We have determined whether changes in PCO(2) above and below eucapnia modulate the precision of the voluntary control of breathing. Twelve trained subjects performed a compensatory tracking task in which they had to maintain the position of a cursor (perturbed by a variable triangular forcing function) on a fixed target by breathing in and out of a spirometer (ventilatory tracking; at 10 l/min). Before each task, subjects hyperventilated for 5 min, and the end-tidal PCO(2) (PET(CO(2))) was controlled; tracking was then performed separately at hypocapnia, eucapnia, and hypercapnia (PET(CO(2)) approximately 25, 37, and 43 Torr, respectively). Ventilatory tracking error was unchanged during hypocapnia (P > 0.05) but was significantly worse during hypercapnia (P < 0.003), compared with eucapnia; arm tracking error, performed as a control, was not significantly affected by PET(CO(2)) (P > 0. 05). In conclusion, ventilatory tracking performance is unaffected by the eucapnic PCO(2). From this, we suggest that resting breathing in awake humans may be independent of chemical drives and of the prevailing PCO(2).