This review summarizes sleep deprivation, breathing regulation during sleep, and the outcomes of its destabilization. Breathing as an automatically regulated task consists of different basic anatomic and physiological parts. As the human body goes through the different stages of sleep, physiological changes in the breathing mechanism are present. Sleep disorders, such as obstructive sleep apnea-hypopnea syndrome, are often associated with sleep-disordered breathing and sleep deprivation. Hypoxia and hypercapnia coexist with lack of sleep and undermine multiple functions of the body (e.g., cardiovascular system, cognition, immunity). Among the general population, athletes suffer from these consequences more during their performance. This concept supports the beneficial restorative effects of a good sleeping pattern.
The mechanism of breathing includes air flow through the passages of the respiratory system due to pressure gradients that are formed by contraction of the diaphragm and the thoracic muscles. Air flows from a region of higher pressure to a region of lower pressure. Respiration involves the interplay between three different pressures: the atmospheric, the interalveolar, and the intrapleural pressure. Inspiration is the active phase of respiration and the result of muscle contraction, and expiration is the passive phase in calm state. Regulation of respiratory system is subconscious and determines rhythmic rotation between inspiration and expiration and ventilation (breathing frequency and depth)
Sleep state is associated with significant changes in respiratory physiology, including ventilatory responses to hypoxia and hypercapnia, upper airway, and intercostal muscle tone, and tidal volume and minute ventilation. These changes are further magnified in certain disease states, such as chronic obstructive pulmonary disease, restrictive respiratory disorders, neuromuscular conditions, and cardiac diseases
Sleep-disordered breathing (SDB), which causes sleep deprivation and intermittent hypoxia, encompasses a broad spectrum of sleep-related breathing disorders, including obstructive sleep apnea (OSA), central sleep apnea (CSA), as well as sleep-related hypoventilation and hypoxemia. Relative hypotonia of respiratory muscles, body posture changes, and altered ventilatory control result in additional physiologic changes contributing to hypoventilation
Hypercapnia, hypoxemia, and negative intrathoracic pressure swings lead to increased sympathetic response in order to maintain the normal air flow followed by hyperventilation.
Breathing is an automatic function and is regulated, according to the metabolic demands, by the autonomic nervous system (ANS) and, more specifically, by the respiratory center (RC), a central pattern generator (CPG) located in medulla oblongata along with the other vital reflexes. Corticalโmedullary circuits furthermore guarantee that voluntary control of breathing is possible
Upon loss of cortical functions without the loss of the medullary CPG, however, control is maintained by the latter.
Breathing is maintained during sleep, but its regulation differs from wakefulness
The progression through sleep stages is accompanied by a sequence of physiological changes based on chemoreceptor and baroreceptor reflexes
Chemoreceptors are divided into peripheral and central. Chemoreflex input consist of peripheral (carotid and aortic bodies), which reflect the concentrations of arterial O2, and of central receptors, which are sensitive to CO2 and H+ changes in the CSF
Consequently, the ventilatory feedback control system of the chemoreflex is vulnerable to rapid fluctuations of this input, similar to those that occur during NREM sleep
Two additional respiratory control centers exist in the medulla: the vasomotor (VMC) that regulates blood pressure and the cardiac center (cardioinhibitory and cardioacceleratory centers) for the regulation of heart rate. The three centers are interconnected to function coordinately for the release not only of the chemoreflex but also for the baroreflex
The baroreceptor reflex is activated when blood pressure is found increased by the baroreceptors in walls of carotid internal artery and of aorta and vasodilation occurs (inhibition of VMC) as well as decreased heart rate (stimulation of cardioinhibitory centers).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8950305/