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

Abstract

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) that 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 implanted with electrodes for electroencephalography (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 (V̇_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-REM sleep. Its increased occurrence during sleep was evidenced by the decreased DIA-to-ADB ratio (1:1 ratio means that each DIA event is followed by an ABD event, indicating a high occurrence of ABD activity). Moreover, V̇_E was also enhanced (P < 0.05) in periods with active expiration. V̇_E had a positive correlation (P < 0.05) with the peak amplitude of ABD_EMG activity. The data strongly demonstrate that hypercapnia-induced active expiration increases during sleep and provide an important functional role to support V̇_E in conditions of increased respiratory demand.

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