What is the Bohr effect?

The Bohr effect is a way to explain the cell’s oxygen release. Red blood cells don’t load oxygen into tissues. Carbon dioxide (CO2) plays a key role in O2 transport due vasodilation. Christian Bohr, a Danish physiologist and father of Niels Bohr, first described the Bohr law in 1904.

Bohr effect in healthy people

Bohr’s effect is normal in healthy people, since healthy people have normal breathing patterns at rest and normal arterial CO2 levels. How does the Bohr law operate? We know that hemoglobin, which is found in red blood cells and called “erythrocytes”, transports oxygen in the blood. How does hemoglobin in red blood cells (called “erythrocytes”) know which areas to release more oxygen and which ones to keep it down? Or, why do they release more oxygen? Why is O2 being released into tissues? Red blood cells detect higher levels of CO2 in tissues, and release oxygen at these locations.

Bohr effect summary. Tissues with higher relative and absolute CO2 values release more oxygen. This is true even for people with normal breathing patterns.

Chronic diseases: The suppressed Bohr effect

Are people with chronic illnesses able to enjoy the normal Bohr effect? Can they still receive oxygen to their brains, hearts, and other vital organs? These medical studies are worth looking at.

Note that advanced stages of some conditions (e.g., asthma and CF) can lead to lung destruction, ventilation-perfusion mismatch and arterial hypercapnia, causing a 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 causes a reduction in oxygen release and cell oxygen tension (Aarnoudse, Monday & Treault, 1980; Gottstein, 1976).

The suppressed Bohr Effect is therefore caused by a low absolute CO2 concentration (see the image to the right), and O2 molecules remain attached to red blood cells. This effect is called “increased oxygen affinity for hemoglobin” by scientists. Hypoxia (CO2 deficiency) can lead to hypoxia (the suppressed Bohr Effect). The oxygen available in vital organs like the brain, heart and kidneys decreases the more we breathe at rest.

Many believe that more oxygen in the air will increase cell’s oxygen content. This is false. In fact, even though breathing is more efficient than usual, it can actually reduce the oxygen content of the arterial blood. Red blood cells are 98% saturated with oxygen in hemoglobin, which is healthy for normal breathing. This number drops to 98% when we hyperventilate (it actually gets lower in real life as most people transition to automatic chest or costal breathing, which reduces arterial blood oxygen levels). However, without CO2 or the Bohr effect, the oxygen is tightly bound to red blood cells and is unable get into the tissues in the required quantities. We now know the reason heavy breathing causes a drop in the cell-oxygen levels of all vital organs.

Our survival depends on the Bohr effect. Why? Some organs and tissues produce more CO2 than others. Red blood cells sense these additional CO2 concentrations and release more O2 to the areas that require it most. This smart self-regulating mechanism allows cells to efficiently transport oxygen.

Bohr effect (medical and scientific explanation).

Christian Bohr said that hemoglobin would be less able to bind oxygen at lower pH levels (e.g. in tissues). According to the Bohr Effect, carbon dioxide is directly in equilibrium with blood protons. This causes hemoglobin to be less able to bind to oxygen in lower pH environments (e.g., tissues or capillaries).

Nearly all textbooks on physiological science contain a description of the Bohr Effect, which is a physiological law. Modern research on the Bohr Effect focuses on more complex topics. See the titles of modern studies below. The Bohr effect’s central idea is that oxygen affinity to hemoglobin is dependent on oxygen concentrations. Lower CO2 values reduce oxygen delivery to the body cells.

Bohr effect, physical exercise

Without the Bohr effect , it would be impossible to walk or run even for 3-5 minutes. Why? Bohr effect: In normal conditions, the Bohr effect causes more oxygen to be released into muscles which produce more CO2. These muscles can still work at a high rate.

Sick people, however, have lower CO2 blood levels. They are more likely to feel chronic fatigue and have poor results in physical fitness tests. This is due to tissue hypoxia, or low cell-oxygen levels.

Professor Henderson on the Bohr effect

This is Professor Henderson, Yale University’s article on the Bohr effect.

“But even in 1885, Miescher (Swiss physician) was inspired by the insight of genius and wrote: “Over O2 supply of body, CO2 spreads it protecting wings.”Yandell Henderson (1873-1944), Henderson Y, carbon dioxide, in Cyclopedia of Medicine ed. H.H. Young, Philadelphia, FA Davis, 1940.

This YouTube video explains why excessive breathing can cause a decrease in cell-oxygen levels.

However, it is known that many of the Bohr Effect studies were conducted in vitro. It is not yet clear whether hyperventilation or arterial hypocapnia (low carbon dioxide) actually cause decreased oxygen transport. I will explain this in the bonus content below.

Vasodilation is more likely to be the main factor in oxygen transport in living organisms than the Bohr Effect. Bohr’s effect has a problem. People hyperventilate which reduces CO2 but also slows down blood circulation (circulation). Overbreathing causes tissues to accumulate more CO2, while the blood flow is slower. The Bohr effect’s true value isn’t as great as people think, but vasodilation reduces O2 and blood supply for all cells.

References

Aarnoudse JG, Oeseburg B, Kwant G, Zwart A, Zijlstra WG, Huisjes HJ, Influence of variations in pH and PCO2 on scalp tissue oxygen tension and carotid arterial oxygen tension in the fetal lamb, Biol Neonate 1981; 40(5-6): p. 252-263.

Braumann KM, Böning D, Trost F, Bohr effect and slope of the oxygen dissociation curve after physical training, J Appl Physiol. 1982 Jun; 52(6): p. 1524-1529.

Böning D, Schwiegart U, Tibes U, Hemmer B, Influences of exercise and endurance training on the oxygen dissociation curve of blood under in vivo and in vitro conditions, Eur J Appl Physiol Occup Physiol. 1975; 34(1): p. 1-10.

Bucci E, Fronticelli C, Anion Bohr effect of human hemoglobin, Biochemistry. 1985 Jan 15; 24(2): p. 371-376.

Carter AM, Grønlund J, Contribution of the Bohr effect to the fall in fetal PO2 caused by maternal alkalosis, J Perinat Med. 1985; 13(4): p.185-191.

diBella G, Scandariato G, Suriano O, Rizzo A, Oxygen affinity and Bohr effect responses to 2,3-diphosphoglycerate in equine and human blood, Res Vet Sci. 1996 May; 60(3): p. 272-275.

Dzhagarov BM, Kruk NN, The alkaline Bohr effect: regulation of O2 binding with triliganded hemoglobin Hb(O2)3 [Article in Russian] Biofizika. 1996 May-Jun; 41(3): p. 606-612.

Gersonde K, Sick H, Overkamp M, Smith KM, Parish DW, Bohr effect in monomeric insect hemoglobins controlled by O2 off-rate and modulated by haem-rotational disorder, Eur J Biochem. 1986 Jun 2; 157(2): p. 393-404.

Grant BJ, Influence of Bohr-Haldane effect on steady-state gas exchange, J Appl Physiol. 1982 May; 52(5): p. 1330-1337.

Gottstein U, Zahn U, Held K, Gabriel FH, Textor T, Berghoff W, Effect of hyperventilation on cerebral blood flow and metabolism in man; continuous monitoring of arterio-cerebral venous glucose differences (author’s transl) [Article in German], Klin Wochenschr. 1976 Apr 15; 54(8): p. 373-381.

Grubb B, Jones JH, Schmidt-Nielsen K, Avian cerebral blood flow: influence of the Bohr effect on oxygen supply, Am J Physiol. 1979 May; 236(5): p. H744-749.

Hlastala MP, Woodson RD, Bohr effect data for blood gas calculations, J Appl Physiol. 1983 Sep; 55(3): p. 1002-1007.

Jensen FB, Red blood cell pH, the Bohr effect, and other oxygenation-linked phenomena in blood O2 and CO2 transport, Acta Physiol Scand. 2004 Nov; 182(3): p. 215-227.

Kister J, Marden MC, Bohn B, Poyart C, Functional properties of hemoglobin in human red cells: II. Determination of the Bohr effect, Respir Physiol. 1988 Sep; 73(3): p. 363-378.

Kobayashi H, Pelster B, Piiper J, Scheid P, Significance of the Bohr effect for body oxygen level in a model with counter-current blood flow, Respir Physiol. 1989 Jun; 76(3): p. 277-288.

Lapennas GN, The magnitude of the Bohr coefficient: optimal for oxygen delivery, Respir Physiol. 1983 Nov; 54(2): p.161-172.

Matthew JB, Hanania GI, Gurd FR, Electrostatic effects in hemoglobin: Bohr effect and ionic strength dependence of individual groups, Biochemistry. 1979 May 15; 18(10): p.1928-1936.

Meyer M, Holle JP, Scheid P, Bohr effect induced by CO2 and fixed acid at various levels of O2 saturation in duck blood, Pflugers Arch. 1978 Sep 29; 376(3): p. 237-240.

Monday LA, Tétreault L, Hyperventilation and vertigo, Laryngoscope 1980 Jun; 90(6 Pt 1): p.1003-1010.

Tyuma I, The Bohr effect and the Haldane effect in human hemoglobin, Jpn J Physiol. 1984; 34(2): p.205-216.

Winslow RM, Monge C, Winslow NJ, Gibson CG, Whittembury J, Normal whole blood Bohr effect in Peruvian natives of high altitude, Respir Physiol. 1985 Aug; 61(2): p. 197-208.