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 O2 (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 (SaO2) >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. Pediatr Pulmonol. 1998; 26:241–249. © 1998 Wiley‐Liss, Inc.