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Contractions and blackouts!

Thread Status: Hello , There was no answer in this thread for more than 90 days.
It can take a long time to get an up-to-date response or contact with relevant users.

sebastien murat

Well-Known Member
May 18, 2004
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Here's another one for you, if you like challenges: do contractions (not splenic contractions but the ones that make you want to breathe) increase the rate of O2 consumption, thus reducing BHD and increasing the risk of a blackout? (Hint: its a trick question).

Seb
 
Well let me try... Firstly - 'Contractions' result in O2 stores being depleted through the use of the basic chemicals that power muscles. That's an easy one one from freediving 101, but, what is BHD?
 
@Shouts: BHD - Breath hold :)

The few times I had the chance to do dry statics and apnea walking with a heartrate monitor I noticed the major reduction in heart rate came with contractions.
I consider my dive response to be relatively untrained and these experiments were done in hot weather (Thailand and Dahab).
An example for my first walk in a session would be:
Rest (standing) - 72bpm,
Walking - rising towards 100bpm,
3 big contractions - down to 42bpm and feeling that I have to breathe.*
In consecutive walks at the same session it would take more conrtactions to get to around the same HR where I would feel I have to stop.*
Seemed to me that the number of steps, time, distance or contractions wasn't as repeatable as the lower cap of 40bpm (in those conditions, while diving I measured lower rates).
Any tips as to why is that?

*I have to point that I think the reasons I stopped are more related to hypercapnia than hypoxia. Signs of hypoxia are not as nearly as pronounced as they can apear in a dive, but it feels like I'm trying to prevent every muscle of my body (bowels included) from shaking uncontrollably. I'm pretty sure it's very different from hypoxic LMC and I produced it in every dry "hypercapnic" max dynamic breathold (apnea stairwalking too) I tried.
 
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What I learned from DB is that the contractions are actually helping with blood circulation, increase blood pressure in the brain, and also in a way "mix" the air in lungs, hence the CO2 saturated air in alveolus may get little bit refreshed with the more rich air deeper out of the alveolus. I assume, the contractions are actually driven by an anaerobic muscle activity and actually allow keeping the same blood pressure with lower heart activity, hence saving oxygen store in the heart muscle. From this point of view it should definitely help prolonging the apnea, and thanks to keeping the blood pressure in brain high, it reduces the risk of BO.
 
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I can answer this question quite objectively since I did many experiments with my oximeters on this subject.

The conclusion I found:

- Resisting contractions always saves more oxygen than allowing contractions
- Having contractions at a slow rate still is a better condition than having no breathing reflex at all, in terms of oxygen consumption
- Having crazy contractions (1 per second) is not beneficial at all, and you would be better off with no breathing reflex

In other words, if I would start a breath-hold with such a high CO2 that I would quickly end up with body buckling contractions at one per second, then I would reach a BO level faster than with less CO2 and fewer contractions.
 
Thanks for the details, Eric. It makes sense. I am just not sure if I understand this properly:
- Resisting contractions always saves more oxygen than allowing contractions
What exactly you mean by resisting and allowing contractions? Resisting them psychically; trying to control the diaphragm muscles; releasing/blocking air out of the lungs; or something else?
 
Thanks Eric,
When you say "resisting contractions" what do you mean? I try to minimize contractions through mental will. This allows them to become less severe and although they may be still coming they reduce in frequency and severity. I would not however classify this as 'resisting' but more a minimising technique.
 
Good timing - someone lent me an oximeter yesterday and i've been doing some holds. Will post some graphs later in the week but interesting to note that for a 5 minute breath hold my %Sp02 fell as far as 77%, I was expecting a lot lower.

Cheers,
Ben
 
Resisting contractions = stopping contractions through one of many known methods.

Various methods
#1 concentration
#2 swallowing
#3 gentling tensing the diaphragm
#4 yogi method-- exhale a micropressure against a pinched nose (blocks contractions forever, and lowers heart rate to <20bpm, but is very excruciating)

Method #4 has the greatest potential, and I have used it in static apnea to block contractions from the 5 minute mark to 7 minute mark, allowing only one contraction at 6 minutes. However, William Trubridge is able to do Method #4 DURING THE DIVE, and that's without fins. That takes insane concentration.

To use method #4 requires that your lungs not be filled to the max. In static I used to pack, and then exhale slightly at 5 minutes just before the 1st contraction, and then start 'blocking' them. If you want to learn the correct exhale pressure, it should be the same exhale pressure that you would use to exhale over a period of 40 seconds. So try doing a 3 minute static, then exhale through one nostril for 40 seconds, WITHOUT USING YOUR THROAT TO CONTROL THE FLOW. Use only the DIAPHRAGM muscle to control the air flow. If you use the diaphragm only, then contractions will stop or never come. Once you have mastered the method while actually exhaling, then do the same but pinch your nose so no air can come out while 'exhaling' against the closed nose.

WARNING: this method can create weird effects on the nervous system, possibly including but not limited to severe depression, sleeplesness, muscle twitches, and other effects. See the thread 'apnea, suicide and depression' and reference my post on 'extreme vagal stimulation.'
 
Thanks Eric for yet another highly informative answer. When are you going to write a book?!!!
You keep mentioning "vagal stimulation" so for those who don't know the definition of this term here it is courtesy of Biology Online. Life Science Reference


vagus nerve
(Science: anatomy, nerve) The vagus nerve enervates the gut (gastrointestinal tract), heart and larynx.
lesions of the tenth nerve usually result in a horse voice, but may also cause difficulty in swallowing or talking.
Synonym: cranial nerve X. A mixed nerve that supplies the pharynx and larynx and lungs and heart and esophagus and stomach and most of the abdominal viscera.One of the cranial nerves in vertebrates found at the floor of the brain that controls many of the parameters involved in the parasympathetic nervous system. The lungs and vocal chords are also the responsibility of the vagus nerve when regarding the nerv.
Retrieved from "http://www.biology-online.org/dictionary/Vagus_nerve"
 
do contractions increase the rate of O2 consumption, thus reducing BHD and increasing the risk of a blackout? (Hint: its a trick question).

The risk of blackout increases only when something increases the chance of hypoxia. Increasing the rate of O2 consumption does not increase the chance of blackout unless you make other assumptions about the conditions of the apnea, such as the person performing apnea is also performing a depth dive and we are comparing the same dive done with contractions and without contractions. Since it was not specified, we can choose another scenario, such as a static, and since an increase in the consumption of O2 also increases the production of CO2, we know the person will have a tougher time holding their breath and therefore we can not assume they will hold their breath to a lower SaO2 than if they had not had contractions; actually we can probably safely assume they will hold their breath without as low of a SaO2, which suggests they are at less risk of blackout.

Therefore, without less ambiguity in the question and its context, we can see that an increase in O2 does not in and of itself suggest an increase in risk of blackout. And therefore, since one part of the question is false, the whole question results in a "no".

If that is not the correct answer and reasons for it, then I feel it is important to mention that the question is riddled with ambiguities and therefore requires clarifications to proceed. For example:

Answering is somewhat putting oneself on the spot until the acronym is assured by the questioner to be what we think it is. I would feel silly being told the statement is false because BHD stands for "blood haemoglobin disease" or something. ;)

Strictly for sentence structure these are the interpretations that have a high possibility of being taken up by the reader:
1. Do diaphragmatic contractions during apnea in a person increase the rate of O2 consumption in the contracting muscles and therefore both, reduce breath hold duration and increase the risk of blackout?
2. Do diaphragmatic contractions during apnea in a person increase the rate of O2 consumption in the contracting muscles and therefore reduce breath hold duration, this reduction increasing the risk of blackout.

It is unknown whether the question is regarding apnea under any possible conditions, specifically while doing a depth dive, specifically while doing a static, or some other specified conditions?
 
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Here's another one for you, if you like challenges: do contractions (not splenic contractions but the ones that make you want to breathe) increase the rate of O2 consumption, thus reducing BHD and increasing the risk of a blackout? (Hint: its a trick question).

Seb

from the beginning

that burning feeling/contraction (hold) will trip vaso constriction reducing O2 consumption, entering DR faster/harder, increase BHD and lessen the risk of BlackOut.

come on Seb we are all waiting. jiji

or is it really a trick question... BHD = Blonde Hair Disorder... constant hyperventilation ,information bouncing off neurons and receptors making it impossible to relax....increasing O2 consumption, iniciating DR = Dumb Response, blackout iminent !! jijii sorry..
 
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Sorry for the delay, I was on the toilet!

Someone wrote: The risk of blackout increases only when something increases the chance of hypoxia. Increasing the rate of O2 consumption does not increase the chance of hypoxia unless you make other [specific] assumptions about the conditions of the apnea.

Your first point is clearly true, but not your second one: increasing the rate of O2 consumption deos increases the risk of hypoxia. Here' why.

-Increasing work output (e.g., swimming or inspiratory muscular contractions against a closed glottis...i.e., our 'contractions') delays the physiological break-point, i.e., there is greater CO2 insensitivity and a delay in the urge to breathe. This is probably a direct result of CO2 muscle buffering (high solubility) under muscular work conditions.

-CO2 insensitivity reduces the reserve margin before a critically dangerous hypoxia to develop, itself increasing the risk of a blackout, under static, dynamic or deep-diving conditions. In other words, you have less margin for error, which increases the risk of a BO; deep-ascents only exacerbate this risk.

- What evidence is there of this? Firstly, HR is a proximate indicator of peripheral vasoconstriction. If HR is elevated, during diving (anxiety issues aside), this is in itself an indication of elevated metabolic rate (e.g., muscular work) and reduced peripheral vasoconstriction. If you increase blood flow to the muscles they will increase O2 consumption. Therefore increased HR indicates increased O2 consumption. Try this simple experiment: BH with facial immersion in water with HR feedback. During the BH HR decreases in line with waht we expect from the DR. When you then experience your contractions, HR increases (i.e., muscular work) as the contractions become more frequent and intense, after which it drops again (even during intense contractions) as hypoxia ensues. Adding exercise at any time increases it again. The lower the absolute HR, the lower the rise in HR during the contraction stage, implying greater protection. Indeed, it is possible to have no rise in HR even during the most intense contractions or exercise bouts provided certain conditions are met.

Finally, my point: contractions may or may not increase O2 consumption and, thus, the risk of a BO, depending on your HR before reaching the contraction stage. Clearly, it is better to have a well developed and strong DR, as well as employing techniques that accentuate it, e.g., E-dives, full-body submersion, etc.

Of course contractions are necessary and helpful, espcially if they occur earlier than too late, at least in this context, as they indicate to us about whether we should surface, if at all, but it is a double-edged sword in that it can also work against us if the DR is not developed enough. Extending the argument, one could state that divers with a more pronounced DR are at reduced risk of BO, all other things being equal.

Cheers
S

PS: BHD = breath-hold duration....I'm not one for cheap tricks!
 
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Someone wrote: The risk of blackout increases only when something increases the chance of hypoxia. Increasing the rate of O2 consumption does not increase the chance of hypoxia unless you make other [specific] assumptions about the conditions of the apnea.
Actually the second sentence was supposed to say "not increase the chance of blackout", correlating to the original question. Not that this affects the focus of your argument.

- What evidence is there of this?...
My interpretation of the statements is that elevated HR indicates elevated metabolic rate and a reduction in peripheral vasoconstriciton and therefore increased O2 consumption. Then it is emphasized that contractions increase HR. According to the first statement, this results in an increased O2 consumption. I do not find the explanation for the suggestion that contractions do not inheritly increase O2 consumption, actually, other than the conclusion it looks like the reasonings are arguing for the opposite? I interpret that the contractions increase HR and the hypoxia induces a lowering of HR. Am I missing something from the explanation?

Finally, my point: contractions may or may not increase O2 consumption and, thus, the risk of a BO, depending on your HR before reaching the contraction stage.
Other than achieving the situation where HR does not rise due to contractions, can you explain how you determine contractions may not increase O2 consumption depending on your HR? As much as I try, I can not deduce it from the elaborations.
 
2 questions that I find relevant:

1) I was under the impression that contractions raise cerebral blood pressure, therefore due to higher ppO2 in the brain you will BO (reach cerebral hypoxia) at lower blood o2 saturation levels. Is there any eveidence supporting/contradicting this?
In this case higher cerebral BP might be able to compensate for increase in O2 consumption due to contractions, no?

2) Maybe a more personal issue, but from the few times I measure HR in dry apnea, the bradicardia arrived with contractions, and I know I'm not the only one it has happened to, does it mean that in this instance of dry apnea the DR wasn't engaged properly?
 
I suppose that the HR is not the whole thing which tells the final answer. I also suggest to check what happens to blood pressure during different kind of apneas. Simple example: check the HR and the blood pressure while packed and without (in the beginning, in the middle and in the end). I may guess that speculations may come more interesting. I suppose some may be surprised what kind of values would be found, even most of us knows that the BP will drop in the beginning of apnea while packed
 
At the break-point, as contractions occur, especially in the dry state, there is generally an increase in HR (-> increase in O2 consumption). The hypoxia-induced reduction in HR has not full taken full hold of the situation. One may consider contractions, at this stage as a form of muscular work, placing it in direct conflict with the DR. Once hypoxia takes hold there is progressive reduction in HR. This can be greatly delayed, say reversed, if some form of work is suddenly carried-out, e.g., standing-up will surely do it. Eventually, it probably wins-out. I've noticed that this tends to be all the more likely if HR is initially elevated, e.g., dry vs. wet, sitting vs. standing, etc. Indeed, when u/w doing statics and swimming off into a dynamic at the break-point, I don't get a rise at all, even if I sprint straight-up; then again my HR is in the low 30s. Though I become progressively more hypoxic and may step-up the speed in the last phase, HR never increases, unless I've decided to bail-out, where it may rise a fraction. I'm begining to believe that to prevent the increase you need several ingredients:
- an initially low HR (i.e., low 30s but most probably dependent on the individual) brought on by a strong DR, minimizing facial equipment, etc;
- submersion; &
- convective (cooling) currents running over the face and body.

I think that if HR is low enough, reflecting a stronger vasoconstriction, then the peripheral resistance increases so much (according to Laplace's principle) that even intense exercise will have a minimal, say insignificant effect, on HR, BP or VO2 (O2 consumption). The problem is that to find the critical HR to prevent a rise with contractions/exercise/work requires individual testing over several days trialing.

Sure CBF (cerebral blood flow) or perfusion pressure may increase with hypercapnia and hypoxia under static conditions, but it deosn't negate the fact that under conditions of work (i.e., contractions), especially if peripheral vasoconstriction is poor, the cardiac output has to be divided between brain and working muscles, reducing CBF.

Regarding packing, the first phase of the breath-hold is poorly indicative of anything that happens during the latter phases. BP is always reduced initially and this is compensated by a rapid increase in HR, to maintain BP.

Cheers
S
 
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