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.