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Obstructive sleep apnoea (OSA) is increasingly recognised as a highly heterogeneous disorder.1 Drivers of the disease process are various and include anatomical traits such as upper airway narrowing related to the interaction of craniofacial structure and obesity, as well as physiological traits such as low arousal threshold (a low level of respiratory stimulus required to trigger arousal), high loop gain (oversensitive respiratory control system) and reduced upper airway muscle responsiveness (diminished ability to prevent airway collapse).2