Cardiac output, O2 delivery and V˙O2 kinetics during step exercise in acute normobaric hypoxia

We hypothesised that phase II time constant (τ2) of alveolar O2 uptake (V˙O2A) is longer in hypoxia than in normoxia as a consequence of a parallel deceleration of the kinetics of O2 delivery (Q˙aO2). To test this hypothesis, breath-by-breath V˙O2A and beat-by-beat Q˙aO2 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%FIO2=11%). Blood lactate ([La]b) accumulation during the exercise transient was also measured. The τ2 for Q˙aO2 was shorter than that for V˙O2A 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 Q˙aO2 kinetics generated the longer τ2 for V˙O2A in hypoxia, with consequent contribution of anaerobic lactic metabolism to the energy balance in exercise transient, witnessed by the increase in [La]b.

► We investigate V˙O2 and Q˙aO2 kinetics in normoxia and hypoxia during moderate intensity exercise.
► Q˙aO2 kinetics is faster than that of V˙O2 in normoxia but not in hypoxia.
► V˙O2 kinetics is slower in hypoxia than in normoxia.
► Blood lactate concentration is larger in hypoxia than in normoxia.
► The slowing of Q˙aO2 brakes V˙O2 kinetics, whence a larger contribution of anaerobic glycolysis.