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An adequate supply of O2 is essential for the maintenance of cellular activity. Systemic or local hypoxia can be experienced during decreased O2 availability or associated with diseases, or a combination of both. Exposure to hypoxia triggers adjustments in multiple physiological systems in the body to generate appropriate homeostatic responses. However, with significant reductions in the arterial partial pressure of O2, hypoxia can be life‐threatening and cause maladaptive changes or cell damage and death. To mitigate the impact of limited O2 availability on cellular activity, O2 chemoreceptors rapidly detect and respond to reductions in the arterial partial pressure of O2, triggering orchestrated responses of increased ventilation and cardiac output, blood flow redistribution and metabolic adjustments. In mammals, the peripheral chemoreceptors of the carotid body are considered to be the main hypoxic sensors and the primary source of excitatory feedback driving respiratory, cardiovascular and autonomic responses. However, current evidence indicates that the CNS contains specialized brainstem and spinal cord regions that can also sense hypoxia and stimulate brain networks independently of the carotid body inputs. In this manuscript, we review the discoveries about the functioning of the O2 chemoreceptors and their contribution to the monitoring of O2 levels in the blood and brain parenchyma and mounting cardiorespiratory responses to maintain O2 homeostasis. We also discuss the implications of the chemoreflex‐related mechanisms in paediatric and adult pathologies. What is the topic of this review?Hypoxia is a life‐threatening condition. Specialized sensory mechanisms in the periphery and CNS respond to reduced O2 levels, triggering ventilatory and haemodynamic responses to enhance O2 uptake and delivery to the tissues.What advances does it highlight?Although anatomically distinct, both peripheral and central mechanisms should be considered when examining the homeostatic responses to hypoxia. Herein, we review past and current research on O2 monitoring in the periphery and CNS, discussing how their sensing mechanisms, pathways and interactions modify respiratory and sympathetic activities. [ABSTRACT FROM AUTHOR]

Key points: Expiratory muscles (abdominal and thoracic) can be recruited when respiratory drive increases under conditions of increased respiratory demand such as hypercapnia. Studying hypercapnia‐induced active expiration in unanaesthetized rats importantly contributes to the understanding of how the control system is integrated in vivo in freely moving animals. In unanaesthetized rats, hypercapnia‐induced active expiration was not always recruited either in wakefulness or in sleep, suggesting that additional factors influence the recruitment of active expiration. The pattern of abdominal muscle recruitment varied in a state‐dependent manner with active expiration being more predominant in the sleep state than in quiet wakefulness. Pulmonary ventilation was enhanced in periods with active expiration compared to periods without it. 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) 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 ABDEMG activity interposed to DIAEMG. Animals were exposed to room air followed by hypercapnia (7% CO2) with EEG, EMG and ventilation ( V ̇ 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 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, V ̇ E was also enhanced (P < 0.05) in periods with active expiration. V ̇ E had a positive correlation (P < 0.05) with the peak amplitude of ABDEMG activity. The data demonstrate strongly that hypercapnia‐induced active expiration increases during sleep and provides an important functional role to support V ̇ E in conditions of increased respiratory demand. [ABSTRACT FROM AUTHOR]