Control and Chemical Regulation of Breathing: Healthy vs. Sick People

What is the most important chemical regulator of respiration? Chemical regulation of respiration is different in healthy and sick people.
Breathing control in healthy people
Any medical or physiological textbook, which discusses breath control or regulation of respiration 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 e-Book "Normal breathing: the key to vital health" (PDF file).
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, that 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.
Conclusion 1. 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 or chemical regulation of respiration in the sick

The breathing of sick people is regulated, in addition to CO2,
by current blood O2 concentrations. The urge for oxygen gets stronger
with the advance of many diseases. This makes sense, since we found
that the key feature of chronic diseases is alveolar hyperventilation
(see Table 1 with 34 medical
research studies about 100% prevalence of hyperventilation in the sick),
while breathing more than the medical norm reduces body
oxygenation due to lack of CO2 in the arterial blood (hence, no conditions for
CO2-induced vasodilation) and suppressed
Bohr effect.
Conclusion 2. The breathing of sick people is regulated chemically by blood and brain CO2 concentrations and O2 drive, that becomes stronger with progression of chronic diseases and increasing cell hypoxia due to increased respiration (elevated minute ventilation).
References: CO2 Effects Web Pages
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 tissues
Cell Oxygen Levels and oxygen transport are controlled by
alveolar CO2 and breathing
Oxygen Transport depends on
breathing and these two effects (Vasoconstriction-Vasodilation and the Bohr
effect) are parts of two diagrams that summarize influences of hypocapnia (low CO2
content in the blood and cells) on circulation and O2 delivery
Free Radical Generation takes
place due to anaerobic cell respiration caused by cell hypoxia. Hence,
antioxidant defenses of the human body are also regulated by CO2 and breathing
Inflammatory Response is controlled by
breathing since hypoxia leads to or intensifies chronic inflammation through over-expression
of the hypoxia-inducible factor 1, while normal
breathing reduces these processes
Nerve stabilization takes place due to calmative or
sedative effects of carbon dioxide in neurons or nerve cells
Muscle relaxation or relaxation of muscle cells
is normal at high CO2, while hypocapnia causes muscular tension, poor posture
and, sometimes, aggression and violence
Brochodilation - dilation of
airways (bronchi and bronchioles) by carbon dioxide, and their constriction due
to hypocapnia
CO2: Best Natural Cough Suppressant
and "home remedy" since it calms urge-to-cough nerve receptors located in the
tracheobronchial tree and larynx
Blood
pH regulation and regulation of other bodily fluids
CO2: Lung Damage Healer: Elevated carbon
dioxide prevents injury and promotes healing of lung tissues
CO2: Skin and Tissue Healer
Synthesis of Glutamine
in the Brain, CO2 fixation, and other chemical reactions
CO2 myth
"CO2 is a toxic waste gas" myth
Breathing control
How is our breathing regulated? Why hypocapnia makes breathing uneven and erratic?
Reference Web Pages: Breathing norms, Medical Graphs and Tables about Breathing Rates (Minute Ventilation) and
Body Oxygen in Healthy, Normal and Sick People
Breathing
norms Parameters, graph, and description of the normal
breathing pattern
6 breathing myths 6
myths about breathing and body oxygenation (prevalence: over 90%)
Hyperventilation Definitions of
hyperventilation: their advantages and weak points
Hyperventilation Syndrome in the
Sick. Table
1. Western scientific evidence about prevalence of CHV
(chronic hyperventilation) in patients with various chronic conditions
(34 medical studies)
Normal Minute Ventilation in
Healthy Subjects: Easy and Light Breathing (14 Studies)
Hyperventilation Prevalence Present in Over 90% of
Normal People (24 medical publications)
HV and hypoxia
How and why deep breathing reduces oxygenation of cells and tissues of
all vital organs
Body oxygen test
How to measure your own breathing and body oxygenation (a simple DIY test)
Body oxygen in healthy
Table 4. CP (body oxygen level) in healthy people (27 medical
studies)
Body oxygen in sick Table 5.
CP (body oxygen level) in sick people (14 medical studies)
Buteyko
Table of Health Zones with clinical description of most common zones
Morning HV Morning
hyperventilation effect or how and why critically ill people are most
likely to die during early morning hours
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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