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

We examined whether slower pulmonary O uptake (V˙O) kinetics in hypoxia is a consequence of: a) hypoxia alone (lowered arterial O pressure), b) hyperventilation-induced hypocapnia (lowered arterial CO 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 O = 12%; lowered end-tidal O pressure [PO] and end-tidal CO pressure [PCO]); iii) hyperventilation (HV; increased PO and lowered PCO); and iv) normocapnic hypoxia (NC-HX; lowered PO and PCO matched to CON). Ventilation was increased (relative to CON) and matched between HX, HV, and NC-HX conditions. During each condition VO˙ was measured and phase II V˙O kinetics were modeled with a mono-exponential function. The V˙O 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 kinetics in hypoxic exercise.