The effect of voluntary hyperventilation-induced hypocapnic alkalosis (RALK) on pulmonary O₂ uptake (VO₂) kinetics and muscle deoxygenation was examined in young male adults (n = 8) during moderate-intensity exercise. Subjects performed 5 repetitions of a step-transition in work rate from 20 W cycling to a work rate corresponding to 90% of the estimated lactate threshold during control (CON; P_ET,CO2 ~ 40 mmHg) and during hyperventilation (RALK; P_ET,CO2 ~ 20 mmHg). VO₂ was measured breath-by-breath and relative concentration changes in muscle deoxy- (HHb), oxy- (O₂Hb) and total- (Hb_tot) haemoglobin were measured continuously using near-infrared (NIR) spectroscopy (Hamamatsu, NIRO 300). The time constant for the fundamental, phase 2, VO₂ response (VO₂) was greater (P < 0.05) in RALK (48 ± 11 s) than CON (31 ± 9 s), while HHb was similar between conditions (RALK, 12 ± 4 s; CON, 11 ± 4 s). The Hb_tot was lower (P < 0.05) in RALK than CON, prior to (RALK, -3 ± 5 µmol/L; CON, -1 ± 4 µmol/L) and at the end (RALK, 1 ± 6 µmol/L; CON, 5 ± 5 µmol/L) of moderate-intensity exercise. Although slower adaptation of VO₂ during RALK may be related to an attenuated activation of PDH (and other enzymes) and provision of oxidizable substrate to the mitochondria (i.e. metabolic inertia), the present findings also suggest a role for a reduction in local muscle perfusion and O2 delivery.