Our study has some limitations. First, the collapsibility of the pharyngeal airway39and the arousal threshold from sleep depend on sleep stage, and older persons tend to experience less slow-wave sleep40 than younger persons. To address this, we standardized the sleep stage by performing airway occlusion only during stage II sleep, which reduced the potential influences of variable sleep depth. However, we cannot rule out the possibility that a decreased arousal threshold during other stages of sleep, or a simple lack of deep sleep in older individuals, contributes to the increased propensity to OSA in this age group. In terms of upper airway collapsibility, our approach of performing measurements only during stage II sleep should have biased the study toward the null hypothesis, but a robust effect of aging was still observed. Second, mask occlusion and naturally occurring upper airway occlusion are not exactly the same, and it might be possible that nasal mechanoreceptors are more stimulated during mask occlusion compared with more physiologic stimuli. Since we applied the same model of airway occlusion throughout the age range, and also measured another variable of upper airway collapsibility (pharyngeal resistance increases during sleep), our study allows us to conclude that increased age is associated with an increase in airway collapsibility during sleep. Third, we may have influenced the outcome of this study by including only healthy older subjects without OSA. The healthy participant effect is a common problem in aging research, since, by excluding OSA and other comorbidities, we may have studied a population of “unusually” healthy older individuals. On the other hand, the study of patients with disease would have not been informative since the increase in pharyngeal collapsibility in patients with OSA is well-known. In addition, airway occlusion during repetitive apnea would not provide meaningful data. Thus, we acknowledge this limitation but point out that studying extremely healthy older subjects would tend to bias toward the null hypothesis and therefore strengthens our findings. This study is cross-sectional in nature. Although our findings are correlative rather than causative, we believe that a more thorough understanding of the pathogenesis of OSA can evolve from these observations. Ultimately, longitudinal studies would be useful to define the natural history of aging on pharyngeal structure and function, although such studies are difficult to complete and likely would be confounded by patients’ weight gain. Despite these limitations, we believe that our new findings importantly add to the existing literature.