Apnea, vasoconstriction, and dynamics

[ggarrett]

Throughout DeeperBlue, vasoconstriction comes up in discussions about the dive reflex and other references. This is the phenomena that during apnea the body will prioritize blood flow in the circulatory system by providing less blood, hence oxygen, to the extremities (toes, legs, etc.) and to less essential lower organs like the intestines, kidneys, bladder, testes, uterus, etc. This allows more blood and oxygen to stay at and flow to the brain, heart, and lungs, thereby compensating for the diminishing amount oxygen due to apnea. Other associated phenomena that occur include increased blood pressure and a splenic reaction that has something to do with amount of red blood cells in the body (if I understand this right).

My curiosity is: how does this vasoconstriction happen?
I tried a search of DeeperBlue and could not find what I was looking for. So, I want to throw this explanation out as a thought.

After a maximum dynamic-no-fins attempt, sometimes I can feel the blood pumping very strong into my abdomen through my diaphragm. In looking at drawings and actual human diaphragms (at the Body World exhibit now traveling around the country- highly recommend it), both the descending aorta (abdominal aorta) and the inferior vena cava pass through the body's main breathing muscle. These two blood vessels are the main artery and the main vein for the greatest percentage of our body mass. The splenic artery also passes through the diaphragm right near the descending aorta.

So, during apnea when the diaphragm starts contracting, it would seem that these vessels could get choked or squeezed, thereby reducing blood flow to everything below the diaphragm. The esophagus gets squeezed closed as well.

This might explain the mechanism for increased blood pressure. It also might explain what triggers the spleen to release more red blood cells. Less blood to spleen means less oxygen. This might tell the spleen that more cells are needed for more oxygen.

In studying drawings of the diaphragm, the main vein, (the inferior vena cava) that returns oxygen-depleted blood back to the heart and lungs, is located more in the center of the diaphragm. The arteries, (the abdominal aorta and the splenic artery) that carry oxygenated blood to the lower body, are located near to the spine and might not be squeezed as much. This makes sense to me that blood flow is constricted by squeezing the inferior vena cava. This would slow the flow of less deoxygenated blood back to heart. It would also allow some oxygen to flow to the lower body. The constriction of the inferior vena cava by the diaphragm would also raise blood pressure.

So, what does this all mean a dynamic apneaist? It explains what I have noticed about the evolution of my strokes in DNF. I found that I get two-thirds of my distance from my arms and one third from my legs. The axilliary arteries and veins that feed the arms come right off the aorta at the top of the heart. They do not pass through any respiratory muscles that I know. The arms are also closer to the heart so blood flows more efficiently to them. I would speculate that not much or any vasoconstriction happens to the hand or arms (sometimes, however, my hands look bluish). So, greater use of the arms in the development of efficient DNF form seems natural and, maybe, logical.

A corollary to this involves the use of the legs, especially near the end of long apnea. If the diaphragm is contracting and squeezing the main vein and the main artery, then heavy use of the legs for kicking would require a higher pressure to pump blood through the vessels at the diaphragm. This would require more energy and oxygen. Additionally, the blood has to travel farther in the leg muscles. Heavy use of the legs might reduce energy-oxygen efficiency in dynamics.

So, for a DNF apneaist like myself, as my form develops in response to greater distances and associated times, I tend to use my arms more and my legs less. When swimming at relaxed pace in a maximum attempt, I find that I use my kick almost more to set up body in a position to maximize my armstroke, rather than for any great burst of propulsion.

Turns present a dilemma since the push off from the wall is all leg muscles. For the DNF apneaist, turns also provide a great opportunity to gain speed and distance while relaxing a bit during the glide. I guess my question in regard to turns is: can the freediver relax his diaphragm during the turn so that he lessens the pressure on the veins and arteries long enough to allow just enough blood to pass into the legs for the push-off from the wall? This would mean relaxing the diaphragm muscle and no contractions. It also might mean having a contraction during the glide after the push-off to allow the body to keep most of the oxygenated blood near the heart and brain once again.

And, what does this mean for the DYF apneaist? In my observation, dynamic apneaists with fins use their lower body almost exclusively while hardly using their arms at all. It would seem that finning with lower body would work against natural vasoconstriction in the diaphragm. While I do not use fins, and, therefore, do not know for sure, I would expect that DYF apneaists might be prone to harder contractions and maybe more contractions as the body tries prioritize blood away from the extremities using the diaphragm. This might also explain why there isn't a bigger margin between DYF records and DNF records despite the enormous gain in propulsion due to the use of fin technology. (WR-DNF = 180m, WR-DYF=212m, or only a 18% increase with fins).

Well, enough of this speculation. When I first heard the term vasoconstriction, I imagined the constriction of all those little capillaries in the feet and toes. I had a hard time imagining little tiny muscles squeezing those little vessels. So, this idea of the diaphragm doing all the work at once seem to answer a lot of questions for me. If someone knows of a thread here in DeeperBlue on the subject, I would welcome the chance to know more about the topic. For anyone who read through this long writing, thanks. It's time to wake up.

Peace,
Glen

 

[sebastien murat]

Actually, the issue of vasoconstriction and apnea has been well researched.

Peripheral vasoconstriction is neurally mediated, in part, by the sympathetic nervous system (Charkoudian et al. 2005). Pulmonary baroreceptors or stretch receptors elicit reflex alterations in sympathetic nervous activity. Stretch receptors are stimulated by ventilatory arrest (Lin et al. 1983b & 1983c; Lindholm 1999). Because the primary function of muscle sympathetic nerve activity (MSNA) in cardiovascular regulation is to control vasoconstriction, systemic blood pressure and muscle perfusion (Ray & Saito 2000), it means that MSNA is inversely related to both blood pressure (BP) and cardiac output (CO), such that when BP or CO is low, MSNA is reduced and vasoconstriction is enhanced, and vice versa (Charkoudian et al. 2005). That being the case, MSNA can limit oxygen uptake by working muscles (Joyner et al. 1992). Obviously, MSNA must be strong enough to over-ride the progressively increasing and potent local accumulation of metabolites in the periphery, known promote active vasodilation (Shepherd & Vanhoutte 1981; Daly & Cook 1999). Interestingly, at the break-point there is a sudden and further increase in vasoconstriction which I would suggest has to do with CO2 reaching some threshold level (can't find the reference at present..sorry).

Seb

 

[cdavis]

Hi Glen,

Fascinating post. I also went to the Body exhibit and was blown away, noticed many of the same things you did and finally understood how the diaphram works.

A fair amount of my work involves fluid flow through hoses. Restricted flow volume is as much a function of the length of the restriction as how small it is. I can readily see how vasoconstriction could increase blood velocity through the diaphram constriction, enabling you to feel it, but don't think it would have much effect on overall flow volume. The length of the restriction looks to be too short to produce enough back preasure to slow things down much.

Connor

 

[Evita]

Great speculation! I don't know nearly enough about this, but your hypothesis that contractions are felt differently and play a different role for DNF versus DYN sounds like it should be explored further. Never thought about any differences between DNF and DYN before (besides the obvious ones), so thanks for the thought food.

 

[efattah]

Glen,

I'm not sure I follow the thinking in your post.

It is well known that seals conserve oxygen by shutting off blood flow to the swimming muscles. The swimming muscles, almost entirely disconnected from the main circulation, rely on stored energy (creatine, myoglobin, and anaerobic glycolysis). This method preserves almost the entire O2 store for the heart & brain.

In a case of perfect and complete vasoconstriction, where absolutely zero blood flowed to any swimming muscles, the length of the apnea swim would be equal to a maximum static apnea attempt, since moving would consume no more oxygen than in a static, since no blood is flowing to the swimming muscles.

I would say that whichever limbs (arms, or legs) are receiving LESS blood, are the limbs we should be using to generate power. Further, I would do everything possible to block or prevent blood from flowing into those limbs. I have found that very tight wetsuits on the legs (or so called sharkskin style suits used by stig, peter p. and others) seem to prevent blood from flowing into the legs, allowing an extension of the apnea swim. I have also imagined using cuffs or bands to prevent blood from flowing into the swimming muscles.

Of course, the more you reduce blood flow to the swimming muscles, the more the swimming muscles are deprived of oxygen. Thus, the more they must rely on stored energy reserves. Without sufficient stored energy, the swimming muscles (in extreme vasoconstriction) would become tired very fast. In the early days of competitive freediving, muscles that became tired early on were thought of as an indicator of poor physical fitness. Now, we know the issue is much more complicated -- it could be poor fitness, or high vasoconstriction.

 

[trullalla]

I would say that whichever limbs (arms, or legs) are receiving LESS blood, are the limbs we should be using to generate power. Further, I would do everything possible to block or prevent blood from flowing into those limbs. I have found that very tight wetsuits on the legs (or so called sharkskin style suits used by stig, peter p. and others) seem to prevent blood from flowing into the legs, allowing an extension of the apnea swim. I have also imagined using cuffs or bands to prevent blood from flowing into the swimming muscles.

i always thought of it in a different way: whichever limb you use for propulsion, you will have less vasoconstriction in.

this is a very interesting topic, and maybe it will help to answer some of my questions. i don't have any experience in dyn and dnf though, because i only train depth.
what i always noticed on my dives is that between constant and free immersion there's a big difference in my body response.
in cw i either feel lactic acid building up during the ascent, or nothing whatsoever if i am very rested and feel strong. so i might assume that is not vasoconstriction that gives me the burning, but my fitness level. on the other hand there must be some bloodshift going on during these deep dives, because at depth i never feel any kind of pressure on my chest.
during fi i feel the vasoconstriction going from around 40 mt on the way down. it starts from the feet and goes up to my hips. on the ascent the feeling of numbness is so strong that i literally don't feel my legs anymore. during the ascent also my arms are affected by that, even though in a less intense way. after surfacing it takes my around a minute to get back to normal.
now, i always assumed that i don't feel like that in cw because i'm actively using my legs and therefore vasoconstriction is not so effective. (but on the other hand i'm not using my arms, and there's still no vasoconstriction going on there.)
these days i'm training a lot of fi, which i dont like so much because not having a fin freaks me out...
and now i'm having this doubt: is it the vasoconstriction that gives me this numbness? what else can it be if not that?
i do exactly the same preparation for cw and fi, and the same breathe-up, so why my body reacts in such different ways?

thanks for any thought on this.

linda

 

[tylerz]

Regarding Seb's references, here are related free online resources:
http://www.physoc.org/publications/pn/issuepdf/62/25-26.pdf - Charkoudian 2006

http://jap.physiology.org/cgi/reprint/87/6/2122 - Lindholm 1999

http://jp.physoc.org/cgi/reprint/540/1/2 - Attenuated sympathetic vasoconstriction in contracting muscles.

http://jap.physiology.org/cgi/reprint/90/4/1516 - Hypoxia augments apnea-induced peripheral vasoconstriction in humans.

 

[sebastien murat]

A tight suit can prevent pooling of (venous) blood in the extremities but it cannot cause peripheral arterial vasocosntriction. For that you'd need a tourniquet.

Tit-bits:
- Vasoconstriction happens simply by just breath-holding, but it can be magnified by hypoxia (not a very helpful effect since it occurs too late in the game).
- At the break-point there is a sudden additional increase in vasoconstriction.
- Surfacing from an extreme dive (i.e, not static) with no burning sensation in the locomotors is an indication of a an ineffective oxygen-conserving dive response. Though this helps recovery en route, permiting more frequent diving, it can critically compromise consciousness.

The different feelings between FI and CW has to do with the way blood volume is distributed around the body with each, largely dependent on the muscle mass used, and the rate at which hypercapnia and hypoxia come on.

Seb

 

[OceanMan]

- Surfacing from an extreme dive (i.e, not static) with no burning sensation in the locomotors is an indication of a an ineffective oxygen-conserving dive response. Though this helps recovery en route, permiting more frequent diving, it can critically compromise consciousness.

I have heard of freedivers doing their maximum depth in CW sometimes with burning legs and sometimes with clear legs.
If the 'no burning' is so detrimental for apnea then why could they successfuly achieve their max depth on these dives?
If it was significantly detrimental shouldn't they have BO at the surface?

Matthias

 

[sebastien murat]

Because their max doesn't reflect their true potential. There are no divers, anywhere, seals included, whose MbO2 stores would be of such an extent to allow them to carry-out maximal effort dives with complete peripheral circulatory arrest while not incuring any locomotor fatigue, though some like elephant seals or toothed whales might come close.

There are many factors that can potentiate a BO. Though reducing the (peripheral vasoconstrictive) dive response increase hypoxia of ascent it does not necessarily mean that it will be of a severity sufficient to trigger a BO.


Seb

 

[DeepThought]

Tit-bits:
- Vasoconstriction happens simply by just breath-holding, but it can be magnified by hypoxia (not a very helpful effect since it occurs too late in the game).
- At the break-point there is a sudden additional increase in vasoconstriction.

To what are you refering as a 'break-point'?

 

[sebastien murat]

Break-point = urge to breathe (1st inspiratory muscle contraction)

Seb

 

[tylerz]

Any references to break-point and its effect on vasoconstriction?

Since the urge to breathe is modifiable by one's degree of hyperventilation, it would be desirable to minimize hyperventilation if the benefits of the vasoconstriction were more O2 conserving than the energy expenditure on contractions. If it were the case, it would explain why some of the longest statics have been done with early contractions. Thoughts?

 

[sebastien murat]

Beside my own work there are no specific references to the break-point and sudden increases in vasoconstriction. However, you may be able to see such an effect by looking at Figure 5 of Andersson & Schagatay (1998) article.

It's also been clearly shown that contractions do not increase the O2-consumption rate (I can't remember the reference off hand sorry!). This can readily be understood by the fact that if an intense vasoconstriction occurs at the break-point, i.e., when contractions occur, then there will be a switch to predominantly anaerobic metabolism in inspiratory muscles.

Some thoughts and myths on hyperventilation (HV), with respect to full-lung dives (F-dives) anyway:

- HV increases PAO2 (in the lungs) and if lung capacity is large this will significantly increase body O2-stores. Because HbO2 is already close to 100%saturated, but not quite, blood O2 carrying capacity will not increase by much despite an increase in PaO2 (in the blood). However, HV may, by rising the cardiac output, potentially increasing the saturation of HbO2 of venous blood (SvO2). Since venous blood makes up as much as 2/3 rds of the total blood volume this would result in a substantial increase in blood O2 stores also. But, HV also increase metabolic rate, in part due to the effort of forceful breathing and increased tissue perfusion, so that its ability to actually increase SvO2 to an important extent is in doubt. On this basis, however, it still makes sense to HV.

BUT

- HV will, unfortunately, reduce tolerance to hypoxia, to a considerable extent in some extreme cases, which makes its usefullness as a tool for maximizing breath-hold duration debatable. On the other hand, as a tool to oppose the vasocontrictive effects and, therefore, the fatiguing effects of the DR on the locomotors, it is hugely beneficial. Such a requirement is commonly encountered during frequent (sub-maximal effort) diving. The problem, however, is having the experience to know how long is too long.

This is where just about everyone, with the exception of maybe one or two, makes the mistake: they prepare for maximum effort dives like serial diving. Make no mistake, they are not the same and the effects they have on the body are, or at least should be, markedly different. The notion of mentally relaxing or undertaking several warm-up dives before a maximum effort dive are contraindications to maximum effort dives.

Unfortunately, it is a big pill to swallow, and as such divers will continue to seek comfort whilst undertaking max effort dives; I guess that's the way most people are. But then one shouldn't expect too much in terms of performance improvements and moreover, not be surprised to experience the odd black-out now and then.


Seb


References:
Andersson, J.P.A. & Schagatay, E.K.A. (1998). Effects of lung volume and involuntary breathing movements on the human diving response. Eur. J. Appl. Physiol. Occup. Physiol. 77(1-2): 19-24.

 

[fogish]

Since I am extremely new to all of this I apologize at the beginning of my post for my ignorance. Could you explain in simpler terms why it is that you would not mentally relax and perform warm up dives before undertaking a max effort dive?

Do the warm up dives use too much Oxygen that is stored in the muscles? Does relaxation mean vasoconstriction takes longer to occur? I would really like to get things sorted out theoretically before I begin application. Why the marked difference between serial diving and maximum effort diving? I would think that what you do in serial diving is just repetitive training for max effort without as much stress on the body.

Thanks for any clarification you can give.

 

[sebastien murat]

Fogish,

You might want to look at some of the other threads in which these issues were previously discussed. It might take a bit of time as ther's a lot out there.

Seb

 

[tylerz]

It's also been clearly shown that contractions do not increase the O2-consumption rate (I can't remember the reference off hand sorry!). This can readily be understood by the fact that if an intense vasoconstriction occurs at the break-point, i.e., when contractions occur, then there will be a switch to predominantly anaerobic metabolism in inspiratory muscles.

Hmm, I would not have thought of vasoconstriction occuring in the diaghragm. I have never noticed during contractions a sense of fatigue or lactic acid in the muscle. Could it be that the diaghragm has a relatively large capacity for anaerobic activity?

- HV increases PAO2 (in the lungs) and if lung capacity is large this will significantly increase body O2-stores. Because HbO2 is already close to 100%saturated, but not quite, blood O2 carrying capacity will not increase by much despite an increase in PaO2 (in the blood). However, HV may, by rising the cardiac output, potentially increasing the saturation of HbO2 of venous blood (SvO2).

And also by the Bohr effect.

Since venous blood makes up as much as 2/3 rds of the total blood volume this would result in a substantial increase in blood O2 stores also. But, HV also increase metabolic rate, in part due to the effort of forceful breathing and increased tissue perfusion, so that its ability to actually increase SvO2 to an important extent is in doubt. On this basis, however, it still makes sense to HV.

The idea came up to hyperventilate first and then finish one's breathe up pattern with a steady breathing that would allow relaxation but steadily continue to breathe, without returning to the body's automated adjustments, to maintain the state. This could overcome the trade off mentioned possibly?

Just as a side note, I thought some of you may find this lightens the subject a little.

1995 - Apneic snout immersion in trained pigs elicits a "diving response".
* Schagatay E,
* van Kampen M.

 

[Will]

Fogish, Seb is referring mainly to stress-induced magnification of the dive response (DR). Since DR is a survival mechanism the higher the level of stress, the greater the response. Three main causes of stress are:
1. hypercapnia
2. no warm-up
3. negative psychology
In my experience 1 & 2 are imperative to max attempts, but I haven't managed to integrate 3 into my regime: it seems that psychological tension during breathe-up increases metabolism through tachycardia etc, lowering Sv02 to the point where even an intense DR cannot stave off hypoxic BO (at least this is the explanation I gave to the failed May WR attempt). However -ve psychology during a dive (e.g. mask leak at 80m) is beneficial, as it has the opposite effect to what it does during the breatheup.
N.B. Serial diving is best done aerobic (less waste products), so you don't want to induce the DR as much.
Will.

 

[sebastien murat]

Tachycardia before a dive is actually very beneficial since it increases cardiac output. Provided that this bradycardia is the result of an emotive response and not one associated with increased oxygen extraction (why would it if there is no physical tension), then, actually, venous blood O2 stores will increase (i.e., SvO2). Unlike Will my best performances have been when the situation is new and surprising and my heart-rate (HR) reaches into the 100s, then the drop in HR upon submerging promptly reaches within the low 30s within 15", before eventually hitting the teens by the time I surface, even in the pool. As I become more familiar with the new conditions, however, I have difficulty in 'fooling' myself that things really are stressful. Often I find that either I cannot equal my previous performance or if I've improved, I can do it with a lesser dive response. That's not ideal, except that I'm not as tired, since the aim is to improve performance.

For someone who only does no prep. singular max. efforts several times a week, I've found that it becomes more and more difficult to find innovative ways of increasing the stress to such a pitch as if I were a novice. And so, I have to dig deep to find the motivation and use such things as drogues or dive not at FRC but closer to RV to gain further improvements. It works well enough, but I'd rather be a novice again!


Seb

 

[wet]

... [Pre-dive] my heart-rate (HR) reaches into the 100s, then the drop in HR upon submerging promptly reaches within the low 30s within 15", before eventually hitting the teens by the time I surface, even in the pool. Seb

Seb, I'm quite interested in the upper part of the ascent. Apparently you maintain full bradycardia right until surface exhaling? AFAIK, seals and dolphins (but not platypus) display anticipatory tachycardia (AT) during ascent (I don't know how near to the surface this begins).

I thought that a human deep diver (employing "wet-sinus, empty-lung, naked- face" diving), would also display AT during the upper part of the ascent, triggered in the facial bio-sensors by one or a combination of pressure differential, temperature differential or light differential between the lower cooler depths and warmer near-surface water. I would expect this to occur while in relatively still, clear, salt-water with very warm surface under bright sunshine, but not in a pool or under cool cloudy conditions. Wearing dark goggles or full mask would reduce or nullify the AT effect, I think, resulting in bradycardia until exhaling.

Although there may be a partial voluntary conscious component to AT (especially among polar seals), I think it is largely an automatic response to tactile & visual sensation in the diver's immediate environment. This is just conjecture on my part. DDeden