COVID-19 can leave behind fatigue, breathing difficulties and neurological symptoms that persist long after the initial infection. Because these effects can also disturb sleep, researchers have questioned whether COVID-19 might alter the physiological mechanisms underlying obstructive sleep apnea.

A new study led by researchers at Koç University suggests that a history of COVID-19 is not associated with meaningful changes in most of the key physiological traits that contribute to obstructive sleep apnea. However, the researchers identified one notable difference: people who had experienced COVID-19 showed a stronger breathing response after brief arousals from sleep.

The study, published open access in the Journal of Clinical Medicine, was conducted by Yeliz Çelik and Professor Yüksel Peker of Koç University in collaboration with Scott A. Sands, Raichel Alex and Susan Redline.

Obstructive sleep apnea occurs when the upper airway repeatedly narrows or collapses during sleep, interrupting breathing and reducing sleep quality. Although it is often discussed as a single condition, its severity can be influenced by several distinct physiological mechanisms.

These include how easily the upper airway collapses, how strongly the respiratory control system reacts to changes in oxygen and carbon dioxide, how readily a person wakes in response to breathing disruption, and how effectively the upper-airway muscles compensate to keep the airway open.

To investigate whether COVID-19 affects these mechanisms, the researchers conducted a matched case-control study involving 120 participants. Sixty people with a history of COVID-19 were compared with 60 controls who had undergone overnight, laboratory-based polysomnography before the pandemic.

Participants were matched according to age, sex, body mass index and the presence of obstructive sleep apnea. The researchers then estimated several physiological traits from the participants' sleep recordings, adjusting their analyses for age, sex, body mass index and apnea-hypopnea index, a conventional measure of sleep apnea severity.

The participants were predominantly male, with an average age of 55 and an average body mass index of 29.4 kg/m².

The analysis found no meaningful differences between the groups in upper-airway collapsibility, ventilatory control stability, arousal threshold or upper-airway muscle compensation. These findings suggest that a previous COVID-19 infection does not substantially alter the principal physiological mechanisms commonly associated with obstructive sleep apnea.

One difference did emerge. Participants with a history of COVID-19 exhibited a greater ventilatory response following arousal from sleep. In other words, their breathing increased more strongly after brief awakenings.

This heightened response could potentially affect how sleep apnea presents or how individuals respond to certain treatments. However, the clinical significance of the finding remains uncertain and will need to be examined in prospective studies.

The results provide a more nuanced picture of the possible relationship between COVID-19 and obstructive sleep apnea. Previous research has suggested that obstructive sleep apnea may increase the risk of poor outcomes during acute COVID-19. Researchers have also considered the reverse possibility: that COVID-19 might initiate or worsen sleep apnea through lasting effects on the respiratory system, nervous system or sleep regulation.

The present findings do not support broad changes in the major physiological traits underlying obstructive sleep apnea among people with a history of COVID-19. They do not, however, rule out the possibility that infection may affect sleep apnea in particular subgroups or through mechanisms not measured in this study.

The case-control design also means that the study cannot establish whether COVID-19 caused the stronger breathing response observed after arousal. Because the control participants' sleep studies were conducted before the pandemic, the findings should be confirmed through longitudinal research that evaluates the same individuals before and after infection.

Further studies could also examine whether the severity of the initial infection, long-COVID symptoms, vaccination status or the time elapsed since infection influences sleep-related breathing mechanisms.

Overall, the findings suggest that the core physiology of obstructive sleep apnea remains largely similar in individuals with and without a history of COVID-19. The increased breathing response to arousal nevertheless points to a potentially important difference that may help guide future research into personalized sleep apnea treatment and post-COVID sleep health.

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