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An Experimental Investigation of the Effects of Acute Sleep deprivation

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Behavior Therapy 40 (2009) 239 – 250
An Experimental Investigation of the Effects of Acute Sleep
Deprivation on Panic-Relevant Biological Challenge Responding
Kimberly A. Babson
Matthew T. Feldner
Casey D. Trainor
Rose C. Smith
University of Arkansas
Prospective research indicates sleep deprivation potentiates
anxiety development, yet relatively little research has
examined the effects of sleep deprivation in terms of specific
types of anxiety. The current study tested the association
between acute sleep deprivation and panic-relevant biological challenge responding among nonclinical participants.
One hundred and two participants were randomly assigned
to either an experimental (acute sleep deprivation) or
control (no sleep deprivation) group. The day prior to and
following the experimental (sleep) manipulation, participants completed a 5-minute 10% carbon dioxide–enriched
air laboratory-based biological challenge. As predicted,
sleep deprivation increased anxious and fearful responding
to the challenge. Findings suggest sleep deprivation may be
an important factor to consider in models of panic
development. There are several areas in this general domain
that warrant additional investigation.
This project also was supported, in part, by a National Institute
of Mental Health National Research Service Award (F31
MH081402) awarded to Kimberly Babson and a Centers for
Disease Control and Prevention contract (U49 CE001248) with Dr.
Address correspondence either to Kimberly A. Babson,
University of Arkansas, 216 Memorial Hall, Fayetteville, AR
72701 (e-mail: [email protected]); or Matthew T. Feldner,
University of Arkansas, Memorial Hall, Fayetteville, AR 72701
(e-mail: [email protected]).
© 2008 Association for Behavioral and Cognitive Therapies. Published by
Elsevier Ltd. All rights reserved.
SLEEP DEPRIVATION IS ONE of the most common health
problems in the United States, with as many as
70 million people reporting sleep deprivation that
results in an estimated $65 billion in health care
costs and lost productivity (U.S. Surgeon General,
2004). Sleep deprivation is associated with multiple
specific sleep disorders. For instance, primary
insomnia is defined by problems falling and staying
asleep or nonrestorative sleep that persists longer
than 1 month and results in functional impairment
(American Psychiatric Association [APA], 2000;
American Sleep Disorders Association, 1990).
Insomnia is the most common sleep problem (cf.
hypersomnia), with prevalence rates ranging from
30% to 35% (Breslau, Roth, Rosenthal, &
Andreski, 1996). There are high comorbidity rates
between chronic (i.e., greater than 6 months) sleep
problems and several types of psychopathology,
including major depression, anxiety disorders, and
substance use disorders (Eaton & Kessler, 1985;
Reiger et al., 1984). Specifically, of those with
chronic sleep problems, 40% met criteria for at
least one psychiatric disorder (Drake, Roehrs, &
Roth, 2003). These data have led researchers to
focus on the effects of sleep deprivation to better
understand its role in the development and maintenance of mental disorders.
Emerging research suggests sleep deprivation
potentiates the development of anxiety. Longitudinal evidence indicates that sleep deprivation is associated with an increased probability of developing
an anxiety disorder (Ford & Kamerow, 1989).
Indeed, sleep problems in childhood and adolescence are related to elevated anxiety symptoms in
adulthood (Gregory, Eley, O'Connor, & Plomin,
babson et al.
2004; Gregory & O'Connor, 2002; Gregory et al.,
2005). For instance, Gregory and colleagues (2005)
examined the relation between persistent sleep
problems in childhood and the development of
anxiety and/or depression in adulthood in a recent
prospective longitudinal study. Participants were
1,037 children who were assessed approximately
every 2 years from age 3 through 26 years. Persistent
sleep problems were defined as parent reports of
child sleep problems during age 5 and/or 7 years and
also at age 9 years. Anxiety and depression were
measured at ages 21 and 26 years with the
Diagnostic Interview Schedule (Robbins, Cottler,
Bucholz, & Compton, 1995). Significantly more
children with than without persistent sleep problems developed anxiety disorders by adulthood
(46% and 33%, respectively). There was not a significant relation between persistent childhood sleep
problems and adult depression. It is important to
note, this line of research does not speak to causal
patterns. In fact, research has suggested a bidirectional relation between sleep problems and
anxiety (Ohayon & Roth, 2003). Although longitudinal research has linked sleep deprivation and
the development of anxiety broadly, the role of sleep
deprivation in specific types of anxiety remains
relatively understudied.
Panic spectrum problems constitute one specific
type of anxiety-related psychopathology that may
be affected by sleep deprivation. Indeed, contemporary work on sleep deprivation and panic development suggest at least two possible avenues by
which sleep deprivation may potentiate panic development. First, sleep deprivation increases basal
levels of anxiety (Sagaspe, Sanchez-Ortuno, &
Charles, 2006) and bodily arousal (Bonnet &
Donna, 2006). The co-occurrence of these two
factors (even in the absence of a panic attack) likely
results in conditioning of anxious responding to
bodily arousal. Second, elevations in basal anxiety
resulting from sleep deprivation likely potentiate
panic attacks, as such anxiety strongly predicts the
occurrence of a panic attack (Coplan et al., 1998;
Ehlers et al., 1986). Sleep-deprived individuals may
be prone to experience panic-related fear along
with bodily arousal, further increasing the conditioning of fear and anxiety to bodily arousal. The
pairing of anxiety and fear with bodily arousal
likely results in interoceptive cues becoming conditioned stimuli that elicit subsequent anxiety and
fear characterized by autonomic arousal, avoidance, and cognitive misinterpretation of bodily
arousal (i.e., catastrophic misinterpretation). These
conditioned responses to bodily arousal are of
central importance to theories of the development
of panic disorder (Barlow, 2002; Bouton, Mineka,
& Barlow, 2001; Clark, 1986; Clark & Ehlers,
Despite the theoretical relevance of sleep deprivation to panic phenomena, the relation between sleep
deprivation and panic has been the focus of limited
empirical investigation. This is particularly noteworthy as sleep complaints are elevated among
persons with panic problems (Babson, Feldner,
Sachs-Ericsson, Schmidt, & Zvolensky, 2008). As
many as 67% of those with panic disorder (PD)
experience clinically significant sleep problems (Mellmann & Uhde, 1990) and 59% of persons with PD
without comorbid depression complain of problems
sleeping (Overbeek, van Diest, Schruers, Kruizinga, &
Griez, 2005). Similarly, 68% of persons with PD
report difficulties falling asleep and 77% report
disturbed and restless sleep (Sheehan, Ballenger, &
Jacobson, 1980). Research in this area has primarily
focused on the relation between PD and specific
parameters of sleep architecture (e.g., durations of
rapid eye movement and slow wave sleep; Lauer &
Krieg, 1992; Mellman & Uhde, 1989; Stein, Enns, &
Kryger, 1993). Generally, this research has suggested
there are relatively few reliable differences in sleep
architecture between persons with and without panic
problems (Stein et al., 1993; Uhde, Roy-Byrne, &
Gillin, 1984). Little investigation has focused on the
effects of sleep deprivation on panic-relevant responding. The only study in this domain (Roy-Byrne, Uhde,
& Post, 1986) examined the effects of one night of
sleep deprivation on responding to a panic-relevant
biological challenge among 12 patients with PD, 10
patients with major depression, and 10 nonclinical
volunteers. During the night of sleep deprivation,
ratings of anxiety and depression were obtained via
patient self-report and nurse observation ratings.
Researchers then used the means of these ratings to
separate PD patients into two subgroups. Specifically,
the “worsening group” showed an increase in mean
self-reported and nurse ratings of anxiety and
depression compared to the control group. In
contrast, “improvers” were individuals with PD that
demonstrated at least a 1-point decrease in selfreported and nurse ratings of anxiety and depression
throughout the night of sleep deprivation. Following
acute sleep deprivation, participants completed a 3minute voluntary hyperventilation challenge. The
well-established hyperventilation procedure was utilized to index the effects of sleep deprivation on panicrelevant responding (see Rapee, 1995; Zvolensky &
Eifert, 2000). The worsening subgroup of participants
with PD (58%) experienced a significant increase in
overall (self and nurse-rated) anxiety levels compared
to the control group. Moreover, 25% of this PD
subgroup reported experiencing a panic attack
following sleep deprivation. These findings were
sleep deprivation and biological challenge responding
specific to this subgroup, as the anxiety ratings and
panic attack frequency for the rest of the PD group
were not different from that of controls. These initial
data suggest that sleep deprivation may potentiate
panic. Indeed, acute sleep deprivation (i.e., 36-hour
deprivation period) appears to increase anxiety
among healthy nonclinical participants (Sagaspe
et al., 2006). Thus, given evidence suggesting relatively
elevated basal levels of anxiety strongly predict greater
anxious and fearful responding to bodily arousal
elicited via panic-relevant biological challenges
(Coplan et al., 1998; Ehlers et al., 1986; Liebowitz
et al., 1984), it is likely that acute sleep deprivation will
potentiate anxious and fearful responding to panicrelevant increases in bodily arousal.
The current study extended research focused on
the panic-relevant effects of acute sleep deprivation
in several novel and significant ways. First, although
the study by Roy-Byrne and colleagues (1986) was a
commendable first step in this research domain, it
may have been insufficiently powered to detect
effects of acute sleep deprivation on responding to
biological challenge. Second, histories of psychopathology can confound results of laboratory-based
studies examining the role of risk-related processes
in psychopathology-relevant responding (Zvolensky, Lejuez, Stuart, & Curtin, 2001), and therefore participants were excluded on the basis of such
histories in the current study. Third, the absence of a
baseline assessment of response to biological
challenge makes it difficult to interpret postmanipulation response patterns. Therefore, the current
study extended the laboratory design to include a
multimodal assessment of panic-relevant responding both pre- and post-sleep manipulation. Fourth,
the absence of a no-sleep deprivation control condition did not allow for drawing conclusions regarding differences in anxious and fearful responding
specific to the effects of acute sleep deprivation. For
this reason, the current study included a no-sleep
deprivation control group. Finally, the current study
utilized the well-established CO2 biological challenge procedure (see Rassovsky & Kushner, 2003),
which elicits greater panic-relevant responding than
the hyperventilation procedure (Rapee, Brown,
Antony, & Barlow, 1992) and therefore likely increases variability in elicited anxiety and panic
symptoms. There were several other advantages to
using a 10% CO2-enriched air biological challenge,
including its ability to reliably produce abrupt
increases in psychological and autonomic responses
comparable to those that are central to learning
theories of panic (Bouton et al., 2001) and the ability
to safely (Prenoveau, Forsyth, Kelly, & Barrios,
2006) and carefully control its administration (i.e.,
onset, timing, dose, and duration) via an automated
delivery system (see Lejuez, Forsyth, & Eifert, 1998,
for a detailed description). Finally, anxious responding to CO2-enriched air biological challenge procedures prospectively predicts panic onset among
young adults (Schmidt & Zvolensky, 2007), suggesting that such responding may mark vulnerability to the development of panic disorder.
It was hypothesized that acute sleep deprivation,
relative to no sleep deprivation, would increase baseline anticipatory anxious arousal (i.e., self-reported
anxiety prior to the post-sleep deprivation CO2 challenge). Furthermore, it was hypothesized that sleep
deprivation, as compared to no sleep deprivation,
would increase panic-relevant responding (i.e., greater
self-reported anxiety and more intense panic symptoms) elicited by the CO2 challenge procedure.
One hundred and two (44 females) adults (Mage =
23.19 years, SD = 8.2) were recruited via fliers and
announcements within the University of Arkansas
and the local Northwest Arkansas community. Of
this original sample, 91 completed all portions of the
protocol. Of this sample of 91, four were removed
due to lost data. Overall, a final sample of 87 (36
female) adults (Mage = 23.41 years, SD = 8.5) completed all portions of the experimental protocol and
was utilized in all analyses. Participants lost to
attrition did not differ from those retained in the
study on any of the variables examined in the
current study, including group assignment. Please
see Table 1 for group demographic information.
Inclusion criteria included age of at least 18 years.
Participants were excluded based on evidence of: (a) a
lifetime history of Axis I psychopathology, including
panic attacks or psychotropic medication use; (b) a
lifetime history of a sleep disorder; (c) a history of
significant medical illness, such as cardiovascular,
endocrine, pulmonary (including asthma), and gastrointestinal illness; (d) limited mental competency and
the inability to give informed, voluntary, written
consent to participate; (e) pregnancy; and (f) suicidality. Participants reporting current Axis I psychopathology, sleep disorder, or suicidality were given
referral information as legally and clinically indicated.
Histories of Axis I diagnoses, past and present
treatment history, and medication use were identified
with the Structured Clinical Interview for DSM-IVNon-Patient Version (First, Spitzer, Gibbon, &
Williams, 1995). Medical screening was conducted
using a structured medical screening interview used
successfully in our prior biological challenge work
(e.g., Feldner, Zvolensky, Eifert, & Spira, 2003;
Feldner, Zvolensky, Stickle, Bonn-Miller, & Leen-
babson et al.
Table 1
Descriptive Data for Demographic Variables and Day 1 and Day 2
Responding as a Function of Group
Education Completed
High school
Two-year college
Partial four-year
Four-year college
Partial graduate
Complete graduate
Smoking Status
Manipulation Checks
Sleep between day 1
and day 2
Change in stimulant use
Nicotine use
Day 1
Baseline SUDs
Post-challenge SUDs
Panic Attack Symptoms
Day 2
Baseline SUDs
Post-challenge SUDs
Panic Attack Symptoms
Experimental M
or n (SD or %)
Control M
or n (SD or %)
19 (43.2%)
21.75 (6.44)
17 (39.5%)
25.11 (9.99)
34 (77.3%)
1 (2.3%)
0 (0%)
9 (20.5%)
33 (76.7%)
1 (2.3%)
0 (0%)
9 (20.9%)
2 (4.5%)
1 (2.3%)
40 (90.9%)
3 (7%)
1 (2.3%)
34 (79.1%)
2 (4.7%)
2 (4.7%)
1 (2.3%)
11 (24.4%)
0.14 (0.78)
7.74 (1.1)⁎
0 (0)
1.1 (2.64)
0 (0)
0.86 (2.74)
0.77 (1.30)
2.04 (1.77)
0.74 (1.65)
2.09 (2.30)
1.52 (1.54)
2.96 (1.93)
1.25 (1.32)
2.76 (1.92)
1.18 (1.87)
2.93 (2.12)
.44 (1.31)⁎
1.74 (1.94)⁎
2.05 (1.94)
3.27 (2.02)
1.01 (1.30)⁎
2.38 (1.63)⁎
Note: N = 87; n for gender reflects women and for smoking status
reflects smokers; SUDS = Subjective Units of Distress Scale
(Wolpe, 1958); sleep between day 1 and day 2 measured in
hours; nicotine use measured via cigarettes smoked.
* = significant difference between group means.
Feldner, 2006) to identify current and/or past history
of chronic physical health conditions. Thirteen
individuals responding to recruitment efforts were
excluded due to positive histories of a medical
condition, 14 were excluded due to current sleep
problems, including the use of prescription sleep
medications, and 54 individuals were excluded on
the basis of other exclusionary criteria.
Structured Clinical Interview for DSM-IV-NonPatient Version (SCID-IV). Lifetime and current
axis I psychopathology and psychotropic medica-
tion use were indexed using the SCID-IV (First
et al., 1995). This instrument also was used to
assess the presence of suicidality and nonclinical
panic attack history. Adequate reliability of the
SCID has been demonstrated (Spitzer, Williams,
Gibbon, & First, 1989). The SCID-IV was administered to all participants by the first author. Training
in SCID-IV administration was conducted by the
second author until mastery of the interview was
demonstrated. Thereafter, six administrations were
audiotaped, and diagnoses were compared with the
second author. The first author began independently administering the interview subsequent to
reaching 100% diagnostic agreement with the
second author. Also, ongoing supervision to correct
for rater drift was conducted throughout the
project. Upon completion of the study, a random
selection of 10% of the administrations were
checked by the third author. Interrater agreement
was 100%.
Sleep Disorders Questionnaire (SDQ). The SDQ
(Violani, Devoto, Lucidi, Lombardo, & Bruni,
2000) is a brief sleep problems questionnaire, consisting of 18 questions that allow for evaluation of
sleep problems based on DSM-IV (APA, 1994)
criteria. Questions index excessive sleepiness, sleep
apnea, parasomnias, and duration of sleep problems. Sample questions include: “In the last
30 days did you suffer from 1 or more of the following problems: did you take more than a half
hour to fall asleep?” and “Did you have problems
staying awake during the day?” Responses are
given as “yes” or “no” answers. Questions focus on
sleeping patterns within the last month as well as
current sleeping habits. Adequate convergent validity has been demonstrated via correlations with
scores on the Pittsburg Sleep Quality Index, a well
established measure of sleep problems (Cohen's
kappa = .78; Violani et al., 2004). In the current
study, the SDQ was utilized to identify, and exclude,
participants endorsing a history of sleep disorders.
Positive and Negative Affect Schedule (PANAS).
The PANAS is a 20-item measure in which respondents indicate on a 5-point Likert-type scale (1 =
very slightly or not at all to 5 = extremely) the extent
to which they generally feel different feelings and
emotions (e.g., “Hostile”). The PANAS is a wellestablished mood measure commonly used in
psychopathology research (Watson, Clark, & Tellegen, 1988). Factor analysis indicates that it assesses
two global dimensions of affect: negative and positive. Both subscales of the PANAS have demonstrated good convergent and discriminant validity.
Additionally, both the negative and positive affect
scales of the PANAS have demonstrated high levels
of internal consistency (range of alpha coefficients:
sleep deprivation and biological challenge responding
.83 to .90 and .85 to .93, respectively). A large body
of literature supports the validity of the PANAS (see
Watson, 2000). In the current study, the negative
affect subscale, which evidenced good internal
consistency (alpha = .75), was utilized to compare
groups on baseline negative affectivity.
Sleep Anticipatory Anxiety Questionnaire (SAAQ).
The SAAQ (Kuo, Racioppo, Bootzin, & Shoham,
1994) is a 10-item questionnaire on which respondents indicate their anxiety about sleep on a 4point Likert-type scale (1 = strongly disagree to 4 =
strongly agree). Example questions include: “My
muscles are tense,” “My heart is beating rapidly,”
and “I worry I will not be able to sleep” (Bootzin,
Shoham, & Kuo, 1994). Two scores are obtained in
the administration of the SAAQ: a total score
measuring overall anxiety about sleep and a subscore measuring self-reports of cognitive and
physical arousal while trying to fall asleep at night.
The SAAQ has demonstrated adequate internal
consistency (Cronbach's alpha = .83 in a student
sample and .83 for individuals with sleep problems;
Bootzin et al., 1994). In line with these data, within
the current study good internal consistency was
demonstrated (alpha = .86). Moreover, scores on the
SAAQ are negatively correlated with self-efficacy
about sleep (Kuo et al., 1994), and it reliably
differentiates between those with and without sleep
problems (Bootzin et al., 1994). The SAAQ was
used in the current study to compare groups in terms
of sleep anticipatory anxiety as a check on random
Subjective Units of Distress Scale (SUDS). The
SUDS (Wolpe, 1958) was used to measure selfreported anxiety elicited by the CO2 challenge.
Ratings were made on an 8-point Likert-type scale
(0 = no anxiety to 8 = extreme anxiety). This measure
is well-established in biological challenge studies
(e.g., Forsyth, Eifert, & Canna, 2000; Karekla,
Forsyth, & Kelly, 2004; Kelly, Forsyth, & Karekla,
2006; Rapee et al., 1992; Schmidt & Zvolensky,
Diagnostic Symptom Questionnaire (DSQ). The
DSQ (Sanderson, Rapee, & Barlow, 1988, 1989) is
a common measure used in challenge experiments
(Zinbarg, Brown, Barlow, & Rapee, 2001; Zvolensky, Lejuez, & Eifert, 1998) to index panic attack
symptoms elicited by a biological challenge procedure. Participants rate each of 13 panic symptoms
on a 9-point Likert-type scale (0 = not at all to 8 =
very strongly felt). Although the DSQ was developed based on the DSM-III-R (APA, 1987) diagnostic criteria for panic attacks, these criteria have
not been substantially altered for DSM-IV. Consistent with past biological challenge studies (Feldner,
Vujanovic, Gibson, & Zvolensky, 2008; Forsyth
et al., 2000; Schmidt, Forsyth, Santiago, & Trakowski, 2002; Zvolensky, Feldner, Leen-Feldner, &
McLeish, 2005), two composite scores were created
which indexed the intensity of cognitive (e.g., fear of
going crazy) and physical (e.g., breathlessness or
smothering sensations) panic symptoms elicited by
the challenge. The DSQ demonstrated good internal
consistency within the current sample for both the
cognitive (alpha = .82) and physical (alpha = .93)
symptom scales.
physiologic stimulus and gas
A physiologic stimulus of 10% CO2-enriched air
(10% CO2, 21% O2, 69% N2) was used. Participants were equipped with a continuous positive
pressure Downs C-Pap Mask (Vital Signs Inc.,
Model No. 9000). For a comprehensive description
of the automated apparatus, see Lejuez and colleagues (1998). Consistent with prior research (Feldner
et al., 2006), participants were administered a single
5-min CO2 presentation.
Laboratory procedures were conducted in a 12-by14-foot experimental room in the Intervention
Sciences Laboratory, housed in the Department of
Psychology at the University of Arkansas. This
room contained a chair, desk, and computer. A twoway mirror, intercom system, and surveillance video
allowed for continuous monitoring and communication between the participant and the experimenter located in an adjacent room. The experimenter room contained a 40-cylinder CO2 tank
filled with 10% CO2 compressed air and a J &J
Engineering recording device transferring information onto a personal computer.
Participants were recruited from the Northwest
Arkansas community, including from the University
of Arkansas. Announcements were made in psychology classes and via flyers announcing the study
placed at various locations in the community (e.g.,
local market place, community bulletin boards).
Interested participants contacted the Intervention
Sciences Laboratory, at which time the SDQ and the
screening portion of the SCID were administered to
initially assess exclusion criteria. Potentially eligible
participants were then invited to attend a laboratory-based individual baseline assessment session
(Day 1). At this session, participants provided
written informed consent and were told that the
purpose of the study was to investigate the effect of
sleep on different health behaviors. All participants
were aware there were two conditions in the
babson et al.
experiment, a sleep deprivation and sleep-asnormal group. Importantly, the informed consent
procedures described possible effects of acute sleep
deprivation (e.g., irritability, difficulty concentrating) but did not include a description of the possible
effects of sleep deprivation on anxiety. Participants
also were informed about the likely effects of the
CO2 procedure (e.g., trouble breathing, sweating,
feeling lightheaded). They were further informed
that these bodily effects are harmless and painless
and that they disappear quickly after returning to
normal breathing. Upon provision of informed
consent, the SDQ, SCID, and medical screening
interview were administered to further evaluate
exclusion criteria. Participants not eligible for
participation at this stage were compensated $10
and thanked for their participation. Eligible participants then completed a battery of self-report
measures and the baseline biological challenge
procedure (Day 1 CO2 challenge; please see below
for procedural details).
After initial screening, informed consent procedures, questionnaire packets, and the biological
challenge were completed, participants were randomly assigned to either the acute sleep deprivation
(experimental) or no sleep deprivation (control)
group. Participants were asked to choose a day and
time when losing sleep for an entire night would not
interfere in their daily life and when they could
attend the second laboratory session the morning
after the night of acute sleep deprivation. Those
assigned to the control group were instructed to
sleep as normal and those in the experimental group
were instructed to stay awake through the night. All
participants were instructed to not change drug use
patterns, including alcohol and cigarette use patterns, relative to normal routines. In an effort to
control for possible differences in drug-related
withdrawal symptoms, they were not instructed to
completely refrain from typical substance use (e.g.,
smoking) patterns. Participants assigned to the
experimental group consented to not drive to the
laboratory for their second appointment to protect
participants against impaired driving that may result from acute sleep deprivation. Within the sleep
deprivation condition, a phone-in digital sleep diary
procedure was implemented in order to monitor
sleep loss. Specifically, participants were instructed
to call the laboratory every hour (calls were digitally
time stamped to check participant compliance)
between 10:00 P.M. and 8:00 A.M. as a manipulation
Upon completion of the randomization procedures and explanation of the instructions for the
night, participants scheduled their Day 2 appointment for the next day, and were compensated $20
for completion of Day 1. All participants completed
Day 1 between 12:00 P.M. and 5:00 P.M. All
participants then returned to the laboratory to
complete Day 2 of the protocol the next day between 6:00 A.M. and 10:00 A.M. The 1-hour Day 2
session included a brief semistructured interview
administered to assess the prior night's sleep level as
well as substance use levels (i.e., cigarettes, caffeine,
stimulants) during the prior night. Participants who
reported changing use of these substances relative to
typical use patterns and those who did not follow
the protocol for acute sleep deprivation or a full
night sleep, were given the option of either (1)
refraining from sleep on a separate night and again
returning to the laboratory to complete the biological challenge procedure or (2) discontinuing participation in the study and receiving an additional $10
compensation. Participants who followed the
experimental directions completed a brief questionnaire packet and the second challenge procedure.
Then, participants were debriefed and compensated
an additional $60 for completion of Day 2.
Biological challenge procedures. During both
laboratory challenges (Day 1 and Day 2), individual
participants sat in front of a computer in the
experimental room. The researcher then fitted the
participant with a C-PAP mask. At this point, the
researcher left the room and began the procedure.
Participants sat alone in the experimental room. The
researcher observed the participant via a two-way
mirror, a video surveillance system, and a bidirectional intercom. Participants first completed a
10-minute baseline period (baseline), which was
immediately followed by a 5-minute 10% CO2enriched air administration. The SUDS was administered via automated computer delivery at the
beginning of the baseline period and immediately
after the challenge procedure (post-challenge period). Upon completion of the CO2 administration,
the DSQ was administered via automated computer
delivery to measure panic attack symptoms experienced during the challenge. After the challenge was
completed, the researcher entered the room and
removed the mask.
manipulation checks
Random assignment. To check the efficacy of
random assignment, differences between groups on
key baseline characteristics were examined. Groups
(experimental, control) were compared in terms of
dichotomous variables (i.e., gender and smoking
status) using chi-square analyses. Continuous variables (i.e., negative affect, nonclinical sleep problem
levels, and sleep anticipatory anxiety) were
sleep deprivation and biological challenge responding
examined using independent samples t-tests. Analyses suggested no pre-experimental group differences (all p's N .1). Please see Table 1 for means and
standard deviations for each of these baseline
CO2 challenge. To examine the efficacy of the
CO2 procedure, paired samples t-tests were utilized
to examine changes in self-reported anxiety (collapsed across group) for both days 1 and 2. Mean
levels of SUDS were compared between the baseline
and postchallenge periods. Analyses suggested that
the CO2 challenge elicited anxiety during both days
1 and 2 [Day 1: t(86) = 5.54, p b .001; Day 2: t(86) =
7.17, p b .01].1
Sleep manipulation. In addition to the methodological checks in place to ensure the efficacy of the
experimental acute sleep manipulation (e.g., hourly
phone calls made during the night by the sleep
deprivation group), participants' adherence to the
experimental instructions (sleep pattern and substance use) was examined using independent samples t-tests that compared groups in terms of selfreported hours of sleep, number of cigarettes
smoked, and caffeinated beverages consumed the
24 hours prior to the Day 2 laboratory appointment. Results suggested participants followed the
experimental directions. Participants in the sleep
deprivation group reported greater sleep loss compared to those in the control group, t(84) = 36.3,
p b .001 (see Table 1). Furthermore, all participants
in the sleep deprivation group completed the phonein digital sleep diary every hour during the night of
sleep loss. Participants in both the sleep deprivation
and control groups reported no change in stimulant
use patterns and both groups used comparable
amounts of nicotine during the night. There were no
significant differences between groups in substance
use levels (all p's N .1).
primary hypothesis tests
Self-reported anxiety. To test the effect of sleep
deprivation on anxious responding to the biological
challenge procedure, a repeated measures analysis
of variance (ANOVA) was conducted. Withinsubject variables included day (Day 1, Day 2) and
measurement point (baseline and postchallenge
SUDS ratings) and the between-group variable was
To examine the efficacy of the CO2 procedure in eliciting
physiological arousal, paired samples t tests were utilized to
examine changes in heart rate and skin conductance level
(collapsed across group) for both days 1 and 2. Specifically, mean
levels of each dependent variable were compared between the
baseline and post-challenge periods. Analyses suggested the CO2
challenge significantly increased heart rate and skin conductance
both on day 1 and day 2 of the procedure.
group (sleep deprivation versus control). In the case
of significant interactions, simple effects t-tests were
conducted to analyze the interaction. A Bonferroni
correction was employed to control for multiple
comparisons yielding a corrected alpha level of .025
for simple effects tests. Effect size was indexed via
eta squared (η2 ).
Results suggested no main effect of day. However,
there was a main effect of group [f (1, 85) = 7.79,
p b .01; η2 = .08] and measurement point [f (1, 85) =
9.06, p b .01; η2 = .09]. A significant interaction between day and group also emerged [f (1, 85) = 11.04,
p b .01; η2 = .12]. Simple effects tests suggested there
was no difference in SUDS ratings (collapsed across
pre- and postchallenge ratings) between groups on
Day 1 [t (85) = 0.54, ns]. However, there was a significant difference in SUDS ratings between groups
on Day 2 [t (85) = 4.32, p b.01]. Specifically, the sleep
deprivation group reported significantly higher
anxiety compared to the control group (please see
Table 1 for means).
Panic attack symptoms. In terms of panic attack
symptoms elicited by the CO2 challenge, two separate repeated measures ANOVAs were conducted to
test the effects of sleep deprivation on physical and
cognitive symptoms of panic. Specifically, the
within-subjects variable was day (Day 1, Day 2)
and the between-group variable was group (sleep
deprivation versus control). A Bonferroni correction
was again employed to control for multiple comparisons, yielding a corrected alpha level of .025 for
simple effects tests. Effect size was indexed via eta
squared (η2 ).
In terms of physical panic symptoms, there was
no main effect of group or day. However, there
was a significant interaction between day and group
[f (1, 85) = 4.43, p b .05; η2 = .05]. Simple effects tests
indicated there were no group differences in physical
panic symptoms on Day 1; however, group differences emerged on Day 2 [t (85) = 2.25, p b .02].
Specifically, the sleep deprivation group experienced
more physical panic symptoms than the control
group on Day 2 (see Table 1 for group means). In
terms of cognitive panic symptoms, a main effect of
group was evidenced [f (1, 85) = 6.50, p b .05;
η2 = .07] such that the sleep deprivation group
reported more intense cognitive panic attack symptoms in response to the challenge procedure than the
control group (see Table 1).
A burgeoning literature documenting that sleep
problems occurring during childhood are related to
elevated anxiety in adulthood (Gregory & O'Connor, 2002; Gregory et al., 2004; Gregory et al.,
babson et al.
2005) suggests (albeit without documenting causal
relations) that sleep loss may potentiate anxiety
development. Relatively less research has examined
the effects of sleep deprivation specifically in terms
of panic-relevant responding, despite a well-established association between panic and sleep problems. Indeed, only one study has been conducted in
this domain (Roy-Byrne et al., 1986), which generally suggested sleep loss may potentiate panic
attacks. Although this study was a commendable
first step in the area, several limitations (e.g., small
sample size, lack of pre- and post-challenge assessments) limited conclusions that could be drawn. The
current study uniquely extended this work (e.g.,
greater methodological power, pre- and post-sleep
manipulation assessments, inclusion of a no-sleep
deprivation control group, more strict inclusion
criteria) to an experimental examination of the role
of acute sleep deprivation in responding to a laboratory-based panic-relevant biological challenge.
Nonclinical participants were randomly assigned
to an acute sleep deprivation or normal night sleep
condition and completed a 2-day laboratory-based
protocol that included repeated 5-min 10% CO2enriched air administrations. Consistent with hypotheses, acute sleep deprivation increased baseline
anxiety and self-reported anxious and fearful responding to the challenge procedure.
Results suggested acute sleep deprivation increased various aspects of panic-relevant anxious
reactivity. First, a significant interaction between
group and day in terms of SUDS ratings suggested
that despite a lack of differences in anxious responding to the challenge on Day 1, the acute sleep
deprivation group reported greater anxiety both
before and after the Day 2 challenge procedure than
the control group. These data support the hypothesis that acute sleep deprivation increased baseline
anxiety prior to the Day 2 CO2 challenge. Acute
sleep deprivation also increased the reported intensity of panic symptoms elicited by the challenge.
Despite a lack of differences between groups in
response to the Day 1 challenge, participants in the
sleep deprivation condition endorsed greater intensity of physical panic symptoms in response to the
Day 2 challenge. In combination with the SUDS
results, these findings suggest that acute sleep
deprivation increased panic-relevant anxious and
fearful responding to the challenge procedures. In
contrast to expectation, although cognitive panic
symptoms were higher overall in the sleep deprivation group, there was not evidence that cognitive
symptom intensity increased among this group as a
result of sleep deprivation. Although the means (see
Table 1) and a statistically nonsignificant trend
toward an interaction between group and day
(p = .07) were in the expected direction, it did not
appear that cognitive panic symptoms (e.g., fear of
going crazy, fear of losing control) were affected by
the sleep manipulation. Given the healthy sample
and consent procedures that informed participants
that the effects of the CO2 challenge are safe and
short-lived, it is likely the magnitude of the effect of
sleep deprivation on these symptoms was too small
to be observed in this study. Nonetheless, these
findings generally suggest that acute sleep deprivation increases anticipatory anxiety about abrupt
increases in bodily arousal and it increases panicrelevant responding to such arousal. It is important
to note that the size of the effects was relatively small
(η2 = .05 to .12), which may be due, in part, to the
conservative nature of the design (e.g., psychologically and physically healthy sample, controlled
environment). Given this conservative test of the
hypotheses, it is likely these small effects are
nonetheless meaningful (Abelson, 1985), demonstrating that, even in a carefully controlled setting,
acute sleep deprivation has panic-relevant effects on
healthy individuals. Importantly, this is a first step,
and future prospective naturalistic research with
participants suffering from panic attacks will
ultimately be needed to directly test the role of
more chronic sleep deprivation in panic development. Moreover, given linkages between elevated
anxiety sensitivity (i.e., fear of the consequences of
anxiety) and sleep problems (Babson, Trainor,
Bunaciu, & Feldner, 2008), extending this work to
participants at risk for panic and anxious reactivity
to the effects of sleep deprivation would likely
amplify the effects of acute sleep deprivation and
increase generalizability to models of the development of panic.
Acute sleep deprivation appears to increase
anxious and fearful responding to abrupt increases
in bodily arousal, which is positively related to panic
onset (Schmidt & Zvolensky, 2007). These results
may have implications, albeit tentative at this early
stage of research, for models of panic development.
Scholars in this area have suggested that panic
attacks among persons with PD are elicited by
conditioned responses to bodily arousal characterized by autonomic arousal, avoidance, and catastrophic misinterpretation of bodily arousal (Barlow,
2002; Bouton et al., 2001; Clark, 1986; Clark &
Ehlers, 1993). The current findings suggest acute
periods of sleep deprivation increase the risk for
anxious and fearful responding to bodily arousal,
perhaps by increasing anxiety and activating interpretive biases leading to catastrophic misinterpretation of bodily arousal. Thus, after acute sleep deprivation, abrupt increases in bodily arousal, which
can be elicited by various activities (e.g., drug use,
sleep deprivation and biological challenge responding
vigorous exercise), may be particularly likely to be
paired with anxiety and fear because sleep-deprived
individuals are at increased risk for fearfully responding to such arousal. Therefore, acute sleep deprivation may “set the stage” for fear-based conditioning of interoceptive arousal. Importantly, as this is a
first step in this domain, this theoretically based
speculation requires additional empirical examination in order to draw etiological conclusions. For
instance, this model would predict that an individual's first panic attack is more likely to occur subsequent to sleep deprivation than after a normal
night of sleep. Similarly, future research could
beneficially extend this work to examination of
psychobiological mechanisms (e.g., learning-based
mechanisms, catastrophic misinterpretation of bodily arousal, hypersensitivity of neuroanatomical fear
circuitry) implicated in panic development. For example, the underlying mechanisms of action discussed in contemporary neuroanatomical accounts
of panic (Gorman, Kent, Sullivan, & Coplan, 2000)
could be tested as mediators of the acute sleep
deprivation–panic-relevant reactivity association.
The specificity (or lack thereof) of the influence of
sleep deprivation on panic as opposed to other
specific anxiety disorders also warrants additional
investigation. For example, given well-established
associations between posttraumatic stress disorder
and sleep deprivation (Spoormaker & Montgomery, 2008), it is possible that acute sleep deprivation
amplifies anxious reactivity among persons suffering from this disorder as well.
Interpretation of the current findings requires
consideration of a number of limitations. First, this
study employed a nonclinical, healthy sample consisting mainly of Caucasian, well-educated, young
adults. Although aspects of this approach were
important for the (prioritized) internal validity of
the study (e.g., screening for histories of psychopathology), our ability to generalize these results to a
more heterogeneous population is constrained. For
instance, it is possible that the effects of sleep
deprivation vary with age as sleep patterns typically
vary across the lifespan (Ohayon, Carskadon, &
Guilleminault, 2004). Future research would benefit
from utilization of a more heterogeneous sample.
Furthermore, this constrained variance may have
restricted the range of reactivity to the challenge
procedure, suppressing effect sizes. Our focus on
internal validity, which reduced the external validity
of these findings, is reasonable at this early stage of
research (Mook, 1983), yet future research would
benefit from including more diverse populations
that would increase generalizability and variability
in responding to the challenge. Second, the laboratory paradigm utilized elicits bodily arousal relevant
to panic, which is helpful for examining risk
processes (Schmidt & Zvolensky, 2007; Zvolensky
et al., 2001). However, this paradigm does not allow
for studying naturalistic panic attacks (e.g., those
experienced as uncued) or naturally occurring sleep
deprivation. Therefore, it will be important to
extend this research to the naturalistic examination
of these factors. For instance, future research could
usefully employ repeated measures of anxiety
throughout a naturalistic period of sleep deprivation (among persons with chronic sleep problems,
for example). This type of design would allow for
drawing conclusions about the pattern of anxiety
development during sleep deprivation and may shed
light on threshold-type issues, such as the degree of
sleep deprivation necessary to potentiate panic
responding. Similarly, it remains unclear how the
panic-related effects of acute sleep deprivation relate
to possible panic-related effects of chronic sleep
deprivation. Although the current study offered a
novel opportunity to experimentally test the effects
of acute sleep deprivation in terms of responding to
abrupt increases in bodily arousal elicited in the
controlled environment of the laboratory, these
conclusions cannot be extended to inferences
regarding the role of chronic sleep deprivation in
panic development. For this reason, future prospective studies would benefit from examining the
relation between chronic sleep deprivation and the
development of anxious and fearful responding to
bodily arousal. Future research also could beneficially integrate a more detailed (laboratory-based)
assessment of sleep parameters to better understand
how specific sleep parameters relate to biological
challenge responding. For instance, it is possible that
reductions in slow wave sleep, in particular, increased anxious and panic-relevant responding.
Indeed, extant research suggests slow wave sleep is
particularly strongly related to anxiety (Arriaga
et al., 1996). Examining continuous indices of this
type of sleep parameter would allow for more
refined conclusions regarding the mechanism(s) of
sleep deprivation that increase anxiety and panic
intensity in this paradigm. Relatedly, the current
study did not include direct observation of sleep
patterns, leaving open the possibility that participants in the sleep deprivation condition were not as
deprived of sleep as they reported. Importantly,
reliance on self-report is consistent with prior
research on the effects of sleep deprivation (e.g.,
Thatcher, 2008) and the digital sleep diary procedure utilized herein helped to ensure the validity of
the sleep manipulation by precluding last-minute
completion of a paper-and-pencil diary, a type of
“faked compliance” observed in studies using selfmonitoring diaries (Litt, Cooney, & Morse, 1998).
babson et al.
Nonetheless, this study would have benefited from
direct observation of sleep in both conditions, which
would further ensure the internal validity of this
type of design. Similarly, we were unable to directly
observe substance use patterns throughout the night
of sleep loss. The structured clinical interview administered on Day 2 to assess substance use during
the previous night is a first step in controlling for the
effects of substance use patterns. However, future
work would benefit from inclusion of direct observation of substance use patterns throughout a
night of sleep loss. Furthermore, participants may
have been aware of the primary aims of the current
study, which may have affected self-reported
responding. Although the current study uniquely
added a pre/post-sleep deprivation assessment and
control group to this area of research and therefore
improved upon previous designs, future research
nonetheless needs to control for the possible role of
experimental demand characteristics. Finally,
although persons lost to attrition in the current
study did not appear to differ from those retained,
decreasing the attrition rate would lead to greater
generalizability of the current results (i.e., decrease
the potential role of self-selection biases).
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