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CPAP does not modify exercise-derived autonomic responses in nonsleepy patients with coronary artery disease and obstructive sleep apnea

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SCHOOL OF MEDICINE
Upper Org Unit

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Glantz, H.

Thunström, E.

Uzel, H.

Azarbarzin, A.

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eng

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N/A

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Abstract

Obstructive sleep apnea (OSA) is associated with autonomic dysfunction and increased cardiovascular risk, but the effects of continuous positive airway pressure (CPAP) on exercise-derived autonomic responses in patients with coronary artery disease (CAD) remain unclear. Methods This study included nonsleepy patients (Epworth Sleepiness Scale score <10) with CAD and OSA (apnea–hypopnea index ≥15 events/h) enrolled in the RICCADSA randomized controlled trial. Of 244 patients randomized at baseline, 204 (CPAP n = 100; no-CPAP n = 104) completed bicycle ergometer exercise testing at both 3 and 12 months and were included. The primary outcome was the change in 1-min heart rate recovery (HRR1) from 3 to 12 months; secondary outcomes included changes in 4-min heart rate recovery (HRR4), chronotropic response, and post-exercise recovery time. Longitudinal changes were analyzed using linear mixed-effects models adjusted for sex, body mass index (BMI), diabetes, and β-blocker use. Results HRR1 remained stable from 3 to 12 months in both groups (approximately 22–23 bpm), with no CPAP or time × treatment effects. HRR4 showed no differential change, remaining around 46–47 bpm. Chronotropic response was unchanged (chronotropic index approximately 0.74–0.76 in both groups). Exercise workload and peak heart rate remained stable over time and did not differ between groups. Post-exercise recovery time shortened significantly in the overall cohort (by approximately 0.3 min from 3 to 12 months) but was not CPAP-specific. Higher BMI and β-blocker use were independently associated with impaired late HRR and chronotropic response. Conclusions In nonsleepy patients with CAD and OSA, CPAP does not modify exercise-derived autonomic or chronotropic responses, underscoring the need for complementary strategies targeting metabolic burden and cardiovascular conditioning.

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Elsevier

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Sleep Medicine

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DOI

10.1016/j.sleep.2026.108954

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