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.