Sleep Apnea and Long COVID: What a Review of 11 Studies Actually Shows

Obstructive sleep apnea and long COVID appear to be intertwined in ways that are real but far messier than headlines suggest, according to a scoping review published in Frontiers in Sleep. A team of respiratory therapy and rehabilitation researchers in Riyadh, Saudi Arabia, systematically combed seven databases for studies published between 2020 and 2026 that examined any relationship between obstructive sleep apnea (OSA) and persistent post-COVID symptoms in adults. Of 184 records identified, only 11 studies survived screening, and those 11 told strikingly different stories depending on which direction of the relationship they measured.

The review, conducted under PRISMA-ScR guidelines and registered on the Open Science Framework, deliberately separated studies into distinct categories rather than pooling them. Some studies asked whether pre-existing OSA raises the risk of developing post-acute sequelae of SARS-CoV-2 infection (PASC). Others looked in the opposite direction, asking whether COVID-19 triggers new-onset sleep apnea. Still others measured how often OSA shows up in patients already attending long COVID clinics, or whether the breathing disorder changes acute COVID-19 severity. Because designs, OSA ascertainment methods, and long COVID definitions varied so widely, the authors declined to merge the findings into a single effect estimate.

An electronic health record analysis spanning three large US networks found that patients with documented OSA before infection had significantly higher adjusted hazard ratios for PASC than those without, an association that persisted after accounting for obesity, acute infection severity, and comorbidities. A separate cross-sectional survey of 24,803 US adults reported that pre-existing OSA was independently associated with roughly a two-fold increased odds of developing PASC, defined as at least three symptoms persisting more than three months, and that treated OSA appeared to attenuate this association in multivariable models. Both studies, however, relied on self-reported or coded diagnoses rather than objective sleep testing.

Objective sleep laboratory data added nuance. Yet the neurocognitive difference lost statistical significance after adjustment for confounders, a detail the review’s authors flagged as central to interpreting the finding. A German study of 20 post-COVID syndrome patients in pulmonary rehabilitation found polysomnography-confirmed sleep apnea in 60 percent, versus 10 percent of healthy controls, though higher body mass index in the patient group remained a potential confounder.

Studies probing the reverse direction produced their own surprises. A Spanish prospective study of 73 patients at a dedicated long COVID clinic in Barcelona found polysomnography-confirmed OSA in 83.6 percent, with 56.1 percent having moderate-to-severe disease, even among patients without daytime sleepiness. But OSA severity was not significantly associated with most long COVID symptoms; insomnia was the only symptom that correlated with apnea-hypopnea index. A Turkish matched case-control study of 304 sleep laboratory patients found that people with a COVID-19 history actually had lower overall OSA prevalence than matched controls, yet a REM-predominant OSA phenotype was significantly more common among them and was independently associated with fatigue. A large retrospective cohort of more than 900,000 US adults found elevated risk of new-onset OSA after COVID-19, with hazard ratios of 1.41 for hospitalized and 1.33 for non-hospitalized patients, persisting up to 4.5 years after infection.

Not every physiological hypothesis survived testing. A Turkish case-control polysomnographic trait analysis found no meaningful differences in upper airway collapsibility, loop gain, arousal threshold, or muscle compensation between adults with and without prior COVID-19 after adjustment. The only significant difference was a higher ventilatory response to arousal in the post-COVID group, suggesting that any COVID-19-related change in OSA pathophysiology may follow a narrower physiological signature than earlier mechanistic theories implied. The review’s authors stressed that intermittent hypoxia, systemic inflammation, autonomic dysregulation, sleep fragmentation, and circadian disturbance should all continue to be treated as hypothesized explanations rather than established causal pathways, because objective mechanistic measurements were scarce across the included studies.

Treatment evidence was the thinnest part of the picture. Only three included studies offered information relevant to OSA treatment, and one of those evaluated positive airway pressure therapy against acute COVID-19 severity rather than long COVID outcomes. That Swedish nationwide register cohort of nearly two million infected adults found that moderate-to-severe OSA increased the risk of severe and critical acute COVID-19, and that longer PAP treatment duration was associated with lower risk of critical disease, though OSA remained associated with severe outcomes even in PAP-adherent patients. For long COVID specifically, the review concluded the available evidence is insufficient to determine whether effective OSA treatment modifies the disease course at all.

The heterogeneity extended to the most basic definitional level. Some studies applied World Health Organization or National Academies criteria for long COVID, some used both frameworks, others used study-specific symptom thresholds, and several, including the new-onset OSA cohort and the trait analysis, did not define long COVID at all because they measured different outcomes entirely. Required symptom durations ranged from one month to three months or went unreported. Acute hospitalization status and severity were inconsistently documented, with ICU admission, mechanical ventilation, and oxygen requirement data missing from most studies. These gaps, the authors argued, make direct comparison between long COVID patients with and without OSA hazardous.

The review also catalogued its own limitations. Eleven studies is a small base, nearly all observational, which means causality in either direction cannot be established. Residual confounding looms large because OSA travels with obesity, cardiovascular disease, hypertension, and metabolic dysfunction, all of which independently worsen COVID-19 outcomes. Overlapping symptoms, including fatigue, impaired concentration, and sleep disturbance, further complicate clinical assessment in both conditions. The authors called for prospective longitudinal studies using standardized OSA and long COVID definitions, objective polysomnography, and clinically meaningful outcomes, along with properly designed trials of interventions such as CPAP therapy.

What the review does support is a practical, carefully hedged message: adults with persistent post-COVID symptoms may warrant evaluation for underlying sleep-disordered breathing, since OSA is common, detectable, and treatable, and untreated OSA emerged as a recurrent risk factor across several analyses. At the same time, the authors were explicit that the direction of the OSA-long COVID relationship remains unclear, that the proposed shared biological pathways are not yet consistently measured, and that nothing in the current evidence base establishes OSA as a proven cause, or a proven consequence, of long COVID. The association is real in the data; its meaning awaits better studies.

Subject of Research: A scoping review of the associations between obstructive sleep apnea and long COVID syndrome in adults

Article Title: Obstructive sleep apnea and long COVID syndrome: a scoping review of current evidence in adults

Article References: Alhotye, M. I., Alotaibi, T. F., Alotaibi, M. M., Alojyri, R. M., Almutairi, A. G., Almutairi, H. A., Alghuraibi, R. S., Alrashdi, A. M., Alruwaili, A. H., & Alqahtani, M. K. (2026). Obstructive sleep apnea and long COVID syndrome: a scoping review of current evidence in adults. Frontiers in Sleep, 5, Article 1990528. https://doi.org/10.3389/frsle.2026.1990528

Image Credits: AI Generated

DOI: 10.3389/frsle.2026.1990528

Keywords: obstructive sleep apnea, long COVID, PASC, scoping review, sleep medicine, intermittent hypoxia, systemic inflammation, CPAP, polysomnography, post-COVID syndrome, observational studies, SARS-CoV-2