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In a previous work we reported discrepancies in the cardiovascular response to arousal from NREM sleep between OSAS patients and healthy controls. The long lasting cardiac sympathetic increase observed in normals was not present in the OSAS group, whereas the peripheral vasculature reaction was similar between the two groups. Analysis of REM arousal revealed that there was a similar temporary cardiac sympathetic impairment in the control group. In this work we have implemented a model-based time domain system identification method to assess the mechanisms involved in this reaction to arousal from both NREM and REM sleep in a group of healthy subjects. The use of time-varying techniques has enabled us to characterize the arousal reaction by analyzing the change in shape of the impulse responses of the system. The mechanisms regulating respiration and vascular effects on heart rate (respiratory sinus arrhythmia or RSA and arterial baroreflex or ABR, respectively) were the most affected by NREM arousal, likely as a result of the return of the wakefulness stimulus. The effect observed on the cardiac influence on the vasculature (circulatory dynamics, CID) was attributed to a change in the dominant mechanism prevailing in its dynamics.