In healthy humans at sea level, alveolar ventilation is precisely regulated to match metabolic rate and maintain pH and arterial partial pressure of dioxygen (O₂) and carbon dioxide (CO₂) at, or close to, resting levels over a wide range of workloads. However, the mechanism that links ventilation to O₂ demand and metabolic CO₂ production remains highly controversial.

The control system that allows regulation of ventilation during exercise with such precision and efficiency consists of three highly integrative levels of control: 1) the central respiratory rhythm and pattern generator (central respiratory controller), 2) distribution and synchronization of respiratory motor output to the appropriate respiratory muscles, and 3) sensory inputs of both peripheral and central origin.

Although controversy remains regarding the primary mechanism regulating exercise hyperpnea, feedback from the active muscles and central command (feedforward) are powerful stimuli capable of substantially modulating the activity of the central respiratory controller and likely contribute to a significant extent to hyperpnea. We propose that these mechanisms dynamically interact to produce adequate ventilation regarding metabolic and gas exchange rates during exercise, with the carotid chemoreceptor adapting the ventilatory response to small changes in arterial CO₂ and acidosis.