Breath Control (Regulation of Respiration): O2 or CO2?
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.
Modern 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.
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
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.
Breath control in the sick: increased role of O2
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).
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.
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.
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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