Regulation of gas exchange

Cellular respiration equation

Oxygen + glucose → water + carbon dioxide + energy (ATP).

Carbonic acid formation

$CO_2 + H_2O \rightarrow H_2CO_3 \rightarrow H^+ + HCO_3^-$ (The process where CO2 becomes acid in the blood).

Hydrogen ions (H+)

A byproduct of CO2 dissolving in plasma; high levels decrease pH (making blood more acidic).

Respiratory center

Located in the medulla oblongata; controls the rate and depth of breathing via inspiration and expiration regions.

Phrenic nerve

The spinal nerve that stimulates the diaphragm to contract.

Intercostal nerves

Spinal nerves that stimulate the external intercostal muscles.

Diaphragm and intercostals

The primary effector muscles responsible for changing thoracic volume to allow breathing.

Central chemoreceptors

Located in the medulla oblongata; highly sensitive to CO2 levels in the blood and H+ ions in cerebrospinal fluid.

Peripheral chemoreceptors

Located in the aortic and carotid bodies; sensitive to O2, CO2, and H+ concentrations in the blood.

Aortic and carotid bodies

Specific groups of cells in the walls of the aorta and carotid arteries that act as peripheral chemoreceptors.

Carbon dioxide concentration

The major factor regulating breathing; even a small increase stimulates receptors to increase breathing rate.

Oxygen concentration

Must fall to very low levels before it significantly stimulates breathing via peripheral chemoreceptors.

pH and H+ ions

An increase in H+ ions (lower pH) directly stimulates the carotid and aortic bodies to increase breathing depth and rate.

Negative feedback loop

Chemoreceptors detect high CO2 -> Respiratory center stimulated -> Effectors increase breathing -> CO2 levels drop

Cerebral cortex control

Allows for voluntary breathing control by bypassing the medulla and sending impulses directly to spinal cord tracts.

Involuntary override

When holding breath, the buildup of CO2 eventually forces the inspiratory center to trigger a breath.

Hyperventilation

Rapid, deep breathing that removes too much CO2, leading to a lack of chemoreceptor stimulation until CO2 levels normalize.

Exercise response

Muscle contraction increases CO2 production, requiring a 10-20 fold increase in gas exchange volume.