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Normal Breathing Defeats Chronic Diseases

Breath Control (Regulation of Respiration): O2 or CO2?

MDs smiling Breath control (or control of respiration) is accomplished chemically, mainly using CO2 and O2 chemoreceptors. The most important chemical regulator of respiration is either CO2 or O2, since the chemical regulation of breathing is different in healthy and sick people.

Control of breathing in healthy people

Any medical or physiological textbook, which discusses breath control in the human body, states that respiration, in healthy people, is mainly controlled by CO2 concentrations in the brain and arterial blood.

CO2: the main chemical regulator of breathing in healthy peopleModern research is focused on specifics and details of this chemical breath control (Binet & Dejours P, 1962; Chernick et al, 1975; Dejours, 1963; Gautier, 2003; Forster & Pan LG, 1994; Heymans C, 1951; Honda Y, 1985; Kiwull-Schöne et al, 1994; Lahiri et al, 1978; Lahiri et al, 2003; Murai et al, 1987; Nattie, 1999; Nye et al, 1983; O'Regan & Majcherczyk, 1982; Richerson et al, 2005; Wennergren & Wennergren, 1983).

The main physiological ideas related to regulation of breathing can be found in Chapter 2. The chemical and physiological mechanisms of immediate regulation of breathing (pages 50-59) of my eBook "Normal breathing: the key to vital health". Here is an extract that includes these pages: Breath Control.

Obviously, should carbon dioxide be poisonous, it would be normal to have it as little as possible, but the situation is opposite, since healthy people have higher CO2 concentrations and the "poison" controls breathing or our outer respiration, the fundamental function of the human body.

CO2 model The breathing centre located near the rear of the brain (medulla oblongata) regulates our breathing movements. This breathing centre (also called the master centre of the body) uses special chemoreceptors to measure CO2 concentrations in the brain and arterial blood. The central chemoreceptors detect changes in the pH of the cerebro-spinal fluid and they are responsible for long-term or slow changes in breathing. Since CO2 dissolves in the blood and can penetrate through the blood-brain barrier, the main reason for pH variations in the brain are changes in CO2 concentrations. Peripheral chemoreceptors monitor immediate changes in CO2, O2, and pH concentrations of the blood and control our breathing in the short run. It is agreed that peripheral chemoreceptors include the carotid and aortic bodies. The carotid bodies, which can sense hypocapnia (low CO2), hypercapnia (high CO2) and hypoxia (low O2) play the main role in humans in comparison with aortic bodies, but immediate changes in CO2 produce the main effects on changes in the involuntary breathing pattern.

Women running during competition The breathing of healthy people during typical daily activities (rest, work, light and moderate exercise, sleeping, etc.) is mainly regulated by the pre-set (or their usual) chemical CO2 concentrations (CO2 breath control).

For example, when a healthy person takes several deep and fast breaths, CO2 in the lungs and blood falls. The breathing centre detects this drop and stops or reduces stimulation and work of the respiratory muscles. The person naturally holds their breath until the CO2 level reaches the initially pre-set value. Conversely, breath holding accumulates more carbon dioxide. The breathing centre senses this increase and intensifies breathing. This overbreathing is going to continue until extra CO2 is removed and the pre-set value is reached again.

We breathe more heavily during physical exercise, when our bodies produce more carbon dioxide. However, the rate of CO2 production matches the rate of CO2 removal in such a fashion that CO2 and O2 values in the arterial blood changes during exercise only slightly.Sick woman with breath control due to low CO2

Breath control in the sick: increased role of O2

Older man breathing oxygen Control of breathing of sick people is done, in addition to CO2, by current blood O2 concentrations. The urge for oxygen gets stronger with the advance of many diseases.

The control of the breathing of sick people is accomplished by blood and brain CO2 concentrations and O2 drive, which becomes stronger with progression of chronic diseases and increasing cell hypoxia due to increased respiration (elevated minute ventilation).

In severely sick people, O2 can become the main factor in regulation of respiration.

The change in air composition during human evolution and evolution of animals on the Earth was the key factor that led to appearance of chronic diseases. This is because hyperventilation was beneficial for creatures living in primitive air with very low O2 content and high CO2 content 1-2 millions of years ago, but overbreathing destroys health now.

This YouTube video "Evolution of Air" features Dr. Artour Rakhimov. He explains the key cause of bronchospasm, spasm of blood vessels, reduced Bohr effects and other effects caused by changes in air and low CO2 in modern air.

Reference pages: Breathing norms and the DIY body oxygen test:
- Breathing norms: Parameters, graph, and description of the normal breathing pattern
- Body-oxygen test (CP test) : How to measure your own breathing and body oxygenation (two in one) using a simple DIY test
.....

References: pages about CO2 effect:
- Vasodilation: CO2 expands arteries and arterioles facilitating perfusion (or blood supply) to all vital organs
- The Bohr effect: How and why oxygen is released by red blood cells in body tissues
- Nerve stabilization: Carbon dioxide has powerful calmative and sedative effects on brain neurons and nerve cells
.....

References

Binet L, Dejours P, The role of arterial chemoreceptors in the control of pulmonary respiration in man [in French], Arch Int Pharmacodyn Ther 1962 Oct 1; 139: p. 328-335.

Chernick V, Faridy EE, Pagtakhan RD, Role of peripheral and central chemoreceptors in the initiation of fetal respiration, J Appl Physiol. 1975 Mar; 38(3): p. 407-410.

Dejours P, Control of respiration by arterial chemoreceptors, Ann N Y Acad Sci. 1963 Jun 24; 109: p. 682-695.

Gautier H, Honoring Pierre Dejours: his contribution to the study of the role of the arterial chemoreceptors in the regulation of breathing in humans, Adv Exp Med Biol 2003; 536: p. 1-7.

Forster HV, Pan LG, The role of the carotid chemoreceptors in the control of breathing during exercise, Med Sci Sports Exerc 1994 Mar; 26(3): p. 328-336.

Heymans C, Chemoreceptors and regulation of respiration, Acta Physiol Scand 1951 Feb 21; 22(1): p. 1-13.

Honda Y, Role of carotid chemoreceptors in control of breathing at rest and in exercise: studies on human subjects with bilateral carotid body resection, Jpn J Physiol. 1985; 35(4): p. 535-544. Review.

Kiwull-Schöne H, Bungart S, Kiwull P, Metabolic acid-base status and the role of carotid chemoreceptors in hyperoxic breathing, Adv Exp Med Biol 1994; 360: p. 261-263.

Lahiri S, Mokashi A, Delaney RG, Fishman AP, Arterial PO2 and PCO2 stimulus threshold for carotid chemoreceptors and breathing, Respir Physiol 1978 Sep; 34(3): p. 359-375.

Lahiri S, Forster RE, CO2/H(+) sensing: peripheral and central chemoreception, Int J Biochem Cell Biol. 2003 Oct; 35(10): p. 1413-1435.

Murai DT, Wallen LD, Lee CC, Clyman RI, Mauray F, Kitterman JA, Effects of prostaglandins on fetal breathing do not involve peripheral chemoreceptors, J Appl Physiol 1987 Jan; 62(1): p. 271-277.

Nattie E, CO2, brainstem chemoreceptors and breathing, Prog Neurobiol 1999 Nov; 59(4): p. 299-331.

Nye PC, Hanson MA, Torrance RW, The effect on breathing of abruptly reducing the discharge of central chemoreceptors, Respir Physiol 1983 Jan; 51(1): p. 109-118.

O'Regan RG, Majcherczyk S, Role of peripheral chemoreceptors and central chemosensitivity in the regulation of respiration and circulation, J Exper Biology 1982 Oct; 100: p. 23-40.

Richerson GB, Wang W, Hodges MR, Dohle CI, Diez-Sampedro A, Homing in on the specific phenotypes of central respiratory chemoreceptors, Exp Physiol 2005 May; 90(3): p. 259-266.

Wennergren G, Wennergren M, Neonatal breathing control mediated via the central chemoreceptors, Acta Physiol Scand 1983; 119(2): p. 139-146.

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