By Dr. Artour Rakhimov, Alternative Health Educator and Author
This is another important detail (to be studied during Buteyko practitioner training) related to biochemical regulation of respiration in healthy people.
Let us consider healthy volunteers, who were asked the following:
- to breathe several times slower or faster while allowing the depth of breathing to regulate itself in a natural manner (their respiration rate could change from normal 12-15 to 3-4 per minute for slow breathing and up to 24-60 per minute for fast breathing);
- to breathe normal air at different barometric pressures (from about .5 to 4 atmospheres);
- to breathe different air mixtures (consisting of from 0.04% to 4-5 % CO2 and from 12% to 80 % O2);
- to walk 3, 5, or 8 km/h.
Was there any common parameter, which regulated breathing for all these situations? Practical experiments revealed that most parameters varied within wide ranges during these tests. For example, minute ventilation, the respiration rate, the volume of a single breath (tidal volume), arterial and venous O2 contents changed two or more times in comparison with corresponding values at rest. However, the carbon dioxide concentration in the arterial blood (aCO2) varied as little as 2-5 % in relation to resting numbers.
These tests were conducted by Yale Professor John Haldane about a century ago when basic ideas about respiration were established. Analyzing these results, Professor Haldane, in his textbook on respiration (probably the oldest one), stated that under normal conditions, exclusive of heavy work, breathing was regulated by the carbon dioxide level in the lungs or arterial blood (Haldane, 1922). These classic experiments have been repeated many times by other researchers.
Therefore, during normal daily activities, the nervous system preserves a certain level of carbon dioxide concentration in the lungs and the arterial blood.
In order to maintain this nearly constant daily CO2 level, the human organism employs, using a feedback mechanism, special groups of nerve cells located in two different places, in the medulla of the brain and near the main arteries close to the heart. This system of cells will be called in this book “the breathing center”. How does this feedback mechanism work?
In normal conditions, the immediate aCO2 value of the person corresponds to aCO2 norm established by the breathing center. However, certain activities can change the aCO2 value in both directions.
For example, during acute voluntary over-breathing, the current aCO2 value becomes smaller than the aCO2 norm. This change is detected by the breathing center. The breathing center instructs (or orders) the respiratory muscles to stop their activity (stop breathing). The organism starts to accumulate carbon dioxide up to the level preset by the breathing center (aCO2). That causes a gradually increasing desire to breathe. Normal breathing is resumed when this preset level is achieved.
In certain other situations, the organism can accumulate excessive (in respect to the preset aCO2 norm) amounts of carbon dioxide. That can happen, for example, during breath-holding started after normal breathing. In both cases, the breathing center senses this gradual aCO2 increase and sends impulses to respiratory muscles to intensify breathing until additional carbon dioxide is removed and aCO2 again stabilizes near the initial norm.
The same situation takes place during speaking while vigorously exercising since ventilation during heavy exercise can be as large as 150-170 litres per minute. Even during yelling or roaring ventilation numbers are significantly less. Hence, speaking while vigorously exercising causes increases in current aCO2 values.
Generally, the drive to increase breathing is proportional to the difference between current aCO2 values and the preset aCO2 norm. When the difference is negative (the current aCO2 values are lower than the aCO2 norm), there is a drive to decrease ventilation, up to its full cessation, as in cases of prolonged voluntary hyperventilation.
The breathing center also monitors oxygenation of the arterial blood using a similar feedback mechanism, but its importance for the above-mentioned tests is almost negligible. Since CO2 forms carbonic acid in the blood, the control of oxygenation is achieved by these cells through sensing hydrogen ions or pH of the blood which is kept, in health, within a narrow range (7.35-7.45). Hence, the breathing center also monitors blood pH, one of the most
important and carefully guarded physiological parameters.
Let us look in more detail at normal physiological responses for these four tests investigated by Professor Haldane.
1. Changing breathing frequency from a normal 12-15 times per minute to 3-4 times per minute caused prolonged inhalations and exhalations in normal people. This naturally produced a slow and deep breathing pattern. The amount of air exhaled during such breathing was almost unchanged. Hence, CO2 elimination from the organism during this slow breathing was also nearly the same (as before the test). Hence, the aCO2 value remains unaffected. Voluntary breathing with high frequencies (24-60 times per minute) resulted in fast shallow breathing also without significant aCO2 changes. Dogs in hot weather cool their bodies using such breathing. Large amounts of water evaporate from their tongues cooling the blood, while the carbon dioxide level remains almost unchanged.
2. Breathing normal air at different barometric pressures (from twice less to four times more, than the normal barometric pressure at sea level) did not have an immediate effect on breathing. Indeed, the CO2 content of the inspired air changed very little in these situations since normal air had only 0.04 % CO2. Hypoxia at the lowest pressures was too small to produce noticeable changes in breathing. Thus, breathing was almost unaffected.
3. When the CO2 content of the inspired air suddenly increased, the CO2 pressure in the lungs and, hence, the arterial blood also increased. The breathing center sensed this aCO2 rise due to blood acidification and that caused increased ventilation. Small increases in inspired air CO2 content (up to about 1%) were almost unnoticeable. Air with around 2% CO2 resulted in a marked increase in ventilation. 4-5% CO2 in inspired air produced labored breathing with minute ventilation over 20 l/min (e.g., Straud, 1959) in order to remove extra CO2 and preserve the preset aCO2.
Variations in O2 concentration of the inspired air produced no sensations in wide ranges (from 15% to 100%). Thus, breathing pure oxygen usually does not result in immediate specific feelings or symptoms. Hyperoxia (excessive oxygen in air) has never been experienced by an animal species during evolution. Indeed, air O2 content on the Earth has always been increasing, except for short historical periods when it has had small drops. Thus, breathing pure O2 is usually not felt, although prolonged breathing is harmful to the lungs and the brain. However, for hypoxia, a slight increase in ventilation and a corresponding aCO2 decrease was detected when air O2 concentration became about 12-15%.
4. Physical exercise required additional energy provided by muscles due to the oxidation of carbohydrates and fats and the generation of additional CO2. This extra CO2 was transported by the venous blood to the lungs and detected by the breathing center. The results were increased breathing frequency and minute ventilation. It is possible for ventilation to reach 100 l/min for moderately heavy physical work, but aCO2 would be virtually the same as at rest (2-5% relative variations in respect to the initial value).
Haldane JS, Respiration, 1922, Yale University Press, New Haven, UK.