Sleeping and Breathing: Sleep Modifies Chemical Control of Breathing (Part 2)

The shift from wakefulness to non-REM sleep is not without effect on chemical control of breathing, however. A dramatic effect appears when chemical stimuli are reduced rather than increased. With mechanically assisted hyperventilation or with hyperventilation induced by hypoxic stimulation of breathing, the respiratory efforts are eliminated when arterial Pco2 decreases 2-4 mm Hg. Although difficult to measure directly, a 10-20 mm Hg decrease is required in awake man. This difference can be depicted on the motor output/Pco2 relationship shown in Figure 2; during wakefulness, the curve has a “hockey-stick” shape, with the bend lying near the eupneic point. During REM sleep, no steep decline occurs in the motor output when arterial Pco2 declines below the eupneic level. Thus, during wakefulness and REM sleep, ventilation is stabilized in the face of transient reduction in arterial Pco2, as would occur during periodic breathing. This appears to contribute to stabilizing breathing while awake but probably contributes little during REM because the gain of the chemical feedback loops is too low to initiate periodic breathing. Nonetheless, breathing is maintained at a level that results in near-normal arterial Pco2 during REM sleep. This would appear to be related to diffuse activation of the higher nervous system that engenders a “behavioral” influence on breathing, as proposed by Phillipson. According to this concept, the chemcial controllers dominate regulation of breathing during non-REM, and nonchemical factors dominate during REM, as depicted in Figure 3. This durable “explanation” principle accounts for the disappearance, during REM, of hypoxia induced periodic breathing in normals and of central apnea in patients. Buy Asthma Inhalers Online


Figure 3. Hypothetical schema of functional interrelationships of the components of the respiratory control system during quiet (non-REM) and active (REM) sleep. Chemical feedback acting through the peripheral (PCR) and central (CCR) chemoreceptors dominate the control of breathing during quiet sleep. Reflexes initiated by upper airway receptors also contribute. During active sleep, these reflex influences controlling breathing are less important, and breathing is heavily influenced by descending influences from higher centers.