Arterial to end-tidal Pco(2) difference during exercise in normoxia and severe acute hypoxia: importance of blood temperature correction

Negative arterial to end-tidal Pco(2) differences ((a-ET)Pco(2)) have been reported in normoxia. To determine the influence of blood temperature on (a-ET)Pco(2), 11 volunteers (21 ± 2 years) performed incremental exercise to exhaustion in normoxia (Nx, P(I)o(2): 143 mmHg) and hypoxia (Hyp, P(I)o(2): 73 mmHg), while arterial blood gases and temperature (ABT) were simultaneously measured together with end-tidal Pco(2) (P(E)(T)co(2)). After accounting for blood temperature, the (a-ET) Pco(2) was reduced (in absolute values) from −4.2 ± 1.6 to −1.1 ± 1.5 mmHg in normoxia and from −1.7 ± 1.6 to 0.9 ± 0.9 mmHg in hypoxia (both P < 0.05). The temperature corrected (a-ET)Pco(2) was linearly related with absolute and relative exercise intensity, VO(2), VCO(2), and respiratory rate (RR) in normoxia and hypoxia (R(2): 0.52–0.59). Exercise CO(2) production and P(E)(T)co(2) values were lower in hypoxia than normoxia, likely explaining the greater (less negative) (a-ET)Pco(2) difference in hypoxia than normoxia (P < 0.05). At near-maximal exercise intensity the (a-ET)Pco(2) lies close to 0 mmHg, that is, the mean P(a)co(2) and the mean P(E)(T)co(2) are similar. The mean exercise (a-ET)Pco(2) difference is closely related to the mean A-aDO(2) difference (r = 0.90, P < 0.001), as would be expected if similar mechanisms perturb the gas exchange of O(2) and CO(2) during exercise. In summary, most of the negative (a-ET)Pco(2) values observed in previous studies are due to lack of correction of P(a)co(2) for blood temperature. The absolute magnitude of the (a-ET)Pco(2) difference is lower during exercise in hypoxia than normoxia.