SLEEP DISORDERED BREATHING
Does Sleep Deprivation Worsen Mild Obstructive Sleep Apnea?
Anup V. Desai, MB BS, PhD, FRACP1,2; Guy Marks, MB BS, PhD, FRACP2,3; Ron Grunstein, MB BS, MD, PhD, FRACP1-4
1Sleep Disorders and Respiratory Failure Unit, Department of Respiratory Medicine, Royal Prince Alfred Hospital; 2Woolcock Institute of Medical
Research; 3Department of Medicine, University of Sydney; 4Sleep Disorders Unit, St. Vincent’s Hospital, Sydney, Australia
Study Objectives: Sleep deprivation is believed to worsen obstructive
sleep apnea (OSA). We assessed the effect of acute sleep deprivation on
polysomnography in a cohort of subjects with mild OSA and a cohort of
subjects without OSA.
Design: Crossover study in which subjects initially had polysomnography
after a normal night’s sleep or after 36 hours of sleep deprivation, followed
by a 2- to 4-week interval, after which subjects were restudied under the
alternate testing condition.
Setting and Participants: 13 subjects with mild OSA and 16 subjects
without OSA were studied in a university teaching hospital sleep laboratory.
Interventions: 36 hours of supervised sleep deprivation.
Measurements: Subjects’ age, body mass index, neck circumference
and Epworth Sleepiness Scale scores were measured; actigraphy and
sleep diaries were used to estimate prior sleep debt before each sleep
study.
Results: Sleep deprivation was found to significantly increase total sleep
INTRODUCTION
OBSTRUCTIVE SLEEP APNEA (OSA) IS VERY COMMON,
AFFECTING APPROXIMATELY 25% OF MIDDLE-AGED MEN.
Most (approximately 60%) of OSA patients have only mild disease (respiratory disturbance index [RDI] 5-15).1,2 Factors that are associated
with acute worsening of OSA include alcohol ingestion or nasal obstruction, and conservative management strategies for OSA often include
alcohol cessation or relief of nasal obstruction.
Sleep deprivation is another factor that may increase OSA severity.
This has been suggested by several studies of sleep-breathing physiology.3-5 Firstly, breathing responses to hypoxia may be decreased after
sleep deprivation5; secondly, sleep deprivation has been shown to have
a depressant effect on upper-airway dilator-muscle activity, which is
important in maintaining upper-airway patency during sleep4; and, finally, sleep deprivation increases rapid eye movement (REM) sleep, where
apneas are more likely to occur.
Some of the earliest work on sleep-disordered breathing commented
on the potential deleterious effect of sleep deprivation on nocturnal
breathing.6,7 This has been further supported by a small amount of published work, showing that sleep deprivation worsens OSA.8-111 In 1981,
Guilleminault and coworkers reported an increase in the mean number
of apneic episodes and a lowering of blood oxygen saturation secondary
to apneic events following acute sleep deprivation of subjects with mild
to moderate OSA.11 However, in this study the numbers were very small
(N = 4).
Disclosure Statement
No significant financial interest/other relationship to disclose.
Submitted for publication May 2003
Accepted for publication August 2003
Address correspondence to: Professor R. Grunstein, E11 Sleep Investigation
Unit, E Block, Royal Prince Alfred Hospital, Missenden Rd, Camperdown,
Sydney, NSW, Australia, 2050; Tel: 02 9515 8630; Fax: 02 9515 7196;
E-mail: [email protected]
SLEEP, Vol. 26, No. 8, 2003
time, sleep efficiency, and rapid eye movement and slow-wave sleep time.
Subjects with OSA showed a lower minimum oxygen saturation after
sleep deprivation. However, subjects did not show a significantly different
respiratory disturbance index, arousal index, or length of the longest
apnea after sleep deprivation.
Conclusions: Acute sleep deprivation did not worsen most OSA parameters as measured by polysomnography. A lower minimum oxygen saturation in mild OSA subjects after sleep deprivation may be important in
patients with significant cardiorespiratory disease. More research is needed to assess whether daytime performance and function (eg, driving,
sleepiness) is more greatly impaired in OSA subjects who are sleep
deprived, compared to normal subjects who are sleep deprived.
Key Words: sleep deprivation, mild obstructive sleep apnea,
polysomnography
Citation: Desai AV; Marks G; Grunstein R. Does sleep deprivation worsen mild obstructive sleep apnea? SLEEP 2003;26(8):1038-41.
More recent work has shown that the loss of 1 night’s sleep results in
a large increase in the RDI of OSA patients.8,9 However, these studies
have compared nocturnal polysomnography with daytime polysomnography after sleep deprivation to assess the effect of sleep deprivation on
breathing during sleep. One study has investigated the effect of chronic
partial sleep deprivation on OSA, revealing an increase in RDI of over
50% and a lowering of the minimum oxygen saturation secondary to
apneic events, but subject numbers were very small (N = 6), and limited
respiratory monitoring was used to measure OSA (Mesam IV, Madaus
Schwarzer Medizin Technik, Munich, Germany, available through
Healthdyne Technologies, Marietta, Georgia).10
Patients often complain that their snoring and sleep apnea appear to
be worsened by sleep loss or sleep deprivation. Given the potential interaction between sleep deprivation and OSA described above, one could
easily imagine a “self-feedback loop,” in which sleep deprivation worsens OSA, which in turn has a negative impact on nocturnal sleep quality and sleep hours, worsening sleep deprivation even further. Hence,
investigating whether the coincidence of OSA and sleep deprivation has
a multiplicative adverse effect on nocturnal breathing disturbances and
daytime function is very important and will have important implications,
for example, with respect to driving.
The aim of this study was to determine the effect of acute sleep deprivation on measured nocturnal sleep and breathing parameters in a cohort
of subjects with mild OSA and a cohort of subjects without OSA.
METHODS
Patients with mild OSA and controls were recruited for this study.
Patients with mild OSA were identified in hospital sleep clinics and then
invited to participate, or alternatively, they were identified through an
audit of recent sleep study results from Royal Prince Alfred Hospital
Sleep Investigation Unit. Controls were recruited from these same
sources and also from advertising among university students.
Twenty-nine subjects (13 with mild OSA, 16 without OSA) underwent polysomnography on 2 occasions: under normal sleeping conditions (baseline testing) and after 36 hours of acute total sleep depriva1038 Does Sleep Deprivation Worsen Mild Obstructive Sleep Apnea?—Desai et al
tion. Subjects were supervised by sleep laboratory staff at all times during their period of sleep deprivation to ensure they did not sleep.
Approximately half of each group (mild OSA and controls) were tested
under baseline conditions first, with the remaining subjects tested under
sleep deprivation conditions first. Generally, both sleep studies were
conducted within 2 to 4 weeks of each other. Age, body mass index, neck
circumference, and Epworth Sleepiness Scale scores were obtained from
the subjects on their first visit. Subjects were instructed to obtain at least
8 hours sleep per night for the 4 nights preceding each occasion of testing to minimize any preexisting sleep debt at the start of a test. Sleep
hours for these 4 nights were also measured objectively using sleep
diaries and actigraphy.
Given the nature of the testing, it was impossible to blind either the
subjects or researchers to the order of testing or to the testing conditions
(baseline or sleep deprivation). However, all the sleep studies were
scored by an experienced technician who was blinded to the patients’
status. The protocol was approved by the Central Sydney Area Health
Service Ethics Committee (RPA zone) and the University of Sydney
Ethics Committee, and informed consent was obtained from each
patient.
Classification of subjects as having OSA or no OSA (ie, control status) was made on the basis of the results of the baseline weekend’s sleep
study. Subjects were regarded as having OSA if their total RDI was at
least 5. Controls had a total RDI less than 5.
Nocturnal Polysomnography
A standard sleep study (polysomnography) setup was used for all subjects. The electroencephalogram placement was according to the 10-20
system with 4 electrodes attached to the scalp (C3, O2, A1 and A2), 2 eye
electrodes (left and right electrooculogram), and 2 submental leads
(electromyography). There were also 2 electrocardiogram leads, 1 near
the right shoulder and a second in the sixth intercostal space on the left
side of the chest. Sensor leads were placed on each leg over the anterior
tibialis for recording leg movements. Breathing was monitored by a
nasal pressure transducer in all studies. Inductive respiratory effort
bands were placed around the chest and abdomen to monitor thoracic
and abdominal wall movement. A position sensor was attached to monitor body position during sleep. A finger probe oximeter continuously
recorded the subjects’ oxygen saturation. Specialized computer software
(Compumedics, Melbourne) was used to acquire, store, and analyze the
collected sleep study data.
Polysomnography Scoring
Sleep stages were scored according to Rechtschaffen and Kales criteria.12 Arousals were scored according to the Atlas Task Force of the
American Sleep Disorders Association.13 For scoring of respiratory
events, thoracic and abdominal bands and nasal pressure were used as
measures of breathing. Apneas and hypopneas were defined as follows:
an apnea involved the cessation of airflow for at least 10 seconds (with
or without a 3% oxygen desaturation or arousal) and a hypopnea
involved a clear reduction (> 20%, compared with the baseline over the
Table 1—Baseline characteristics* of the study groups
Age, y
BMI, kg/m2
Neck circumference, cm
Epworth Sleepiness Scale score
†Sleep time, h
Controls
n, 16
OSA
n, 13
38 ± 14.7
25.5 ± 5.1
38.9 ± 2.5
7 ± 4.2
7.1 ± 0.5
45 ± 14.8
30.3 ± 4.2
41.4 ± 2.6
9 ± 6.0
6.6 ± 0.5
*Data are presented as mean ± SD.
†Sleep time is the average number of hours of sleep per night recorded during the 4 nights
preceding the study.
BMI refers to body mass index.
SLEEP, Vol. 26, No. 8, 2003
preceding 2 minutes) in 1 of the measures of breathing during sleep for
at least 10 seconds in association with at least a 3% oxygen desaturation
or an electroencephalographic arousal (or both).
In addition, snoring or flattening in the nasal pressure trace terminating in an arousal was scored as a subcriterion respiratory event. These
were not included in the total RDI but formed part of the total arousal
index score.
Estimates of Prior Sleep Hours
Actigraphy
Mini-Mitter Actiwatches (AW64 series; Cambridge Neurotechnology
Cambridge U.K/Mini-Mitter, Sunriver, Ore, USA) were used in this
study. Subjects were asked to wear the Actiwatch for the 4 nights and
days prior to their presentation to the sleep laboratory. They were asked
to press the round event marker on the front of the watch at the time of
significant sleep-wake events, such as getting into bed, attempting sleep,
waking in the middle of the night, and waking in the morning.
Sleep Diary
Sleep diaries were sent to subjects prior to their polysomnography.
Subjects were asked to complete the sleep diary each morning for 4
mornings before their sleep laboratory attendance. The sleep diary
sought subjective information about the previous night’s sleep, such as
the estimated time of getting into bed, turning off the light and attempting sleep, any known wake periods during the night, and final time of
awakening and getting up in the morning. Any daytime naps could also
be recorded on the sleep diary.
Using the manufacturer supplied Mini-Mitter software, together with
the sleep diary data, researchers manually marked nighttime sleep onset,
overnight wake periods, morning wake time, and any daytime nap periods on the downloaded actigraphic trace. Total sleep duration was then
accurately estimated using the software’s automatic analysis program.
Statistical Analysis
Differences in preceding sleep hours were assessed with t tests, and
results were expressed as mean differences with 95% confidence intervals. The effect of sleep deprivation on polysomnographic measures in
subjects with and without OSA was evaluated using 2-way analysis of
variance. All interactions were tested and are reported. Pairwise comparisons between levels of each factor were assessed. Effect sizes (differences) with 95% confidence intervals were calculated. P values <.05
were considered statistically significant.
Posthoc power calculations were performed to assess whether this
study was adequate to detect clinically important differences in
polysomnography outcome variables between control and sleepdeprived states in all subjects and within the subgroups. For the outcome
variable total RDI, there was 80% power to detect a difference between
control and sleep-deprived states equal to 3.9 per hour or greater in all
subjects, or equal to 5.8 per hour or greater in the OSA subgroup. The
data analysis was undertaken using the SPSS statistical package 10.0.05
(SPSS Inc., Chicago, Ill, USA).
RESULTS
Table 1 presents the baseline characteristics of the 2 study groups.
Subjects with OSA were more overweight, as indicated by an increased
body mass index and neck circumference. The mean Epworth Sleepiness
Scale Score for both groups was less than 10. Both groups slept less than
8 hours on average for the 4 nights preceding the testing.
There was no difference in average sleep hours during the preceding
4 nights in the subjects prior to the 2 tests (6.7 hours sleep per night prior
to baseline test compared to 6.9 hours sleep prior to sleep deprivation
test; difference 0.3 hours, 95% confidence interval -.006 to 0.6).
1039 Does Sleep Deprivation Worsen Mild Obstructive Sleep Apnea?—Desai et al
Baseline Polysomnography
This study controlled for prior sleep hours before the 2 polysomnograms. All subjects were instructed to obtain at least 8 hours sleep per
night for the 4 nights preceding each occasion of testing, and subjects
also completed a sleep diary and wore actigraphs during this period.
Analysis of these recordings showed that there was no statistically significant difference in the amount of sleep the subjects had prior to their
2 polysomnograms. Hence, differences in polysomnographic measures
between the 2 testing conditions would not be expected to be explained
by differences in sleep debt from the days immediately prior to the subjects’ sleep studies.
Sleep measurement by actigraphy and sleep diary showed that our
subjects were partially sleep deprived preceding the test nights (6.7 to
6.9 hours of sleep per night, on average). This may have limited the ability to detect an effect of acute sleep deprivation. However, this level of
chronic partial sleep deprivation is very frequent in society.14,15 A major
strength of this study is that we requested subjects avoid sleep deprivation, measured prior sleep hours by 2 different methods, and found this
not to differ significantly between groups or testing conditions.
An attempt was made to reduce clinic selection biases in the control
group by recruiting university students via an advertisement. However,
part of the control group was still recruited from patients seen at hospital sleep clinics or from patients who had had negative laboratory sleep
studies. These ‘controls’ are therefore unlikely to be totally disease free.
Table 2 shows that although the total RDI was less than 5 in the control
group’s baseline polysomnography, their mean REM RDI was 8. As a
consequence of selection biases, the presence of simple snoring or mild
REM OSA in the control population may have biased the study against
finding a difference between the 2 study groups. However, these selection biases would not be expected to affect the response to sleep deprivation in the study subjects. Because a single technician scored all sleep
studies, differences in scoring between studies would be very small,
eliminating this potential bias.
In this study, subjects with OSA showed a lower minimum oxygen
saturation after sleep deprivation. A reduction in minimum oxygen saturation in OSA patients after sleep deprivation has been noted previously.11 This is likely to be of marginal clinical significance for healthy
Table 2 presents the baseline polysomnography results of the 2 study
groups. Subjects with OSA had a mean total RDI of 12, compared to a
mean total RDI of 2 in the control group. Similarly, there was a difference between the groups in other measures of sleep-disordered breathing, especially non-REM RDI, arousal index, and minimum oxygen saturation. Based on these polysomnographic results, OSA subjects had
mild disease, whereas controls, by definition, had no OSA.
Effect of Sleep Deprivation on Polysomnography
Table 2 illustrates that, after sleep deprivation, subjects slept longer,
had greater sleep efficiency, and increased amounts of REM and slowwave sleep. However, RDI, arousal index, and the length of the longest
apnea were not significantly different. The effect of sleep deprivation on
minimum oxygen saturation differed according to OSA status. Subjects
with OSA showed a lower minimum oxygen saturation after sleep deprivation, whereas control subjects did not.
DISCUSSION
The aim of this study was to determine the effect of acute sleep deprivation on measured nocturnal sleep and breathing parameters in a cohort
of subjects with mild OSA and a cohort of subjects without OSA. Sleep
deprivation was found to significantly increase total sleep time, sleep
efficiency, and REM and slow-wave sleep time. Subjects did not show a
significantly different RDI, arousal index, or length of the longest apnea
after sleep deprivation. However, subjects with OSA showed a lower
minimum oxygen saturation after sleep deprivation.
Because the order of the sleep studies was balanced, with approximately half of the subjects of each group (mild OSA and controls) tested under baseline conditions first, with the remaining subjects tested
under sleep deprivation conditions first, the differences in polysomnographic outcomes due to sleep deprivation could not be due to first-night
effects (subjects sleeping worse on their first weekend of testing because
of unfamiliarity).
Table 2—Polysomnographic data at baseline and after sleep deprivation.
Variable
Subjects
Total
N, 29
Sleep time,
min
Total
REM
S1
S2
SWS
SE, %
RDI
Total
During
REM
During
NREM
AI
SRE
Longest
apnea, s
Min O2
sat, %
Interaction*
OSA
n, 13
Control
n, 16
Baseline†
Difference‡
P value
Baseline†
Difference‡
P value
Baseline†
Difference‡
P value
344 (50.6)
62 (24.4)
22 (12.2)
195 (28.7)
63 (21.5)
82 (11.6)
53 (15 to 91)
17 (4 to 30)
-8 (-13 to -2)
15 (-9 to 40)
19 (7 to 32)
9 (6 to 13)
0.01
0.01
0.01
0.20
0.01
0.00
343 (50.3)
62 (24.3)
22 (12.2)
194 (28.6)
63 (21.4)
81 (11.6)
51 (-6 to 107)
22 (3 to 41)
-4 (-12 to 4)
19 (-17 to 55)
17 (-3 to 36)
11 (5 to 16)
0.08
0.02
0.28
0.29
0.09
0.00
345 (50.3)
63 (24.3)
23 (12.2)
196 (28.6)
63 (21.4)
82 (11.6)
55 (4-106)
12 (-6 to 29)
-11 (-18 to -4)
12 (-20 to 44)
22 (5 to 40)
8 (3 to 13)
.04
0.176
0.00
0.449
0.01
0.00
0.91
0.40
0.22
0.78
0.65
0.41
7 (5.4)
1.0 (-2 to 4)
0.50
12 (1.4)
0.5 (-4 to 5)
0.79
2 (5.1)
1 (-2 to 5)
0.47
0.77
14 (12.8)
-1 (-6 to 4)
0.62
20 (12.7)
-0.2 (-7 to 7)
0.95
8 (12.7)
-2 (-9 to 4)
0.51
0.69
5 (6.1)
13 (6.1)
2 (1.4)
1 (-2 to 4)
-2 (-5 to 1)
-0.4 (-0.9 to 0.2)
0.33
0.14
0.23
10 (6.1)
17 (6.0)
2 (1.4)
0.6 (-4 to 5)
-3 (-7 to 2)
-0.3 (-1.2 to 0.6)
0.78
0.24
0.45
1 (6.1)
9 (6.0)
1 (1.4)
2 (-2 to 6)
-2 (-6 to 2)
-0.4 (-1.2 to 0.4)
0.25
0.37
0.34
0.58
0.78
0.94
23 (16.4)
0.0 (-7 to 7)
1.0
29 (18.3)
0.6 (-11 to 12)
0.91
17 (16.6)
-0.6 (-10 to 9)
0.90
0.87
91 (2.3)
-1.1 (-2.4 to -0.02)
0.047
89 (2.6)
-2.5 (-4.3 to -0.7)
0.01
92 (2.4)
0.1 (-1.3 to 1.6)
0.85
0.03
*Interaction, significance test on the difference in the effect of sleep deprivation between patients with mild OSA and control subjects.
†Data are presented as mean (SD).
‡Data, presented as mean (95% CI), are the difference between baseline and sleep deprivation conditions.
OSA refers to obstructive sleep apnea; REM, rapid eye movement sleep; S1, stage 1 sleep; S2, stage 2 sleep; SE, sleep efficiency; RDI, respiratory disturbance index (the number of apneas
and hypopneas per hour of sleep); NREM, non-rapid eye movement sleep; AI, arousal index (the number of arousals per hour of sleep); SRE, the number of subcriterion respiratory events
per hour of sleep; Min O2 sat, the minimum oxygen saturation.
SLEEP, Vol. 26, No. 8, 2003
1040 Does Sleep Deprivation Worsen Mild Obstructive Sleep Apnea?—Desai et al
patients but may be more relevant in patients with significant cardiorespiratory disease.
This study did not show significant differences in RDI, arousal index,
and length of the longest apnea after sleep deprivation in the subjects
with OSA. This is in contrast to previous studies with small patient numbers,10,11 which have utilized short periods of daytime polysomnography
after 1 night without sleep8,9 or that have used limited respiratory monitoring to measure OSA.10 Although this study has essentially shown that
acute sleep deprivation does not worsen OSA severity, the effect of
chronic sleep deprivation has not been examined and may differ from
that of acute sleep deprivation.
This study showed that normal subjects do not develop OSA acutely
as a result of sleep deprivation. Several studies of sleep-breathing physiology3-5 suggest plausible physiologic reasons why this might occur.
However, other studies suggest sleep fragmentation has more profound
effects on upper-airway collapsibility16 and ventilatory drive17 than total
sleep deprivation.
This study was adequately powered to detect clinically important differences in the outcome variables after sleep deprivation (eg, there was
an 80% power to detect a difference in total RDI of 5.8 per hour or
greater in the OSA subgroup). Smaller differences due to sleep deprivation are unlikely to have been detected in this study. A larger study would
be needed to detect smaller differences, especially with respect to the
interactive effects of sleep deprivation between subjects with and without OSA.
Subjects with OSA in this study had relatively mild disease, with an
average RDI of 12.1 (range, 9.2-15.0). Importantly, these subjects in
general did not report excessive daytime sleepiness, as measured by the
group’s mean Epworth Sleepiness Scale score (9 ± 6.0). Hence our study
subjects with OSA are more representative of those patients with OSA
alone (snoring, nocturnal apneas, obstructive respiratory events on
polysomnography), rather than those with sleep apnea syndrome (clinical combination of OSA and excessive daytime sleepiness).18 It is not
known whether these 2 different groups of OSA patients differ in other
respects, such as in their response to sleep deprivation. It also is
unknown as to whether the results of this study can be extrapolated to
subjects with moderate or severe OSA.
Larger studies with a broader range of OSA subjects that address this
same research question are needed to further our knowledge of the effect
of sleep deprivation on OSA. These studies should also examine whether
daytime performance and function (eg, driving, sleepiness) are more
severely impaired in OSA subjects who are sleep deprived, compared to
normal subjects who are sleep deprived. This will have important clinical implications, especially with regard to advice about sleeping habits
for high-risk groups of OSA patients (eg, commercial drivers).
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Stoohs RA, Dement WC. Snoring and sleep-related breathing abnormality during partial
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ACKNOWLEDGEMENTS
This study and the researchers were supported by funds from the
Australian National Health and Medical Research Council, Community
Health and Tuberculosis Australia Association, NSW Motor Vehicle
Accidents Authority, and Sydney’s St. Vincent’s Hospital.
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1041 Does Sleep Deprivation Worsen Mild Obstructive Sleep Apnea?—Desai et al