Arousal intensity during the night may contribute to obstructive sleep apnoea - but it's not what you may be thinking!

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1. Summary

Obstructive sleep apnoea (OSA) is a highly prevalent disorder that occurs when the upper airway (throat region) repeatedly narrows or closes during sleep, thus limiting breathing. These obstructed breathing events result in decreases in blood oxygen levels and cortical arousals (or “brief awakenings”). Cortical arousals from sleep are assumed to be vitally important in restoring airflow by stimulating the upper airway muscles that act to keep the airway open. However, our findings reveal that different levels or intensity of arousal may in fact further contribute to OSA.

 

The study found that higher arousal intensity causes a greater response in upper airway dilator muscle activity and minute ventilation. At first thought, more air in may be considered a good thing. However, unnecessarily large increases in ventilation can destabilise breathing control and promote subsequent airway obstruction. Specifically, hyperventilation can lead to excessive reductions in CO2 (the primary driver of breathing during sleep). This is followed by hypoventilation, which can reduce upper airway dilator muscle activity and perpetuate unstable breathing and OSA.

 

Importantly, the study also demonstrated that arousal intensity was not related to any of the primary stimuli for respiratory associated arousals (e.g. level of inspiratory effort). This indicates that arousal intensity is an individual trait, and those with higher arousal intensity may be at greater susceptibility to airway obstruction during sleep.

 

Further to advancing understanding into the mechanisms of cortical arousal, their physiological consequences and contribution to OSA, the current findings raise the potential for development of new therapies that target arousal intensity in patients in whom arousals play a major role in their OSA. Future studies will also look to determine if the efficacy of current OSA treatments are hindered, or perhaps even helped, in those with a higher arousal intensity trait.

2. Share a PubMed or DOI link to article

https://www.ncbi.nlm.nih.gov/pubmed/27784404

3. Do you have any ideas to expand upon this research? Are you looking for collaborators?

In addition to its contribution to OSA pathogenesis and potential influence on OSA treatment, arousal intensity may also help explain daytime consequences of OSA and their variability between patients. For instance, does someone with high arousal intensity have greater daytime sleepiness or cognitive impairments, such as reduced concentration, memory and learning? These are important questions that future research into arousal intensity may help answer.

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