The Limits of Breath Holding - Scientific America

supplement:

How the Dive Reflex Extends Breath-Holding: Scientific American

The article is about the breakpoint of breath holding. It’s a popularized version of a review article from 2006 by the same author. It questions what causes the uncomfortable urge to breathe after even only a minute or two, and why humans can’t generally BH long enough to black out.

Parkes cites some literature suggesting that it is not oxygen or carbon dioxide levels alone, although these must play some role. Blocking carotid chemoreceptors doesn’t prolong BH time. Blocking chest volume receptors (spinal anesthesia) or lung volume receptors (transplant patients) doesn’t prolong BH time. But rebreathing your own exhaled gas does seem to allow longer BH time beyond the usual breakpoint. There is not a single gas-dependent determinant of breakpoint. It doesn’t seem to be tied to a specific high CO2 level or low O2 level, although other studies have indeed quantified threshold curves.

The author hypothesizes that the uncomfortable urge is related to some kind of stimulus originating in the diaphragm. Temporarily paralyzing the diaphragms of some brave volunteers did prolong BH time. Either the diaphragm senses gas levels directly and communicates this to the brain, or it simply cannot tolerate prolonged absence of movement. He also suggests that the diaphragm sustains a contracted state throughout a breath-hold.

Their work also demonstrated that neuronal oscillators in the respiratory centre of the brainstem continue to cycle during apnea. This was seen as subtle rhythmic oscillations in heart rate, known as sinus arrhythmia. This would suggest that deliberate over-riding of the natural urge to breathe must occur somewhere between the brainstem oscillators and synapses on the phrenic nerves. It is not known if diaphragmatic contractions occur when this block becomes weakened, or if they originate within the diaphragm itself.

Very interesting post Fitz-Clarke. One question that comes to my mind is, would causing voluntary contraction on ascend decrease the risk of shallow water black out?

To Azrael3000:

Try it and find out!

I've noticed that "riding" my contractions, i.e. helping them along when they occur (so, not entirely voluntarily induced) during static BH relaxed me. I tried it later on during my dives - again, not inducing them voluntarily - and it made me feel more comfortable.

Then again... I've never blacked out, so I don't know if this delays the process. My aim in freediving is to always come up fresh, and be happy with whatever depth/time I've done.

(What is a "voluntarily induced" contraction? It seems to me to be too fake to be of any benefit.)

I did try it out that's why I was asking whether there is any scientific background on that. Also I never had a BO, so can't comment on any delay or so.

So for me a "voluntarily induced" contraction is a voluntary upwards movement of the diaphragm. This obviously contracts the lungs. So my question is basically linked to: Does this maneuver increase the partial O2 of the blood? Which would mean that the chances of SWBO are lower. Or am I wrong here?

Edit: This is in my opinion also related to the technique of hook breathing after surfacing. As you there try to keep the lungs under pressure (exchanging used air rather slowly).

I think voluntarily pushing your diaphragm up doesn't give the same "punch" as a real one. And I believe your theory about increasing pp O2 sounds good, but what about the O2 expenditure on the muscle power you need to voluntarily push up your diaphragm. Plus the O2 your brain needs to think of pushing up your diaphragm. That's why I say 'let the body do it's thing":king

When speaking about "voluntary diaphragmatic contractions" in freediving, one usually refers to contractions induced when equalizing ears with the Valsalva maneouvre during the descent. The contractions at the end of a breathold are typically involuntary, though some relatively rare freedivers do not experienced any, hence they might try inducing them voluntarily.

A "hook breath" is the contraction of thoracic and abdominal muscles, with the primary purpose of keeping up the blood pressure after the exhale. When you exhale after a BH the blood pressure abruptly drops, worsening so the already progressed cerebral hypoxemia. Increasing the pressure in lungs helps keeping the BP and hence the supply of the brain on sufficient level. The increase of PaO2 in lungs helping the gas exchange is a related but a different effect, probably less important than the prevention of the blood pressure drop.

Properly spoken, the contraction of a diaphragm results in a inspiratory movement (diaphragm goes outwards), so decreasing the pressure in lungs. However, the involuntary diaphragmatic contractions are in fact contractions of larger groups of respiratory muscles, not only of the diaphragm, so they induce both compressing and expanding movements. It was proven that the contractions help with the oxygenation of the brain (there is a study adressing this issue, but I can't locate it right now)

thanx Trux for explaining the different types of voluntary contractions.
Valsalva maneouvre? In freediving? Aren't we past that? I guess that's why I didn't think of those.
And that's the best explanation of why one should hook breathe on recovery I've ever read.

Thanks for the explanation Ivo. Clarifies a lot of things to me.

The study you refer to Ivo is Dujic et al. 2009 from Croatia (1). They looked at dry static apnea. Diaphragmatic contractions began after 2 or 3 minutes, and increased in frequency. Negative pressure spikes in the chest increase venous return of blood to the heart and thereby increase stroke volume. There was no change in peripheral vascular resistance, so the increased cardiac output largely goes to the brain. It is like reverse CPR that pulls extra blood into the chest every few seconds.

It would be difficult to do a control study in the absence of contractions to see if contractions actually prolong BH time, since this would require paralyzing the diaphragm and chest muscles. However, contractions probably do buy a little extra time by raising brain O2 levels during the middle and later stages of apnea. This would be true only if apnea time is limited by hypoxic black out. It would not be expected to affect CO2 levels significantly, so the effect on urge-related breakpoint is not so clear. But as discussed in the SciAm article, breakpoint may be further prolonged by the mechanical effect alone of diaphragm movement. It should be pointed out that there was no facial immersion or cold stimulus in this study, and hence no diving response.

It’s not so clear what role contractions might play during a dive because there are many other factors involved, such as different lung volumes, blood shift, diving response, hyperbaric gas levels, etc. But the same effect likely does happen, and one would expect a small increase in cerebral blood flow due to contractions. Again, this would presumably be beneficial only if the diver is close to hypoxic black out. The time gained however might be offset by the increased oxygen cost of muscle contraction.

(1) Dujic Z, Uglesic L, Breskovic T, Valic Z, Heusser K, Marinovic J, Ljubkovic M, Palada I. Involuntary breathing movements improve cerebral oxygenation during apnea struggle phase in elite divers. J Appl Physiol. 2009 Dec;107(6):1840-6.