Baroreflex control of heart rate (HR) is impaired following chronic intermittent hypoxia (CIH). However, the location and nature of this response remain unclear. We examined baroreceptor afferent, vagal efferent, and central components of the baroreflex circuitry. Fischer 344 (F344) rats were exposed to room air (RA) or CIH for 35-50 days, and were then anesthetized with isoflurane, ventilated, and catheterized for measurement of mean arterial blood pressure (MAP) and HR. Baroreceptor function was characterized by measuring percent (%) changes of integrated aortic depressor nerve activity (Int ADNA) relative to the baseline value in response to nitroprusside- and phenylephrine-induced changes in MAP. Data were fitted to a sigmoid logistic function curve. Heart rate responses to electrical stimulation of the left aortic depressor nerve and the right vagus nerve were assessed under ketamine-acepromazine anesthesia. Compared to RA controls, CIH significantly increased maximum baroreceptor gain or maximum slope (Gmax), maximum Int ADNA, and Int ADNA range (maximum - minimum ADNA), whereas other parameters of the logistic function were unchanged. In addition, CIH increased the maximum amplitude of bradycardic response to vagal efferent stimulation and decreased the time from the stimulus onset to the peak response. In contrast, CIH significantly reduced the maximum amplitude of bradycardic response to left aortic depressor nerve stimulation and increased the time from the stimulus onset to the peak response. Therefore, CIH decreased central mediation of the baroreflex, but augmented baroreceptor afferent function and vagal efferent control of HR.