The matching of muscle O₂ delivery (Q) to muscle O₂ consumption (mVO₂) is a key determinant of the ability to sustain exercise [1]. During exercise at VO₂max, respiratory muscle activity may necessitate redistribution of cardiac output from locomotor to respiratory muscles [2]. Near-infrared spectroscopy (NIRS) provides a non-invasive mVO₂/Q estimate via measurement of [deoxyhaemoglobin] change (Δ[HHb]), yet the relative contribution of VO₂ and Q to Δ[HHb] is typically not interpretable. However, a plateau in pulmonary O₂ uptake (pVO₂) during ramp-incremental exercise (RI) provides a scenario by which Δ[HHb] largely reflects changes in Q, assuming mVO₂ remains constant. Thus, the aim of this study was to examine mVO₂/Q matching in the vastus lateralis (VL) during a pVO₂ plateau. We hypothesised that, at VO₂max, Δ[HHb] would increase consequent to a redistribution of Q away from the locomotor muscles. Six healthy males (24 ± 4 yr; 185 ± 2 cm; 76 ± 6.3 kg), identified as exhibiting a pVO₂ plateau [cf. 3], completed RI cycle ergometry (20 W.min^-1) to the limit of tolerance. pVO₂ was measured breath-by-breath (mass spectrometry and turbinometry) and VL Δ[HHb] was measured using NIRS (NIRO-200). Δ[HHb]peak was determined from repeated maximal isometric contractions. The Δ[HHb] profile during RI was characterised by a sigmoid [4]: Δ[HHb] = A₀ + A / (1 + e^{-[-c + (d*t)]}). The fitting window for Δ[HHb] spanned from RI onset to 60 s prior to the pVO₂ plateau, whence the model was projected forward to volitional exhaustion. This allowed comparison of the measured Δ[HHb] with the predicted value: A relative hypo- or hyper-perfusion state being estimated from an under- or over-prediction of the model, respectively. The pVO₂max plateau (4.08 ± 0.45 L.min^-1) averaged 69 ± 31 s (range 34 – 126 s) before termination. Ventilation (V_E) increased by 19.0 ± 10.6 L.min^-1 during this time, reaching a peak of 178 ± 16 L.min^-1. The Δ[HHb] response to RI was well characterised by a sigmoid (R² = 0.92 – 0.99). At the limit of tolerance the predicted Δ[HHb] was 102 ± 4 % of the measured value, but with a Δ[HHb] ‘reserve’ demonstrated by Δ[HHb]peak (135 ± 21%). These data indicated mVO₂/Q matching in the VL during exercise at VO₂max, despite increased energetic demands from both the locomotor and respiratory muscles. The VO₂ requirement of the respiratory muscles at high V_E has been estimated to be >3 mL.min^-1 VO₂ per L.min^-1 V_E [5]. In the present investigation this equates to ~15% of the VO₂ increment in RI, which may be expected to manifest in a delivery-to-consumption mismatch in the locomotor muscles [2]. Conversely, these data suggest that in healthy young males mVO₂/Q in the VL is maintained at the limit of tolerance during cycling at pVO₂max despite the increased energetic demands of both locomotor and respiratory muscles.