sled diving within AIDA

[sebastien murat]

How many divers can actually undergo complete alviolar collapse without suffering lung squeeze?

Is the question rhetorical?
How many dive really deep, or on empty, and how many have had lungs squeeze?
Lungs squeeze is due to a combination of things, not just diving deep, e.g., prior packing, but diving deep can help trip it...then we call it a squeeze because we were diving deep

 

[Kars]

Sebastien, have you got any wild guess, what the cross-over depth is?

I mean from what depth is it more beneficial to start diving FRC?

To what depth can one dive FRC without the need for wet O2 decompression?

 

[Siku]

Is the question rhetorical?

No I'm genuinely asking. Is complete collapse not the province of the super flexible? I mean without sufficient chest flexibility squeeze is going to happen before collapse, no? (I know blood shift plays a part too by supporting the chest cavity).

I understood squeeze was caused by negative pressure in the lungs (and e.g. sudden movements or major contractions while negative), and that packing would offset this, or postpone it till deeper. So interesting you say packing is a CAUSE of squeeze. Can you explain more?

Kars doesn't that rather depend on when residual volume is reached? I mean with half as much air in the tank RV's at half the pressure, right?

But mouthfill/frenzel would continue to work AFTER alviolar collapse. Eric has said that theoretically a good mouth fill can EQ deeper than current CWT, and that's regardless of what's left in the lungs.

Still a DCS risk associated with mouthfill though. Damn.

 

[rddk]

A dan research was looking for a relation between lung squeeze and genetic predisposition, because some people can suffer of lungs squeeze even on shallow dives withouth packing.
Btw i dived with seb in France to 46 mt on a sled and was empty withouth any warm up and no lungs squeeze at all, also i did repetitive dives to 40+ metres on empty and didn't have any squeeze, one guy that was with us was going on full and had squeeze at same dept, that's ironc...

 

[sebastien murat]

Sebastien, have you got any wild guess, what the cross-over depth is?

I mean from what depth is it more beneficial to start diving FRC?

To what depth can one dive FRC without the need for wet O2 decompression?

Its individual. It depends on lots of things, but the most obvious that come to mind are:
- lung capacity on full vs. empty
- swimming efficiency (e.g., fins vs. no fins, poor technique)
- (surface) buoyancy, i.e., fat and wetsuit
- ability to invoke the DR
- ability to invoke an exercise response
- activity level and what you are doing `down there´
- blood volume
- dive depth and
- dive duration, when coupled to surface intervals, i.e., fatigue

The only way you can know is by doing lots of dives under constant conditions and tweaking it a little. I had the opportunity to literally undertake +10,000 empties over the last dozen years so I'm pretty well atuned to what works and what doesn't. BUT, sometimes I dive on full if I know my burn rate is going to be high because of, say, the need to get down there quickly, perhaps several times, and the need to keep my arms and legs aerobic with essentially no fatigue.....then some people say to me "but you said &@&%!". Like I keep saying over and over the recipe varies on the occasion and one situation may require an altogether different approach.

I understand O2 deco, but in my opinion its all wrong cause you shouldn't mix low metabolic rates with elevated O2 levels. The only way it can work is if the two are matched, but if you are on the slippery DCI slope then what choice do you have. My risk of DCI is probably next to nothing even on deep NLs. I have a low N2 load because of a:
- low N2 uptake due to:
- low cardiac output (because of a strong and prompt DR)
- pulmonary shunt and collapse at fairly shallow depths (because of the low lung volume)
- low N2 load, because I don't carry much
.....a tell-tale sign is the complete absence of N2 narcosis at any depth


On the issue of `squeezes´:
my understanding is that lungs are collapsed regularly during surgery so collapse per se is not necessarily the problem. I've had several squeezes (nothing major). All occurred when I did empties, then packed and then dived deep. Similar depth dives on empties, for me, did not result in any such experiences. I believe that `densifying´ the lungs by engorging them with blood (the blood pooling that comes with immersion, especially empties), followed by stretching them by packing is probably the culprit; obviously they're not so elastic then. You can probably get the same effect without doing empties first, if you over-stretch the membranes ....a bit like over-stretching rubber past the the point where all the stretch is recoverable. Of course, the system adapts, so that if your max packing pressure now no longer reaches this point then it may be ok.

The other BIG problem I have with packing is that if you combine it with the blood shift, which also dilates your heart (in a big way) you can do damage to the heart muscles, as has been shown by Andersson and Liner. I don't think you want to mess with that considering the state of your heart and what you probably put it through. But hey people still smoke knowing its bad for them. It's just all a little hard to respect what people do when I see them consciously doing things that damage their bodies (and minds) because they have a too willful will and want to prove something to themselves (or others) by chasing that pathetic little tag at the bottom of some line. I say this because I've screwed up a lot and have had lots of time to reflect. I'm certainly not proud or don't respect anything I've personally done that was geared in that way. But if we're talking exploration, then I'm all ears.

 

[Kars]

Reading this stuff makes me wish I had a place nearby to explore.

Thanks Sebastien, talks like these are very motivational to me.

 

[sebastien murat]

Out of interest, did this absent-minded chap (hate that "oops, I've just offed another marine mammal" feeling) happen to replicate the seal's normal dive profile?

here's the break-down: seal was dropped to 300 m in 3 min and ascended in 9 min ...... presumably at a constant rate....which would indicate a more or less similar `natural´dive profile as far as descent is concerned, but the ascent rate took somewhat longer than normal; seals always ascent slower than they sink.

 

[efattah]

My dive response isn't that great. Having said that, I got zero narcosis on FRC dives to 72m, where dives to the same depth with packing produce significantly noticeable narcosis. When diving 'for fun' in dark cold water, with packing, I get narcosis as shallow as 40m, and at 45m it is severe. FRC diving 'for fun' in cold dark water, 40m-45m gives zero narcosis. This would imply lower N2, but it could also be due to the fact that I produce almost no CO2 on the descent. Either way my risk of DCS was basically the same, in fact I would say I was more likely to get bent on the FRC dives because I could take a much shorter surface interval (my typical surface interval between deep/fun FRC dives is 3:30 to 5:00, versus 6:30 to 8:30 between packing dives). The long surface interval from packing dives is needed to blow off the extra CO2 that I absorb at depth.

On 'line' dives, I can do two dives to 60m with a 10-12 minute interval, either with packing or at FRC and I am pretty safe as long as I don't ascend at a sprint. Increase that to 70m (x2) or 60m (x3) and the symptoms appear very reliably. A single dive to 65m can give me small symptoms if I bolt up at a breakneck pace.

Adding 'apnea deco' on air following each dive, and I could do 60m x 4 and get very minor symptoms, versus more severe symptoms at 60m x 4 with no deco at all. O2 deco seems more effective than apnea deco but has other disadvantages that Seb mentioned.

 

[sebastien murat]

"FRC diving 'for fun' in cold dark water, 40m-45m gives zero narcosis. This would imply lower N2, but it could also be due to the fact that I produce almost no CO2 on the descent."

Your CO2 production would be lower than on full but it would not be almost zero, because the DR takes time to kick in and fully develop. Even then, if you have a poor response then your burn rate will still be high, especially if it doesn't take long to reach the bottom or if you engage in any swimming during descent, or shiver. Also, the lungs aren't much of a viable sink for CO2 on empties, because of the much reduced initial volume and additional compression, so any CO2 produced likely becomes stored in tissues, including blood, which would tend to fast track reaching hypercapnia, i.e., compared to fulls metabolic considerations aside. So, the lack of narcosis, I would say, is due almost entirely to a lack of N2 rather than CO2.

It's also important to appreciate that if one's DR is poor, which I recall yours is (correct me if I'm wrong), then rate of N2 uptake (via a reduced cardiac output) wont be prompt enough before you reach a substantial shunt or collapse, so you'll probably absorb a not inconsiderable amount of N2. If you've suffered a previous DCI then you're also at increased risk.

Based on what you just described, I guess there's no more deep diving for you...?

 

[chrismar]

Simple as I am, can you please explain to be why total volume of N2 (or any other gas) would affect absorption rate? Gas partial pressure dictates this sort of thing, so I fail to see how, why or where volume comes into it until you actually start running out of molecules. Lower total volumes allow bigger shifts in gas ratios for gasses getting consumed or produced (O2, CO2), but the N2 % just isn't going to shift in any meaningful way.

 

[sebastien murat]

Two ways:
-a low lung volume will result in your lungs experiencing an earlier collapse/ shunt, resulting in a reduced/restricted uptake. I should expand here. basically, your upper airways separate from your lower airways earlier (at a lower partial pressure difference), so that the absolute amount of gas that can enter the system is reduced
-a low lung volume invokes a more prompt and pronounced DR, which slows the rate at which the blood picks-up gases from your lungs, and also the extent this gassed-up blood can reach peripheral sites, e.g., joints, non-working muscles, etc. In other words, uptake and delivery slow down, which reduces the risk


....in short!

 

[sebastien murat]

Since someone asked me why you shouldn't jump on O2 after breath-hold diving, I though to post more widely:

If you deco or resuc on anything greater than about > 20% O2 you're probably doing yourself and the victim a great dis-service.

During the recovery period the sustained and lowered nervous system temperature (i.e., that includes your brain by the way) post breath-holding provides neuroprotection against the NOT insignificant and damaging effects of free, reactive O2 radicals; it also slows the rate at which N2 comes out of solution. The requirement or suggestion of administering 100% O2 (or greater, during in-water deco) is just plain dangerous and wrong , as you simply accelerate radical damage, aggravate re-perfusion injury, and bubble formation. Bottom line: plain old air is good enough and best. Actually, expired air resuc may possibly be better, since its compatible with a < 20% O2, and the higher CO2 is known to be neuroprotective. If you're the designated (educated) responsible and administer anything > 20% air, you are in breach of your duty of care to yourself or anyone else.

 

[trux]

Very interesting! I wonder though why O2 deco is common at scuba including tech diving too, and why DAN and other authorities advise administering O2 at decompression accidents. Or am I wrong?

If it is true, the information should be consulted with the medical comission of AIDA, since I believe the O2 decompression is a recommended procedure not only at sled dives, but also at

 

[sebastien murat]

Note: I specifically referred to breath-hold diving and not diving with breathing apparatus. BHD generates altogether different conditions in metabolic status

Having said that, we're also working on a means of inducing a down-regulated metabolic state (short-term torpor), with associated core temperature cooling, for conventional diving, as this would greatly slow the rate of N2 uptake, narcosis, hypercapnia, intolerance of hypoxia, etc., during diving; apart from restricting the rate of bubble formation during ascent/post-dive surface interval/ascent to altitude. Importantly, we've managed to induce this state during normal breathing, in a non-diving subject at rest (me), and I'm now looking at packaging this as a gadget or integrating it conventional equipment for an active SCUBA (or whatever) diver. Even more interesting perhaps is that it seems to result in a shift to fat metabolism with suppressed appetite and inactivity, just like in hibernating animals. Exciting times I think since its awfully difficult to get overweight/obese people to lose fat by adhering to an eat less + exercise regime.


PS: this is not a DAN sponsored project...its purely commercial but, nonetheless, a collaborative project with academia. We're looking to publish the results of these experiments, shortly, possibly in a high impact journal like Nature i.e., if they settle with a one-case study, otherwise we'll have to recruit more subjects or settle for a lesser journal. The results are being presented at an MRI conference in Colorado, in March. These results have broad and major implications that go well beyond diving, hence why advising other divers indirectly via AIDA doesn't rank high on my list of must dos. Moreover, I prefer a more direct, not necessarily politically correct approach. Anyway, does the medical arm of AIDA even dive?? Last thing: I'd have no interest in addressing yet another bunch of busy-body bureaucrats, with arm-chair opinions, trying to bolster their CVs .... no disrespect intended but been there, done that.

 

[trux]

Seb, I fail to see the difference between scuba and breath-hold diving in this case. You tell that it is the O2 free radicals that cause the damage to the nervous system and accelerate the bubble forming. The radicals will be there in both cases, at an O2 deco after scuba as well as after a breath-hold. You tell the damage will be bigger because of the lower brain temperature at a freediver, but I am not quite persuaded that after 3 minutes of a freedive the brain will be much cooler than after an hour of scuba diving (despite the continuos breathing and higher metabolism).

EDIT: Please also note that not all freedivers use your method of pre-dive supercooling of their brains, that I I've read you alegedly do. So does your advice not to use O2 for deco goes just to the freedivers diving in the same style as you, or generally?

EDIT: And as for the protective role of CO2 - the level of CO2 will be still higher at a freediver even after a few breaths, than at a scuba diver, so from this point of view it should be then even worse for a scuba diver, or not?

Do you have any data that would back your claims? I'd love to see them, because it sounds interesting, but so far I am not very persuaded it is not just a hypothesis.

 

[Kars]

I'm wondering, can one (learn) to induce this hibernation state in a glance?

You hint about a device for scuba divers too?

In find this stuff fascinating, and am keen on learning to do and understand it.
Can it also mean longer full lung static breath holds?

Learning that those free radical O2 indeed are kept at bay by exhale, hibernation dives is very interesting, and indeed it points towards that the next level is reduced lung volume dives, possibly enriched with the hibernation technique.

Great stuff, keep it coming! I'm a dry sponge here...

Love, Courage and Water,

Kars

 

[sebastien murat]

You tell that it is the O2 free radicals that cause the damage to the nervous system and accelerate the bubble forming. The radicals will be there in both cases, at an O2 deco after scuba as well as after a breath-hold. You tell the damage will be bigger because of the lower brain temperature at a freediver, but I am not quite persuaded that after 3 minutes of a freedive the brain will be much cooler than after an hour of scuba diving (despite the continuos breathing and higher metabolism).

EDIT: Please also note that not all freedivers use your method of pre-dive supercooling of their brains, that I I've read you alegedly do. So does your advice not to use O2 for deco goes just to the freedivers diving in the same style as you, or generally?




You've misunderstood.

The genetic blueprint for torpor or metabolic down-regulation, in this instance triggered by the threat of hypoxia, already exists in you; its common to all aerobic life. Moving on....let's not get to esoteric

Cold increases solubility of gases in tissue, which reduces bubble size, and probably nucleation based on what I've seen on very superhydrophobic surfaces. Radicals, as far as I know, have nothing to do with bubble growth dynamics.

Radical damage occurs because of the `excess´O2 vis-a-vis a lowered metabolic rate. Some regions are ischemic and when you reperfuse them the elevated O2 does the damage, not the ischemia. Brain temperature drops promptly as soon as you hold breath and it is magnified by the DR. The rate is as high as 1 degree C/minute (in my case) and with no external DR magnifiers, like cold face, etc. It takes time for the effect to reverse and if you dive before the temperature returns to baseline you just step-down progressively. The animal data backs all of this (i.e., birds, mammals, reptiles). My physiology is no different to yours intrinsically. Maybe a strong DR, but that's all.

Your brain will not cool during scuiba, unless you lose your ability to shiver, in which case you are no hypothermic, in which case your toast unless you have brown fat kicking in or someone/something warms you up. This torpor is full regulated and not hypothermia.

The CO2 protects against hypoxia, i.e., during low MET state, but all bets are off if you jump on O2. Need to think about your question to this one...give me a day....I'm writing at light speed with no time

The data goes out to reviewers then you get to see it, like everyone else...sorry...their rules, not mine.

To be continued...got to go.

 

[sebastien murat]

continuing....

Cooling occurs during BHD diving, but you can get a head start with the device. This would mean reduced N2 load, etc.

The ability to invoke torpor probably varies with individual and their state, just like everything else in life.

Trux, this is not a hypothesis or data from some test-tube or even trial on rodents, this is in-human observation spanning several years, and these observations are corroborated by direct in-animal data on diving animals (birds and mammals). In fact, our rate of cooling was more prompt and faster than even the dive animal data and, moreover, faster (over the range we looked at) then what can be achieved by cardiopulmonary by-pass. We didn't even attempt to induce a full-blown response with face cooling. In fact we covered much of the face with foam pads, since the real world seldom has cold water on stand-by when you need it.

With regards to SCUBA and CO2: by cooling the brain tissue, more CO2 can be dissolved (Henry's law) before it has an adverse effect. In fact CO2 is the reason why MET drops. Furthermore, tolerance of hypercapnia is enhanced because the MET rate is lower (time/dose response curve is more gentle and forgiving)

Also, from a SCUBA point of view, a lower MET means enhanced tolerance to O2 toxcity, which would mean deeper and longer on air or O2. How much more? Don't know. Could be insignificant actually.

 

[sebastien murat]

This is not something you learn, this is something you do! YOU ARE ALREADY DOING IT WHEN YOU DIVE, but some do it better than others.

The term hibernation is a misnomer that conjures up sci-fi, pseudo science and space travel, of which I have no interest. All hibernation is, is conservation of energy along an energy continuum, such that some engage in it to a lesser or greater extent over shorter or longer periods. Typically wehn one refers to hibernation one means something on the order of a (winter) season) but the line is fuzzy. In fact, its an artificial construct with no real founding in reality. And no, it does not involve lowering body temperature to near-freezing temperatures or loss of consciousness in human or human-sized animals; lucky for us otherwise you'd be paralyzed and worse. In (adult) humans, the maximum drop in MET you'll get is no more than about 70-75% below basal rates, and that is associated with only a modest drop in temperature (4-5 degrees). There are several ways you could attempt to trigger this, but the threat of asphyxic hypoxia, i.e., BHD, is an omnipotent trigger. Not surprising really since O2 stores are small, strictly limited, and MET rates at the start of diving are not exactly that of blue whale (its slow).

Yes Kars, it will mean a long static. To get a really long static, I mean something on the order of say maybe 20-25' (?? haven't tried or crunched the numbers...ask Peter Lindholm.....he's knows the numbers as well as anyone) you'd have to start off in a torpid state already. To maximally affect this condition before a dive, could be done, but the issue is how do you induce this state when you're breathing and how long will it take. Firstly, you have to stack the situation in your favor, e.g., cold periphery, fasting, rest, diet, time of day, etc. You also have to understand that even in the best human-sized hibernators it can takes some time. Anyway, so now we are talking about a long wind-up time. And, we are talking about a stunt, and I can feel my interest starting to wane!

A low MET produces less radicals (and you'll probably live longer too judging from the latest research (in humans and animals), but if your O2 need is actually over-matched by an excessive O2 supply then this where the radicals really kick-in. The important thing is that supply must be matched to demand, otherwise you'll get reperfusion injury once that blood re-enters those previously rendered vasoconstricted tissues. It can get all pretty too confusing, I know, but if you keep in mind that its (in most cases) not low oxygen levels per se that does tissue damage, but rather a re-supply with too much O2, and too quickly, that does the real damage you'll appreciate that a slow top-up is the way to go. Anyway, all this IS known...just dig-around the literature. Indeed, there's a move (if it hasn't already happened) to not administer 100%O2 to hypoxic neonates.

Having said all this, if you suffer a DCI hit, what do you do? Not talking about prevention here, but treatment. Do you add O2 to wash-out the N2 or do you try to lower MET?
- best not to get the hit in the first instance
- if you cool things with MET reduction, the bubbles will shrink, which in some ways is akin to recompression therapy, but with enhanced neuroprotection since the gas wont come out of solution so quickly and the inflammatory response is mitigated by cold.
- I'm not an expert on HBOT, so someone else can comment on that, but I'm always keen to go head to head to find better ways of doing things (but not if I sense show boating coming on)


Careful with the "dry sponge", sponges can get over-saturated, after which they become pretty useless unless you squeeze the water out of them!

 

[trux]

As to the reoxigenation damage of ischemic tissue, I looked it up and this is indeed a known problem in the clinic medicine. It is called Reperfusion Injury. But it is a question to which extent we can speak about ischemic tissue at a freediver, and to which extent the use of pure O2 will make a difference to normal air. The reperfusion injury happens at reoxygenation of the tissue (not necessarily only after administering pure O2). When there is 5 times more O2 in the lungs, it does not mean at all that there will be 5 times more O2 in the blood, and 5 times more free radicals. In other words, if the reperfusion injury is to happen to the hypoxic tissue, I am uncertain what difference the use of O2 in comparison to plain air will make. If you have any data on this, it would be highly appreciated.

Anyway, thanks to brining it up. I understand you have no interest to communicate with AIDA, but I think it is important that it is at least reported to them, and that they decide for themselves whether to look at it closer or no.