The brain requires well-regulated cerebrovascular perfusion to match metabolic demand. Regional coupling of perfusion to metabolic rate is termed neurovascular coupling (NVC). NVC remains stable during blood gas perturbations upon ascent to altitude, where individuals are exposed to the antagonistic effects of hypoxia and hypocapnia. Few studies have addressed the effects of acute hypocapnia and respiratory alkalosis independently. We aimed to assess the specific effects of acute steady-state hypocapnia on NVC magnitude in a laboratory setting. We recruited 17 healthy participants and instrumented the posterior cerebral artery (PCA) with a transcranial Doppler ultrasound. NVC was elicited using a standardized strobe light stimulus (6 Hz; 5x30sec on/off), and both peak and mean absolute responses from baseline (BL) were quantified. Participants were coached to hyperventilate to reach steady-state hypocapnic steps of Δ-5 and Δ-10 Torr end-tidal (PET)CO2 from baseline levels. PETCO2 levels were significantly decreased from 36.7±3.2 (baseline) to 31.6±3.9 Torr (∆-5) and 26±4.0 (∆-10) Torr (P<0.001). There was a significant reduction in NVC magnitude (ΔPCAv) from BL during controlled hypocapnia at both Δ-5 and Δ-10 in peak ΔPCAv (P=0.044 and P=0.037, respectively), but no significant decrease in mean ΔPCAv (P=0.193). Our study demonstrates that acute respiratory alkalosis attenuates peak NVC magnitude at Δ-5 Torr PETCO2, without further attenuation at Δ-10. Although peak NVC magnitude was attenuated, our data suggests that NVC is remarkably stable in acute respiratory alkalosis given (a) the magnitude of reduction in peak NVC was small and (b) NVC was unchanged in mean responses to visual stimulation.