The purpose of the present study was to investigate the contribution of ventilation to arterial O2 desaturation during maximal exercise. Nine untrained subjects and 22 trained long-distance runners [age 18-36 yr, maximal O2 uptake (V̇O(2 max) 48-74 ml · min-1 · kg-1] volunteered to participate in the study. The subjects performed an incremental exhaustive cycle ergometry test at 70 rpm of pedaling frequency, during which arterial O2 saturation (Sa(O2)) and ventilatory data were collected every minute. Sa(O2) was estimated with a pulse oximeter. A significant positive correlation was found between Sa(O2) and end-tidal PO2 (PET(O2); r = 0.72, r2 = 0.52, P < 0.001) during maximal exercise. These statistical results suggest that ~50% of the variability of Sa(O2) can be accounted for by differences in PET(O2), which reflects alveolar PO2. Furthermore, PET(O2) was highly correlated with the ventilatory equivalent for O2 (VE/V̇O2; r = 0.91, P < 0.001), which indicates that PET(O2) could be the result of ventilation stimulated by maximal exercise. Finally, Sa(O2) was positively related to V̇E/V̇O2 durimg maximal exercise (r = 0.74, r2 = 0.55, P < 0.001). Therefore, one-half of the arterial O2 desaturation occurring during maximal exercise may be explained by less hyperventilation, specifically for our subjects, who demonstrated a wide range of trained states. Furthermore, we found an indirect positive correlation between Sa(O2) and ventilatory response to CO2 at rest (r = 0.45, P < 0.05), which was mediated by ventilation during maximal exercise. These data also suggest that ventilation is an important factor for arterial O2 desaturation during maximal exercise.
ASJC Scopus subject areas