Yes, the do mention CO2 in that part. Their claim PAO2 chemorecptors are playing more important role than pH and PACO2 chemoreceptors (as I already wrote) rather surpirsed me. That should be very easily verifiable, so I wonder that they would claim something like that if it was not true. On the other hand, I know very well, that hypercapnia alone (with no hypoxia associated to it) leads to bradycardia too, so I have rather serious doubts about their claim.
EDIT:
There is nothing wrong with the data, and nothing wrong with the experiments. The purpose of the experiments was not showing the influence of CO2, but the influence of facial thermo sensors and apnea. In this document they simply did not go into the depths to analyze hypoxia and hypercapnia in apnea separately, which itself would not be too bad. The only surprising is the menitoned claim about the PAO2 receptors, but since I do not now what led the to the conclusion, I cannot comment.
I've no criticism of the data or experiments per se. Respiration, whether pneic or apneic, is consumption (O2) and production (CO2) with many variables. I was surprised to see that the production side of respiration was so relatively insignificant in the written paper. They include many references to other things, virtually nothing about CO2.
DDeden