will all go away...it never does
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Trux,
On the topic of cerebral vasodilation, it makes sense. The other problem is that when the vasodilation is lost, so too is the cooling. We saw this loss of cooling effect in the tests we did measuring brain temperature. Consequently, there would be an increased rate at which gases would come out of solution. If you can vent off this gas quickly enough then the risk of CAGE should increase. On exhale the post-dive vasodilation is sustained for longer, in my case for example, the (bradycardic) DR is sustained for up to 20-30 seconds post-dive. This means plenty of time to re-oxygenate without loses to peripheral tissues and perhaps sufficient time to off-gas the vital organs.
On the topic of cerebral vasodilation, it makes sense. The other problem is that when the vasodilation is lost, so too is the cooling. We saw this loss of cooling effect in the tests we did measuring brain temperature. Consequently, there would be an increased rate at which gases would come out of solution. If you can vent off this gas quickly enough then the risk of CAGE should increase. On exhale the post-dive vasodilation is sustained for longer, in my case for example, the (bradycardic) DR is sustained for up to 20-30 seconds post-dive. This means plenty of time to re-oxygenate without loses to peripheral tissues and perhaps sufficient time to off-gas the vital organs.
Seb, this discussion is very interesting, and I agree with a lot of your argumentation, including that about the N2 absorbtion in sinus (I posted similar concern in the thread about Herbert's record attempt). I just wanted to tell that Eric is not completely wrong, although with his exhale on the ascent he does not profit from the FRC effects all along. By exhaling he will not get moe hypocapnic than before it, simply because the PP of CO2 will not change. The difference in transpulmonary pressure while submerged, altough driving the gas exchange on surface, is completely negligible at this depth in the respect of the ambient pressure.
On the other hand I completely agree that the exhaling will reduce the O2 stores, But that again prevents offloading of the CO2 from blood (Haldane effect). Additionally, the DR is strongly hypoxically driven, so I do not think that exhaling on the ascent would reduce the DR. In contrary, I agree here with Eric that it should make it stronger.
There's a lot at stake here, call it social responsibility, because if the interpretation is mistaken but believed diver's lives could be at risk:
Trux,
You have to distinguish between gas solubility and partial pressures, as the two are very different. Partial pressure is the all important factor in keeping one conscious.
Let's go back to basics:
1. During ascent with breath-hold: alveolar pO2 (PAO2) decreases with depth, until it equals the (mixed) venous pO2, at which point the usability of the lungs as an O2 store ceases. Indeed, if PAO2 drops below PvO2 the lungs act as an O2-sink, precipitating the development a critical hypoxia (i.e., loss of consciousness). I know that if you ascent very quickly desaturation can be extreme, so easy does it there (cf. Schaefer and Carey, 1962). Now, if you exhale, at least from a ventilatory (not maybe cardiovascular) perspective you achieve little, and may actually aggravate the hypoxia. Let's see why: in the face of decreasing pressure, to maintain lung volume constant, you have to give something. So, gas is removed by exhaling. That keeps the ideal gas law more or less happy and balanced. Now, if you remove/decrease the lung gas, then the fractional concentration of these gases in the lungs must decrease. Consequently, the partial pressure (of O2) must also decrease. One way or the other pO2 will decreases and you simply can't circumvent this problem at all. I think we all agree there..??
2. From the point of view of CO2 during ascent the following occurs: an increase in arterial pCO2 is blunted by the Haldane effect, i.e., because blood CO2 solubility increases (cf. Muth et al. 2005). Couple this to the loss of alveolar CO2 associated with exhaling, which for similar reasons given above for pO2, lowers the pCO2 even more. Therefore, the arterial pCO2 decreases that Muth et al. actually measured would decrease maybe even more. Sprinting up would only magnify the effect. The influx of CO2 into the lungs during ascent is regulated, at least in part, by the speed of ascent (Schaefer and Carey 1962) and/or the amount of exhaling.
My understanding is that what's important, from the point of view of hypoxia, is the partial pressure of O2 and CO2, since this is the driving force for gas transport to tissues and to keeping them `alive´. Therefore, a low arterial pO2 combined with a low arterial pCO2 will increase the risk of LOC, pretty dramatically if you ascend quickly and engage in exhalation behavior using this model.
The issue then becomes on of: despite the above happening could I rely on cardiovascular effects associated with exhaling at depth to see me through. I think we're all pretty much agreed upon the idea of limiting lung volume expansion to ensure venous return during at least the last stages of ascent. So, can I head-off a lung-induced decrease in cerebral blood flow. It seems reasonable, but you can't simply put the pulmonary/respiratory effects discussed previously aside. It has to, in the end, be reintegrated back into its whole.
By the way, on the issue of DCI: granted better vital organ N2 off-loading would be ensured by exhaling. Still, what of the peripheral tissues that picked-up a lot of N2 at the start under a poor DR and the work of swimming down. How do you then get it out of the joints and muscles? So, you head off vital organ DCI but take a peripheral hit. Hmm, starting to get complicated again. And, if that's the case Eric's Xen + deco stops (if you can handle them) may be you're only remaining strategy. I guess the analogy is: I recognize smoking could be bad for me, but if I use a filter (or two) its should at least be a bit better. If you believe that then you should buy a Xen. I mean it, really, cause its your only hope. I would.
Is there a flaw in my argument? I'm quite happy to keep this thread alive, take a few hits, even change my position, as long as a clear and unequivocal outcome is reached. The problem is that we've only anecdotal info and nothing concrete.
Trux,
You have to distinguish between gas solubility and partial pressures, as the two are very different. Partial pressure is the all important factor in keeping one conscious.
Let's go back to basics:
1. During ascent with breath-hold: alveolar pO2 (PAO2) decreases with depth, until it equals the (mixed) venous pO2, at which point the usability of the lungs as an O2 store ceases. Indeed, if PAO2 drops below PvO2 the lungs act as an O2-sink, precipitating the development a critical hypoxia (i.e., loss of consciousness). I know that if you ascent very quickly desaturation can be extreme, so easy does it there (cf. Schaefer and Carey, 1962). Now, if you exhale, at least from a ventilatory (not maybe cardiovascular) perspective you achieve little, and may actually aggravate the hypoxia. Let's see why: in the face of decreasing pressure, to maintain lung volume constant, you have to give something. So, gas is removed by exhaling. That keeps the ideal gas law more or less happy and balanced. Now, if you remove/decrease the lung gas, then the fractional concentration of these gases in the lungs must decrease. Consequently, the partial pressure (of O2) must also decrease. One way or the other pO2 will decreases and you simply can't circumvent this problem at all. I think we all agree there..??
2. From the point of view of CO2 during ascent the following occurs: an increase in arterial pCO2 is blunted by the Haldane effect, i.e., because blood CO2 solubility increases (cf. Muth et al. 2005). Couple this to the loss of alveolar CO2 associated with exhaling, which for similar reasons given above for pO2, lowers the pCO2 even more. Therefore, the arterial pCO2 decreases that Muth et al. actually measured would decrease maybe even more. Sprinting up would only magnify the effect. The influx of CO2 into the lungs during ascent is regulated, at least in part, by the speed of ascent (Schaefer and Carey 1962) and/or the amount of exhaling.
My understanding is that what's important, from the point of view of hypoxia, is the partial pressure of O2 and CO2, since this is the driving force for gas transport to tissues and to keeping them `alive´. Therefore, a low arterial pO2 combined with a low arterial pCO2 will increase the risk of LOC, pretty dramatically if you ascend quickly and engage in exhalation behavior using this model.
The issue then becomes on of: despite the above happening could I rely on cardiovascular effects associated with exhaling at depth to see me through. I think we're all pretty much agreed upon the idea of limiting lung volume expansion to ensure venous return during at least the last stages of ascent. So, can I head-off a lung-induced decrease in cerebral blood flow. It seems reasonable, but you can't simply put the pulmonary/respiratory effects discussed previously aside. It has to, in the end, be reintegrated back into its whole.
By the way, on the issue of DCI: granted better vital organ N2 off-loading would be ensured by exhaling. Still, what of the peripheral tissues that picked-up a lot of N2 at the start under a poor DR and the work of swimming down. How do you then get it out of the joints and muscles? So, you head off vital organ DCI but take a peripheral hit. Hmm, starting to get complicated again. And, if that's the case Eric's Xen + deco stops (if you can handle them) may be you're only remaining strategy. I guess the analogy is: I recognize smoking could be bad for me, but if I use a filter (or two) its should at least be a bit better. If you believe that then you should buy a Xen. I mean it, really, cause its your only hope. I would.
Is there a flaw in my argument? I'm quite happy to keep this thread alive, take a few hits, even change my position, as long as a clear and unequivocal outcome is reached. The problem is that we've only anecdotal info and nothing concrete.
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I think we've entered the age of technical freediving, which Eric foresaw with his Xen. Well done Eric
Speaking as a spectator (since I'm unlikely to do deep diving on any regular basis - much beyond 40m or so) this is a fascinating thread. I appreciate everyone's tolerate for discourse and disagreement amongst such informed views is fascinating.
There is no escape. You may not suffer narcosis but your not out of the woods with DCI if you do lots even 30m with short breaks, or SWB on any long dive/high metabolic rate.
Already this has changed my thinking - when last I was at Dean's I did quite a few dives past 30-40m consecutively - though I did generally allow awhile between them. While I never felt anything odd - and was not close to blackout (near as I can tell!!) I think now I would be more conservative.
It is, however, not often that I have the right circumstance for such depths.
It is, however, not often that I have the right circumstance for such depths.
Unfortunately, DCI is a very insidious condition: suddenly there it is. I've seen people come up with freediving tables before, but the fact of the matter these are speculative at best, not even empirical, so you've no guarantees. Moreover, they don't/can't factor in the effects of variable cardiac outputs and redistribution of blood-flow to/away from various tissues. If they try to convince you otherwise, they're full of s**t.
This I gathered. Like as not I'd not notice DCS unless it bit me pretty hard. I think it would be an issue were I a competitive diver. As it is I really enjoy going deep, but seldom have an opportunity. (around here there is not much to see down there - and I'm short qualified safety divers) From this discussion however I gather even exhale dives may or may not mitigate the risk. So it is a matter for edge-of-the-envelope exploration by the likes of you and Eric.
For me the result of depth work has been more relaxed dives <30m.
For me the result of depth work has been more relaxed dives <30m.
Don't be mistaken, I'm not the type that blindly goes, that's why Eric and I are still here. Exploration for me doesn't happen in great leaps, its all inch by inch stuff. I've a more NASA like approach and I don't knowingly place myself in harms way, not unless I absolutely have to, which is pretty rare these days since I don't teach much. Hardly exploration at all really if I look at the way others do things.
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I'm familiar enough with your work, and Eric's, to know you are both very systematic and conservative. This incremental approach is what makes your observations useful.
The rapidity with which your heart rate drops is amazing - how does that feel?
In my pool work with exhale dives (not full - probably 2/3 to 4/5ths exhaled) I found the dives very comfortable - but they were getting too long for the lifeguards..
The rapidity with which your heart rate drops is amazing - how does that feel?
In my pool work with exhale dives (not full - probably 2/3 to 4/5ths exhaled) I found the dives very comfortable - but they were getting too long for the lifeguards..
It feels really good 
I think if you don't dive with a good quality heart rate monitor you're selling yourself short in you development (one that measures beat-to beat or R-R). I learnt a lot from it. It should also tell you if you're genetically in the high or low SWB risk. In my experience, if you're not getting into the 30s or less (about +50% decrease) then you're probably in the high risk category, and so should work to sensitize the response.
I'm presently working on a product that helps you achieve just this. Not talking beta blockers, etc. This stuff only kicks in when you dive and has no side effects. Guess it would be performance enhancing, but considering that BOs are a risk why would one not use it. By the way, its separate to the stuff that lowers your metabolic rate, i.e., torpor inducing.
I think if you don't dive with a good quality heart rate monitor you're selling yourself short in you development (one that measures beat-to beat or R-R). I learnt a lot from it. It should also tell you if you're genetically in the high or low SWB risk. In my experience, if you're not getting into the 30s or less (about +50% decrease) then you're probably in the high risk category, and so should work to sensitize the response.
I'm presently working on a product that helps you achieve just this. Not talking beta blockers, etc. This stuff only kicks in when you dive and has no side effects. Guess it would be performance enhancing, but considering that BOs are a risk why would one not use it. By the way, its separate to the stuff that lowers your metabolic rate, i.e., torpor inducing.
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For me its a two stage event:
reflex to get into the low/mid 30s, followed by another jumb into teens during hypoxia/hypercapnia. But if I get really (dis)stressed then its all out and I hit single digits. I don't purposely try to do that of course because it's really not achieved pleasantly. I know of a girl who hits single digits without even trying just placing her face in the water...lucky her
reflex to get into the low/mid 30s, followed by another jumb into teens during hypoxia/hypercapnia. But if I get really (dis)stressed then its all out and I hit single digits. I don't purposely try to do that of course because it's really not achieved pleasantly. I know of a girl who hits single digits without even trying just placing her face in the water...lucky her
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Exactly. And I insist that by exhaling, you will reduce neither the PpCO2 nor the CO2 in the blood. The alveolar PpCO2 will remain identical to the level prior the exhale, because the transpulmonary pressure difference between full and empty lungs is several orders lower than the ambient pressure and hence has no meaningfull impact. So no change in alveolar PpCO2 due to the exhale. And since the lung volume is reduced after the exhale, the PaCO2/PACO2 (arterial/alveolar) diffusion will equalize quicker with less volume of CO2 extracted from the blood. That means then, that in fact by exhaling you may increase your arterial PpCO2, not reducing it, gaining so more tolerance against hypoxia.
Still, apart from the question of PpCO2, I completely agree that the total effect of the exhale at the acent as described by Eric is highly speculative, depending on the individual body response, and can be very dangerous for inexperienced divers. I trust Eric's experiments and believe that in his case this method triggers the needed response, but am not persuaded it is an universally usable method, and would not try recommending it to anyone without any deeper research and experiments on a wider sample of subjects.