Hyperventilation

[azapa]

Originally Posted by TRITON

Since i started breathing like this i haven't had an LMC or a blackout and regularly feel burning in my legs and hands at the end of the dive as a sign of the diving reflex kicking in.

Hi Alex, I am pretty sure the leg burn is nothing more than o2 depletion /co2 build up in those big leg muscles, and has nothing to do with DR. Please correct me if I'm wrong. To be honest on a recreational freedive, I would not be too happy regularly getting to the burn point as it would probably mean I'm over extending my dive. On supervised personal best dives my legs burn like crazy though, to the point of hating the dive and thinking of giving my safety diver the head shake....

Waaay of topic but all good fun...

[billieball]

Well, let's see what Blaine does.
As for the FIT stance on hyperventilation, I know it is discouraged (or at least that is how I interpreted that which I was taught in Level II). By "hyperventilation," I am referring to the breathing method that is most commonly associated with the term...not the all-encompassing term that would include any breath outside of a "normal" one. Anyway, splitting hairs I suppose. And when we "purge" before a dive, we do indeed resume normal, slowed breathing before the dive.
Peace,
Billie

[trux]

Originally Posted by azapa

Hi Alex, I am pretty sure the leg burn is nothing more than o2 depletion /co2 build up in those big leg muscles, and has nothing to do with DR. Please correct me if I'm wrong.

Muscle burn means acid lactic production, and acid lactic production mean anaerobic metabolism. As long as the core and brain feels fine, it indeed signals a strong diving response. If you feel like blacking out (or you do black out), it may simply mean general hypoxemia.

[chrismar]

Originally Posted by trux

Muscle burn means acid lactic production, and acid lactic production mean anaerobic metabolism. As long as the core and brain feels fine, it indeed signals a strong diving response. If you feel like blacking out (or you do black out), it may simply mean general hypoxemia.

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]

" the hypocapnia messes up your diving response and in the end-effect it leads to a quicker oxygen stock depletion."

Do you have a guess as to how much time one might lose, Trux? 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.

[trux]

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]

Originally Posted by trux

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]

Originally Posted by Bill

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]

Originally Posted by Fattah

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]

Originally Posted by trux

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]

Originally Posted by efattah

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]

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:

Originally Posted by efattah

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]

Originally Posted by trux

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]

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]

Originally Posted by efattah

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.