Hyperventilation

[trux]

Re: David Blaine again!

Bill, I did not really see any statistical data that would tell you the difference. Perhaps Eric Fattah could serve with some data. However, I am afraid that it is quite individual. There are likely people who have good diving response even with moderate hyperventilation, and on the other hand you have people with weak response even in hypercapnia.

Additionally, as ADR correctly noted, the hyperventilation is certain trade-off - it has some advantages too - very slightly higher starting oxygen saturation, and later onset of contractions (which consume some oxygen too). So the final result depends on many factors.

The higher oxygen saturation thanks to hyperventilation - normal oxygen saturation is between 97% and 99% (95% are still clinically accepted in a patient with normal hemoglobin level). So with hyperventilation you can manage to increase the saturation only approximately by some 0% to 3%. The effect of prolongating the comfort phase may be more important - both physiologically and psychically, and it only depends on the strenght of the diving response you have with and without hyperventilation, and on the total lenght of the breath-hold, to know how much you lose or save.

 

[efattah]

Re: David Blaine again!

The higher oxygen saturation thanks to hyperventilation - normal oxygen saturation is between 97% and 99% (95% are still clinically accepted in a patient with normal hemoglobin level). So with hyperventilation you can manage to increase the saturation only approximately by some 0% to 3%.

Unfortunately this is one of the biggest misconceptions amongst freedivers and even some physiologists.

Arterial oxygen saturation is an extremely poor indicator of the oxygen state of the blood, because it only analyzes blood as it has left the lungs. Venous blood comprises a huge fraction of your blood, and it is very desaturated as it returns to the lungs through the veins (not the arteries).

During hyperventilation, arterial oxygen saturation barely changes (as Trux noted), but venous oxygen saturation increases DRAMATICALLY, from around 50-60% to 80% or more. So, the total oxygen content of the blood does actually increase quite dramatically. Whether this is enough to counter the low-CO2 effect is another debate.

In my experience, if all possible methods and tricks are used to initiate a dive response, it is possible to get a very good dive response even with extremely low CO2, making for an effective but still comfortable dive. However, high CO2 will probably always get the best result.

 

[naiad]

Re: David Blaine again!

I gave up hyperventilation when I had a static blackout a few years ago but started doing it again. I figured that since I have no problem holding until the start of samba even when too warm, that the CO2 depletion wasn't making things any more dangerous and starting contractions 1-2 minutes later than normal today felt so good that it must help my O2 consumption. There's certainly no shortage of CO2 at the end.

Same with me.

 

[trux]

Re: David Blaine again!

During hyperventilation, arterial oxygen saturation barely changes (as Trux noted), but venous oxygen saturation increases DRAMATICALLY, from around 50-60% to 80% or more.

It is true that the topic is more complicated, but this claim is not entirely correct either. The entering volume of oxygen (arterial saturation) is about the same (almost 100%), and the consumption too, so it means the venous saturation could be increased only by quicker blood circulation.

This indeed happens during hyperventilation - the heart rate increases and there is vasodilatation in extremities. Hence the blood flow, and the venous saturation in extremities increases seriously. So you are right - if you measure the venous saturation in extremities, you will be able to detect a dramatical increase.

But quite the opposite happens in brain - during hyperventilation the carotids are constricted and the cerebral venous oxygen saturation drops sharply (from 66% ± 3% to 56% ± 3% measured in this study). Also the lungs and the core may show similar effect (though probably not as strong as at the brain - I have no data at hand right now).

So if you sum it all up, you will end with about the same amount of oxygen in your blood anyway. Well, the final oxygen volume may be little bit higher than what the change of arterial saturation signals, but definitely not as high as the change of the venous saturation in extremities.

Anyway, the higher heart-rate and the vasodilatation caused by the hyperventilation that helps increasing the venous saturation, has also a disadvantage - it also increases the consumption, so the little advantage you gain, you start quickly losing once you begin your breath-hold.

 

[efattah]

Re: David Blaine again!

It is true that the topic is more complicated, but this claim is not entirely correct either. The entering volume of oxygen (arterial saturation) is about the same (almost 100%), and the consumption too, so it means the venous saturation could be increased only by quicker blood circulation.

I disagree -- blood vessels in the whole body will vasoconstrict due to the hypocapnia, reducing the entire body's access to oxygen. So even if the arterial saturation is similar, the hyperventilating person will have blood which returns to the lungs with very little oxygen drained from it.

Then, once the dive starts, a strong dive reflex maintains the vasoconstriction, continuously denying the rest of the body with oxygen, except the brain, which then vasodilates and receives oxygen.

I have actually tested this by using a transcutaneous O2/CO2 monitor. The transcutaneous sensor on my chest detects a dramatically higher PO2 when I hyperventilate.

 

[trux]

Re: David Blaine again!

I disagree -- blood vessels in the whole body will vasoconstrict due to the hypocapnia, reducing the entire body's access to oxygen. So even if the arterial saturation is similar, the hyperventilating person will have blood which returns to the lungs with very little oxygen drained from it.

Sorry Eric, but it could not work. If you reduce the throughput (vasoconstriction), while keeping the consumption on the same level (the cells still need the same amount of oxygen), it would have the exact opposite effect of what you suggest - the venous oxygen saturation would drop dramatically against the normal state. To increase the O2 saturation, you need increasing the throughput.

The reality is different. Although CO2 is vasodilatant (hence its lapse activates vasoconstriction), the effect of hyperventilation is mixed - there are both vasoconstriction and vasodilatation in different parts of the organism. This is a quotation from http://www.umds.ac.uk/physiology/BDS1B/1B33.htm

Carbon dioxide is a vasodilator, so the low level of carbon dioxide in the body will have a direct effect on arterioles, constricting them and reducing the blood flow to the organs they supply. Carbon dioxide also stimulates the vasomotor center so the low level of carbon dioxide will produce less activity in sympathetic constrictor fibres, making arterioles dilate. Organs which normally have a high level of sympathetic activity, such as the skin, will show the vasodilatation and the faces of subjects who are hyperventilating may be red; organs like the brain in which the arterioles have very little sympathetic activity to be inhibited, will obviously show the vasoconstriction, because of the direct effect of the low carbon dioxide. The brain becomes hypoxic but this has less effect on the cerebral arterioles than the low partial pressure of carbon dioxide, so the blood flow remains low despite the hypoxia, producing dizziness and tunnel vision.

The tingling and picking in extremities you feel after hyperventilation is not a consequence of vasoconstriction as some people may mistakenly assume, but the effect of reduced free calcium concentration influencing the nerve fibers. And in fact it is also another disadvantage of hyperventilation, I did not mention yet. The high depolarization of nerve fibers causes muscle tension and muscle contractions (or even tetanism), which again will negatively influence the oxygen consumption shortly after the hyperventilation.

 

[trux]

Re: David Blaine again!

Well, this discussion is very much off-topic in this thread but I think it is quite interesting. It might be worth of moving it to a separate thread (best into the new planned section for sciences, once it is created)

I forgot to react to this one:

I have actually tested this by using a transcutaneous O2/CO2 monitor. The transcutaneous sensor on my chest detects a dramatically higher PO2 when I hyperventilate.

Yes, that's not surprising at all, and exactly for the reason I mentioned - blood vessels in skin vasodilatate due to the hyperventilation, hence there is increased blood flow and the blood has less time to get desaturated. In no way it means that the venous saturation is on the same level inside the body too!

 

[efattah]

Re: David Blaine again!

Sorry Eric, but it could not work. If you reduce the throughput (vasoconstriction), while keeping the consumption on the same level (the cells still need the same amount of oxygen), it would have the exact opposite effect of what you suggest - the venous oxygen saturation would drop dramatically against the normal state.

If what you are describing is correct, then the moment the dive reflex (vasoconstriction) kicks in, then oxygen drain from the lungs would soar as the blood reaching the lungs is profoundly desaturated. In the case of an empty lung dive, blackout would occur almost immediately, implying the dive reflex would have a negative effect.

I am theorizing that the blood flows through a closed loop without ever reaching any cells. The effect is very similar to using cyanide. When I eat apricot kernels and then do static, my arterial oxygen saturation remains immensely high even at the end of the breath hold, even just before a blackout, because the cells are unable to use the oxygen. It just flows in a closed loop.

 

[efattah]

Re: David Blaine again!

I would also add that it was Peter Lindholm, an expert in physiology, would explained to me how venous saturation increases dramatically with hyperventilation.

 

[trux]

Re: David Blaine again!

If what you are describing is correct, then the moment the dive reflex (vasoconstriction) kicks in, then oxygen drain from the lungs would soar as the blood reaching the lungs is profoundly desaturated. In the case of an empty lung dive, blackout would occur almost immediately, implying the dive reflex would have a negative effect.

No, it would not, because the vasoconstriction is selective (and partially inverted) in both cases (hyperventilation and diving response) and not global. So while in the constricted area the cells take percentually more oxygen from the blood, in global volume it represent less (because there is little blood available), hence having little impact on the part where the blood is needed. But that's not the point of what I was telling. I am telling that measuring blood saturation on places strongly impacted by the vasoconstriction or vasodilatation will simply not tell you the real global values, but only the state in that very place.

 

[trux]

Re: David Blaine again!

I would also add that it was Peter Lindholm, an expert in physiology, would explained to me how venous saturation increases dramatically with hyperventilation.

I do believe that the increase of venous saturation is higher than the arterial one (although not as high as your oximeter indicates). I doubt though that it makes any dramatic difference in the total amount of oxygen available to the organism after hyperventilation. And any positive difference is further diminished by the negative effects of hyperventilation (muscle tension, vasodilatation, high heart-rate, possible later onset of diving response)

 

[azapa]

Re: David Blaine again!

If two or three hook breaths pressurize the torso and avoid rapid a decrease in saturated O2 after a dive, could they also increase saturated 02 before a dive without affecting CO2 levels?

 

[trux]

Re: David Blaine again!

Perhaps telling it more clearly: assuming you are in rest, and with constant heart-rate, the venous oxygen saturation will be high in dilated parts, while low in constricted parts. This is perfectly shown in the above mentioned examples where the venous saturation in brain drops by 10% after hyperventilation, while on your skin it climbs dramatically. You would need to measure the venous O2 saturation in the heart to have little bit better clue, but even that would not really tell you how much more O2 you have in all blood volume of your body. That's because on the place you measure (even in the heart) you indeed get more of the high saturated blood from dilated parts, while there is only little coming from the possibly big volume of desaturated blood from constricted parts (i.e. the head) that flows slower hence not influencing immediately the measured level.

And since the vasoconstriction and vasodilatation are to great degree inverted at hyperventilation vs. diving response, the vasoconstriction kicked in by hyperventilation won't directly morf into the vasoconstriction you need.

 

[trux]

Re: David Blaine again!

If two or three hook breaths pressurize the torso and avoid rapid a decrease in saturated O2 after a dive, could they also increase saturated 02 before a dive without affecting CO2 levels?

I think not really, because the arterial blood is already practically saturated, and to saturate the venous blood, you need blood throughput higher than normal. So maybe if you managed accelerating your heart rate in the same time, but without physical effort (consuming the oxygen), it might have some effect. Actually packing may have such effect - it creates both increased alveolar pressure and higher heart rate. The problem is that when you pack, you are in fact already in apnea, hence the gain won't be interesting since it is anyway oxygen that you already have and don't get more.

EDIT: stress is a good agent for the saturation - it increases the heart rate, and accelerates blood flow. But it causes hyperventilation too, so we are back where we were. So I'd tell artificial controlled stress. That's finally what FRC experts like Seb Murat (and I believe Eric Fattah too) teach

 

[TRITON]

Re: David Blaine again!

Maybe I wasn't precise enough in my previous post....
The "leg burn" i mentioned happens only on max attempts or close to max dives and i'm pretty sure that's DR.

I suspect Triton was referring to the feeling of blood shift coming on. For me it happens at a certain point during a dive (in a static, usually around two and a half minutes) where my arms and legs get hot, start tingling (NOT hypocapnia!) and it feels to me like the blood is leaving. Your response is a good one either way.

 

[Bill]

Re: David Blaine again!

Azapa
I think that hook breathing has more to do with blood pressure than O2. One breath is enough to get O2 (like we were taught a long time ago) but if the blood pressure drops, it will take a while to get to the head. Much better to stay awake than to wake up face down.

 

[ADR]

Re: David Blaine again!

Trust a pilot to correctly point that out !

Hi Bill...its been a while pal, hope you are well

 

[hteas]

Re: David Blaine again!

Trux and EricF - Please keep this up, but maybe on a separate thread. It is straying (sort of), but there are those of us on the edge of our seats trying to keep up (seriously). It really has potential to help a lot of practicing freedivers to increase their times, as well as understanding what's going on inside during the attempt.
Howard

 

[trux]

Re: David Blaine again!

Trux and EricF - Please keep this up, but maybe on a separate thread. It is straying (sort of), ...

Yes, exactly. I already wrote we are getting a lot off topic with it, but am persuaded that the discussion is interesting not only for us who are involved in it. Although this discussion about hyperventilation is directly coming from the controversial article referenced in the initial post, it indeed deserves an independent thread. I suggested moving it to the Science subforum as soon as it is created (as was already pre-announced by Papa Smurf). Once the new forum is up, we should suggest more such threads (or parts of them, like in this case) to be moved there.

 

[trux]

Re: David Blaine again!

Well, I'll continue about the topic of hyperventilation here before I forget some details that just came to my mind, and hope it will be all indeed moved to a separate thread later.

As for the saturation of the venous blood - I just realized that there is also another effect that helps increasing it, not only the higher throughput (through increased heart-rate and vasodilatation in some parts). We all know that when hyperventilating, the CO2 level drops, and the pH climbs. And the pH has an important effect on the way hemoglobin binds oxygen. At high pH (low CO2) it binds it very strongly (hence pulling more of it from lungs and saturating the blood), and oppositely at high CO2 (low pH) it binds it worse, and releases the oxygen easier (it helps oxygenating the cells even at progressing hypoxemia).

Still, alone it would not really help increasing the venous saturation more than the arterial one. And since the arterial saturation is close to maximum already at normal ventilation, only the above mentioned increased throughput could help. But, now the high pH not only helps loading the O2 from lungs to blood, it also makes the discharging more difficult. It means that the blood despite being saturated to the max, is unable to deliver and release the oxygen where it is needed. The consequence then indeed is the increased venous oxygen saturation.

But that's not all! The problem is that despite the high O2 saturation, cells are starved of oxygen above normal, and cumulate oxygen debt. And I do not even speak about the brain or some other parts that are starved even more severely because of vasoconstriction of some arteries, and build so oxygen debt more quickly. And that's of course just another factor playing against hyperventilation in freediving, because although you may manage to increase slightly the O2 content in your blood, the organism is in fact deprived of normal flow of oxygen from blood to cells, and will then need to take it from the blood later during the breath-hold, when the unloading becomes easier with the decreasing pH.

EDIT: the strenght of the effect of the oxygen debt building will depend on the length and level of the hyperventilation. Normally it won't be too serious, because the system is self-balancing, but it may be sufficient to eliminate at least part of the little extra oxygen you managed to get by the hyperventilation. So from this point of view, on my mind, the only real "advantage" of hyperventilation is not really much higher O2, but the lowering of CO2 and the consequent prolongation of the comfort phase of the breath-hold. And you all know why I've put the word advantage into double quotes.