In conscious normal humans after a brief hypoxic ventilatory stimulus ventilation slowly decays to baseline and does not undershoot though the subjects are hyperoxic and hypocapnic. This phenomenon is attributed to short-term poststimulus potentiation (STP), which may be an important factor promoting ventilatory stability by preventing periodic breathing. It has been proposed that obstructive sleep apnea (OSA) is a variant of periodic breathing, with obstruction occurring when ventilatory drive is low. If this were the case, patients with OSA might have reduced STP. To test this, seven normal adults and 12 patients with OSA (mean apnea index, 52.4 +/- 6.9 SE events/h) were studied. Ventilation (VI) was measured in awake seated subjects during 30 to 45 s of exposure to hypoxia (end-tidal O2: 50 mm Hg) followed by hyperoxia. A total of 57 hypoxic-hyperoxic runs were analyzed (36 in the patients and 21 in the normal subjects). During hypoxia VI increased and end -tidal CO2 decreased by similar amounts in both groups. In normal subjects after hypoxia there was a gradual decay in VI to prehypoxic levels without an undershoot. In patients, there was on average a ventilatory undershoot at 35 s of hyperoxia, with a mean VI of 83% of baseline. The undershoot was due mainly to a decrease in tidal volume, which wes significantly lower than that of the normal subjects for several seconds. These changes were particularly prominent in seven patients who were not different from the others in terms of baseline characteristics, hypoxic responses, and OSA severity. Our results indicate that a significant number of patients with OSA have reduced STP after brief hypoxia, a finding that may be of relevance to the pathogenesis of OSA.
