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This brief review addresses the characteristics, lability and the mechanisms underlying the hypocapnic-induced apnoeic threshold which is unmasked during NREM sleep. The role of carotid chemoreceptors as fast, sensitive detectors of dynamic changes in CO2 is emphasized and placed in historical context of the long-held debate over central vs. peripheral contributions to CO2 sensing and to apnoea. Finally, evidence is presented which points to a significant role for unstable, central respiratory motor output as a significant contributor to upper airway narrowing and obstruction during sleep.