Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8650810 | Respiratory Physiology & Neurobiology | 2018 | 29 Pages |
Abstract
We examined whether slower pulmonary O2 uptake (VËO2p) 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 O2â¯=â¯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 VO2pË was measured and phase II VËO2p kinetics were modeled with a mono-exponential function. The VËO2p time constant was different (pâ¯<â¯0.05) amongst all conditions: CON, 26â¯Â±â¯11s; HV, 36â¯Â±â¯14s; HX, 46â¯Â±â¯14s; and NC-HX, 52â¯Â±â¯13s. Hypocapnia may prevent further slowing of VËO2p kinetics in hypoxic exercise.
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Physiology
Authors
Daniel A. Keir, Michael Pollock, Piramilan Thuraisingam, Donald H. Paterson, George J.F. Heigenhauser, Harry B. Rossiter, John M. Kowalchuk,