Scientific American: "The Limits of Breath Holding"

I'm not a free diver except in the most rudimentary and trivial sense, but I find it fascinating in several dimensions, and I've followed a number of threads about it here on SB. There's an article in the April 2012 (current) issue of Scientific American The Limits of Breath Holding by Michael J. Parkes, a lecturer in applied physiology at the University of Birmingham, UK.

An abstract is at The Limits of Breath Holding: Scientific American

Contrary to my impression from reading here on SB and elsewhere, the limiting factor for the "break point" is neither direct O₂ or CO₂ sensing, nor lung volume sensing.
"The best hypothesis is that the diaphragm sends signals to the brain about how long it has been contracted and how it is biochemically reacting to depleted levels of oxygen or rising levels of carbon dioxide. Initially those signals cause mere discomfort, but eventually the brain finds them intolerable and forces breathing to start again."

A search didn't find mention of it here, and I thought there might be some interest, particularly by serious free diving practitioners. I don't know if this article, or the underlying research, might inform improvements in free diving, and that's not directly addressed in the article. But that seems at least plausible.

I believe that I made mention of that form of "need to breathe" detection and control back in one of my early posts here. We use that as part of our breathing exercises and have long taught repeated diaphragmatic contractions as a good way to stave off air hunger.

Thalassamania:

...//...have long taught repeated diaphragmatic contractions as a good way to stave off air hunger.

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Please elaborate.

Did anyone read that Scientific American article? I'm not subsribed to it, can anyone in a few words say what's in there?

I've started swimming and snorkeling before I even went to school and was doing so every day, 6 times a week for 9 years till I was too old for my parents to push me continue doing that. I've had a lot of time in the pools to practice holding my breath. What worked for me was: sit down for a few min and fully relax, hyperventilate for a bit, take a deep breath and go. Swimming technique has a lot to do how long you last and how far you go, but when you start feeling the urge to take a breath, do so but don't let the air out of the mouth, just move it from the lungs to your mouth and back, it kind of imitates the breathing and I last a lot longer this way.

What one can do to see if it works, take a plastic bag, take a full breath and exhale into the bag, then just keep breathing in/out of the bag. The longer I do it, the faster I start breathing but I don't get that same feeling when I just try to hold my breath.

My wife put it in front of me a week or so ago then took it away before I could read it I have no idea where she hid it.

There was a box at the bottom of the 1st page of the article that suggested to me that the CO2 sensing was not wholey ruled out, but not having actually read the body of the article I did not have the opportunity to reconcile the two statements.

Shurup:

Did anyone read that Scientific American article? I'm not subsribed to it, can anyone in a few words say what's in there?
...

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Did you try reading the online abstract I linked to in the OP, or the summary I quoted there?

gcarter:

My wife put it in front of me a week or so ago then took it away before I could read it I have no idea where she hid it.

There was a box at the bottom of the 1st page of the article that suggested to me that the CO2 sensing was not wholey ruled out, but not having actually read the body of the article I did not have the opportunity to reconcile the two statements.

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That's what I quoted in the OP.

Note I'm not the author, or more than an interested layman about physiology, but I'll try to make the distinction that the article does:

There are sensory structures in the body that react to blood levels of O₂ (in the carotid arteries) and CO₂ (in the carotids and brain stem). The article asserts that these have been ruled out as the controllers of break point because blood gas concentrations (presumably directly measured by instrumentation) do not predict break point, and because severing the nerve connections to these blood gas receptors does not disable the break point effect.

As I quoted in the OP though,
"The best hypothesis is that the diaphragm sends signals to the brain about how long it has been contracted and how it is biochemically reacting to depleted levels of oxygen or rising levels of carbon dioxide. ..."
which allows for O₂ and/or CO₂ levels to be an indirect cause insofar as they might contribute to the "fatigue" of the diaphragm.

Since I find myself paraphrasing more of the article than I originally intended, I'll add that another ruled-out hypothesis for break point is sensing lung volume, also because of cases where nerves had been severed.

For any more than that, you'll just have to find where your wife hid your magazine ...

Just read it - important to note that this is not a research paper but a more of a cherry-picked review. Most of the research that "supports" his view are experiments from the 50s and 60s, one of which used curare to paralyze patients (exept for 1 arm) to see how long they could withstand simulated breath holds (they were on life support and the breathing was turned off). Anyways they lasted 4 minutes and didn't report ill effects; however, he says that other studies trying the same thing since then ended much much earlier. The other one was a study that said that people could continue breath holds a second and a third time shortly after a first breath hold if they took in an asphyxiating gas even though gas levels (o2 and a co2) were getting worse. And that was apparently support for the idea that it is tension on the diaphram that stimulates breathing. I haven't read those papers (if there are even published papers on it) so I have no idea what the methodological quality of the papers were like but the first one at least is such an artificial environment I fail to see it's utlility (there are so many confounding factors given that you are basically shutting down every organ system while trying to isolate and examine the effect of one). I just skipped through it and I can think of one very common freediving exercise that makes the hypothesis seem like nonsense - if you do a static exhale, where you breathe in a big breath and then exhale fully (or close to it), your breath hold is FAR less than a regular breath hold and you don't get contractions/urge to breathe later -- yet there is no tension placed on the diaphram.

Doesn't include any research that i would consider good peer reviewed research (granted I don't really know the freediving literature all that well - other than the stuff that is practically relevant) and scientific american is not a peer reviewed journal.

Anyways basically move along nothing to see here.