Hypercapnia-induced active expiration increases in sleep and enhances ventilation in unanaesthetized rats

Expiration is passive at rest but becomes active through recruitment of abdominal muscles under increased respiratory drive. Hypercapnia- induced active expiration has not been well explored in unanaesthetized rats. We hypothesized that (i) CO2-evoked active expiration is recruited in a state-dependent manner, i.e. differently in sleep or wakefulness, and (ii) recruitment of active expiration enhances ventilation, hence having an important functional role in meeting metabolic demand. To test these hypotheses, Wistar rats (280-330 g) were implantedwith electrodes for EEG and electromyography EMG of the neck, diaphragm (DIA) and abdominal (ABD) muscles. Active expiratory events were considered as rhythmic ABD(EMG) activity interposed to DIA(EMG). Animals were exposed to room air followed by hypercapnia (7% CO2) with EEG, EMG and ventilation ((V)over dot(E)) recorded throughout the experimental protocol. No active expiration was observed during room air exposure. During hypercapnia, CO2-evoked active expiration was predominantly recruited during non-rapid eyemovement sleep. Its increased occurrence during sleep was evidenced by the decreased DIA-to-ADB ratio (1: 1 ratio means that eachDIA event is followed by an ABD event, indicating a high occurrence of ABD activity). Moreover, (V) over dot(E) was also enhanced (P < 0.05) in periods with active expiration. (V) over dot(E) had a positive correlation (P < 0.05) with the peak amplitude of ABD(EMG) activity. The data demonstrate strongly that hypercapnia-induced active expiration increases during sleep and provides an important functional role to support. (V) over dot(E) in conditions of increased respiratory demand. (AU)