This study assessed whether respiratory rates (RRs) correlate with urinary growth hormone (U-GH) excretion and sleep architecture in infants with chronic neonatal lung disease (CNLD) in early (1 month), middle (6 months), and late (10 months) infancy. Twenty-three preterm infants (CNLD = 16, controls = 7) were studied on 51 occasions. CNLD infants were stratified according to mean non-REM sleep respiratory rate (NREM RR) in early infancy into ''High RR CNLD'' infants (mean NREM RR >2 SD higher than controls) and ''Normal RR CNLD'' infants (mean NREM RR within 2 SD of controls' mean).
''High RR CNLD'' infants (RR >45) had a lower mean birthweight (P = 0.015), current weight (P = 0.042), current length (P = 0.02), and growth velocity in early infancy (grams/week gained: P = 0.042) than ''Normal RR CNLD'' and control infants. Mean (95% CI) U-GH excretion (ng U-GH/g urinary creatinine) was higher in ''High RR CNLD'' infants in air or their usual O 2 (1,932 [459, 3,406]) than ''Normal RR CNLD' ' (394 [147, 642]) and controls (320 [147, 492]) (P = 0.024). With resolution of tachypnea by mid-infancy, hemoglobin oxygen saturation (SaO 2 ) >93%, mean growth parameters and U-GH excretion for the ''High RR CNLD'' group were not significantly different from ''Normal RR CNLD'' and control groups. CNLD infants demonstrated increased sleep efficiency (P = 0.016), whereas controls had similar sleep efficiency between early and middle infancy (P = 0.452). Mean percent time in REM sleep (REM%) and slow wave sleep (SWS%) were not significantly different between early and middle infancy and did not vary in relation to respiratory rate. We conclude that tachypneic infants with CNLD have slower growth and elevated U-GH excretion in early infancy. With resolution of tachypnea, growth improved, U-GH excretion decreased, and sleep consolidation occurred. An elevated U-GH in tachypneic CNLD infants may reflect stress, compromised nutrition (GH resistance), or a feedback loop involving a direct effect of GH on lung growth and repair.