The early time course of adaptation of pulmonary O₂ uptake (VO_2p) (reflecting muscle O₂ consumption) and muscle deoxygenation kinetics (reflecting the rate of O₂ extraction) were examined during highintensity interval (HIT) and lower-intensity continuou (END)training. Twelve male volunteers underwent 8 sessions of either HIT (8-12 x 1 min intervals at 120% VO_2max separated by 1 min rest) or END (90-120 min at 65% VO_2max). Subjects completed step-transitions to a moderate-intensity work rate (90% estimated lactate threshold) on 5 occasions throughout training, and ramp incremental and constant-load performance tests at pre-, mid- and post-training. VO_2p was measured breath-by-breath by mass spectrometry and volume turbine. Deoxygenation ([HHb]) of the vastus lateralis muscle was monitored by near-infrared spectroscopy. The fundamental phase II time constant for VO_2p ( VO₂) and deoxygenation kinetics (effective time constant, ' = (TD + ) [HHb]) during moderate-intensity exercise were estimated using nonlinear least-squares regression techniques. The VO₂ was reduced by ~20% (p < 0.05) after only 2 training sessions and by ~40% (p < 0.05) after 8 training sessions (i.e., post-training), with no differences between HIT and END. The '[HHb] (~20 s) did not change over the course of 8 training sessions. These data suggest that faster activation of muscle O₂ utilization is an early adaptive response to both HIT and lower-intensity END training. That [HHb] kinetics (a measure of fractional O₂ extraction) did not change despite faster VO_2p kinetics suggests that faster kinetics of muscle O₂ utilization were accompanied by adaptations in local muscle (microvascular) blood flow and O₂ delivery, resulting in a similar "matching" of blood flow to O₂ utilization. Thus faster kinetics of VO_2p during the transition to moderate-intensity exercise occurs after only 2 days HIT and END training, and without changes to muscle deoxygenation kinetics, suggesting concurrent adaptations to microvascular perfusion.