Part 3. Effects of unnoticed increased breathing on cellular oxygenation (or how our slight over-breathing influences breathing of cells)

When a person starts to over-breathe or hyperventilate (breathe more air per minute), blood oxygenation in the lungs has negligible changes. Why? During normal breathing human blood has 98-99% O2 saturation. Hence, big breathing cannot increase the blood oxygenation in any significant degree.

What are the other effects, if a healthy person starts to breathe more or deeper?
- More carbon dioxide is removed from the lungs with each breath and therefore the level of CO2 in the lungs immediately decreases.
- In 1-2 minutes, the CO2 level falls below the normal levels in all the blood due to its circulation through the lungs.
- In 3-5 minutes most cells of the body (including vital organs and muscles) due to CO2 diffusion experience lowered CO2 concentrations;
- In 15-20 minutes, the CO2 level in the brain is below the norm due to slower diffusion rate.

Hence, too much CO2 is removed from all cells. When the breathing is big all the time, the CO2 level in all body cells is chronically low. How can CO2 influence oxygenation of the tissues? There are two direct CO2 effects on the oxygenation of tissues.

A. Vasodilation-vasoconstriction effect

Imagine that a person at rest starts to hyperventilate or breathe very heavy and very fast. What would happen? The person would feel dizzy and can faint or pass out. Why? It cannot be due to too much oxygen, since their blood is almost fully saturated with O2 with very shallow (or normal) breathing at rest.

This scan below shows brain oxygenation in two conditions: normal breathing and after 1 minute of hyperventilation. The red color represents the most O2, dark blue the least. Brain oxygenation for overbreathing is reduced by 40%. (Litchfield, 2003).



This result is quoted in many medical textbooks (e.g., Starling & Evans, 1968) since the effect is well documented and has been confirmed by dozens of professional experiments. According to the Handbook of Physiology (Santiago & Edelman, 1986), cerebral blood flow decreases 2% for every mm Hg decrease in CO2 pressure. Why?

CO2 is a dilator of blood vessels (arteries and arterioles). Arteries and arterioles have their own tiny smooth muscles that can constrict or dilate depending on CO2 concentrations. When the breathe more, CO2 level becomes smaller, blood vessels constrict and vital organs (like the brain, heart, kidneys, liver, stomach, spleen, colon, etc.) get less blood. As physiological studies found, blood flow to these organs is proportional to blood CO2 concentrations. The less we breathe, the more blood and oxygen can reach the tissues of vital organs.

Since hyperventilation is an important part of our “fight-or-flight” response, during hyperventilation the blood is generally diverted from the vital organs to the large skeletal muscles. Indeed, studies found decreased perfusion of the heart (Okazaki et al, 1991), brain (discussed above), liver (Hughes et al, 1979; Okazaki, 1989), kidneys (Okazaki, 1989), and colon (Gilmour et al, 1980).
 

Why did Nature provide us with this physiological reaction: vasoconstriction due to hyperventilation? Breathing is closely connected with blood flow to all vital organs, sensitivity of the immune system, permeability of cellular membranes, and many other functions. As soon as vital organs (the brain, heart, stomach, kidneys, liver, etc.) are under stress (chemical, viral, bacteriological, etc.), or inflammation, or injury, the breathing gets heavier.

That helps to prevent:
- excessive bleeding (as in cases of open injuries, cuts, bruises, etc.),
- quick spread of bacterial and viral infections,
- excessive amounts of toxic products in the blood from injured or polluted tissues,
- damage to vital cleansing organs (e.g., liver and kidneys).

All these preventive effects can save the life of the organism in the short run. At the same time, it is not normal to be in a state of stress (or fight-flight mode) all the time. Our breathing, if there is no emergency, should be normal. In order to normalize breathing (or to retrain the breathing centre), all organs and tissues should be gradually repaired, restored and rebuilt.

B. The Bohr effect

The description of the Bohr law (discovered over a century ago) can be found in standard physiological textbooks since it was confirmed by dozens of professional studies.

What is the Bohr effect? As we know, oxygen is transported in the blood by hemoglobin cells. How do these red blood cells know where to release more oxygen and where less is needed? Or why do they unload more oxygen in those places where more is required? For example, at rest the heart muscle requires more oxygen, but blood travels everywhere.

The hemoglobin cells sense higher concentrations of CO2 (end product of energy production) and release oxygen in such places. The effect strongly depends on the absolute CO2 values in the blood and the lungs.

If the CO2 concentration is low, O2 cells are stuck to the red blood cells. Hence, CO2 deficiency leads to hypoxia or low oxygenation of the body cells (the suppressed Bohr effect). The more we breathe at rest, the less the oxygenation of our cells in the vital organs, like brain, heart, liver, kidneys, etc.

The Bohr effect is crucial for our survival. Why? At each moment of our lives, some organs and tissues work harder and produce more CO2. These additional CO2 concentrations are sensed by the hemoglobin cells and cause them to release more O2 in those places where it is most required. This is a smart self-regulating mechanism for efficient O2 transport.

For example, without the Bohr effect, you could not walk or run even for 3-5 minutes. Why? In normal conditions, due to the Bohr effect, more O2 is released by red blood cells in those muscles, which generate more CO2. Hence, these muscles will get more O2 and can continue to work with the same high rate.

Western studies confirmed that hyperventilation compromises oxygenation of vital organs, like liver and kidneys (Hughes et al, 1979; Okazaki et al, 1989), and heart (Okazaki et al, 1991) (e.g., Hughes et al, 1979; Hashimoto et al, 1989; Okazaki et al, 1991).

Conclusions: Even slight unnoticed over-breathing or increased ventilation decreases blood and oxygen supply for all vital organs causing tissue hypoxia and poor perfusion.

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References for part 3

Gilmour DG, Douglas IH, Aitkenhead AR, Hothersall AP, Horton PW, Ledingham IM, Colon blood flow in the dog: effects of changes in arterial carbon dioxide tension, Cardiovasc Res 1980 Jan; 14(1): 11-20.

Hashimoto K, Okazaki K, Okutsu Y, The effects of hypocapnia and hypercapnia on tissue surface PO2 in hemorrhaged dogs [Article in Japanese], Masui 1989 Oct; 38(10): 1271-1274.

Hughes RL, Mathie RT, Fitch W, Campbell D, Liver blood flow and oxygen consumption during hypocapnia and IPPV in the greyhound, J Appl Physiol. 1979 Aug; 47(2): 290-295.

Litchfield PM, A brief overview of the chemistry of respiration and the breathing heart wave, California Biofeedback, 2003 Spring, 19(1).

McArdle WD, Katch FI, Katch VL, Essentials of exercise physiology (2-nd edition); Lippincott, Williams and Wilkins, London 2000.

Okazaki K, Hashimoto K, Okutsu Y, Okumura F, Effect of arterial carbon dioxide tension on regional myocardial tissue oxygen tension in the dog [Article in Japanese], Masui 1991 Nov; 40(11): 1620-1624.

Okazaki K, Okutsu Y, Fukunaga A, Effect of carbon dioxide (hypocapnia and hypercapnia) on tissue blood flow and oxygenation of liver, kidneys and skeletal muscle in the dog, Masui 1989 Apr, 38 (4): 457-464.

Santiago TV & Edelman NH, Brain blood flow and control of breathing, in Handbook of Physiology, Section 3: The respiratory system, vol. II, ed. by AP Fishman. American Physiological Society, Betheda, Maryland, 1986, p. 163-179.

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© 2008 Artour Rakhimov (If you copy the content of these pages for educational purposes, please, indicate the site address and author's name).