Bohr Effect Explained: Healthy vs. Sick People
Bohr effect (medical or scientific explanation is down below)
The Bohr effect explains cells oxygen release or why red blood cells unload oxygen in tissues, while carbon dioxide (CO2) is the key player in O2 transport due to vasodilation and the Bohr effect (or Bohr law). The Bohr effect was first described in 1904 by the Danish physiologist Christian Bohr (father of famous physicist Niels Bohr).
What is Bohr effect in simple terms?
Bohr effect in healthy people
The Bohr effect is a normal process in healthy people since healthy people have normal breathing at rest and normal arterial CO2 levels. How does the Bohr effect work? As we know, oxygen is transported in blood by hemoglobin cells. How do these red blood cells know where to release more oxygen and where less? Or why do they unload more oxygen at all? Why is O2 released in tissues? The hemoglobin cells sense higher concentrations of CO2 in tissues and release oxygen in such places.
Bohr effect summary. More oxygen is released in those tissues that have higher absolute and/or relative CO2 values. Note that this is true for healthy people who have normal breathing pattern.
Suppressed Bohr effect in people with chronic diseases
Can people with chronic diseases enjoy the normal Bohr effect and normal oxygen delivery to the brain, heart and all other vital organs? Consider these medical studies.
Minute ventilation rates (chronic diseases)
| All references or
click below for abstracts
|Normal breathing||6 L/min||-||Medical textbooks|
|Healthy Subjects||6-7 L/min||>400||Results of 14 studies|
|Heart disease||15 (~+mn~4) L/min||22||Dimopoulou et al, 2001|
|Heart disease||16 (~+mn~2) L/min||11||Johnson et al, 2000|
|Heart disease||12 (~+mn~3) L/min||132||Fanfulla et al, 1998|
|Heart disease||15 (~+mn~4) L/min||55||Clark et al, 1997|
|Heart disease||13 (~+mn~4) L/min||15||Banning et al, 1995|
|Heart disease||15 (~+mn~4) L/min||88||Clark et al, 1995|
|Heart disease||14 (~+mn~2) L/min||30||Buller et al, 1990|
|Heart disease||16 (~+mn~6) L/min||20||Elborn et al, 1990|
|Pulm hypertension||12 (~+mn~2) L/min||11||D'Alonzo et al, 1987|
|Cancer||12 (~+mn~2) L/min||40||Travers et al, 2008|
|Diabetes||12-17 L/min||26||Bottini et al, 2003|
|Diabetes||15 (~+mn~2) L/min||45||Tantucci et al, 2001|
|Diabetes||12 (~+mn~2) L/min||8||Mancini et al, 1999|
|Diabetes||10-20 L/min||28||Tantucci et al, 1997|
|Diabetes||13 (~+mn~2) L/min||20||Tantucci et al, 1996|
|Asthma||13 (~+mn~2) L/min||16||Chalupa et al, 2004|
|Asthma||15 L/min||8||Johnson et al, 1995|
|Asthma||14 (~+mn~6) L/min||39||Bowler et al, 1998|
|Asthma||13 (~+mn~4) L/min||17||Kassabian et al, 1982|
|Asthma||12 L/min||101||McFadden, Lyons, 1968|
|Sleep apnea||15 (~+mn~3) L/min||20||Radwan et al, 2001|
|Liver cirrhosis||11-18 L/min||24||Epstein et al, 1998|
|Hyperthyroidism||15 (~+mn~1) L/min||42||Kahaly, 1998|
|Cystic fibrosis||15 L/min||15||Fauroux et al, 2006|
|Cystic fibrosis||10 L/min||11||Browning et al, 1990|
|Cystic fibrosis*||10 L/min||10||Ward et al, 1999|
|CF and diabetes*||10 L/min||7||Ward et al, 1999|
|Cystic fibrosis||16 L/min||7||Dodd et al, 2006|
|Cystic fibrosis||18 L/min||9||McKone et al, 2005|
|Cystic fibrosis*||13 (~+mn~2) L/min||10||Bell et al, 1996|
|Cystic fibrosis||11-14 L/min||6||Tepper et al, 1983|
|Epilepsy||13 L/min||12||Esquivel et al, 1991|
|CHV||13 (~+mn~2) L/min||134||Han et al, 1997|
|Panic disorder||12 (~+mn~5) L/min||12||Pain et al, 1991|
|Bipolar disorder||11 (~+mn~2) L/min||16||MacKinnon et al, 2007|
|Dystrophia myotonica||16 (~+mn~4) L/min||12||Clague et al, 1994|
Note that advanced stages of some conditions (e.g., asthma and CF) can lead to lung destruction,
ventilation-perfusion mismatch and arterial hypercapnia causing further reduction in body oxygen levels.
Overbreathing or hyperventilation in the sick causes hypocapnia or reduced CO2 tension in the lungs and arterial blood (since ventilation-perfusion mismatch is not a common finding in the sick). This leads to hampered oxygen release and reduced cells oxygen tension due to the suppressed Bohr effect (Aarnoudse et al, 1981; Monday & Ttreault, 1980; Gottstein et al, 1976).
Hence, for the suppressed Bohr effect, the absolute CO2 concentration is low (see the picture of the right side), and O2 molecules are stuck with red blood cells. (Scientists call this effect “increased oxygen affinity to hemoglobin”). Hence, CO2 deficiency (hypocapnia) leads to hypoxia or decreased cell-oxygen levels (the suppressed Bohr effect). The more we breathe at rest, the less the amount of available oxygen in the cells of vital organs, like the brain, heart, liver, kidneys, etc.
Many people believe that breathing more air increases oxygen content in cells. This is not true. Generally, breathing more even reduces oxygen content even in the arterial blood. Indeed, hemoglobin cells in normal blood for very small normal breathing are about 98% saturated with O2. When we hyperventilate this number is about the same (in real life it gets less since most people make a transition to automatic costal or chest breathing that reduces arterial blood O2 levels), but without CO2 and the Bohr effect, this oxygen is tightly bound with red blood cells and cannot get into the tissues in required amounts. Hence, now we know one of the causes why heavy breathing reduces the cell-oxygen level of all vital organs.
The Bohr effect is crucial for our survival. Why? During 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 cells oxygen transport.
Bohr effect (medical or scientific explanation)
Christian Bohr stated that at lower pH (more acidic environment, e.g., in tissues), hemoglobin would bind to oxygen with less affinity. Since carbon dioxide is in direct equilibrium with the concentration of protons in the blood, increasing blood carbon dioxide content, according to the Bohr effect, causes a decrease in pH, which leads to a decrease in affinity for oxygen by hemoglobin (and easier oxygen release in capillaries or tissues).
The description of the Bohr effect, which is a physiological law, can be found in nearly all physiological textbooks. Modern studies related to the Bohr effect are devoted to more advanced topics (see the titles of studies for modern research below). It is the central proposition of the Bohr effect that oxygen affinity to hemoglobin depends on absolute CO2 concentrations and reduced CO2 values decrease oxygen delivery to body cells.
Bohr effect and physical exercise
For example, without the Bohr effect, we could not walk or run for even 3-5 minutes. Why? In normal conditions, due to the Bohr effect, more O2 is released in those muscles, which generate more CO2. Hence, these muscles can continue to work with the same high rate.
However, sick people have reduced CO2 blood values. Hence, they are likely to experience symptoms of chronic fatigue, and poor results for physical fitness tests due to tissue hypoxia (low cell-oxygen levels).
Professor Henderson about Bohr effect
This is what Professor Henderson from the Yale University wrote about the Bohr effect,
"But even as early as 1885, Miescher (Swiss physiologist) inspired by the insight of genius wrote: "Over the O2 supply of the body, CO2 spreads its protecting wings" Yandell Henderson (1873-1944), in Henderson Y, Carbon dioxide, in Cyclopedia of Medicine, ed. by H.H. Young, Philadelphia, FA Davis, 1940.
Here is YouTube video that considers the Bohr effect and explains the mechanism why overbreathing decreases cell-oxygen level.
Another web page related to oxygen transport and cell oxygenation: Vasodilation (expansion of arteries and arterioles due to higher CO2 values) or why breathing less improves perfusion or blood flow to all vital organs.
Click here for references used on this page.
* Illustrations by Victor Lunn-Rockliffe
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