Slow V ˙ O 2 kinetics in acute hypoxia are not related to a hyperventilation-induced hypocapnia

We examined whether slower pulmonary O₂ uptake (V˙O_2p) kinetics in hypoxia is a consequence of: a) hypoxia alone (lowered arterial O₂ pressure), b) hyperventilation-induced hypocapnia (lowered arterial CO₂ pressure), or c) a combination of both. Eleven participants performed 3-5 repetitions of step-changes in cycle ergometer power output from 20W to 80% lactate threshold in the following conditions: i) normoxia (CON; room air); ii) hypoxia (HX, inspired O₂ = 12%; lowered end-tidal O₂ pressure [P_ETO₂] and end-tidal CO₂ pressure [P_ETCO₂]); iii) hyperventilation (HV; increased P_ETO₂ and lowered P_ETCO₂); and iv) normocapnic hypoxia (NC-HX; lowered P_ETO₂ and P_ETCO₂ matched to CON). Ventilation was increased (relative to CON) and matched between HX, HV, and NC-HX conditions. During each condition VO_2p˙ was measured and phase II V˙O_2p kinetics were modeled with a mono-exponential function. The V˙O_2p time constant was different (p < 0.05) amongst all conditions: CON, 26 ± 11s; HV, 36 ± 14s; HX, 46 ± 14s; and NC-HX, 52 ± 13s. Hypocapnia may prevent further slowing of V˙O_2p kinetics in hypoxic exercise.