The Bohr effect characterizes the binding ability of oxygen to hemoglobin as a function of PH and carbon dioxide partial pressure. It is largely responsible for gas exchange in organs and tissues. Respiratory diseases and improper breathing affect blood PH via the Bohr effect and disrupt normal gas exchange.
What is the Bohr effect?
The Bohr effect ensures oxygen supply to the body by transporting oxygen with the help of hemoglobin. The Bohr effect is named after its discoverer Christian Bohr, the father of the famous physicist Niels Bohr. Christian Bohr (1855-1911) recognized the dependence of the oxygen affinity (ability to bind oxygen) of hemoglobin on the PH value or the carbon dioxide or oxygen partial pressure. The higher the PH the stronger the oxygen affinity of hemoglobin and vice versa. Together with the effect of cooperative binding of oxygen and the influence of the Rapoport-Luebering cycle, the Bohr effect enables hemoglobin to be an ideal oxygen transporter in the organism. These influences change the steric properties of hemoglobin. Depending on the environmental conditions, the ratio between the poorly oxygen binding T-hemoglobin and the well oxygen binding R-hemoglobin adjusts. Thus, oxygen is normally taken up in the lungs, whereas oxygen is usually released in the other tissues.
Function and role
The Bohr effect ensures oxygen supply to the body by transporting oxygen with the help of hemoglobin. In this process, oxygen is bound as a ligand to the central iron atom of hemoglobin. The iron-containing protein complex has four heme units each. Each heme unit can bind one oxygen molecule. Thus, each protein complex can contain up to four oxygen molecules. By changing the steric properties of heme due to the influence of protons (hydrogen ions) or other ligands, the equilibrium between the T-form and the R-form of hemoglobin shifts. In oxygen consuming tissues, oxygen binding to hemoglobin weakens by lowering the PH. It is better released. Therefore, in metabolically active tissues there is increased oxygen release by increasing the hydrogen ion concentration. The carbon dioxide partial pressure of the blood increases at the same time. The lower the PH value and the higher the carbon dioxide partial pressure, the more oxygen is released. This continues until there is complete deoxygenation of the hemoglobin complex. In the lungs, the carbon dioxide partial pressure decreases due to expiration. This leads to the increase of the PH value and thus to the increase of the oxygen affinity of the hemoglobin. Therefore, in the lungs, oxygen uptake by hemoglobin occurs simultaneously with carbon dioxide release. Furthermore, the cooperative binding of oxygen depends on the ligands. The central iron atom binds protons, carbon dioxide, chloride ions and oxygen molecules as ligands. The more oxygen ligands present, the stronger the oxygen affinity at the remaining binding sites. However, all other ligands weaken the affinity of hemoglobin for oxygen. This means that the more protons, carbon dioxide molecules or chloride ions are bound to hemoglobin, the more easily the remaining oxygen is released. However, a high oxygen partial pressure favors oxygen binding. In addition, a different pathway of glycolysis takes place in erythrocytes than in other cells. This is the Rapoport-Luebering cycle. During the Rapoport-Luebering cycle, the intermediate 2,3-bisphosphoglycerate (2,3-BPG) is formed. The compound 2,3-BPG is an allosteric effector in the regulation of oxygen affinity to hemoglobin. It stabilizes T-hemoglobin. This promotes rapid oxygen release during glycolysis. Thus, oxygen binding to hemoglobin is weakened by decreasing PH, increasing the concentration of 2,3-BPG, increasing carbon dioxide partial pressure, and increasing temperature. As a result, oxygen delivery increases. Conversely, the increase of PH, the decrease of 2,3-BPG concentration, the decrease of carbon dioxide partial pressure and the decrease of blood temperature promotes.
Diseases and ailments
Accelerated breathing in the context of respiratory diseases such as asthma or hyperventilation due to panic, stress, or habit leads to an increase in PH via increased carbon dioxide exhalation due to the Bohr effect. This results in the enhancement of the oxygen affinity of hemoglobin. Oxygen delivery in the cells becomes more difficult. Therefore, ineffective breathing patterns lead to an undersupply of oxygen to the cells (cell hypoxia). The result is chronic inflammation, weakening of the immune system, chronic respiratory diseases and many other chronic diseases. According to general medical knowledge, cell hypoxia often triggers diseases such as diabetes, cancer, heart disease or chronic fatigue. According to Russian physician and scientist Buteyko, hyperventilation is not only a consequence of respiratory diseases, but is also often caused by stress and panic reactions. In the long term, according to him, over-breathing becomes a habit and is the starting point of various diseases. Therapy involves consistent nasal breathing, diaphragmatic breathing, prolonged breathing pauses, and relaxation exercises to return breathing to normal in the long term. Several studies have shown that the Buteyko method can reduce the use of anticonvulsant medications by 90 percent and cortisone by 49 percent. When there is insufficient exhalation of carbon dioxide as part of hypoventilation, the body becomes overly acidic (acidosis). Acidosis occurs when the blood PH is below 7.35. The acidosis that occurs during hypoventilation is also called respiratory acidosis. Causes may include paralysis of the respiratory center, anesthesia, or rib fractures. Typical of respiratory acidosis are shortness of breath, blue coloration of the lips and increased fluid excretion. Acidosis can cause cardiovascular disturbances with low blood pressure, cardiac arrhythmias, and coma.
