DCI and freediving

[efattah]

If at -25m my lungs have 8% CO2, 6% O2, and the balance as nitrogen, then after exhaling I will still have 8% CO2, 6% O2 and the balance as nitrogen, except the total volume is less. I don't follow or see any method how this could decrease arterial CO2 levels; in fact, after exhaling my urge to breathe increases dramatically, so much so that I am afraid to exhale every time and must force myself to do it, because an already straining urge to breathe becomes much worse. Regardless of the calculations, I always follow the results of actual experiments, and in my particular case this maneuver helps, but *only* if accompanied by the abdominal pressure maneuver. Without that I'm doubtful as to how much it would help. If you try a dry static, and exhale even a few liters near the end, notice how the urge to breathe explodes in intensity.

With the Xen, the complexities of deco with incomplete blood circulation are hopelessly complicated, which is why I chose an experimental method to 'fit' the algorithm to the existing freediving DCS data.

 

[growingupninja]

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

When this has happened to you (distress=sudden single digits) did you experience any physical 'symptoms' such as cramping? I have read some of your posts on stress and apnea and read the study on forced immersion of juvenile seals, but don't currently have a HR monitor I can dive with. From tests on dry land and cold water facial immersion though I get a pretty solid dive response.

In my own experience with extreme distress while diving I was spearing near a large underwater mesa. Not particularly deep but it was winter and know I would be experiencing some mild DR (probably about 15% bradycardia) from water temp, despite full lungs and a mask. I was poking about near the table top at about 30' when a very powerful and unexpected deep swell caught me and slammed me headfirst into a rock. I was caught completely unaware and impact was hard enough to rattle my teeth, and had my tounge been in a different position I would have bitten through it. My dive hood saved my life or at least a very, very nasty head wound. Stupid thick skull was also in my favor.

But in seconds following impact as adrenaline flooded my body, nearly every muscle I could feel began to cramp. Cramps faded quickly and I felt my head, collected myself, etc, and it occurred to me that I might have been under for a while even though I did not feel even faintly hypoxic so I went up. I did not have a HR monitor but the results would be fascinating and it is not a repeatable experience. Training dry exhale dynamics, I frequently get cramps as extreme bradycardia and vasoconstriction as measured by a pulse O2 monitor kick in, but not suddenly and to that extent.

 

[sebastien murat]

No, I did not get cramps.

When this has happened to you (distress=sudden single digits) did you experience any physical 'symptoms' such as cramping? I have read some of your posts on stress and apnea and read the study on forced immersion of juvenile seals, but don't currently have a HR monitor I can dive with. From tests on dry land and cold water facial immersion though I get a pretty solid dive response.

In my own experience with extreme distress while diving I was spearing near a large underwater mesa. Not particularly deep but it was winter and know I would be experiencing some mild DR (probably about 15% bradycardia) from water temp, despite full lungs and a mask. I was poking about near the table top at about 30' when a very powerful and unexpected deep swell caught me and slammed me headfirst into a rock. I was caught completely unaware and impact was hard enough to rattle my teeth, and had my tounge been in a different position I would have bitten through it. My dive hood saved my life or at least a very, very nasty head wound. Stupid thick skull was also in my favor.

But in seconds following impact as adrenaline flooded my body, nearly every muscle I could feel began to cramp. Cramps faded quickly and I felt my head, collected myself, etc, and it occurred to me that I might have been under for a while even though I did not feel even faintly hypoxic so I went up. I did not have a HR monitor but the results would be fascinating and it is not a repeatable experience. Training dry exhale dynamics, I frequently get cramps as extreme bradycardia and vasoconstriction as measured by a pulse O2 monitor kick in, but not suddenly and to that extent.

 

[sebastien murat]

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.

There are two things here which we must separate: 1. does ascending per se lower hypoxia tolerance? and, 2. does exhaling counteract this effect, thereby maintaining or even enhancing hypoxia tolerance?

In the first instance:
The data from Líner et al (1993) clearly demonstrates that PACO2 decreases during ascent. Presuming there is rapid equalization between PACO2 and paCO2, as you suggest, this would point to a reduction in PaCO2 also. Further, their data clearly demonstrates that a large quantity of CO2 is mobilized into the lungs upon decompression. This CO2 coming out of the blood. The additional graphs the offer, on gas exchange, further demonstrates this very well, and I quote from this reference:
"...during the ascent, the PACO2 decreased,..."
"...after leaving the bottom, CO2 moved into the alveoli at an [accelerating ] rate reaching 218 +/- 13 ml/m/m2 ... late in the ascent."

You can see this also from Lanphier & Rahn (1963) article: CO2 moves back into the lungs and PACO2 drops. Fig.7 clearly shows PaCO2 dropping.
"...PCO2....decreases rather abruptly on ascent."
"The volume of CO2 is low at the outset .... until the beginning of ascent, when a relatively large increase occurs."
"... unexpectedly low values of PCO2 found upon surfacing from dives."
"The volume of CO2 transferred to the lungs ...... modifies the fall in PCO2 to a considerable extent."

And, elsewhere, in Hong et al. (1963):
"Upon return to the surface CO2 leaves the blood...". Fig. 7 of this publication clearly shows movement of CO2 out of the blood and into the lungs and this processing accelerating with the rate of decompression, i.e., with decreasing depth. The only thing the dropping pCO2 does is offer subjective/relative relief in the urge to breathe, not enhanced hypoxic tolerance. Indeed, hypoxia tolerance would decrease



In the second instance: it sounds plausible, but let's measure it!
I propose that someone with a flow-though CO2 gas analyzer do the following very simple test: breath-hold at TLC until contractions start, after which you exhale progressively, measuring pACO2 continuously as you exhale to FRC

 

[sebastien murat]

If at -25m my lungs have 8% CO2, 6% O2, and the balance as nitrogen, then after exhaling I will still have 8% CO2, 6% O2 and the balance as nitrogen, except the total volume is less. I don't follow or see any method how this could decrease arterial CO2 levels; in fact, after exhaling my urge to breathe increases dramatically, so much so that I am afraid to exhale every time and must force myself to do it, because an already straining urge to breathe becomes much worse.

Sure reducing lung volume, in itself, reduces BH ability all other things equal. Normally, however, if you hold breath and then release there is prolongation of BH. Try it by BH at TLC ? contractions and then exhaling (progressively or in one hit). The decrease in the urge to breathe is due to either:
- unloading of lung stretch receptors (see Flume et al. 1995); and/or,
- a drop in PA/aCO2

I'm interested in whether the second possibilityexists.

 

[Fondueset]

Possible
A: mild concussion
B: transient compression of neck/base of skull.

When this has happened to you (distress=sudden single digits) did you experience any physical 'symptoms' such as cramping? I have read some of your posts on stress and apnea and read the study on forced immersion of juvenile seals, but don't currently have a HR monitor I can dive with. From tests on dry land and cold water facial immersion though I get a pretty solid dive response.

In my own experience with extreme distress while diving I was spearing near a large underwater mesa. Not particularly deep but it was winter and know I would be experiencing some mild DR (probably about 15% bradycardia) from water temp, despite full lungs and a mask. I was poking about near the table top at about 30' when a very powerful and unexpected deep swell caught me and slammed me headfirst into a rock. I was caught completely unaware and impact was hard enough to rattle my teeth, and had my tounge been in a different position I would have bitten through it. My dive hood saved my life or at least a very, very nasty head wound. Stupid thick skull was also in my favor.

But in seconds following impact as adrenaline flooded my body, nearly every muscle I could feel began to cramp. Cramps faded quickly and I felt my head, collected myself, etc, and it occurred to me that I might have been under for a while even though I did not feel even faintly hypoxic so I went up. I did not have a HR monitor but the results would be fascinating and it is not a repeatable experience. Training dry exhale dynamics, I frequently get cramps as extreme bradycardia and vasoconstriction as measured by a pulse O2 monitor kick in, but not suddenly and to that extent.

 

[trux]

There are two things here which we must separate: 1. does ascending per se lower hypoxia tolerance? and, 2. does exhaling counteract this effect, thereby maintaining or even enhancing hypoxia tolerance?

1. Of course, the ascent lowers the PpCO2, there is no doubt about it, and nobody disputes it here. However, the drop in pressure is present and identical regardless whether you are on full lungs, empty lungs, or whether you exhale at certain depth.

What makes the difference, is the lung volume - the bigger it is the more CO2 diffuses from the blood stream into lungs at the ascent. So therefore, of course, we all agree that FRC protects from the SWB better than full lungs, but in the same time the method Eric described offers this advantage too.

2. Yes, it does, because you lower the volume into which the CO2 difuses from the blood, hence slowing down the diffusion rate. The question whether the loss of O2 will be sufficiently compensated by the effect of a stronger DR, is an entirely different topic, that is not the subject of this dispute - I believe there are too many variables to incline to one or the other side without a detailed research, but I believe Eric that it works in his case.

Sure reducing lung volume, in itself, reduces BH ability all other things equal. Normally, however, if you hold breath and then release there is prolongation of BH. Try it by BH at TLC ? contractions and then exhaling (progressively or in one hit). The decrease in the urge to breathe is due to either:
- unloading of lung stretch receptors (see Flume et al. 1995); and/or,
- a drop in PA/aCO2

Both of this happens only on the surface:

- The unloading of stretch receptors is not bad in itself, and won't impact the hypoxic tolerance, but it won't happen much at 20m depth anyway (the lungs are not really stretched at that depth).

- the drop in PACO2/PaCO2 happens due to the reduced transpulmonary pressure after the exhale. On the surface the transpulmonary gradient is small, but still measurable. Submerged a few decimeters it is already completely negligible in comparison to the ambient pressure, hence will not have any measurable influence in depth. From the physical point of view, I see no way the PaCO2 or PACO2 could drop at depth after the exhale.

 

[growingupninja]

Possible
A: mild concussion
B: transient compression of neck/base of skull.

I don't think it was concussion; I had a bump on my head but no symptom and am familiar with concussions from ring sports. Could have been other factors at work--cold, mild dehydration, sudden defensive/unconsciouss muscular contraction. Neck compression is interesting. Now that you mention it, I think the one other time I remember taking that kind of impact at that angle (stalling out of a backflip while on a gymnastics springfloor) I might have gotten immediate unexplained leg cramps. Somewhat comforting to know that the body maintained a diving state even if other involuntary reactions happen--I didn't lose air or inhale or seem to suffer any sudden O2 demand, although my lungs were in a very comfortable neutralish state.

I do want to get a HR monitor I can dive with; I have never felt a huge need for monitoring time or depth since as primarily a spearfisherman my dive profiles are very erratic but from dry training with a pulse meter I have come to realize that HR could be very useful to me. I am not exactly doing 70m dives but correlation between HR and DCS also makes a lot of sense, as Seb maintains.

Thanks all for this discussion.

 

[Fondueset]

For sure spinal compression can have weird effects like that.

 

[sebastien murat]

I don't think it was concussion; I had a bump on my head but no symptom and am familiar with concussions from ring sports. Could have been other factors at work--cold, mild dehydration, sudden defensive/unconsciouss muscular contraction. Neck compression is interesting. Now that you mention it, I think the one other time I remember taking that kind of impact at that angle (stalling out of a backflip while on a gymnastics springfloor) I might have gotten immediate unexplained leg cramps. Somewhat comforting to know that the body maintained a diving state even if other involuntary reactions happen--I didn't lose air or inhale or seem to suffer any sudden O2 demand, although my lungs were in a very comfortable neutralish state.

I do want to get a HR monitor I can dive with; I have never felt a huge need for monitoring time or depth since as primarily a spearfisherman my dive profiles are very erratic but from dry training with a pulse meter I have come to realize that HR could be very useful to me. I am not exactly doing 70m dives but correlation between HR and DCS also makes a lot of sense, as Seb maintains.

Thanks all for this discussion.

Its not just that there's a correlation between HR and DCI, but perhaps more importantly, is that heart rate during BHD reflects your metabolic rate (MR; your rate of oxygen consumption). Your metabolic rate directly reflect not only your ability to dive for longer but also more safely, since hypoxia tolerance (dose/timer tolerance) is largely determined by MR and, hence, your risk of BO. With a heart rate monitor, you can do many things:
- see if your are genetically predisposed to BO, i.e., poor DR, and what you can do to sensitize the DR
- monitor how various conditions and dive strategies influence your risk, e.g., varying lung volume, water/air temperature, ascent rate, work effort and timing, diet type and timing, etc.
- instructors would be identify students at higher risk of BO, i.e., low DR responders

In short and innumerable number of things.

In this respect being able to correctly measure HR, especially instantaneous (beat-to-beat) HR will be crucial. I'm hopeful that something soon will be available specifically for freedivers from Uwatec. In my humble opinion, it would be the single most important practical measure of a diver's status, especially if employed in conjunction with (high HR) alarm. I can't wait. And, I'm not plugging UWATEC because I use a Galileo....just stating fact.

Gees I haven't been active on DB as much as this in years!

 

[growingupninja]

Its not just that there's a correlation between HR and DCI, but perhaps more importantly, is that heart rate during BHD reflects your metabolic rate (MR; your rate of oxygen consumption). Your metabolic rate directly reflect not only your ability to dive for longer but also more safely, since hypoxia tolerance (dose/timer tolerance) is largely determined by MR and, hence, your risk of BO. With a heart rate monitor, you can do many things:
- see if your are genetically predisposed to BO, i.e., poor DR, and what you can do to sensitize the DR
- monitor how various conditions and dive strategies influence your risk, e.g., varying lung volume, water/air temperature, ascent rate, work effort and timing, diet type and timing, etc.
- instructors would be identify students at higher risk of BO, i.e., low DR responders

In short and innumerable number of things.

In this respect being able to correctly measure HR, especially instantaneous (beat-to-beat) HR will be crucial. I'm hopeful that something soon will be available specifically for freedivers from Uwatec. In my humble opinion, it would be the single most important practical measure of a diver's status, especially if employed in conjunction with (high HR) alarm. I can't wait. And, I'm not plugging UWATEC because I use a Galileo....just stating fact.

Gees I haven't been active on DB as much as this in years!

I tend to agree with what Will said about taking too much from marine mammal studies; they are just so different from us, but one of the seal studies mentioned a trend--it seems the freeranging seals dived at a variety of depths and durations, but total number of beats per dive stayed relatively consistent on a seal to seal basis. I wonder if we will see a freedive computer at some point which just counts beats and warns when you are exceeding your limit? This is something you could test--have trained divers do breathholds accompanied by various exertions and record the TOTAL number of beats before O2 sat reaches likesay 85%. Exertions might vary; ie in know in my case once I begin to experience DR from hypoxia/hypercapnia a rise in exertion level results in lactic acid penalties but no rise in HR. I don't have a device to measure total beats but if I did I'd experiment.

Re: HR while diving as a way for instructors to quickly identify students who might be extremely susceptible to blackout. There is guy I have trained with in the pool who is a beginner and to my knowledge he has ended any max dynamic in samba, and usually at a distance that seems short given his reasonable fitness level. He says he does not experience contractions except had one once right before samba and he doesn't seem to be hyperventilating. I have wanted to see what his pulse looks like during a breathhold. I suspect he doesn't experience hypoxia/hypercapnic DR.

 

[sebastien murat]

I tend to agree with what Will said about taking too much from marine mammal studies; they are just so different from us, but one of the seal studies mentioned a trend--it seems the freeranging seals dived at a variety of depths and durations, but total number of beats per dive stayed relatively consistent on a seal to seal basis. I wonder if we will see a freedive computer at some point which just counts beats and warns when you are exceeding your limit? This is something you could test--have trained divers do breathholds accompanied by various exertions and record the TOTAL number of beats before O2 sat reaches likesay 85%. Exertions might vary; ie in know in my case once I begin to experience DR from hypoxia/hypercapnia a rise in exertion level results in lactic acid penalties but no rise in HR. I don't have a device to measure total beats but if I did I'd experiment.

Re: HR while diving as a way for instructors to quickly identify students who might be extremely susceptible to blackout. There is guy I have trained with in the pool who is a beginner and to my knowledge he has ended any max dynamic in samba, and usually at a distance that seems short given his reasonable fitness level. He says he does not experience contractions except had one once right before samba and he doesn't seem to be hyperventilating. I have wanted to see what his pulse looks like during a breathhold. I suspect he doesn't experience hypoxia/hypercapnic DR.

I'm familiar with that particular literature. There not so different. Most of the essential difference is that everything in them is juiced-up. If you look over all the literature on cardiovascular diving reflexes , spanning mammals (including humans), reptiles, and birds you'll see what I mean. This stuff is hard-wired from way back when. Some people look for differences and then see only differences. I look for similarities and see lots of similarities, but not only similarities. There's a world of difference studying diving animals and not freediving yourself and studying diving and also diving. For example, years ago I remember that they found out and were surprised to discover that diving animals glide on the way down to save energy. If they bothered to ask any competent human freediver or actually freedived it would have been bloody obvious. I see this kind of stuff all the time and I have a hard time taking it serious. Bit like being an expert fisherman I guess but only in theory.

Total number of beats could clarify the picture, but more importantly is the way the HR responds in the ascent and shortly after surfacing. I mean, you can have a few overall number of beats but a dramatically increasing HR during ascent and upon surfacing, which wouldn't be ideal from the point of view of hypoxia tolerance on an extreme dive.

This fella, he sounds like he has a high metabolic rate all the way through (=> poor DR), in which case stimulation from hypercapnia (=> contractions) is greatly depressed, because CO2 is very soluble in peripheral tissue, or like you suggest he's CO2-insensitive...either way not good...but HR monitoring should id the problem.

 

[Fitz-Clarke]

I disagree that the sinuses play any significant role in gas exchange during a dive. Human sinus blood flow is only about 0.8 to 1.2 ml/min (1). Total for all sinuses would be on the order of 5 ml/min. Compare this with 800 ml/min blood flow to the brain. Furthermore, the sinuses receive most of their blood supply from branches off the internal carotid arteries, which are already nearly saturated with nitrogen coming directly from the lungs. Even if you had total pulmonary shunt due to complete lung collapse with zero exchange in the lungs, the half-time for perfusion-limited uptake of nitrogen from the sinuses to equilibrate a circulating blood volume of 6 litres would be Ln2 * 6/.005 = 831 min. Gas uptake from the sinuses would be negligible on a BH dive of several minutes.

Despite the diving response, brain blood flow actually increases during apnea, mainly due to increasing carbon dioxide. This is a consistent finding in studies looking at carotid or cerebral blood flow in humans and diving mammals (2,3). In humans during static apnea it rises from about 750 to 800 ml/min. The drop in cardiac output pretty well matches the degree of peripheral vasoconstriction. This coordinated response between bradycardia and vasoconstriction keeps blood pressure from rising or falling too much. But the brain is exempt from the diving response, so the diving response alone cannot provide any protection from neurological DCS.

Although you guys speak confidently about nitrogen kinetics in the peripheral tissues, there is no data on nitrogen washout kinetics after BH diving and role of diving response. It has never been measured. In fact it would be very difficult to measure. Xenon washout kinetics has been measured in dog muscle after single exposure (4), but without vasoconstriction from a diving response. You could look at recovery of muscle oxygen kinetics with NIRS as a surrogate of blood flow, but not nitrogen. Rate of vasoconstriction onset has been measured in humans with face immersion, but not the time constant of flow recovery afterwards. Heart rate recovery would give an approximation, but says nothing about blood flow distribution to specific organs and tissues during or after a dive.

So it would be very difficult to say much about gas exchange in the peripheral tissues after a dive or over repetitive dives without pure speculation. If you are building conservatism into a decompression algorithm, you would have to assume little or no washout between dives. This is essentially what the military did in early procedures for repetitive diving in the 1950s, giving no credit for surface intervals. If the model is designed to avoid brain DCS, existing open-circuit scuba algorithms may come close for routine freediving, although they don’t account for the small increase in brain perfusion, rapid ascents, and unknown carbon dioxide effects on bubble nucleation or growth.

A major point in this discussion seems to be that exhale dives enhance diving response and reduce gas uptake. I would still like to see some numbers. I do believe it because there is published data to support greater diving bradycardia at lower lung volume (5,6). But it would still be nice to see some data, particularly effects on gas levels.

This brings the discussion to pulmonary shunt and its role in DCS protection. As I pointed out in one of my papers (7), shunt is related to the diffusion-perfusion ratio of the lungs. Since both D (lung compression) and Q (cardiac output) decrease during a dive, it is the degree of mismatch, expressed as the drop in ratio D/Q, that determines alveolar-arterial equilibration (A-a) gradient. Although an important concept, it is still an over-simplification, and various other lung factors need to be incorporated. Basically, regional alveolar collapse is related to the gravitational gradient, while blood flow has a fractal distribution. Calculating shunt in a heterogeneous compressing lung requires a more elaborate theory. I have worked out much of this in a revised model, but haven’t had time to write it up. But exhaled gas measurements under varying degrees of lung volume in an appropriately designed experiment might allow inverse solution or reverse engineering of the necessary parameters.

(1) Aust R, Bäcklund L, Drettner B, Falck B, Jung B. Comparative measurements of the mucosal blood flow in the human maxillary sinus by plethysmography and by xenon. Acta Otolaryngol. 1978 85:111-5.
(2) Palada I, Obad A, Bakovic D, Valic Z, Ivancev V, Dujic Z. Cerebral and peripheral hemodynamics and oxygenation during maximal dry breath-holds. Respir Physiol Neurobiol. 2007 157:374-81.
(3) Zapol WM, Liggins GC, Schneider RC, Qvist J, Snider MT, Creasy RK, Hochachka PW. Regional blood flow during simulated diving in the conscious Weddell seal. J Appl Physiol. 1979 47:968-73.
(4) Weathersby PK, Mendenhall KG, Barnard EE, Homer LD, Survanshi S, Vieras F. Distribution of xenon gas exchange rates in dogs. J Appl Physiol. 1981 50:1325-36.
(5) Hong SK, Moore TO, Seto G, Park HK, Hiatt WR, Bernauer EM. Lung volumes and apneic bradycardia in divers. J Appl Physiol. 1970 29:172-6.
(6) Andersson J, Schagatay E. Effects of lung volume and involuntary breathing movements on the human diving response. Eur J Appl Physiol Occup Physiol. 1998 77:19-24.
(7) Fitz-Clarke JR. Lung compression effects on gas exchange in human breath-hold diving. Respir Physiol Neurobiol. 2009 165:221-8.

 

[sebastien murat]

Hi.

I've attached a profile I did, demonstrating the difference between full lungs to vital capacity (no packing) and empty lungs under very controlled and all but equivalent conditions, i.e., same depth and duration. The exhales dives were effected by passively sinking to depth whilst the full lungs required swimming for much of the way. The difference is pretty dramatic. Points 1 and 4 are start of dive, point 2 and 5 are start of ascent, point 3 and 6 surfacing. Once again not that it takes some time for HR to come back up after surfacing (can't see it very well on this resolution). Typically for me it takes 20-30" post surface to get a rise. The steep rise in HR before a full lung dive is due to to an anticipatory exercise response, due to the fact that to effect descent swimming (= work) will have to take place to overcome buoyancy. I also measured end-dive exhaled (mixed) lung pO2. This is also pretty typical for me. Anyway, works for me. I've seen others with a poor response, doing a similar set of dive profiles and the difference varies from poor to marginal.

The are some studies demonstrating a decrease in BP and peripheral vasodilation with lung inflation during breath-holding with DR, and at variable CO2 levels. For more detailed info you should look up such authors as de Burgh Daly, Angell-James. Most of the work was done in the 70s and 80s if I recall correctly. There were studies on seals, cats, dogs, and even frogs (?) (see Jones, on this early works). There is also a single human observation involving BH during decompression in a chamber in which BP was measured. Its in one of the hyperbaric publications.

 

[Simos]

Hi.

I've attached a profile I did, demonstrating the difference between full lungs to vital capacity (no packing) and empty lungs under very controlled and all but equivalent conditions, i.e., same depth and duration. The exhales dives were effected by passively sinking to depth whilst the full lungs required swimming for much of the way. The difference is pretty dramatic. Points 1 and 4 are start of dive, point 2 and 5 are start of ascent, point 3 and 6 surfacing. Once again not that it takes some time for HR to come back up after surfacing (can't see it very well on this resolution). Typically for me it takes 20-30" post surface to get a rise. The steep rise in HR before a full lung dive is due to to an anticipatory exercise response, due to the fact that to effect descent swimming (= work) will have to take place to overcome buoyancy. I also measured end-dive exhaled (mixed) lung pO2. This is also pretty typical for me. Anyway, works for me. I've seen others with a poor response, doing a similar set of dive profiles and the difference varies from poor to marginal.

The are some studies demonstrating a decrease in BP and peripheral vasodilation with lung inflation during breath-holding with DR, and at variable CO2 levels. For more detailed info you should look up such authors as de Burgh Daly, Angell-James. Most of the work was done in the 70s and 80s if I recall correctly. There were studies on seals, cats, dogs, and even frogs (?) (see Jones, on this early works). There is also a single human observation involving BH during decompression in a chamber in which BP was measured. Its in one of the hyperbaric publications.

Is the difference in HR due mainly to the fact that you had to swim down you think? i.e. if you just had more weight on while on full lunch and you could sink to the bottom, how would the grapb look?

 

[growingupninja]

Hi.

I've attached a profile I did, demonstrating the difference between full lungs to vital capacity (no packing) and empty lungs under very controlled and all but equivalent conditions, i.e., same depth and duration. The exhales dives were effected by passively sinking to depth whilst the full lungs required swimming for much of the way. The difference is pretty dramatic. Points 1 and 4 are start of dive, point 2 and 5 are start of ascent, point 3 and 6 surfacing. Once again not that it takes some time for HR to come back up after surfacing (can't see it very well on this resolution). Typically for me it takes 20-30" post surface to get a rise. The steep rise in HR before a full lung dive is due to to an anticipatory exercise response, due to the fact that to effect descent swimming (= work) will have to take place to overcome buoyancy. I also measured end-dive exhaled (mixed) lung pO2. This is also pretty typical for me. Anyway, works for me. I've seen others with a poor response, doing a similar set of dive profiles and the difference varies from poor to marginal.

The are some studies demonstrating a decrease in BP and peripheral vasodilation with lung inflation during breath-holding with DR, and at variable CO2 levels. For more detailed info you should look up such authors as de Burgh Daly, Angell-James. Most of the work was done in the 70s and 80s if I recall correctly. There were studies on seals, cats, dogs, and even frogs (?) (see Jones, on this early works). There is also a single human observation involving BH during decompression in a chamber in which BP was measured. Its in one of the hyperbaric publications.

I know depth and duration were the same but to clarify, you were doing wet eq on the full lung dives as well? In my past limited and less scientific experiments (ahem, face dunks in bowl of cold water) I had no signficant difference in bradycardia (about 45% within a minute) between full lungs, frv, and less than frv. Snorting water in my nose seemed to accelerate everything though.

For the record though when doing dry exhales I start to experience mild bradycardia almost immediately, and full lung dry static no real bradycardia until blood O2 is low eighties, a while into the hold. I have no way to sample HR while diving, and cold water DR is certainly not applicable everywhere (for me bradycardia definitely fell off when I repeated the experiment with warmer water).

 

[turtle]

Is the difference in HR due mainly to the fact that you had to swim down you think? i.e. if you just had more weight on while on full lunch and you could sink to the bottom, how would the grapb look?

not main factor, DR is just much stronger on empty lungs. try taking pulse and doing static on full vs empty and you will see big difference! also on empty dives, pulse keeps dropping even during ascent work phase, where you would expect to lose benefit of an easy/heavy descent.

 

[turtle]

I know depth and duration were the same but to clarify, you were doing wet eq on the full lung dives as well?

i sort of doubt either would've been wet equalisation given the depth (15m) and that seb is quite comfy at btv.

 

[growingupninja]

i sort of doubt either would've been wet equalisation given the depth (15m) and that seb is quite comfy at btv.

I rarely do full exhale in the ocean and do not think I have the chest flexibilty to do 15m after a full, complete, purge at the surface, but I have done btv my entire life and it has never failed me. By about 25' after absolute exhale I am doing throat gymnastics to eq. If such is the case, comfortable handsfree with air at 15m is as impressive as anything else in this thread. Maybe I just need to play with mouthfill from the surface. But my question was basically, wet eq with a full lung, could we gain better DR but still have plenty of gas in the tank?

 

[turtle]

for empty, read frc not full exhale. I've watched seb playing around, doing exhales in 15-20m, handsfree eq with a mask all the way and very much relaxed with it.

i'd imagine wet eq would give better DR than covering face with a mask though, whether on full or empty lungs, both from stress and from water contact.