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Psychosomatic Medicine 65:857-864 (2003)
© 2003 American Psychosomatic Society

ORIGINAL ARTICLES

Psychophysiological Reactivity and Coping Styles Influence the Effects of Acute Stress Exposure on Rapid Eye Movement Sleep

Anne Germain, PhD, Daniel J. Buysse, MD, Hernando Ombao, PhD, David J. Kupfer, MD and Martica Hall, PhD

From the Departments of Psychiatry (A.G., D.J.B., H.O., D.J.K., M.H.) and Statistics (H.O.), School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania.

Address reprint requests to: Martica Hall, PhD, University of Pittsburgh School of Medicine, Department of Psychiatry, 3811 O’Hara Street, E-1121, Pittsburgh, PA 15213. Email: hallmh{at}msx.upmc.edu


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
OBJECTIVE: The goal of the present study was to investigate the roles of situational (ie, psychophysiological reactivity to acute stress) and dispositional variables (ie, neuroticism, coping styles) in shaping the effects of acute stress exposure on REM sleep.

METHODS: Sixty-three healthy young adults slept in the laboratory after being randomized into CTL or EXP. Measures of psychophysiological reactivity (state anxiety, stress level, and mean arterial blood pressure) were collected before and immediately after randomization. All subjects completed the Neuroticism-Extroversion-Openness-Personality Inventory Revised and the Ways of Coping Checklist.

RESULTS: A significant stress exposure by REM period interaction was found, and average RCs in the last REM period were significantly lower in EXP compared with CTL subjects (p = .005). The global slope of increase in average RC across successive REM sleep periods was less steep in EXP compared with CTL subjects (p = .02). Late-night RC was mediated by changes in subjective stress level from baseline to task notification, whereas REM latency was predicted by changes in state anxiety. Neuroticism and coping style did not directly moderate the effects of acute stress exposure on REM sleep. Rather, social coping and avoidance moderated psychological reactivity.

CONCLUSIONS: The findings suggest that attenuation of REM sleep phasic activity after stress exposure may reflect adaptive regulation of waking emotional arousal. Mediation and moderation models are more informative than traditional bivariate approaches to investigating the relation between stress exposure and sleep alterations.

Key Words: acute stress, • REM sleep, • moderation, • mediation.

Abbreviations: ANCOVA = analysis of covariance;; BDI = Beck Depression Inventory;; CTL = control condition;; EXP = acute stress exposure condition;; FNE = first night effect;; MAP = mean arterial blood pressure;; NEO-PI-R = Neuroticism-Extroversion-Openness Personality Inventory—Revised;; NREM = nonrapid eye movement;; RC = rapid eye movement count;; REM = rapid eye movement;; %REM = percentage of rapid eye movement sleep;; REML = rapid eye movement latency;; STAI-S = Spielberger State-Trait Anxiety Inventory;; VAS-Stress = visual analogue scale for subjective stress ratings.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Situational (eg, state anxiety, cardiovascular reactivity) and dispositional factors (eg, neuroticism, hardiness) shape the relationship between stress exposure and waking physical or psychological well-being (eg, Refs. 1–8). However, the contributions of situational and dispositional factors in shaping the effects of acute stress exposure on sleep parameters remain scarcely explored. Examining the role of such factors in healthy people may provide further insights into the mechanisms underlying the development and maintenance of REM sleep disturbances in people experiencing transient stressful life events (9–13) and chronic posttraumatic stress disorder (review, Ref. 14).

Previous studies investigating the effects of acute stress exposure on sleep in healthy samples have generally found that REM sleep alterations are more frequent than NREM sleep alterations. However, bivariate models (ie, between-group comparisons) have failed to demonstrate a consistent and robust linear relationship between stress exposure and REM sleep alterations in healthy cohorts. Acute stress exposure has been inconsistently associated with increased %REM and REM sleep duration and decreased REML (15–21). Most studies have reported no changes in REM density after acute stress exposure (15, 17, 18, 20, 22–24). These findings contrast with reports of REM sleep alterations in people undergoing transient or chronic life events with and without comorbid depression (eg, Refs. 9, 12–14) and provide little insight into the potential factors that may clarify these equivocal findings.

Readdressing the effects of acute stress exposure on REM sleep using mediation and moderation models (25–27) may elucidate the role of situational and dispositional factors in preventing or facilitating the development REM sleep alterations after acute stress exposure. Mediation supposes that the predictor variable influences the outcome variable both directly and indirectly via an intermediate variable or mediator. The mediator is conceptualized as a process internal to the organism, one that is independent from the experimental design. For instance, psychophysiological reactivity may mediate the relationship between stress and REM sleep. Accordingly, different levels of psychophysiological arousal would be expected to induce different levels of REM sleep alterations. State anxiety, perceived stress, and mean arterial blood pressure are well documented measures of psychophysiological reactivity to acute stressors. Score differences between baseline and task notification on these three measures were thus used as measurements of psychophysiological reactivity.

Alternatively, moderation implies that the interaction between two independent variables (the predictor and the moderator) significantly influences the direction and strength of relationship to the outcome variable. For instance, acute stress exposure (the predictor) and neuroticism (the moderator) may both independently predict REM sleep profiles. In the latter case, neuroticism is a dispositional factor independent from acute stress exposure (ie, an effect modifier that is not predicted by stress exposure, as opposed to psychophysiological reactivity in the previous mediation example) that can modify the effects of acute stress exposure on REM sleep. Additionally, the interaction between acute stress exposure and neuroticism may also influence the outcome variable. For example, people with high neuroticism exposed to an acute stressor may exhibit different REM sleep parameters compared with people with low neuroticism exposed to the same acute stressor, or compared with people with high neuroticism who are not exposed to the stressor.

Only two studies have used mediation models to investigate the relationship between stress and sleep. One study showed that situation factors, such as psychological distress (28), mediate the relationship between perceived stress level and subjective sleep quality. In the recent study, we showed that autonomic tone during NREM sleep after acute stress exposure was correlated with subjective and objective sleep quality (M. Hall, R. Vasko, D. J. Buysse, J. Thayer, H. Ombao, Q. Chen, J. D. Cashemere, D. Kupfer, unpublished data). Autonomic tone during REM sleep after acute stress exposure, however, was not correlated with subjective sleep quality or expression of REM sleep parameters. The latter observation suggests that the investigation of waking psychophysiological reactivity to stress may be a more potent mediator of REM sleep parameters after acute stress exposure. Previous studies that investigated the effects of acute stress exposure on REM sleep have not examined whether psychophysiological reactivity to the stressor influences this relationship. In the present study, the term psychophysiological reactivity refers to changes in subjective reports of anxiety, perceived stress, and the physiological measurement of mean arterial blood pressure from prestress to poststress exposure. Because psychophysiological reactivity to the stressor should be predicted by acute stress exposure, we first hypothesized that psychophysiological reactivity would mediate alterations of REM sleep parameters after acute stress exposure. Based on previous studies, we specifically hypothesized that REM density, REML, %REM, and REM duration would be predicted by both group assignment (control stress condition vs. acute stress exposure) and psychophysiological reactivity.

Previous correlational data suggest that two dispositional factors, neuroticism and repression, may moderate the effects of acute stress exposure on REM sleep. Specifically, REM density, %REM, and REML have been shown to vary as a function of neuroticism and repression after acute stress exposure (19, 20, 30). Because these two factors should be independent from stress exposure, the second hypothesis was that neuroticism and coping styles (a similar but broader construct than repression) would moderate the effects of acute stress exposure on these REM sleep parameters. Figure 1 illustrates the two hypotheses.



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  		Fig. 1. Proposed models of the mediation and moderation of REM sleep parameters after acute stress exposure.

 

   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects
The results reported here are one component of a study that investigated the effects of presleep acute stress on autonomic tone during sleep (M. Hall, R. Vasko, D. J. Buysse, J. Thayer, H. Ombao, Q. Chen, J. D. Cashemere, D. Kupfer, unpublished data). Sixty-three subjects (32 men, 31 women; age range, 18–24 yr; mean age, 19.6 ± 1.8) enrolled in this study. Most were recruited from the Department of Psychology undergraduate subject pool at the University of Pittsburgh. The subjects received 5 hours of extra credit toward their introductory psychology class. Six additional subjects were recruited from other undergraduate classes, and each received $50. Subjects were included if they reported no significant sleep disturbances as determined by their global score on the Pittsburgh Sleep Quality Index (31). To control for their potential influence on sleep, tobacco use, self-reported current psychiatric diagnosis, and substance use problems were exclusion criteria. All subjects provided written informed consent. They were asked to refrain from consuming alcoholic beverages and drugs during the 24 hours preceding their appointment at the sleep laboratory and to refrain from intense exercising and consuming caffeine, alcohol, and other substances during the day of their appointment. A self-report questionnaire was used to evaluate caffeine, alcohol, medication, and drug use and exercise levels for the day preceding and the day of the experimentation.

Measures
Subjects arrived at the Clinical Neuroscience Research Center at Western Psychiatric Institute and Clinic at 8:00 PM. After instrumentation for sleep recordings, subjects completed the questionnaire battery, composed of the BDI (32), the Spielberger State-Trait Anxiety Inventory (33), the VAS-Stress, the NEO-PI-R, (34), and the Ways of Coping questionnaire (35).

The BDI assesses the severity of behavioral, cognitive, and emotional symptoms associated with current depression. The Spielberger State Anxiety Index is a self-report measure of anxiety endorsed in a given situation. The ambient stress level before and immediately after experimental acute stress exposure was assessed using the VAS-Stress measure. Subjects placed a mark on four separate 10-cm lines to represent how uptight, tense, distressed, and stressed they were. Responses were summed to yield the VAS-Stress score. Subjects also completed the Ways of Coping questionnaire. This 42-item questionnaire measures the use of five different coping styles: avoidance, problem-focused, seeking social support, self-blame, and wishful thinking. The Pittsburgh Sleep Quality Index encompasses seven areas of sleep quality (subjective sleep quality, sleep latency, duration, efficiency, disturbances, use of sleep medication, and daytime dysfunction) in the preceding month. Finally, subjects completed the 255-item NEO-PI-R, which assesses five personality dimensions labeled neuroticism, extraversion, openness to experience, agreeableness, and conscientiousness. As mentioned, correlational data suggest that neuroticism may modulate the effects of stress on REM sleep. Therefore, only the neuroticism subscale was used for analyses in the present study. After completing the questionnaire battery, subjects were allowed to relax, watch television, or study until approximately 15 minutes before their habitual bedtime.

Baseline measures of MAP were conducted during a 5-minute baseline phase. After the baseline period, three MAP measures were taken within a 6-minute period during and after task notification. Changes between MAP at baseline and at task notification ({Delta}MAP) were used as correlates of physiological reactivity.

Experimental Manipulation
The experimental manipulation was delivered immediately before bedtime in two phases: a 5-minute baseline phase and a stress manipulation phase. During the baseline phase, subjects were comfortably seated in a chair in the bedroom with their eyes closed. As previously described, a blood pressure cuff was placed on the subject’s nondominant arm, with electrodes connected. After the initial 5-minute baseline period, three MAP measures were taken within a 6-minute period.

At this point, a randomized group assignment card was opened, and subjects were notified of their group assignment. Task instructions were then played on a tape recorder. All subjects heard the same male voice. CTL subjects (N = 31) were told that they would have the opportunity to a read popular magazine in the morning, whereas the EXP group (N = 32) was told that they would give a speech in the morning, and that their performance would be evaluated. Task instructions lasted 23 seconds for the control condition and 53 seconds for the stress condition. Two MAP samples were collected at 2-minute intervals before, during, and immediately after task notification. Immediately after hearing the instructions, subjects also completed the VAS-Stress and the STAI-S again. The blood pressure cuff was removed, and subjects were told "to get a good night of sleep in order to perform well on your task in the morning." Lights out signaled the beginning of the Polysomnographic recordings.

Manipulation checks were conducted by comparing the differences between baseline and task notification levels immediately after group assignment on the three reactivity measures: {Delta}STAI-S, {Delta}VAS-Stress, and {Delta}MAP.

Sleep Recordings
Each participant slept in the laboratory for 1 night. Bedtimes were scheduled to correspond to self-reported habitual bedtimes. Similarly, subjects were awakened at their self-reported habitual rising time in the morning. Sleep recordings were performed using referential electroencephalogram (C3, C4, and O1, each referenced to tied mastoids), bilateral electro-oculogram, electromyogram (bipolar submental leads), and electrocardiogram. Grass model 7P511J AC amplifiers (Astro-Med Inc., West Warwick, RI) were used to acquire data, with 60-Hz notch filters applied to the signals. Data were collected in analog and digital formats and scored both visually and digitally in 30-second epochs according to the standard criteria of Rechtschaffen and Kales (36) by experienced technicians who were unaware of the study hypotheses.

Sleep latency was computed as the number of minutes to reach the first minute of a period beginning with and containing a minimum of 8 minutes of stage 2 sleep, delta sleep, or REM sleep within a 10-minute period after lights out. Sleep efficiency was computed as the ratio of minutes spent asleep divided by the total number of minutes between lights out and good morning time. REM latency was defined as the number of minutes elapsed between sleep onset and the first 30-second epoch of REM sleep minus minutes of wakefulness during this interval. An automated measure of REM density, RC, for each REM period was computed as the number of REMs identified by automated detection algorithm divided by the number of REM minutes (37). A whole-night average RC value was also computed (ie, total REMs automatically detected/total REM duration in minutes).

Statistical Analyses
Group comparability was determined using independent t tests. Manipulation checks were performed using ANCOVAs with baseline measures as covariates. Differences between the two groups on overall sleep profiles and REM sleep measures were conducted with ANCOVAs, using baseline VAS-Stress as the covariate. To reduce the skewness in the distributions, square root transformations were applied to all REM sleep variables except average RC, which was normally distributed. Logarithmic transformations normalized sleep stage percentage and sleep efficiency data. To control for type I errors, Bonferroni corrections were applied to each variable cluster: 1) for questionnaire measures, the level of statistical significance was set at p = .004 (0.05/12 comparisons); 2) for global sleep parameters, the level of statistical significance was set at p = .005 (0.05/10 comparisons); and 3) for REM sleep parameters, level of statistical significance was set at p = .01 (0.05/4 comparisons).

Separate univariate hierarchical regression models were fit to each of the REM sleep parameters of interest while controlling for baseline VAS-Stress to determine whether psychophysiological reactivity, neuroticism, and coping styles mediate and moderate REM sleep parameters. All analyses were performed with SPSS 10.1 (SPSS Inc., Chicago, IL).

To compare average RC group differences across successive REM sleep periods, a linear mixed effects model was fit. The model assumed that average RC profiles for the two groups were linear. The mixed model included both fixed and random effects. The fixed effects included the intercept and the slope of the RC profile for each of the two groups. The fixed effect parameter estimated the group or population profiles. A formal test for the difference in the fixed parameters can be performed with mixed models. In particular, we tested whether the difference between the slopes and intercepts of the two groups were statistically significant. In mixed models, the subject-specific intercept and slope parameters are random because individual subjects are assumed to be randomly selected from their respective populations. Thus, each subject has unique intercept and slope parameters. Logistic regression models were then used to determine whether psychophysiological reactivity, neuroticism, and coping styles predicted individual RC slopes in the two groups. SAS system (SAS Institute Inc., Cary, NC) for mixed models (39) was used to perform these computations.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
None of the subjects reported significant consumption of caffeine, alcohol, medications, or drugs the day preceding their appointment. On the day of the appointment, none reported intense exercise or significant consumption of caffeine, alcohol, medications, or drugs. The two groups did not differ at baseline in terms of self-reported sleep quality, depressive symptoms, state or trait anxiety, and coping styles (Table 1). However, baseline VAS-Stress was greater in subjects later assigned to the CTL group than in those assigned to the EXP group [t(61) = 4.57, p < .001]. Baseline ambient stress was thus used as a covariate in subsequent analyses.


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  		TABLE 1. Means (SD) for the Questionnaire Measures for Control and Experimental Groups
 
Manipulation checks confirmed the potency of the stressor. After controlling for baseline ambient stress and MAP, STAI-S [F(1,62) = 6.58, p = .01], VAS-Stress [F(1,62) = 18.16, p < .001], and MAP [F(1,60) = 5.08, p = .03] were significantly higher in the EXP group than in the CTL group after task notification compared with baseline.

Forty-one subjects (18 CTL and 23 EXP) exhibited four REM periods. There was a significant stress exposure by REM period interaction [F(3,114) = 2.65, p = .05] for RC across REM periods (Figure 2). Post hoc independent t tests revealed that RC was significantly higher in the CTL group than in the EXP group (12.96 ± 6.49 vs. 7.74 ± 4.88; p = .005) during the last REM period. Average RC across the first three REM periods did not differ for these 41 subjects when compared with the entire sample. This was confirmed by the linear mixed effect analysis, which allows all subjects to be included despite missing data. Specifically, the linear mixed effect analysis corrected for baseline MAP and baseline VAS-Stress revealed that the slope of increase of average RC across REM periods was significantly steeper in the CTL group than in the EXP group (3.27 for CTL vs. 3.27–1.47 for EXP, p = .02). Therefore, although both groups started at comparable average RC values early in the night, a significant difference between the two groups slowly developed across subsequent REM sleep periods, and this deviation became statistically significant during the last REM sleep period (Figure 2). Other REM parameters did not differ between the two groups (Table 2).



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  		Fig. 2. Interaction between stress exposure (control vs. experimental) and REM sleep period for automated average REM counts. Error bars represent standard deviations.

 

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  		TABLE 2. Mean (SD) Scores on Polysomnographic Sleep Measures for the Two Study Groups
 
Hierarchical regressions controlling for baseline VAS-Stress revealed that average RC in the fourth REM period was predicted by stress exposure (ß = -.42, p = .02) and by {Delta}VAS-Stress (ß = -.49, p = .02). Stress exposure, in turn, predicted {Delta}VAS-Stress (ß = .41, p < .001). Furthermore, when controlling for baseline VAS-Stress and {Delta}VAS-Stress, stress exposure was no longer a significant predictor of late-night average RC (ß = -.24, NS), indicating full mediation. In other words, the change in self-rated stress from baseline to posttask notification completely accounted for the relationship between stress exposure and average RC in the fourth REM period. {Delta}MAP (ß = .05, NS) and {Delta}STAI-S (ß = .25, NS) were not significant predictors of late-night average RC. Logistic regression models showed no relationship between measures of psychophysiological reactivity and the average RC slopes in the two groups.

Consistent with the lack of group differences observed for the other REM sleep parameters, stress exposure did not predict REML, %REM, or REM duration. Nevertheless, hierarchical regressions controlling for stress exposure and baseline VAS-Stress revealed that REML was best predicted by {Delta}STAI-S (ß = .36, p = .01), whereas {Delta}MAP (ß = .23, NS) and {Delta}VAS-Stress (ß = -.46, NS) did not further contribute to the model. Neither psychological nor physiological measures of reactivity predicted %REM sleep or REM duration.

Neuroticism and coping styles did not moderate effects of acute stress exposure on REM sleep parameters (Table 3). However, these dispositional factors could more remotely moderate REM sleep parameters by shaping psychophysiological reactivity to stress. Therefore, post hoc analyses were conducted to explore whether neuroticism and coping styles moderated psychophysiological reactivity. Two sets of hierarchical regressions were conducted to determine whether {Delta}VAS-Stress and {Delta}STAI-S (psychological reactivity measures previously shown to mediate RC and REML, respectively) were predicted by neuroticism and coping styles, while controlling for group assignment and their respective baseline values (STAI-S1 and VAS-Stress1). {Delta}VAS-Stress was predicted by the interaction between group assignment and coping with social support (ß = .26, p = .04; Figure 3). This interaction indicated that people in the EXP group with high social coping exhibited greater {Delta}VAS-Stress than EXP subjects who exhibited endorsed less social coping; subjects in the CTL groups who reported high social coping reacted slightly less than CTL subjects who used low social coping. {Delta}STAI-S was also predicted by the interaction between group assignment and social coping (ß = .22, p = .02); this interaction was similar to that observed for {Delta}VAS-Stress. In addition, the interaction between group assignment and avoidance coping predicted {Delta}STAI-S (ß = .22, p = .02; Figure 4). People in the EXP who reported greater use of avoidance as a way of coping showed greater {Delta}STAI-S than EXP subjects who endorsed less use of avoidance. The latter group showed {Delta}STAI-S levels comparable with those exhibited by CTL subjects.


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  		TABLE 3. Standardized ß Coefficients From Hierarchical Regression Analysis Controlling for Baseline Perceived Stress and Stress Exposure for Mediators and Moderators of REM Sleep Parameters
 


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  		Fig. 3. Moderated mediation of the effects of stress exposure on late-night average RC. Subjective stress ratings mediate the effects of acute stress exposure on late-night average RC. Subjective stress ratings, in turn, are partially determined by the interaction between stress exposure and seeking social support as a way of coping.

 


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  		Fig. 4. Partial mediation of REML by changes in presleep state anxiety. Changes in state anxiety predict REML. Changes in state anxiety, in turn, are partially moderated by the interactions between stress exposure and seeking social support, and the interaction between stress exposure and avoidance.

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
ACKNOWLEDGMENTS
 REFERENCES
 
The goal of this study was to investigate the roles of situational (ie, psychophysiological reactivity to acute stress) and dispositional factors (ie, neuroticism and coping styles) in shaping the effects of acute stress exposure on REM sleep. Automated average RC significantly differed between groups, but other REM sleep alterations were not observed in this sample of healthy young adults. Subjects in the acute stress exposure showed lower late-night average RC and slower rate of average RC increase across REM periods than subjects in the control condition. Late-night average RC and REML were preceded and predicted by psychological reactivity to the stressor, but not physiological reactivity according to {Delta}MAP measurements. Contrary to the moderation hypothesis and to previous correlational data, neuroticism and coping did not directly influence the effects of acute stress exposure on REM sleep. Rather, because there was an interaction between stress exposure and seeking social support, the latter partially moderated psychological reactivity, which in turn predicted late-night RC and REML. These results demonstrate that the effects of acute stress exposure on REM sleep are influenced directly by situational factors and indirectly by dispositional factors. The present findings reinforce the need to examine concurrent state-dependent and trait-dependent factors that may prevent or facilitate successful stress recovery.

The observed increase in average RC across REM periods in both groups is consistent with previous reports (9, 40, 41). The finding that average RC is altered after stress exposure is also consistent with previous studies that investigated the effects of experimental acute stress exposure or transient and chronic stressful life events on REM sleep (9, 11–14). Although studies conducted with people experiencing transient or chronic stress often report an increase in REM density (the analogue visually scored measure of average RC), healthy subjects exhibited a decrease in late-night average RC and a slower rate of increase across successive REM periods immediately after stress exposure. Phasic REM sleep activity thus may be a correlate of adaptability to a stressor. Specifically, average RC suppression after acute stress exposure may reflect functional regulation of waking emotional arousal during sleep, whereas increased phasic REM activity in clinical samples exhibiting chronic stress reactions may represent failure or inability to downregulate waking emotional arousal during sleep. Several observations reinforce the suggestion that attenuation of phasic REM sleep activity after acute stress exposure may indicate adaptation to stress: 1) increased REM density is a correlate of diurnal affect intensity in divorced, bereaved, and depressed subjects (11, 42, 43); 2) persistent elevated REM density in both depressed patients and alcoholics has been shown to predict relapse (44) and failure to remit with psychotherapy (40, 41, 45, 46); and 3) decreases in REM density parallel reductions in affect intensity and remission with psychotherapy in depressed patients (43, 46, 47) . Conversely, intensification of phasic REM sleep activity seems to be a specific marker of an underlying emotional dysregulation. The relationship between neural mechanisms involved in the induction of phasic REM sleep activity and those involved in regulation of emotional arousal during sleep remains unclear.

Despite the fact that bivariate analyses revealed no group difference for REML, predictive analyses nevertheless showed that elevated presleep state anxiety predicted longer REML. This finding is consistent with clinical studies that have reported prolonged REML in patients with anxiety disorders (48–52) and in people for whom the onset of a depressive episode was preceded by an acute life event (11). Because stress exposure did not predict REML, an increase in norepinephrine release during the evening preceding sleep recording (associated with elevated base-line perceived stress in the CTL group and stress exposure in the EXP group) may constitute one of the possible underlying neurochemical mechanisms associated with increased REML (eg, Refs. 53, 54). Alternatively, increases in REML may be attributable to subtle disruptions during the preceding NREM sleep period (29). Further investigations are required to determine the significance of REML alterations in nondepressed subjects exposed to acute stress.

The finding that coping with social support and avoidance had indirect effects on late-night average RC and REML through their influence on psychological reactivity indicated that dispositional factors are remote, albeit influential, factors of these REM sleep parameters. Interestingly, studies now show that reduced social support and increased avoidance may foster psychological distress, which in turn has been associated with sleep complaints (28, 55–57). Therefore, a closer examination of the moderating effects of coping styles on waking reactivity may provide valuable insights into dispositional factors that may increase vulnerability to both psychological distress and sleep disruption. Although neuroticism was not found to be a significant predictor of REM sleep parameters or psychophysiological reactivity, it remains possible that other personality traits that are more concisely defined may moderate the effects of stress on REM sleep.

Certain limitations must be acknowledged. First, there is the possibility that the combination of acute stress exposure and the FNE cannot be determined and may confound the present results regarding the effects of acute stress exposure on REM sleep. The FNE refers to the sleep changes observed on the first night compared with the second recording night in the laboratory that reflect adaptation to the novel sleep environment. In healthy subjects, reported FNEs on REM sleep consist of delayed REM latency and decreased REM percentage and REM sleep duration (eg, Refs. 58–60). The lack of differences between the two groups on REML, %REM, and REM duration may indeed be attributable to the robust FNE on these REM sleep parameters in healthy subjects. Additionally, although both groups were subjected to the FNE, only EXP subjects exhibited lower late-night average RC values. The slope of increased average RC across REM periods was also less steep in the EXP group compared with the CTL group. Therefore, we are confident that attenuated average RC values indeed reflect a genuine effect of acute stress exposure on REM sleep. It remains possible, however, that the FNE and acute stress exposure have synergistic effects on average RC. Notably, two studies now suggest that trait and state anxiety may influence the FNE on sleep parameters in healthy controls (61) and insomnia patients (62), reinforcing the need for considering experimental, situational, and dispositional factors simultaneously to characterize better the effects of waking experiences on sleep parameters. By the same token, the design of the present study did not permit us to investigate the occurrence of additional or different REM sleep alterations over the course of subsequent nights. Alternatively, the acute stress exposure may have only short-term effects on REM sleep parameters in healthy young people. Investigating how acute stress exposure influences sleep longitudinally may be especially valuable in understanding the development of persistent REM sleep alterations, which are reported in chronically stressed samples. A third limitation relates to the initial group difference on the baseline mean level of perceived stress. This initial group difference is unlikely to represent a greater disposition to experience stress in the CTL group compared with the EXP group because of the lack of group difference at baseline on the Spielberger Trait Anxiety measure, which is a more direct measure of predisposition to stress. In addition, VAS-Stress scores in the CTL group were significantly reduced after task notification, whereas VAS-Stress scores were significantly increased after task notification in the EXP group. If the CTL group was indeed more predisposed to experience stress in the new laboratory environment, the reduction in state anxiety scores in the CTL group would indicate that they were also able to rapidly adapt to the new environment and therefore were less likely to experience REM sleep disruption. Finally, it was not possible to examine within-subject changes in REM sleep parameters across multiple study nights. Within-subject REM sleep changes from baseline to stress exposure, rather than REM sleep profile immediately after acute stress exposure, may have been more revealing of the interactions between acute stress exposure and dispositional factors.

Despite these limitations, the present study illustrates that mediation and moderation models are more informative than traditional bivariate approaches to investigate the relationship between acute stress exposure and REM sleep alterations. The contributing roles of situational context and dispositional factors in shaping the effects of acute and chronic stress on REM sleep in patients demonstrating REM sleep alterations (eg, depression, posttraumatic stress disorder) need to be investigated further.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
REFERENCES
 
This work was supported by the Fonds de la Recherche en Santé du Québec, RR00056, MH30915, AG00972, MH01554, MH24652, MH62298, NSF DMS 0102511. Special thanks to the sleep technologists, data managers, and statisticians who made this study possible.

Received for publication March 25, 2002.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 

  1. Bohnen N, Nicolson N, Sulon J, Jolles J. Coping style, trait anxiety and cortisol reactivity during mental stress. J Psychosom Res 1991; 35: 141–7.[CrossRef][Medline]
  2. Burns JW, Friedman R, Katkin ES. Anger expression, hostility, anxiety, and patterns of cardiac reactivity to stress. Behav Med 1992; 18: 71–8.[Medline]
  3. Carlier IV, Lamberts RD, Gersons BP. The dimensionality of trauma: a multidimensional scaling comparison of police officers with and without posttraumatic stress disorder. Psychiatry Res 2000; 97: 29–39.[CrossRef][Medline]
  4. Lazarus RS, Folkman S. Stress, appraisal, and coping. New York: Springer; 1984.
  5. Fichera LV, Andreassi JL. Cardiovascular reactivity during public speaking as a function of personality variables. Int J Psychophysiol 2000; 37: 267–73.[Medline]
  6. Regehr C, Hill J, Glancy GD. Individual predictors of traumatic reactions in firefighters. J Nerv Ment Dis 2000; 188: 333–9.[CrossRef][Medline]
  7. Yehuda R. Biological factors associated with susceptibility to posttraumatic stress disorder. Can J Psychiatry 1999; 44: 34–9.[Medline]
  8. Vollrath M. Personality and stress. Scand J Psychol 2001; 42: 335–47.[CrossRef][Medline]
  9. Cartwright RD. Rapid eye movement sleep characteristics during and after mood-disturbing events. Arch Gen Psychiatry 1983; 40: 196–201.
  10. Cartwright RD, Wood E. Adjustment disorders of sleep: the sleep effects of a major stressful event and its resolution. Psychiatry Res 1991; 39: 199–209.[CrossRef][Medline]
  11. Monroe SM, Thase ME, Simons AD. Social factors and the psychobiology of depression: relations between life stress and rapid eye movement sleep latency. J Abnorm Psychol 1992; 101: 528–37.[Medline]
  12. Reynolds CF, Hoch CC, Buysse DJ, Houck PR, Schlernitzauer M, Pasternak RE, Frank E, Mazumdar S, Kupfer DJ. Sleep after spousal bereavement: a study of recovery from stress. Biol Psychiatry 1993; 34: 791–7.[CrossRef][Medline]
  13. Reynolds CF, Hoch CC, Buysse DJ, Monk TH, Houck PR, Kupfer DJ. REM sleep in successful, usual, and pathological again: the Pittsburgh experience 1980–1993. J Sleep Res 1993; 2: 203–10.[Medline]
  14. Pillar G, Malhotra A, Lavie P. Posttraumatic stress disorder and sleep—what a nightmare! Sleep Med Rev 2000; 4: 183–200.[CrossRef][Medline]
  15. Baekeland F, Koulack D, Lasky R. Effects of a stressful pre-sleep experience on electroencephalograph-recorded sleep. Psychophysiology 1968; 4: 436–43.[Medline]
  16. De Koninck J, Koulack D. Dream content and adaptation to a stressful situation. J Abnorm Psychol 1975; 84: 250–60.[CrossRef][Medline]
  17. Foulkes D, Rechtschaffen A. Pre-sleep determinants of dream content: effects of two films. Percept Mot Skills 1964; 19: 983–1005.
  18. Koulack D, Prevost F, De Koninck J. Sleep, dreaming, and adaptation to stressful intellectual activity. Sleep 1985; 8: 244–53.[Medline]
  19. McGrath MJ, Cohen DB. REM drive and function: a study of the interactive effects of personality and pre-sleep condition. J Abnorm Psychol 1980; 89: 737–43.[Medline]
  20. Cohen DB. Eye movement density during REM sleep: the influence of personality and pre-sleep condition. J Pers Soc Psychol 1975; 32: 1090–3.[Medline]
  21. Goodenough DR, Witkin HA, Lewis HB, Koulack D, Cohen H. Repression, interference, and field dependence as factors in dream forgetting. J Abnorm Psychol 1974; 83: 32–44.[Medline]
  22. Cohen DB, Cox C. Neuroticism in the sleep laboratory: implications for representational an adaptive properties of dreaming. J Abnorm Psychol 1975; 84: 91–112.[Medline]
  23. Cartwright RD, Luten A, Young M, Mercer P, Bears M. Role of REM sleep and dream affect in overnight mood regulation: a study of normal volunteers. Psychiatry Res 1998; 81: 1–8.[CrossRef][Medline]
  24. Lauer C, Riemann D, Lund R, Berger M. Shortened REM latency: a consequence of psychological strain? Psychophysiology 1987; 24: 263–71.[Medline]
  25. Baron RM, Kenny DA. The moderator-mediator variable distinction in social psychological research: conceptual, strategic, and statistical considerations. J Pers Soc Psychol 1986; 51: 1173–82.[CrossRef][Medline]
  26. Judd CM, Kenny DA, McClelland GH. Estimating and testing mediation and moderation in within-subject designs. Psychol Methods 2001; 6: 115–34.[CrossRef][Medline]
  27. Kraemer HC, Stice E, Kazdni A, Offord D, Kupfer D. How do risk factors work together? mediators, moderators, independent, overlapping and proxy risk factors. Am J Psychiatry 2001; 158: 848–56.
  28. Paulsen VM, Shaver JL. Stress, support, psychological states and sleep. Soc Sci Med 1991; 32: 1237–43.
  29. Deleted in proof.
  30. Cohen DB. Dysphoric affect and REM sleep. J Abnorm Psychol 1979; 88: 73–7.[Medline]
  31. Buysse DJ, Reynolds CF, Monk TH, Berman SR, Kupfer DJ. The Pittsburgh Sleep Quality Index: a new instrument for psychiatric practice and research. Psychiatry Res 1989; 28: 193–213.[CrossRef][Medline]
  32. Beck AT, Ward C, Mendelson M, Mock J, Erbaugh J. An inventory for measuring depression. Arch Gen Psychiatry 1961; 4: 561–7.
  33. Spielberger CD. State-Trait Anxiety Inventory for Adults. Palo Alto (CA): Consulting Psychologists Press; 1968.
  34. Costa PT, McCrae RR. Revised NEO Personality Inventory (NEO-PI-R) and NEO-Five-Factor Inventory (NEO-FFI) professional manual. Odessa (FL): Psychological Assessment Resources; 1992.
  35. Vitaliano PP, Russo J, Carr JE, Maiuro RD, Becker J. The Ways of Coping checklist: revision and psychometric properties. Multivariate Behav Res 1985; 20: 3–26.
  36. Rechtschaffen A, Kales A. A manual for standardized terminology, techniques and scoring system for sleep stages of human subjects. Los Angeles (CA): UCLA Brain Information Service, Coleman; 1968.
  37. Doman J, Detka C, Hoffman T, Kesicki D, Monahan JP, Buysse DJ, Reynolds CF III, Coble PA, Matzzie J, Kupfer DJ. Automating the sleep laboratory: implementation and validation of digital recording and analysis. Int J Biomed Comput 1995; 38: 277–90.[CrossRef][Medline]
  38. Deleted in proof.
  39. Deleted in proof.
  40. Buysse DJ, Kupfer DJ, Frank E, Monk TH, Ritenour A, Ehlers CL. Electroencephalographic sleep studies in depressed outpatients treated with psychotherapy, I: baseline studies in responders and nonresponders. Psychiatry Res 1992; 42: 13–26.[Medline]
  41. Buysse DJ, Tu XM, Cherry CR, Begley AE, Kowalski J, Kupfer DJ, Frank E. Pre-treatment REM sleep and subjective sleep quality distinguish depressed psychotherapy remitters and non-remitters. Biol Psychiatry 1999; 45: 205–13.[CrossRef][Medline]
  42. Newell PT, Cartwright RD. Affect and cognition in dreams: a critique of the cognitive role in adaptive dream functioning and support for associative models. Psychiatry 2000; 63: 34–44.[Medline]
  43. Nofzinger EA, Schwartz RM, Reynolds CF, Thase ME, Jennings JR, Frank E, Fasiczka AL, Garamoni GL, Kupfer DJ. Affect intensity and phasic REM sleep in depressed men before and after treatment with cognitive-behavioral therapy. J Consult Clin Psychol 1994; 62: 83–91.[CrossRef][Medline]
  44. Clark CP, Gillin JC, Golshan S, Demodena A, Smith TL, Danowski S, Irwin M, Schuckit M. Increased REM density at admission predicts relapses three months in primary alcoholics with a life time diagnosis of secondary depression. Biol Psychiatry 1998; 43: 601–7.[Medline]
  45. Buysse DJ, Hall M, Begley A, Cherry CR, Houck PR, Land S, Ombao H, Kupfer DJ, Frank E. Sleep and treatment response in depression: new findings using power spectral analysis. Psychiatry Res 2001; 103: 51–67.[Medline]
  46. Buysse DJ, Kupfer DJ, Frank E, Monk TH, Ritenour A. Electroencephalographic sleep studies in depressed outpatients treated with psychotherapy, II: longitudinal studies at baseline and recovery. Psychiatry Res 1992; 42: 27–40.[CrossRef][Medline]
  47. Thase ME, Reynolds CF, Frank E, Jennings RJ, Nofzinger E, Fasiczka AL, Garamoni G, Kupfer DJ. Polysomnographic studies of unmedicated depressed men before and after cognitive-behavioral therapy. Am J Psychiatry 1994; 151: 1615–22.[Abstract/Free Full Text]
  48. Reynolds CF, Shaw D, Newton TF, Coble PA, Kupfer DJ. EEG sleep in outpatients with generalized anxiety: a preliminary comparisons with depressed outpatients. Psychiatry Res 1983; 8: 81–9.[Medline]
  49. Glaubman H, Mikulincer M, Porat A, Wasserman O, Birger M. Sleep of chronic post-traumatic patients. J Trauma Stress 1990; 3: 255–63.
  50. Hefez A, Metz L, Lavie P. Long-term effects of extreme situational stress on sleep and dreaming. Am J Psychiatry 1987; 144: 344–7.[Abstract/Free Full Text]
  51. Kramer M, Kinney L. Sleep patterns in trauma victims with disturbed dreaming. Psychiatr J Univ Ott 1988; 13: 12–6.[Medline]
  52. Schlosberg A, Benjamin M. Sleep patterns in three acute combat fatigue cases. J Clin Psychiatry 1978; 39: 546–9.[Medline]
  53. Netzer NC, Kristo D, Steinle H, Lehmann M, Strohl KP. REM sleep and catecholamine excretion: a study in elite athletes. Eur J Appl Physiol 2001; 84: 521–6.[Medline]
  54. Lorenzo JL, Barbanoj MJ. Variability of sleep parameters across multiple laboratory sessions in healthy young subjects: the very first night effect. Psychophysiology 2002; 39: 409–13.[CrossRef][Medline]
  55. Hanson BS, Östergren PO. Different social network and social support characteristics, nervous problems, and insomnia: theoretical and methodological aspects on some results from the population study "Men Born in 1914," Malmö, Sweden. Soc Sci Med 1987; 25: 849–59.
  56. Shaver JLF, Lentz M, Lands CA, Heitkemper MM, Buchwald DS, Wodds NF. Sleep, psychological distress, and stress arousal in women with fibromyalgia. Res Nurs Health 1997; 20: 247–57.[CrossRef][Medline]
  57. Urponen H, Vuori I, Hasan J, Partinen M. Self-evaluations of factors promoting and disturbing sleep: an epidemiological survey in Finland. Soc Sci Med 1988; 26: 443–50.
  58. Browman CP, Cartwright RD. The first night effect on sleep and dreams. Biol Psychiatry 1980; 15: 809–12.[Medline]
  59. Le Bon O, Staner L, Hoffmann G, Dramaix M, San Sebastian I, Murphy JR, Kentos M, Pelc I, Linkowski P. The first night effect may last more than one night. J Psychiatr Res 2001; 35: 165–72.[CrossRef][Medline]
  60. Toussaint M, Luthringer R, Schaltenbrand N, Carelli G, Lainey E, Jacqmin A, Muzet A, Macher JP. First-night effect in normal subjects and psychiatric inpatients. Sleep 1995; 18: 463–9.[Medline]
  61. Kajimura N, Kato M, Sekimoto M, Watanabe T, Takakashi K, Okuma T, Mizuki Y, Yamada M. A polysomnographic study of sleep patterns in normal humans with low- or high-anxiety personality traits. Psychiatry Clin Neurosci 1998; 52: 317–20.[Medline]
  62. Riedel BW, Qinfield CF, Lichstein KL. First-night effect and reverse first night effect in older adults with primary insomnia: does anxiety play a role? Sleep Med 2001; 2: 125–33.[CrossRef][Medline]




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