Apnea, vasoconstriction, and dynamics

[Will]

...also, from what we know of altitude medicine hypoxic cerebral vasodilation overrides hypocapnic cerebral vasoconstriction (allowing climbers to oxygenate the brain even though they are hyperventilating and blowing off CO2).
On the flipside, reasearch in normobaric conditions shows that among the major factors controlling cerebral blood flow (CBF) - cerebral perfusion pressure (CPP), arterial partial pressure of oxygen (PaO2), cerebral metabolism, arterial partial pressure of carbon dioxide (PaCO2), and cardiac output (CO), the effect of PaC02 is peculiar in being independent of autoregulatory CBF mechanisms and it allows to explore the full range of the CBF.
About 70% increase (or even less) in arterial PaCO2 may double the blood flow (Sokoloff, 1989).
Is it possible that hypoxia overrides hypocapnia, but hypercapnia overrides hyperoxia, as far as CBF is concerned..? This seems like the only explanation for the two apparently conflicting observations. In fact Mintun et al state that "experimental measurements of CBF during controlled hypoxia in human subjects show that a large increase in CBF begins as pO2 is reduced to 30–35 mmHg." This could be the threshold at which hypoxic vasodilation overrides the other factors.

 

[Shallow russian]

Seb, thank you for answering.
Shallow in nickname means first of all not perfect english. Sorry for that.

IT also means that the deepest mark here im Moscow we can achieve is 6 meters on bottom of our pools. Other places have visibility less then 1 meter even in winter.

Shallow also indicates the very low level of theoretic discussion we have here in Russia in comparance to practical achievements of some of our athletes.

And I am looking for training basis to overcome in winter my shallow depth mark in the sea - 45 meters.

 

[sebastien murat]

A Russian witha sense of humour, they must be pretty rare in your neck of the woods.

Wise man said: He who cuts too many corners does a full circle!

I'll most definitely have to disagree with you on that one Will: I would most definitely not seek out CO2 narcosis. Moreover, contractions are believed to be associated with excessive -ve intrathoracic pressures at depth, predisposing to bleeds. Moreover, the O2-conserving effects of the DR will always be more accentuated with E- than F-dives, because lung volume and work output are minimized...guaranteed

The cerebral vessels are more sensitive to decreases in PaCO2 (Blaber et al. 2003), the cardiovascular responses during hypocapnic hypoxia involve vasodepression and insufficient cerebral perfusion (Daly & Hazzledine 1963; Scott 1966; Ott & Shepherd 1971 & 1973; Ott et al. 1972; 1975; Gandevia et al. 1978a; Huang et al. 1987; Blaber et al. 2003). More particularly, there is cerebral vasoconstriction (Ketty & Schmidt 1946; Blaber et al. 2003), hypotension (Pelletier 1972), and peripheral vasodilation (Shapiro et al. 1970; Richardson et al. 1972). Considering that the normal brain ordinarily receives 20 % of the , despite the fact that it contributes only 2.5 % to the total body mass (Sokoloff 1976), a repartitioning of cardiac output to the periphery may itself adversely affect cerebral perfusion. Even if the hypocapnia was only mild this would still be enough to blunt or abolishes the vasodilatory stimulus of severe hypoxia (Shapiro et al. 1970).

No matter how you configure it just don't stack-up! Its probably no coincidence that a variety of animals have been found E-diving. These include: seals (Scholander 1940), sea-otters (Snyder 1983), sea-snakes (Murdaugh & Jackson 1962), alligators (Andersen 1961), and a variety of diving-birds (Eliassen 1960; Ross 1976; Tome & Wrubleski 1988; Sato et al. 2002).

Back at you....

Seb

 

[Will]

contractions are believed to be associated with excessive -ve intrathoracic pressures at depth, predisposing to bleeds

Are you talking about rate of change of -ve intrathoracic pressure? (i.e. a quick descent to 40m brings on contractions, whereas a slow dive to 80m doesn't). This might apply, but doesn't quite fit the shoe with my diving, where the relationship between initial CO2 and descent contractions is dependable. As you mentioned, hyperventilation before a fast sled descent minimises 'the uglies' (contractions etc), so it is probably more dependant on PaCO2 or rate of change of PaCO2. I've never even had a tickle in the lungs, let alone a bleed, so I'd be surprised if it was absolute -ve intrathoracic pressure that's doing this.
What's wrong with CO2 narcosis? If PaCO2 is the greatest stimulator of vasocontriction then narocosis is merely an indicator of an accurate breathe-up and enhanced bloodshift. If max depth is increased gradually in warm, clear water CO2 blackouts shouldn't ever be a danger, and I have never experienced even slight mechanical impairment even during acute (relatively speaking) narcosis.

So PaCO2 is the omnipotent factor in CBF. The study that I read at http://www.high-altitude-medicine.com/ which stated that hypoxic vasodilation overrided hypocapnic vasoconstriction must have been erroneous... Incidentally almost all of these studies (Blaber, Sokoloff, Shapiro etc) were conducted in normobaric or hypobaric conditions, often with specific application to Altitude medicine. Is it certain that they apply also to our ballpark, where we are climbing down from Everest in a matter of seconds?

You know my stance on freediving animals: other than the reptiles (which I know nothing about - do they dive at all deep?) the animals that exhale dive are without exception all very buoyant. For buoyant animals and many humans, especially female, exhale diving is the most energy efficient strategy; while for less buoyant animals, and some (few?) humans, inhale diving is more energy efficient (since I can practically 'inhale and sink,' even in the salty old Red Sea, exhaling for me is like strapping on a weightbelt).
So which comes first: does nature select for oxygen efficiency or energy efficiency?

Don't forget to pack your gas analysers for September - I am keen to see just how much hypocania I am hitting on ascents. Would it be enlightening to analyse exhaled gas at 20m and again at the surface in an ascent from say 60m CNF?

 

[cebaztian]

My god, so many intelligent people in the same place. Thanks for your discussion - which as always when Murat or Fattah is involved takes quite a lot of concentration. Will is not making it easier

I have though tried to make it easier:
http://www.fridykning.se/freediving/features/muratarticle1.html

I also hope that we can find those last participants needed for a Murat clinic in Sweden 1-3 september.

http://www.fridykning.se/freediving/features/muratclinic.html

SebastiAn
Sweden

PS. Do you guys do any diferantion between hypoxi (general) or hypoxemia (brain) low O2.

 

[cdavis]

Makes my brain ache to read this stuff, but it sure is interesting.

Just to throw an additional idea into the debate, mountain climbers spend a lot of time (several weeks?) getting aclimated to high altitude. Is it possible that altitude medical studies are seeing a learned response? i.e. Does the body learn to overcome a natural tendency towards contracting the carotid arteries when hyperventiating at altitude in order to get enough 02? Such a learned response might be a bridge between these, apparently disagreeing, studies. Just from a common sense aspect, there must be some explaination for mountain climbers breathing very fast and not passing out as a result.

Connor

 

[sebastien murat]

Sebastian, you can have peripheral and, or central hypoxia. When there is central hypoxia, it stands to reason that there must also be peripheral hypoxia, but the converse is not necessarily true. For example, the vasocosntrictive effects of the DR eventually result in hypoxia of the tissues distal to the site of constriction, while the blood may even be hyperoxic. So, when referring to hypoxia it is important to refer to distinguish between peripheral and central.

Will, the problem with one-off dives is that they hardly reflect the wider reality, i.e., most peole do more than just one dive, consequently, CO2 retention becomes an issue especially if exercise is involved. Not only does CO2 output increase but hypoxia at the break-point is more severe reducing the safety margin (easy demo for you in Dahab). During deep dives in which contractions occur at depth, because of the shallow-pressure gradient, it will be some time before the lungs expand enough to take-up the CO2. Consequently contractions may occur for some time, resulting in excessive -ve intrathoracic pressures. Contractions can of course occur with E-dives but their frequency is reduced.

Narcosis is a problem to the extent that your mind is functioning on less than all cylinders. I would also suggest that excessive CO2 retention which is to be expected to be greater with F-dives, would predispose to vascular headaches post-diving.

You've quoted 30-35 mmHg as being the point at which large increase in CBF occur. This seems an awfully low value since unconsciousness occurs typically in the range of 25-40 mmHg (PAO2), depending on CO2.

The buoyancy issue is the cornerstone of whether a diver will choose to E- or F-dive. Most people do not sink on an F-dive from the surface, irrespective of vital capacity. Indeed, many have problems sinking in seawater on E-dives. Are you able to sink at VC from the surface? Furthermore, because the lung-shrinkage effect is much greater with F- than E-dives, it means that relatively speaking buoyancy losses are greater with F-dives so that ascents are not that much more costly in terms of energy, let alone aerobic energy, since the DR is maintained.

Nature selects for what is needed. For survival (=max performance) efficiency is achieved by metabolic down-regulation (e.g., hypothermic and hypoxic hypometabolism) even if this means a reduced oxygen storage capacity and increased anaerobic burden. In this respect this is the most efficient for what the task at hand.

I'll get back to you about this seeming conflict in the literature...give me a week or so.

Seb

 

[sebastien murat]

Here’s the latest from the horses mouth:
“The smaller vasodilatation to hypoxia and larger vasoconstriction to hypoxic hypocapnia at high altitude suggest that cerebrovascular responses may be impaired at the high altitude, i.e. a maladaptation (Nordcliffe et al. 2005)

[Breath-hold diving to depth results in an] unexpectedly low value of PCO2 … upon surfacing …(Lanphier & Rahn 1963)

My own experiment and those of others also confirm this.

By the way, you’ve already submitted several samples if you recall. Your end-dive, end-expiratory F-dives: 43 +/- 2 mmHg, which is within the normal range when simply resting on the surface, i.e., isocapnic.

 

[sebastien murat]

Here’s the latest from the horses mouth:
“The smaller vasodilatation to hypoxia and larger vasoconstriction to hypoxic hypocapnia at high altitude suggest that cerebrovascular responses may be impaired at the high altitude, i.e. a maladaptation (Nordcliffe et al. 2005)

[Breath-hold diving to depth results in an] unexpectedly low value of PCO2 … upon surfacing …(Lanphier & Rahn 1963)

My own experiment and those of others also confirm this. CO2 values lie below (hypocapnic) or within (isocapnic) the normal range. The normal range meaning simply resting at the surface.


Seb

Seb

 

[Will]

Will is not making it easier

I am in way over my head... however the quickest way to learn is to ask questions and make challenges (wise man et al, c. 1000 bc)
Damn, just write a huge reply, but lost it when I pressed send. Will have to try again tonight...

 

[Will]

I take it we are talking exclusively about 'one-off' dives - as we all know these are the only way to acheive maximum performances.

The two reasons why I relate descent contractions with rate of change of PaCO2 (rather than absolute PaCO2) are:
- the faster you descend the earlier they come
- if you interrupt the descent the contractions vanish instantly
With adequate diaphragmatic and thoracic flexibility I don't think -ve intrathoracic pressure should be a problem. Once, when my mask flooded at 78m, I registered a gut-wrenching contraction (I hate mask floods), but didn't have so much as a tickle in the lungs upon surfacing. Furthermore don't contractions help squeeze the little red suckers out of the spleen?

Mental impairment is the only symptom of narcosis that really concerns me too, but I have found that through 'programming the unconscious' (visualisation, positive affirmation etc) prior to the dive all actions at depth become automatic, and you can even provide for contingencies.

The 30-35mmHg was from a study for altitude medicine, a topic of which I am becoming increasingly suspicious.

My buoyancy: in fresh water I am -ve at VC, in very salty water I am slightly positive, but sink easily from 10m (a couple of strokes). Don't underestimate the difference in energy cost of E and F ascents: for my particular physiology (mean body density 1.08kg/L) and for a target depth of 80m I will consume 30% more energy overcoming buoyancy by diving at FRC as opposed to VC, and 40% more than if I pack. On the other hand someone who is neutral on the surface after exhaling (i.e. very buoyant) would use 50% less energy overcoming buoyancy when diving on FRC.
I am trying to create a more accurate mathematical model that takes into account drag-related energy loss: hope to have it ready for Blue Spirit.

Cheers for the Nordcliffe reference - that settles that one! To throw another cat in the cage, when confronted with hypoxia cerebral vasodilation isn't the brain's only defence; in fact the first thing that happens is a reduction of O2 rediffusion back into the blood. In conditions of repose CBF supplies a surplus of O2, and some of this passes back from brain cells into capillaries. During hypoxia this backflow is inhibited, allowing greater oxygen extraction from the same CBF. There is no reason why this process should be influenced by hypocapnia, so it should take some of the edge off cerebral vasoconstriction. How much is anyones guess...

 

[sebastien murat]

Will,

The onset of contractions is related to the speed of descent and obviously the initial PACO2. If descent is rapid much CO2 will eneter the blood stream resulting in a rapid increase in the PaCO2, stimulating the chemoreceptors which stimulate the urge to breathe. If descent is interrupted this urge dissipates, as the CO2 is largely bufffered, only to return later as the PaCo2 inevitably increases.

Agree, that for a trained diver contractions at depth should not be a problem, but there are also trained divers such as Stig and Lotte for example who do not tolerate someone pressure well, because of unusually elevated RV. For them contractions would probably aggravate their bleeds.

The analogy with altitude physiology is speculative at best. For this reason, I'll be doing some specific (invasive) testing later this year, looking at arterial blood gases.

There is potentially another problem with a loss in the DR during ascent: ischemic damage. Ridgeway et al (2005) suggest that cognitive impairment is unlikely to occur because the DR increase CBF. But this is not the case during ascent from diving so that damage could occur, which probably explains the vagueness and (short-term) memory loss I repeatedly here about from divers. What about DCI?

Will, about your maths model: will it incorporate gas-exchange related effects on buoyancy? I ask this because the 'lung-shrinkage effect', due to inequities in CO2/O2 gas-exchange, is such that the buoyancy losses during the course of F-dives are much larger than with E-dives, which would considerably affect the accuracy of model predictions. Indeed, the larger the initial lung volume and the longer the dive the greater the losses. I've calculated that the difference in the loss in buoyancy between F- and E-dives can be as much 1.5-2.5 kg. This does not even account for differences in the rate of lung shrinkage due to difference in metabolic rate between F- and E-dives.


Seb

 

[cebaztian]

I have a question/comment I think some of you can comment.

In my practical knowledge of the "Murat way" of diving I have discovered that (when you still are a beginner in this style) you need to have some "blind faith".

I have to tell myself that even though I feel bad, I am alright.

Signs like contractions, lactic acid, feeling of cold or stress use to be signs to STOP your maximum dive - now you should be happy for them to appear as early as possible in a dive.

In this way I can dive deeper than I could before (about 10% right now). In a deepdive this is a bit scary - because I set of to a depth that I will make ONLY if I get the diveresponse going (otherwise BO at the end).

BUT...

If I cheat with the PRINCIPLES of this alternative style: I take to much air, I ventilate a bit too much, I move too much in the descent. Then I end up somewhere with a "semi Murat kind of dive".

Since different approaches have different advatages and disadvantages: can I end up in a situation where I only reap only the disadvantages of both styles.

Have you Will (or anyone), for instance found youself halfway down to 75 CNF realizing that you havent got the bodily response needed for the dive - and then aborted?

Sebastian
Sweden

 

[sebastien murat]

One has to remember that I too started off using conventional diving techniques and for many years.

Seb

 

[BennyB]

Seb, do you think your athletic background has/had any bearing on your ability to adapt and continually improve your adaption to FRC diving?

Cheers,
Ben

 

[sebastien murat]

No, but motivation is a powerful trigger for the development of the DR. For the last few years I've been doing one dive per day, nor warm-ups, anywhere from 4-6 dives per week. These are, however, highly intensive, very specific and very stressful, but thankfully it doesn't last too long. Mental recovery is also very important. Certainly, just looking at me you would bank on it. This training system is based on 1980s Russian/East-German training principles regarding athletic training.

Seb

 

[Will]

Have you Will (or anyone), for instance found youself halfway down to 75 CNF realizing that you havent got the bodily response needed for the dive - and then aborted?

I rarely miss target depths or have to abort dives, and I think this is mainly due to the elimination of variables from pre-dive routine and physiology. If everything is the same as the previous max attempt (sleep duration, breakfast, warm-up, breathe-up, time of day, descent line, water temp & suit config, safety diver etc etc...) then there should be no reason I can't make the same depth.
Knowing this helps a lot with the psychology, and allows me to basically 'shut down' during the descent. Everything is programmed through visualisation, and I very rarely actually make a decision during a dive. Works for me (other than when I am poisoned...)

I've calculated that the difference in the loss in buoyancy between F- and E-dives can be as much 1.5-2.5 kg.

Wow. In what circumstances is there a difference this great? A margin of 1.5-2.5kg between VC and FRC dives would have to involve an absolute buoyancy change of 3-5kg between duckdive and surfacing for the VC dive. I know for a fact this doesn't apply to me as I am no more than a couple of litres positive at the start of a CNF dive, and yet I still float easily to the surface from 5-8m at the end of the dive - i.e. max absolute buoyancy change of 1kg, therefore max difference to an E-dive of 0.5kg. This may be because I have a very short aerobic phase during the ascent, and the rest of the dive is either freefall or anaerobic (predominantly).
At any rate there is no hope of being able to put it into the model: even though it is based on first principles, deriving the formula involves very difficult (for me) integration and maximisation - chucking a physiological variable into the mix would overheat my mainframe!

One has to remember that I too started off using conventional diving techniques and for many years.

Yes, but were you ever human, or born to the family pinnepedia?

 

[efattah]

When I dive without my wetsuit in Vancouver waters (low salinity), I use only a 4lb neck weight. After a lot of experimentation, I determined that this was the optimal amount of weight for BOTH my inhale+packing dives, and my FRC dives.

However, given that when packing I start the dive with 11L of VC, vs. 5L for FRC, then I'm starting with a buoyancy difference of 6kg.

I this config I let myself sink after the tuck dive on FRC, and on full packing I let myself sink at 35m.

 

[Mullins]

Has the FRC approach been represented at all in CW competitions yet? Presumably this would be acid test of its value for max dives, if not for serial diving.

Although it's still comparatively young as a methodology it sounds like several world-class inhale freedivers have been playing with it for long enough to begin putting it into practice. I haven't heard any reports yet, apart from a couple of fairly positive ones regarding training performances.

 

[sebastien murat]

I think I may not have been clear enough regarding losses in buoyancy between the beginning and end of a dive. Let me elaborate:

Because the O2 stores needed for metabolism involves taxing the lungs O2 stores to a greater extent than blood O2 stores (at least until PO2 reaches 80 mmHg, whereby there is a rapid desaturation in HbO2 as a result of the shape of the O2 dissociation curve), it means that a large initial lung volume will correspondingly result in a greater decrease in volume over the course of a dive. Admittedly the loss in buoyancy will most notably be felt, not so much a depth, but more so upon approaching the surface, because of the steep nature of the ambient pressure-to-lung volume relationship upon approaching the water surface. These losses will magnified by increases in cardiac output and O2 extraction rate by the tissues, in short, elevated metabolic rates , dive duration and depth. In other words the deeper you can dive the greater the loss in buoyancy from start to finish. Because of the considerably reduced lung volume associated with E-dives the potential for further reductions in lung volume is much more reduced, relatively speaking. With an E-dive, and according to my calculations, the loss in buoyancy is in the order of 0.5 kg, at the extreme (hardly noticeable?) In contrast with F-dives the loss can be as high as 2.5 kg or more. Indeed, the greater you lung capacity and initial lung volume on diving, provided you dive deep and long (e.g., max dive) the greater the penalty. Corriol (2002) suggested that losses in buoyancy equivalent of up to 25 % of the initial lung volume can be incurred.

The loss in buoyancy is not just related to inequities between O2 uptake and CO2 off-gassing but also due to to the asymetrical nature of N2 uptake and release; N2 uptake is always greater than off-gassing. Although N2 uptake is fortunately slow in comparison to the other gases, its sheer volume will make a significant impact on the loss of buoyancy incurred.

The problem with attempting record E-perfs. is that the issue of equalization and tolerance to high pressure has to become a non-issue. In addition, the DR must be more more pronounced (considerably?) in comparison to F-dives. Having a high [Hb] and blood volume would undoubtedly be helpful. It is questionable whether a big F-diver could switch over to E-dives and expect comparable perfs. I for one don't believe so. I think it takes some time, possibly several years since an elevated VO2max and possibly efficient exercise response tend to undermine one's tolerance to pressure and one's O2-conserving ability, respectively. Having said that, the % rate of improvent with E-dives can be much greater than F-dives since high CO2 tensions with F-dives tends to prevent divers from willingly (psychologically) undertaking max dives on a regular basis, e.g., 4-5 week, thereby reducing the stimulus for increasing [Hb] and blood volume, i.e., through incurring sufficient hypoxia, and sensitizing the DR.


Seb