SlowV˙O2kinetics in acute hypoxia are not related to a hyperventilation-induced hypocapnia
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abstract
We examined whether slower pulmonary O2 uptake (V˙O2p) 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 [PETO2] and end-tidal CO2 pressure [PETCO2]); iii) hyperventilation (HV; increased PETO2 and lowered PETCO2); and iv) normocapnic hypoxia (NC-HX; lowered PETO2 and PETCO2 matched to CON). Ventilation was increased (relative to CON) and matched between HX, HV, and NC-HX conditions. During each condition VO2p˙ was measured and phase II V˙O2p kinetics were modeled with a mono-exponential function. The V˙O2p 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˙O2p kinetics in hypoxic exercise.
