Purpose: Patients suffering from sleep disordered breathing present with a reduced cerebral vascular reactivity (CVR) [1]. The severity of this reduction is shown to be related to the number of arousals per night [2]. These changes in CVR and the fragmentation of sleep could play a role in the respiratory changes observed in this patient population. Hypotheses: We hypothesized that the change in CVR following a night of artificially fragmented sleep when compared to the CVR change following a normal night. Furthermore, we predicted a decline in respiratory CO2 sensitivity. Methods: Participants visited the laboratory on two occasions for an overnight stay. One visit included a normal night’s sleep (control) and the other visit included a night of fragmented sleep (fragmentation). During fragmentation micro-arousals were elicited during all sleep stages using a 500ms auditory stimulus played every minute. Continuous polysomnography was recorded throughout each night. CVR was assessed before and after each night using transcranial Doppler ultrasound of the middle cerebral artery. During the assessment of CVR participants were exposed to three five-minute steps of hypercapnia: 4, 7 and 10 mmHg above normal end-tidal partial pressures of CO2(PETCO2). A hypercapnic (10 mmHg>normal PETCO2) multi-frequency binary sequence test was completed following each night to assess central and peripheral chemosensitivity. A dynamic end-tidal forcing system was used for gas control during each assessment. Results: The mean (±S.E.) change in CVR following fragmentation is reduced across all three steps of hypercapnia when compared to the CVR change after the control night; -2.23±4.36%, -2.55±2.45% and -9.13±1.89%, respectively. We also observed a reduction in total CO2 chemosensitivity following fragmentation, -41.97±20.25%. Additionally, peripheral chemosensitivity remained unchanged following fragmentation -6.20±16.62%. However, central chemosensitivity was markedly reduced -35.77±6.02%. Discussion: These results support our hypothesis of parallel alterations in breathing and cerebral vascular control following a night of disrupted sleep. The poor quality of sleep effecting patients suffering sleep disordered breathing could potentially play a role the respiratory control changes seen in this population, which may ultimately promote the further development of the disease.