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The long-term impairment of pulmonary function during exercise was assessed in 12 children, aged 6 to 12 yr, who developed BPD after prematurity (gestational age 30 +/- 2 wk [mean +/- SD] and birth weight 1,400 +/- 335 g) and 16 age-, sex-, and physical activity-matched healthy children born at term, who served as controls. The children performed pulmonary function tests at rest and a maximal stepwise exercise on a treadmill. Oxygen consumption (VO2), carbon dioxide output (VCO2), and minute ventilation (VE) were monitored during the run. Baseline mean spirometric values (% of predicted) were in the normal range for both groups but were lower in BPD children with respect to control children (p < 0.05). At rest, arterial oxygen saturation (SaO2) was > or = 98% in all BPD children, but at peak exercise, 4 of them had a SaO2 fall > or = 4%. The postexercise FEV1 fall, with respect to the baseline, was 8 +/- 6%, in BPD and 2 +/- 1% in control children (p < 0.01). Maximum VO2 and VE were significantly lower in BPD children with respect to the control group (25.2 +/- 10.3 versus 37.1 +/- 10.4 ml/min/kg and 20.8 +/- 9.4 versus 30.7 +/- 7.9 L/min, respectively, both p < 0.01). Also, at submaximal levels of exercise dynamic, VO2 and VE responses were significantly lower in the BPD group (ANOVA, p < 0.001), with a ventilatory pattern characterized by lower tidal volumes. Anaerobic threshold was 20.6 +/- 9 in BPD and 28.8 +/- 8.6 ml O2/min/kg in healthy children (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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Santuz et al. (1995) studied this question.
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