ABSTRACT
Breathing is normally an unconscious activity due to automatic command by groups of neurons in the brainstem that control the cyclic contraction and relaxation of the respiratory muscles. A neurobiological model provides a framework for understanding the perception of dyspnea in parallel with the control of breathing. Airway inflammation, a prominent feature of both asthma and chronic obstructive pulmonary disease, may contribute to dyspnea as evidenced by results of laboratory and clinical studies. Afferent impulses from sensory receptors are transmitted to brainstem respiratory centers that automatically adjust breathing to provide direct appraisal of blood gas, acid–base, and mechanical status of the respiratory system. Integration and processing of respiratory inputs from sensory receptors occurs in the central nervous system that subsequently produces efferent output via the phrenic and thoracic spinal nerves to the diaphragm and intercostal muscles, respectively. Endogenous opioids are the only neuropeptides that have been shown to modulate the perception of dyspnea.
