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wake and sleep (typically maintained in a 2:1 ratio) deviate from the normal
24-h day (e.g., 20- or 28-h days), such that the subject's biological clock is
unable to entrain to this schedule. The subject experiences two distinct
influences simultaneously—the schedule of predetermined sleep and waking
times representing the homeostatic system and the rhythm of the subject's
unsynchronized (i.e., free-running) circadian system. Neurobehavioral
functions are assayed during the waking periods. By folding the data over
either the free-running circadian rhythm or the imposed sleep-wake cycle,
the other component can be balanced out. Thus, the separate effects of cir-
cadian rhythms and wake duration (i.e., homeostatic drive for sleep) on neu-
robehavioral variables can be assessed.
Forced desynchrony studies have found that both the circadian and
homeostatic processes influence sleepiness and performance. 26,27 The inter-
action of the two systems is oppositional during diurnal wake periods (from
approximately 0700 h until 2300 h), such that a relatively stable level of
alertness and performance can be maintained throughout the day. 89,90 This
explains why in many studies of alertness and performance, very little tem-
poral variation is observed during the waking portion of a normal day, espe-
cially when there is no sleep deprivation 24 ( Fig. 7.2 ) .
The interaction of the homeostatic and circadian processes is believed to
be nonlinear (i.e., nonadditive). 90,92 Therefore, the separation of circadian
and homeostatic influences on neurobehavioral variables presents a concep-
tual and mathematical challenge, and it is difficult, if not impossible, to quan-
tify the relative importance of the two influences on neurobehavioral
functions. Moreover, their relative contributions may vary across different
experimental conditions 55,90 and among subjects. 93
5. INTERINDIVIDUAL VARIABILITY IN CIRCADIAN
RHYTHMS
Healthy adults show interindividual differences in the free-running cir-
cadian period (tau), 94-98 which shows robust stability within individuals. 97
Subjects also demonstrate interindividual differences in circadian ampli-
tude 58,99 and circadian phase 57,58,95,99 which are in part due to genetic influ-
ences. 99 There are several standardized methods for assessing interindividual
differences in circadian rhythms. One newer method, using molecular tech-
niques, can determine individual differences in tau, amplitude, and phase-
resetting, which relate to diurnal phase preference, using cultured human
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