SLEEP-INDUCED BREATHING INSTABILITY

We present a view of the neuromechanical regulation of breathing and c auses of breathing instability during sleep. First, we would expect tr ansient increases in upper airway resistance to be a major cause of tr ansient hypopnea. This occurs in sleep because a hypotonic upper airwa y is more susceptible to narrowing and because the immediate excitator y increase in respiratory motor output in response to increased lends is absent in non-REM sleep. Secondly, sleep predisposes to an increase d occurrence of ventilatory ''overshoots'', in part because abruptly c hanging sleep states cause transient changes in upper airway resistanc e and in the gain of the respiratory controller. Following these venti latory overshoots, breathing stability will be maintained if excitator y short-term potentiation is the prevailing influence. On the other ha nd, apnea and hypopnea will occur if inhibitory mechanisms dominate fo llowing the ventilatory overshoot. These inhibitory mechanisms include : a) hypocapnia--if transient, will inhibit carotid chemoreceptors and cause hypopnea, but if prolonged will inhibit medullary chemoreceptor s and cause apnea; b) a persistent inhibitory effect from lung stretch ; c) baroreceptor stimulation, from a transient rise in systemic blood pressure immediately following termination of apnea or hypopnea may p artially suppress the accompanying hyperpnea; d) depression of central respiratory motor output via prolonged brain hypoxia. Once apneas are initiated, reinitiation of inspiration is delayed even though excitat ory stimuli have risen well above their apneic thresholds, and these p rolonged apneas are commonly accompanied by tonic EMG activation of ex piratory muscles of the chest wall and upper airway.