The magnitude of the Bohr effect profoundly influences the shape and position of the blood oxygen equilibrium curve.

For the past century, the importance of the Bohr effect for blood oxygen delivery has been deemed secondary to the influence of the uptake of carbon dioxide when the blood is deoxygenated (the Haldane effect). This is, however, not the case. The simultaneous oxygen and proton binding to hemoglobin can be modelled by a two-ligand, two-state formulation, while the resulting changes in acid-base status of the surrounding solution can be assessed according to Stewart's model for strong ion difference. This approach shows that an abolishment of the Bohr effect (by either equalizing pKa values of the Bohr groups of T and R states, or by removing the Bohr groups in the calculations) dramatically increases oxygen affinity, and that the Bohr effect plays a crucial role in determining the overall position and shape of the oxygen equilibrium curve. Thus, the magnitude of the Bohr effect (the Bohr factor) and oxygen affinity are directly related, and any change in hemoglobin structure that affects the Bohr factor will inevitably influence hemoglobin oxygen affinity. The modelling approach also emphasizes that pH, PCO and PO in capillaries are dependent variables, determined by arterial blood gases, the Bohr effect, the respiratory quotient (RQ) of tissue metabolism and the buffer capacity of blood. Thus, the full extent of the Bohr effect cannot be appreciated by comparing oxygen equilibrium curves made at constant PCO or pH, but only by comparing curves at constant proton saturation of the Bohr groups. This is because, it is the protons bound to the Bohr groups that directly influence hemoglobin‑oxygen binding.