A highly collapsible or narrow airway is an important cause of obstructive sleep apnoea (OSA). It can be quantified during sleep using the gold standard pharyngeal critical closing pressure (Pcrit) technique. However, Pcrit is too complex and time-consuming to be performed clinically. A simple alternative to Pcrit could guide targeted therapy for OSA. Chapter two introduces a new method to quantify upper airway collapsibility in OSA. This involves a simple intervention applied during a routine continuous positive airway pressure (CPAP) titration study. The intervention involves simply turning off the CPAP device to atmospheric pressure for 5 breaths/efforts from the therapeutic level ~5-10 times throughout the night and measuring the flow response. 35 participants completed this simple intervention and a follow-up physiology study to quantify Pcrit. The clinical intervention modestly correlated with Pcrit (r=-0.7). However, the same intervention during the physiology night strongly correlated with Pcrit (r=-0.9). Chapter three explores an alternate methodology, the Upper Airway Collapsibility Index (UACI). This test involves delivering brief pulses of negative pressure to the upper airway via a nasal mask in early inspiration during wakefulness and quantifying the pressure difference across the collapsible portion of the upper airway. I found that this 10-15min test relates closely to Pcrit in 34 people with OSA (r=0.8). This is useful, as the methodology described in chapter one requires CPAP, which many people are unable to tolerate. Chapter four was a proof-of-concept study in 25 people with OSA in whom the UACI test was performed with and without a mandibular advancement splint. A small but significant improvement in the UACI of 7% was detected with the mandibular advancement splint. Chapter five uses the UACI to study how collapsibility varies across the breathing cycle. Genioglossus muscle activity and reflex responses were also quantified in 12 people with OSA. I found that: 1) the upper airway was most collapsible during expiration, 2) this was associated with lower genioglossus muscle activity and 3) the reflex response to negative pressure was attenuated during expiration. Collectively, these studies provide new insight into OSA pathogenesis and simplified tools to estimate upper airway collapsibility.