[4] Once activated, they send action potentials through large myelinated fibers[5] of the vagus nerve to the inspiratory area in the medulla and apneustic center of the pons.
Josef Breuer and Ewald Hering reported in 1868 that a maintained distention of the lungs of anesthetized animals decreased the frequency of the inspiratory effort or caused a transient apnea.
The neural circuit that controls the Hering–Breuer inflation reflex involves several regions of the central nervous system, and both sensory and motor components of the vagus nerve.
Thus, an increase in pulmonary stretch receptor activity leads to inhibition of the CVMs and an elevation of heart rate (tachycardia).
Early physiologists believed the reflex plays a major role in establishing the rate and depth of breathing in humans.