Control Pause Question

How do we know a long control pause is brought on by good carbon dioxide tolerance rather than just a very low rate of production of carbon dioxide? Thanks.

 

Maybe by measuring other parameters. If u have a control pause say about 15 and you improve to say 30 but your temps and heartrate are still the same then you may have improved your carbon dioxide tolerance.

 

low rate of CO2 = low CP.

Higher CO2 allows more oxygenation of tissues = longer CP.

Lower CO2 production allows less oxygenation, tissue hypoxia, and low CP.

 

But the breathing instinct is triggered by carbon dioxide sensors, not by cellular oxygenation.

 

And thats why one need to get to the "airhunger" in the buteyko exercise.

 

Yeah I guess that's the only way to be sure you're filled with carbon dioxide... but maybe if one is all glycolysis he could use up oxygen before even raising carbon dioxide... and get air hunger from oxygen sensors...

 

Why is the controlled pause done after expiration rather than inhalation?

 

yes maybe. haven´t found the quote but i read that to get airhunger from oxygen is very rare..

 

It is a kind of backup system I think.

 

Then it would take ten minutes to check...

 

exhalation gives you your body's response to its existing CO2 stores without the benefit of the oxygen from the lungs.

 

It would be the same it would just take longer... but I guess it helps standardize results across different lung volume to body ratio.

 

But we're blowing out the excess carbon dioxide with the exhalation, aren't we? I recall reading that decreasing lung volume through exhalation allows CO2 to passively diffuse into the blood, so I guess even blowing out all that CO2 still allows it to rise faster than after a full inhalation. Anyway, I've done the standard Buteyko breath holding exercise, but I still like holding the inhale sometimes instead. I've noticed I can get down to a couple inhalations per minute and continue pretty comfortably that way, assuming I'm inactive. Perhaps it's doing no good, though.

 

There may be a problem because holding breath after Inhalation is linked to a stress "state" and also the CP is meant as a measurement only not a exercise to raise co2

 

Okay, well I'll abandon the inhalation holds then. When I do the pauses on exhalation I typically only go 5 to 10 seconds at a time for each hold, it's not a full CP which would be longer.

 

My take away is to check ETCO2 / morning temperature for good metabolism (which indicates good co2 production) whilst at the same time checking CP. Ideally have high in both.
I think where Peat disagrees with Buteyko is that you're right, control pause can get higher with a reduction in metabolism. But you want a high metabolism too.

a recent email response from Peat:

"Lots of the Buteyko people are now using devices, essentially tubes to increase the dead space, which I think are more practical than the timing method. Since metabolic rates vary tremendously, unless there’s a device to measure the end tidal CO2, it’s hard to tell whether a person’s CO2 retention is increasing, or their metabolic rate is decreasing. My end tidal CO2 is typically about 6%, while I’m breathing much faster than average, using much more oxygen. Breathing in a bag, or sitting in a plastic bag or bathtub full of CO2 (it’s heavier than air, so it stays in), is another way to get the body to adapt to a higher CO2. When someone’s tissues are loaded with the antithyroid polyunsaturated fatty acids, it’s a long process to get their lactate production down, CO2 production and retention up.

Eur J Clin Invest. 1989 Feb;19(1):65-71.
Adenosine receptor mediated stimulation of ventilation in man.
Jonzon B(1), Sylvén C, Beermann B, Brandt R.
(1)Department of Clinical Pharmacology, Huddinge University Hospital, Stockholm,
Sweden.
We wanted to examine how adenosine stimulates ventilation in man. Bolus doses of
adenosine were given i.v. in an antebrachial vein in multiples of 2.65 mg. The
minute ventilation was increased by adenosine 5.3 to 15.9 mg (median values) from
control 12.6 +/- 1.9 l min-1 to 42.5 +/- 4.7 l min-1 in a dose-dependent manner.
The adenosine receptor antagonist theophylline, 58.3 +/- 3.3 (mean +/- SEM) mumol
l-1 plasma, inhibited the response by approximately 25%. Dipyridamole 10 mg, an
adenosine uptake blocker, enhanced the effect of adenosine by approximately 60%.
The ventilation was not affected by metoprolol, atropine, naloxone or cromolyn
sodium but was attenuated by hyperventilation. The respiratory stimulation
started before chest pain and cardiovascular effects such as AV-block were
encountered. It is concluded that this respiratory stimulation shows
characteristics of adenosine receptor mediated responses but the location of such
adenosine receptors is uncertain. The findings are compatible with a stimulatory
or facilitating effect of adenosine on afferent pathways."

 

I've found that this isn't how it works.

Artour at normal breathing says that buteyko practitioners often score low on ETCO2.

I follow Peat principals and have a high metabolism, my ETCO2 is between 5.7-6% (the normal being from 4-6% kPa), however my CP is low around 10-12 seconds.

 

Yes, I think thats the main reason.

 

Speculating: If CO2 gets low, cells are more likely to be in hypoxic conditions, therefore more likely to go to glycolysis, which produces less CO2, continuing the reinforcing cycle. This could well be part of what makes it hard to get out of (along with lowered CO2 set point when it gets chronic).

 

This may be true but it isn't what buteyko or Artour teach. They emphasize the cp as the primary way to measure results in increasing co2 levels and therefore better tissue oxygenation. I studied under Artour for quite awhile.