We proposed that the higher incidence of sleep fragmentation, sympathovagal imbalance and baroreceptor reflex impairment during quiet sleep may play a critical role in late-sleep-related cardiovascular events. Polysomnographic recording was performed through wireless transmission using freely moving Wistar-Kyoto rats over 24h. The low-frequency power of arterial pressure variability was quantified to provide an index of vascular sympathetic activity. Spontaneous baroreflex sensitivity was assessed by slope of arterial pressure-RR linear regression. As compared with early-light period (Zeitgeber time 0-6h), rats during the late-light period (Zeitgeber time 6-12h) showed lower accumulated quiet sleep time and higher paradoxical sleep time; furthermore, during quiet sleep, the rats showed a lower δ% of electroencephalogram, more incidents of interruptions, higher σ% and higher β% of electroencephalogram, raised low-frequency power of arterial pressure variability value and lower baroreflex sensitivity parameters. During the light period, low-frequency power of arterial pressure variability during quiet sleep had a negative correlation with accumulated quiet sleep time and δ% of electroencephalogram, while it also had a positive correlation with σ% and β% of electroencephalogram and interruption events. However, late-sleep-related raised sympathetic activity and sleep fragmentation diminished when an α1-adrenoceptor antagonist was given to the rats. Our results suggest that the higher incidence of sleep fragmentation and sympathovagal imbalance during quiet sleep may play a critical role in late-sleep-related cardiovascular events. Such sleep fragmentation is coincident with an impairment of baroreflex sensitivity, and is mediated via α1-adernoceptors.