OverviewResponse to hypercapniaCentral chemoreceptors ◦ Peripheral chemoreceptors

This may be what you are looking for if Neural control of breathing wasn't.


Minute ventilation (V̇E; in litres/minute) is controlled by the respiratory centre in the medulla oblongata, which receives sensory input from chemoreceptors in the carotid bodies as well as those in the brain. These reflexes act quickly to keep the arterial partial pressure of CO2 (PaCO2) within the normal range, despite the demands we put on the body.

Response to hypercapnia

Hypercapnic drive dominates the control of minute ventilation. It seems odd that CO2 is more important than O2, but CO2 governs blood pH and blood pH influences the behaviour of every chemical process in the body (see Hyperventilation). When you hold your breath for long enough, the strong impulse to breathe isn’t your body screaming for oxygen, it’s the chemoreceptors in your brain wanting to get rid of CO2 (and, therefore, acid) before the pH of your cerebrospinal fluid gets any lower. There is a reflex that responds to hypoxia (see below), but it is sluggish and doesn’t kick in until your arterial partial pressure of oxygen (PaO2) gets lower than 8 kPa (usually 10-13 kPa). On a typical day at sea level it’s more likely that changes in PaCO2 will drive your breathing more than PaO2.

Central chemoreceptors

The chemoreceptors in your brain are located on the ventral surface of the medulla. They are not structures that are identifiable to the plain eye or under a microscope, but merely regions of the brain that respond to changes in the pH of the cerebrospinal fluid (CSF). Central chemoreceptors are not sensitive to changes in O2, or CO2 for that matter. However, they indirectly detect changes in CO2 via the effect PaCO2 has on the pH of CSF. These chemoreceptors respond to any change in pH, whether it is an increase or decrease.

central chemoreceptors

Figure 1: Central chemoreceptors detect CO2 levels indirectly by its effect on cebrebrospinal fluid (CSF) pH. Hydrogen ions (H+) cannot cross the blood-brain barrier (BBB; the endothelial cells of the brain capillaries) because they are charged. CO2 on the other hand crosses easily. Once dissolved in the CSF, CO2 has a profound effect on CSF pH since CSF is only buffered by HCO3- and a small increase in H+ increases pH more that it would in the better-buffered blood in the capillaries.

Remember: central chemoreceptors don't detect blood pH, they indirectly detect blood PaCO2. When the body is in metabolic acidosis (such as lactate acid accumulation during exercise) these chemoreceptors can't "see" the effect on blood pH.

Peripheral chemoreceptors

The chemoreceptors in the periphery that contribute to the control of breathing are located in the carotid bodies, pea-sized lumps at the bifurcation of the common carotid artery. Specialised sensory cells in the carotid bodies respond to:

Low PaO2
High PaCO2
Low pH

When the body is hypercapnic, carotid chemoreceptors contribute about 25% of the drive to breathe, while central chemoreptors contribute about 75% (such things are determined in nerve lesion experiments in animals). On the other hand, when PaO2 is persistently low (as in a chronic condition like COPD) only the peripheral chemoreceptors can sense this. Similarly, it is only the peripheral chemoreceptors that can detect acidaemia, since the central chemoreceptors don't sense blood pH.

reflex control of breathing

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