Heart-rate variability (HRV) is mediated by at least three primary mechanisms: (a) vagal feedback from pulmonary stretch receptors ("PSR"); (b) central medullary coupling between respiratory and cardiovagal neurons ("RCC"); and (c) arterial baroreflex-induced fluctuations ("ABR"). We employed a noninvasive experimental protocol in conjunction with a minimal model to determine how these sources of HRV are altered in obstructive sleep apnea syndrome (OSAS). Respiration, heart rate and blood pressure were monitored in 8 normals and 9 untreated OSAS patients in relaxed wakefulness, stage 2 and REM sleep. A computer-controlled ventilator delivered inspiratory pressures that varied randomly from breath to breath. Application of the model to the corresponding subject responses allowed the delineation of the three components of HRV. In all states, RCC gain was lower in OSAS vs. normals (P<0.04). ABR gain was also reduced in OSAS (P<0.03). Both RCC and ABR gains increased from wakefulness to sleep (P<0.04). However, there was no difference in PSR gain between subject groups or across states. The findings of this study suggest that the adverse autonomic effects of OSAS include impairment of baroreflex gain and central respiratory-cardiovascular coupling, but the component of respiratory sinus arrhythmia that is mediated by lung vagal feedback remains intact.