Abstract Introduction Obstructive sleep apnea (OSA) is associated with an increased risk for major adverse cardiovascular events (MACE), such as sudden cardiac death. MACE is more frequent in the morning in the general population but more frequent in the middle of the night in people with OSA. Whether these differences are associated with changes in circadian rhythms of blood pressure regulation is unknown. We tested if circadian rhythms in systolic blood pressure (SBP) during rested wakefulness and in response to a standardized mild exercise are disturbed in people with OSA compared to healthy controls (HC). Methods We studied 39 participants (HC [n=25, age 52.8±7.8 {mean±SD} years], (OSA [n=14, 50.6±6.6 years]) during ten identical recurring 5-h 20-min behavioral cycles in dim light and in an environment free of time cues. SBP was measured in the supine position during rested wakefulness followed by while seated at rest and during mild-intensity (heart rate at 50% heart rate reserve using the Karvonen formula) exercise on a static cycle ergometer. Circadian phases were determined relative to the dim-light melatonin onset. We performed mixed-model cosinor analyses to test whether the groups differed in their SBP rhythms during rested wakefulness and in their BP responses to exercise. Results Melatonin levels or phases relative to clock time were not different between groups (p=0.17), suggesting similar timing of central circadian clock outputs. There was an overall rhythm (p< 0.001) and a trend to group x circadian phase interaction for resting SBP (p=0.10). A separate group analysis showed a significant circadian rhythm in SBP in HC (p< 0.001) with a peak in the evening but no evident circadian rhythm in people with OSA (p=0.17). There was no circadian phase x exercise reactivity interaction between groups, but overall, exercise reactivity of SBP was significantly higher in people with OSA (+4mmHg, p=0.001). Conclusion OSA is characterized by a blunted circadian rhythm in resting blood pressure and an exaggerated blood pressure reactivity to exercise. Mechanisms for these rhythm changes should be investigated further. Support (if any) Support: NIH F32HL163232, R01HL125893, R01HL163232, R35HL155681, R01HL156948, ULTR00128, Oregon Institute of Occupational Health Sciences.