Acute sleep restriction (4 h time in bed) impairs the link between neural activity and cerebral blood flow (i.e., neurovascular coupling, NVC). Nitric oxide (NO) is an important mechanism in the NVC response. Insufficient sleep increases reactive oxygen species (ROS) and reduces NO bioavailability. Resveratrol, a polyphenol with antioxidant properties, reduces ROS and improves vascular function. We hypothesized that NVC following acute sleep restriction would be improved with acute oral resveratrol supplementation. Sixteen adults (8 M/8 F, age: 28 ± 7 yr, 25 ± 3 kg/m) completed two morning visits following a night of normal (NS; 449 ± 46 min) or restricted (RS; 243 ± 12 min) sleep. During each visit, middle (MCAv) and posterior (PCAv) cerebral artery velocity (transcranial Doppler ultrasound) were measured before and 45 min following oral resveratrol (250 mg) during: ) a validated visual search paradigm (Where's Waldo) and ) 5-min carbogen (95% O, 5% CO) air breathing. The peak cerebral blood velocity response to visual stimulation was reduced following sleep restriction (MCAV: NS 16 ± 7%, RS 11 ± 7%, = 0.017; PCAv: NS 43 ± 13%, RS 32 ± 14%, = 0.017) and restored with resveratrol in the PCA (RS + resveratrol: 40 ± 17%; = 0.028), but not the MCA (RS + resveratrol: 9 ± 5%; = 0.391). There was no effect of oral resveratrol on the peak response to visual stimulation following normal sleep. There was no effect of sleep restriction nor oral resveratrol on cerebrovascular response to carbogen air breathing. One night of RS (4 h time in bed) impairs NVC and resveratrol mitigates this impairment, particularly in the PCA. These results enhance our mechanistic understanding of sleep-associated impairments in NVC. Herein, we demonstrate that one night of restricted sleep (4 h time in bed) impairs the link between neural activity and cerebral blood flow (i.e., neurovascular coupling, NVC) of both middle and posterior cerebral arteries, and oral resveratrol supplementation may mitigate these impairments, particularly in the posterior cerebral artery. These results enhance our mechanistic understanding of sleep-associated impairments in NVC and advance our knowledge of neurovascular dysfunction occurring after restricted sleep.