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The effects of body temperature and oxygen consumption on sleep architecture


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Jordan, Joanne Elizabeth (1994) The effects of body temperature and oxygen consumption on sleep architecture. PhD thesis, University of Tasmania.

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Two related theories have had a substantial impact on our
understanding of the nature and function of sleep. These are the
energy conservation and restorative theories of sleep. Both theories
predict an increase in both slow wave sleep (sws) and sleep duration
following increased energy expenditure. These predictions form the
background to the empirical work of this thesis, and it is the effect of
wake-period metabolism on both sleep metabolism and architecture
that holds the main research focus.
Three studies were designed to evaluate the effects of either
metabolic rate (MR), body temperature (Tb), or both, on sleep
architecture, in particular sws. The first and second studies imposed
variations in waking activity in order to assess the effects of MR and
Tb on sleep architecture. The first study actively increased MR by
physical exercise, while the second study used passive heating in a
warm bath. The third study compared T b , MR and sleep in endurance
athletes and sedentary individuals.
In the first study, the first sleep cycle of 10 young fit subjects (mean
age = 21.8 years) was assessed after a 19km run, either immediately
before bedtime or a few hours before retirement. There were four
conditions: a no exercise condition; a late afternoon exercise session
with evening meal; a late afternoon exercise session without evening
meal; and a late evening exercise session with an evening meal. The
results showed no evidence of an exercise-induced sws effect, and
found that exercise transiently increased wake-period MR which
returned to control levels by bedtime. Furthermore, there was some
evidence to suggest that a rise in wake-period energy expenditure
may have a negative effect upon sleep properties. The second study investigated the effect of passive heating on sleep
architecture by using a method similar to that described by Horne
and Staff (1983), Sewitch (1987) and Berger and Phillips (1988a,b). It also tested the hypotheses that sws levels increase following
heating due to either a compensatory drop in Tb at sleep onset
(Sewitch, 1987), or a sustained elevation in absolute Tb at sleep
onset, and during sleep (Berger & Phillips, 1988; Berger, Palca,
Walker & Phillips, 1988). Five healthy young male subjects (mean
age = 20.4 years) were passively heated in a 42-43 0c warm bath to
induce elevated Tb and MR. A repeated measures design with two
conditions was employed. These conditions included a control (no
passive heating), and a passive heating condition in the late
afternoon. Rectal temperature (Tre ) was monitored from the early
afternoon until the awakening period on the following morning.
Metabolic rate was recorded for 20 minutes prior to, and immediately
after the passive heating, and then across the sleep period. Sleep
recordings also were monitored over the night. Results showed that
passive heating significantly increased T re, MR and sws levels. Rectal
temperature increases were sustained into, and across the sleep
period, whereas MR increases were only transient and did not
continue into the sleep period. sws levels were significantly elevated
in the first 150 minutes of sleep. The direct relationship of Tb to sws
supported the theory proposed by Berger and Phillips (1988a,b). The third and final study determined whether the characteristically
higher sws levels and longer sleep durations of endurance athletes
(Trinder, Paxton, Montgomery & Fraser, 1985) may be attributable
to the effect of Tb on sleep. It was designed to assess the role of Tb on
sleep by comparing the laboratory sleep of endurance athletes and
sedentary individuals with Tb at sleep onset held constant between
the two groups based upon evidence from another study (Hedges,
1989) that showed higher average Tres and earlier sleep onset times in
athletes compared to sedentary individuals. It was thus considered
that the higher Tres reported for athletes in this study may have been
a consequence of their earlier sleep onset times. In the final study
eight male endurance athletes (mean age = 21.5 years) and eight
male non-athletes (mean age = 22.6 years) were compared under
conditions of no-exercise. The results showed sws levels to be higher and sleep duration longer
in the endurance athletes as compared to sedentary subjects, despite
Tb at sleep onset being the same for the two groups, as a result of
sleep onset being held constant. The results suggest elevated Tb at
sleep onset may not be the mechanism causing particular sleep
characteristics of endurance athletes. Rather it is proposed that the
sleep properties of endurance athletes are due to a phase delay of the
circadian oscillator, which in this group is achieved by an advance of
the sleep-wake cycle (earlier usual sleep onset time).
In conclusion, it is argued that there is a relationship between
metabolism and sleep architecture where sws can be facilitated by
either (a) high metabolism during sleep onset and the early part of
sleep; or (b) the phase angle in the circadian temperature rhythm at
sleep onset, or both.

Item Type: Thesis (PhD)
Keywords: Sleep, Sleep, Body temperature, Oxygen
Copyright Holders: The Author
Copyright Information:

Copyright 1991 the Author - The University is continuing to endeavour to trace the copyright
owner(s) and in the meantime this item has been reproduced here in good faith. We
would be pleased to hear from the copyright owner(s).

Additional Information:

Thesis (Ph.D.)--University of Tasmania, 1994. Includes bibliographical references (leaves 147-176)

Date Deposited: 19 Dec 2014 02:32
Last Modified: 01 Dec 2016 05:07
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