In contrast to adults, newborn infants breathe from an elevated end-ex
piratory lung volume, determined by the interaction of airflow retarda
tion (braking) by the diaphragm and larynx, and expiratory duration. T
o determine the effect of hypercapnia on this strategy, we examined ch
anges in respiratory muscle activity and the ventilatory response to C
O2 breathing in eight premature infants 33-34 wk gestational age in th
e first 3 postnatal days. We recorded tidal volume, airflow, and elect
romyograms (EMG) of the laryngeal abductor [posterior cricoarytenoid (
PCA)I, which abducts the vocal cords, and diaphragm during behaviorall
y determined quiet sleep in room air and during steady-state inhalatio
n of 2% CO2 in air. As expected, tidal volume increased (P < 0.0005) w
ithout a change in inspiratory duration with hypercapnia. Unexpectedly
, in all subjects, expiratory duration was longer during CO2 inhalatio
n (P < 0.001), accompanied by marked changes in expiratory flow patter
ns consistent with increased expiratory braking. Diaphragm postinspira
tory EMG activity increased with hypercapnia (P < 0.005) with no chang
e in baseline diaphragm or PCA EMG activity. Peak inspiratory EMG acti
vity of the diaphragm and PCA increased with CO2 (10 and 37%, respecti
vely; P < 0.05). We conclude that the mechanisms used to elevate end-e
xpiratory lung volume are enhanced during hypercapnia in premature inf
ants. This breathing strategy may be important in maintaining gas exch
ange in infants with lung disease.