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) CO -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 implanted with electrodes for EEG and electromyography EMG of the neck, diaphragm (DIA) and abdominal (ABD) muscles. Active expiratory events were considered as rhythmic ABD activity interposed to DIA . Animals were exposed to room air followed by hypercapnia (7% CO ) with EEG, EMG and ventilation ( ) recorded throughout the experimental protocol. No active expiration was observed during room air exposure. During hypercapnia, CO -evoked active expiration was predominantly recruited during non-rapid eye movement 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, was also enhanced (P< 0.05) in periods with active expiration. had a positive correlation (P< 0.05) with the peak amplitude of ABD activity. The data demonstrate strongly that hypercapnia-induced active expiration increases during sleep and provides an important functional role to support in conditions of increased respiratory demand.

Cardiovascular and respiratory profiles during the sleep–wake cycle of rats previously submitted to chronic intermittent hypoxia

“…Other studies, however, have reported different results concerning the occurrence of active expiration during sleep. Although Leirão, Silva, Gargaglioni, and da Silva () have demonstrated that NREM sleep is accompanied by robust active expiration in hypercapnia‐exposed rats, these authors showed that rats breathing room air did not present active expiration during this sleep state. Likewise, we did not observe expiratory abdominal muscle recruitment during sleep in our recordings.…”

Active expiratory oscillator regulates nasofacial and oral motor activities in rats

“…The pre‐Bötzinger complex (pre‐BötC), located in the ventral medulla, is responsible for generating the active inspiratory motor behaviour (Smith, Ellenberger, Ballanyi, Richter, & Feldman, ). During high chemical drive, such as increases in CO 2 (hypercapnia) and/or in [H + ] (acidosis), expiratory muscles contract to force exhalation during stage 2 of expiration, thereby enhancing pulmonary ventilation (Abdala, Rybak, Smith, & Paton, ; Leirao, Silva, Gargaglioni, & da Silva, ; Magalhaes et al., ; Pisanski & Pagliardini, ). This phenomenon is mediated by phasic late‐expiratory (late‐E) neurons located in the parafacial respiratory group (pFRG), adjacent to the ventrolateral portion of the facial nucleus in rats (Abdala et al., ; Pagliardini et al., ).…”

Adrenergic C1 neurons are part of the circuitry that recruits active expiration in response to hypoxia

“…This effect seems to be exclusive to hypoxia, because ablation of the C1 cells did not affect the generation of active expiration elicited by hypercapnia. These results suggest that recruitment of Abd muscles by chemosensory drives could be mediated through different neuromodulatory systems (Leirão et al, 2018;O'Halloran, 2018).…”