Upper airway dilator muscle generate inspiratory pressure that balances subatmospheric pharyngeal pressure gene-rated by diaphragmatic contraction leading to reduce upper airway patency. Neural control of upper airway dilator muscles involve several categories of receptors such as vagal pulmonary receptors, upper airway mecanoreceptors, baroreceptors, chemoreceptors. Upper airway resistances increase during sleep and upper airway inspiratory muscle activity decrease especially during bursts of rapid eye movements in REM sleep. Sleep-related upper airway obstruction occurs when upper airway dilator pressure does not balance subatmospheric pharyngeal pressure. Several variables are involved in the pathophysiology of obstructive apneas such as upper airway anatomical factors, structural muscular dysfunction, changes in neural drive.