Administration of 100% O-2 to preterm Infants induces an apnea that is usually central. We hypothesized that this apnea may be ''mixed'' at times with an obstructive component appearing late during the respiratory pause. In addition, we reasoned that obstruction would depend on the duration of the apnea. Thus, we gave 100% O-2 to 61 healthy preterm infants. Group 1 was greater than or equal to 1,500 g [birth wt 1.8 +/- 0.1 (SE) kg, gestational age 32 +/- 1 wk, postnatal age 19 +/- 2 days, n. = 26] and group 2 was <1,500 g [birth wt 1.2 +/- 0.1 kg, gestational age 29 +/- 1 wk, postnatal age 30 +/- 4 days, it = 35]. Ventilation was measured using a flow-through system. Respiratory efforts in the absence of flow were detected using chest and abdominal displacements or diaphragmatic electromyography. In group 1, 19% of the central apneas became obstructive at 17 +/- 3 s, whereas in group 2, 34% did so at 12 +/- 2 s. Mixed apneas were longer than those without obstruction (28 +/- 3 vs. 12 +/- 1 s; P = 0.0001). The incidence of mixed apneas was 0, 14, and 66% in group I and 0, 27, and 69% in group 2 in apneas of 3-10, 11-20, and >20 s, respectively. These findings suggest that 1) a percentage of the central apneas induced by inhaling 100% O-2 became obstructive, 2) the incidence of the obstructive component increased with the duration of apnea, and 3) smaller infants became obstructed sooner and had a higher incidence of obstruction than larger infants. We speculate that the obstructive component is facilitated by the loss of airway motor tone induced by central respiratory inhibition and possibly by the action of high O-2 on the thyroarytenoid muscles. This would be more evident the longer the apnea.