Effect of controlling CO₂ on peripheral hypercapnic chemosensitivity at exercise intensities above the respiratory compensation point

A rapid change in arterial CO 2 tension causes changes in ventilation, referred to as peripheral hypercapnic chemosensitivity (PHC). The PHC increases from rest to low-intensity exercise yet is not further augmented at higher exercise intensities, where additional ventilatory stimulants are present. During supra-respiratory compensation point (RCP) exercise, as arterial CO 2 tension falls, so does PHC, which may mask the effect of other ventilatory stimuli. Twenty healthy subjects ( n=10 females) completed a maximal exercise test and on subsequent days (2 and 3) had PHC measured at rest, 40% of maximal work rate (Wmax), and supra-RCP exercise intensities. On one experimental day, participants were kept isocapnic, and on the other, end-tidal carbon dioxide (P ET CO 2 ) declined naturally during supra-RCP exercise (poikilocapnia). PHC was measured as the quotient between the change in ventilation and P ET CO 2 after two breaths of hypercapnic (10% CO 2 ) gas delivered 3-5 times during each condition. There was a significant increase in PHC during supra-RCP intensities with isocapnia, compared to poikilocapnic exercise (+11.2±6%) ( p=0.0015). Yet during the isocapnia day, there was still no significant increase in PHC from 40% intensity to supra-RCP ( p=0.96). A repeated measures correlation demonstrated a significant relationship between PHC and P ET CO 2 during poikilocapnia ( r=0.49, p<0.001), with no significant relationship during isocapnia ( r=0.06, p=0.57). We conclude that the metabolic milieu associated with supra-RCP exercise does not impact PHC and there is a CO 2 -dependent relationship in which P ET CO 2 influences PHC independent of the initial exercise sensitization.