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EFFECTS ON SLEEP 47
The parasympathetic autonomic nervous system seems to be responsible for the
bradycardia observed in non-REM sleep and mainly in tonic REM sleep through the
increase in vagal activity (Guazzi et al., 1968). The variability of heart rate in REM
sleep could be placed under the same control, as vagotomy strongly reduced the
heart rate instability (Baust and Bohnert, 1969). During falling asleep, respiration is
unstable and alternates between hypo- and hyperventilation episodes. This respiration,
called “periodic respiration” (Mosso, 1886), disappears when stable sleep
occurs (stage 2). The main hypotheses concerning this periodic ventilation refer to
metabolic control and chemoreceptor responses to levels of PaCO 2 and PaO 2
(Chapman et al., 1988). In stable non-REM sleep, respiration is regular in amplitude
and frequency, although ventilation per minute is lower than during awakening. In
REM sleep, respiration appears irregular with sudden variations in amplitude and
frequency. This irregularity appears to be not modifiable by metabolic factors and,
therefore, it is possibly linked to mechanisms leading to REM expression. The nonhabituation
of the cardiovascular responses would be explained by the absence of an
inhibitory influence on the part of the arousal system that affects the centres regulating
the autonomous response.
3.1.4 EEG RESPONSE
The sleep polygraph continuously records EEG activity, eye movement (EOG) and
muscle tone (EMG). These data are used to classify sleep into various stages, and to
assess times of falling asleep and waking up. Also, sleep variables such as total sleep
time and total time spent in SWS (consisting of sleep stages 3 and 4, the stages of
deep sleep) and in the REM stage (also called dream or paradoxical sleep) can be
assessed on the basis of sleep polygraph recordings. Polygraphic indicators of
responses to individual noise events are changes from a deeper to a less deep sleep
and EEG awakening. Several field studies (Pearsons, Bennett and Fidell, 1973;
Vernet, 1979; Vallet et al., 1983; Hume, Van and Watson, 2003; Basner et al., 2004)
have been conducted regarding noise-induced changes in sleep stage and awakening
using EEG recordings. Transition from a deep stage of sleep to a shallower sleep
stage can be the direct consequence of a nocturnal noise event. Although not perceived
by the sleeper, these transitions modify the sleep architecture and may reduce
the amount of SWS (Carter, 1996; Basner et al., 2004) and the amount and rhythmicity
of REM sleep may be markedly affected (Naitoh, Muzet and Lienhard, 1975;
Thiessen, 1988). In addition to their results from a laboratory study, Basner et al.
(2004) present results from a field study with valid data for 63 subjects (aged 18–65
years) with 15 556 aircraft noise events included in the final analyses. They established
a curve that gives the probability of awakening as a function of L Amax with a
model that assumed a background noise level just prior to the aircraft noise event of
27 dB(A). The L Amax threshold for noise-induced awakenings was found to be about
35 dB(A). Above this threshold the probability of noise-induced awakenings increases
monotonically up to circa 10% when L Amax = 73 dB(A). This is the extra probability
of awakening associated with the aircraft noise event, on top of the probability
of awakening spontaneously in a 90 second interval.
Some arousals provoked by noise events are so intense that they induce awakening.
Frequent awakening leads to sleep fragmentation and overall sleep disturbance. The
noise threshold for awakening is particularly high in deep SWS (stages 3 and 4) while
it is much lower in shallower sleep stages (stages 1 and 2). In REM sleep the awakening
threshold is variable and depends on the significance of the stimulus. Total
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