We hypothesised that phase II time constant (2) of alveolar O2 uptake (VO2A ) is longer in hypoxia than in normoxia as a consequence of a parallel deceleration of the kinetics of O2 delivery (QaO2 ). To test this hypothesis, breath-by-breath VO2A and beat-by-beat QaO2 were measured in eight male subjects (25.4±3.4 yy, 1.81±0.05 m, 78.8±5.7 kg) at the onset of cycling exercise (100 W) in normoxia and acute hypoxia (FIO2=11%). Blood lactate ([La]b) accumulation during the exercise transient was also measured. The 2 for QaO2 was shorter than that for VO2A in normoxia (8.3±6.8 s versus 17.8±3.1 s), but not in hypoxia (31.5±21.7 s versus 28.4 5.4±5.4 s). [La]b was increased in the exercise transient in hypoxia (3.0±0.5 mM at exercise versus 1.7±0.2 mM at rest), but not in normoxia. We conclude that the slowing down of the QaO2 kinetics generated the longer 2 for VO2A in hypoxia, with consequent contribution of anaerobic lactic metabolism to the energy balance in exercise transient, witnessed by the increase in [La]b.