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| Year : 2006
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: 8 | Issue : 30 | Page
: 30-39 |
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| Waking levels of salivary biomarkers are altered following sleep in a lab with no further increase associated with simulated night-time noise exposure |
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David S Michaud1, Susan M Miller1, Catherine Ferrarotto1, Anne TM Konkle2, Stephen E Keith1, Kenneth B Campbell3
1 Consumer and Clinical Radiation Protection Bureau, Health Canada, Ottawa, Canada
2 University of Maryland, School of Medicine, Physiology Department, Baltimore, USA
3 University of Ottawa, Department of Social Sciences, School of Psychology, Ottawa, Canada
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The goals of this study were twofold. First, we assessed if waking salivary hormone profiles are altered by nighttime noise exposure in a laboratory environment. Second, we evaluated the potential influence that sleeping in the lab in itself may have had on salivary biomarkers, by comparing results obtained following sleep at home. Twelve adults (7 males, 5 females) between 19-25 yrs slept at home and in a sleep laboratory. Subjects provided six saliva samples during waking hours on the day prior to sleep in the lab, on both days after sleeping in the lab and on the day following the resumption of sleep at home. Following one night of adaptation, subjects were exposed throughout the 2 nd night to simulated backup alarms that consisted of trains of 5 consecutive 500 ms duration audible tones. The time between the onset of each tone was 1 s and the time between trains (offset to onset) was 15 to 20 s. When compared to home conditions, cortisol and melatonin levels were higher following sleep in the laboratory 30 minutes after awakening. However, no significant differences were noted for any salivary biomarker between the 1 st and 2 nd night in the sleep lab, suggesting that these endpoints were not influenced by exposure to noise on the 2 nd night. Waking profiles of alpha-amylase were not influenced by where the subjects slept. Subjective reports of sleep disturbance following sleep in the lab were also obtained. For most of the day there was no apparent influence of the laboratory noise exposure. However, subjects did report more sleepiness during the evening (8 pm) following the 2 nd night in the laboratory. In general, overall sleep quality was rated slightly higher upon awakening from sleep at home. Factors that might have contributed to the observations in this study are discussed, including those related to the potentially non-representative sample. Keywords: Salivary biomarkers, sleep disturbance, night-time noise
How to cite this article:
Michaud DS, Miller SM, Ferrarotto C, Konkle AT, Keith SE, Campbell KB. Waking levels of salivary biomarkers are altered following sleep in a lab with no further increase associated with simulated night-time noise exposure. Noise Health 2006;8:30-9 |
How to cite this URL:
Michaud DS, Miller SM, Ferrarotto C, Konkle AT, Keith SE, Campbell KB. Waking levels of salivary biomarkers are altered following sleep in a lab with no further increase associated with simulated night-time noise exposure. Noise Health [serial online] 2006 [cited 2023 Jun 3];8:30-9. Available from: https://www.noiseandhealth.org/text.asp?2006/8/30/30/32465 |
| Introduction | |  |
There are clear deleterious consequences associated with accumulated sleep deficit that suggest sleep serves both a psychological and a physical restorative function. [1],[2],[3] These range from an increased sense of fatigue [4] and impaired task performance [5],[6] to an overall sense of general malaise. [7] Evidence that sleep disturbance can influence stress-sensitive biomarkers, such as cortisol and catecholamines, [8] provides a potential biological link between sleep disturbance and stress-related disorders. The sleep loss threshold for adverse health outcomes is certainly not well-established. However factors that contribute to impaired sleep are known; including alcohol consumption, [9] hormonal fluctuations, [10],[11] stress/anxiety disorders, [12],[13] shift work [14] and age. [15],[16] Environmental variables, such as noise, can also contribute to sleep disturbance. [17],[18]
Much of the research on environmental noise-induced sleep disturbance (EN-ISD) has focused on noise from transportation sources, such as aircraft, road traffic and rail. [19],[20] Construction noise has received less attention, but a recent finding indicates that the major complaint from residents living near the construction of the central artery tunnel in Boston was the nighttime use of backup alarms on construction vehicles. [21] An acoustic backup alarm consists of a series of repetitive on-off tones that are emitted while the vehicle is reversing. When the vehicle ceases to reverse and subsequently advances, the alarm is not sounded. Backup alarms may be particularly intrusive to sleep because they are intended to be distinguished from background sounds.
Regardless of the source, studies on EN-ISD do not always yield consistent results with respect to the objective or subjective parameters of sleep disturbance. Furthermore, there is concern in this area that one's response to simulated noise exposures in the sleep laboratory may not be applicable to EN-ISD in the home environment.
Analysis of several field and laboratory studies has shown that the threshold for noise-induced awakenings was lower in the laboratory environment, likely because of the novelty associated with the sleep environment. It has also been suggested that in the natural environment people habituate to noise-induced awakenings. [22],[23],[24] There is support for the "novelty influence" on laboratory results insofar as the environmental context, specifically the degree of novelty, has been shown to increase the immediate salivary cortisol response to moderate psychological stress (Trier social stress test). [25] Therefore, the novel environment of the sleep lab might result in elevated cortisol that could interfere with sleep by increasing cortical arousal and decreasing slow wave sleep. [8] For laboratory sleep studies, most researchers in the field of noise and sleep exclude the 1 st night of analyses from laboratory experiments, to avoid the so-called first night effect (FNE). [26] However, due to the small scale of this study, the 1 st night was included to reduce costs and make the overall experiment shorter.
No study to date has directly assessed how sleeping in a laboratory (compared to sleeping at home) may influence changes in cortisol and catecholamines throughout the day, over-and-above any impact that nighttime noise exposure may have on them. There is a wide-spread interest in salivary cortisol, particularly the "awakening response", whereby elevated levels can be suggestive of an overactive hypothalamic pituitary adrenal (HPA) axis. Elevated morning levels have been associated with chronic stress in general, including workplace stressor exposure; [27] morning cortisol levels are also elevated in patients who suffer from depression. [28] On the other hand, blunted morning cortisol levels have been observed in people suffering from burnout [29] and a recent laboratory study showed a suppressed morning cortisol response in individuals exposed to nighttime low frequency noise. [30] While cortisol represents the endocrine arm of the stress response, more recent studies have shown that salivary alpha-amylase levels are highly positively correlated with the activity of the sympathetic nervous system. [31],[32] Together, salivary cortisol and alpha-amylase profiles provide a comprehensive assessment of the stress response without requiring multiple urinary and/or plasma sampling. Furthermore, to our knowledge, the influence of the sleeping environment on melatonin levels has not yet been reported, despite the knowledge that melatonin is sensitive to disrupted sleep patterns [33],[34],[35] and associated with subjective measures of sleep disturbance. [36]
In the present study, we investigated the effect of night time exposure to a simulated backup alarm on salivary biomarkers and subjective reports of sleep disturbance in a sleep lab. Further, we directly assessed the impact that sleeping in a laboratory has on the waking salivary cortisol, alpha-amylase and melatonin profiles by comparing (within the same subjects) patterns on days following sleep at home to those following sleep in the laboratory.
| Materials and Methods | | |
Subjects: Twelve subjects (7 males, 5 females) between the ages of 19 and 25 volunteered to participate in this study. Subjects were recruited from the university population without regard for their sleep environment at home. While sleeping at home they were not exposed to any of the experimental conditions carried out in the sleep laboratory (see below). Subjects were instructed to sleep at home as they normally would. No subject reported a history of psychiatric, neurological or audiological disorder. Additionally, no one reported disordered sleep as indicated by the Pittsburgh sleep quality Index. [37] All subjects were asked to read and sign a consent form that provided details of the experimental paradigm and procedures. Each subject received an honourarium for their participation in this study. This study was conducted according to ethical guidelines established by the Canadian Tri-Council (natural, medical and social sciences) Research board and approved by the human research ethics boards at the University of Ottawa and Health Canada.
Laboratory sleep environment: Each subject spent two consecutive nights in the windowless sleep chamber that measured approximately 4 x 3 m. The room, which was similar to a dormitory, was equipped with a dim reading light and a main overhead light. The walls were sound insulated to attenuate sounds originating from the adjacent sleep recording room.
Salivary sampling procedure: To the extent possible, we tried to minimize putative circa-septan (weekly) rhythms in salivary cortisol. [38] The 4 consecutive sampling days began on Friday for 6 of the subjects, on Sunday for 2 subjects, Monday for 2 subjects and Wednesday for 2 subjects. Subjects were provided with instructions of the procedure to follow for the collection of saliva samples for each of the 4 day sampling periods. The four days were, Baseline, representing samples taken following normal sleep at home (before going to the lab), Lab1 and Lab2, corresponding to samples taken following both respective sleep periods in the lab and PostLab, referring to samples taken once subjects resumed sleep at home. Subjects were instructed to refrain from eating and drinking alcoholic beverages at least 30 min and 12 hr, respectively, before providing the sample. Also, they were instructed to rinse their mouth with water 10 min before providing the sample. Subjects were instructed to provide saliva samples on six occasions: immediately upon awakening (awakening), 30 minutes after awakening (+30 min), ninety minutes after awakening (+90 min), noon, 5 pm and before going to bed. Subjects also recorded the actual sampling time so that variations in sampling times could later be assessed. The sampling regimen was selected to ensure that potential changes over the course of the day would be detectable. Saliva samples were collected by having subjects place Salivettes (Sarstedt, Inc., Rommelsdorf, Germany) in their mouth for a period of 1-2 min. Samples were temporarily refrigerated at ~4șC for up to 7 days , after which they were transported to the lab and immediately centrifuged at 4șC (1000 x g for 5 min). To avoid potential multiple freeze-thaw effects on biomarkers, samples were fractioned and stored at -30șC until cortisol, alpha-amylase and melatonin assays were conducted (about 2-3 weeks later).
Enzyme immunoassay (EIA): Commercially available salivary hormone EIA kits were used to determine saliva levels of cortisol, alpha-amylase (Salimetrics Inc., PA, USA) and melatonin (Alpco Diagnostics, NH, USA). According to manufacturers' specifications, alpha-amylase levels were determined in singles, while cortisol and melatonin were assayed in duplicates. For all assays, samples were thawed, re-centrifuged (21000 x g, 2 min @ 4șC) and the supernatant aliquoted as unknowns into the assay. The physiological half-life for cortisol, melatonin and alpha-amylase is <1 hr, ~40 min and 2 hr, respectively.
Auditory stimuli: The impact of exposure to a series of simulated backup alarms on evoked potentials (presented as a separate manuscript, [39] waking salivary biomarkers and subjective sleep parameters was assessed by exposing subjects to a train of five consecutive 1000 Hz, 500 ms pure tones that were presented monaurally to the right ear of each subject on the 2 nd night in the sleep lab (Lab2). An Eartone 3A foam-padded earphone insert produced the auditory stimuli (25 cm of standard plastic tubing, 2.5 mm in diameter). The insert earphone was used to control for consistency of stimulus presentation in spite of head movement and ear position during the night. The offset-to-onset period of the tones was also 500 ms. In order to simulate typical backup alarms, each tone had a 2 ms rise-and-fall time. The sound pressure level (SPL) of the stimulus was set at either 80 or 60 dB in different conditions. The delay between trains of 5 consecutive stimuli (offset to onset) varied between 15 and 20 s. A total of 30 trains of stimuli (i.e., 150 total stimuli) were presented in a block. On average approximately 15 blocks were presented to each subject over the entire night. The auditory stimuli were synthesized using a 16-bit waveform generator card. Stimulus level was verified using a Bruel and Kjaer 2209 sound level meter and Bruel and Kjaer 4152 artificial ear with 2 cm 3 coupler. The calibration of the artificial ear was checked with a Bruel and Kjaer 4220 pistonphone. Background sound levels in the sleep room on both nights were less than 35 dBA during sleeping hours.
The first night in the lab (Lab1) was considered the adaptation night so subjects could acclimatize to the EEG electrodes and earphone. Subjects were informed that the stimuli would be presented at different times during the sleep period on both nights in the lab. In actual fact, stimuli were only presented during the second sleep night (Lab 2). Following lights out, subjects spent 480 min (+5 min) in bed. On the second night of the study, stimulus presentation did not begin until at least 10 min had been spent in definitive sleep (stage 2 or SWS). The stimuli were terminated if the subject awoke. During sleep, the time between stimulus presentation blocks was randomized to be between 10 and 30 min. At least two blocks of stimuli were presented in stages 2, 3 and 4 (combined to form SWS) and REM sleep.
Subjective reports: Subjects were asked to complete two questionnaires that described the quality of their sleep in the laboratory. The Stanford sleepiness scale (SSS) [40] was completed following both nights of sleep at 08:00, 12:00, 16:00 and 20:00. This consists of a 7 point scale in which 1 = feeling alert and wide awake to 7 = sleep onset soon; lost struggle to remain awake. Subjects were also asked to complete a questionnaire indicating how many times they recalled awakening during the night, the duration of each recalled awakening, whether they recalled hearing the sounds and to what extent the sounds disturbed them (1= not at all; 3 = a great extent). In addition, subjects rated overall sleep quality on a 7-point Likert scale in which 1=extremely poor to 7=excellent, upon awakening from sleep in the lab and sleep at home.
Statistical analyses: All statistical analyses were carried out using the STATISTICA software package version 6.1 (StatSoft, OK, USA). The levels of cortisol, melatonin and alpha-amylase were not correlated, which justified separate analyses for each hormone. Hormone concentrations were evaluated via a factorial within-subjects measures design. The two repeated factors were Location with four levels (Baseline, Lab1, Lab2 and PostLab) and Sampling Time with six levels (awakening, +30 min, +90 min, noon, 5 pm, before sleep). Data points that were deemed to be too low for detection were replaced by a value representing the lowest level of analytical sensitivity of the assay. For missing values, the average hormone concentration across all other subjects was substituted. Note that analysis of the alpha-amylase concentrations was performed on log transformed data in order to minimize the effects of the standard deviations being proportional to the means. To permit comparisons with other reports, the raw data for alpha-amylase is also presented in [Table - 1]. All analyses were corrected for violations to the assumption of sphericity by the Huynh-Feldt (H-F) procedure. [41]
Further probing of the data consisted of conducting simple effects analyses in the case of a significant interaction, followed by appropriate pair-wise comparisons; a Bonferroni correction factor was applied to these analyses. Statistical analyses of subjective sleep disturbance ratings obtained from the two questionnaires filled out following sleep in the lab (Lab1 vs. Lab2) were conducted using t -tests. Friedman's ANOVA was used to analyze the subject's ratings of sleep quality on the 7-point Likert scale upon awakening following sleep at home and sleep in the lab. Friedman's rank test was used to conduct the non-parametric analyses on subjects' reported sampling times for each of the 6 daily saliva samples, provided across all four locations.
| Results | | |
Salivary cortisol: Overall analysis of the cortisol concentrations revealed a significant interaction of sampling time and location (F 7,72 = 3.01; P = 0.009, H-F correction applied). Closer investigation of the data suggested that the difference in cortisol levels between the different testing locations appeared to be at the morning sampling times. Analyses of the simple effect of location at the first sampling time (awakening) revealed a significant difference (F3,9 = 3.91; P = 0.048) between Locations. Analysis of the data associated with the second morning sample (+30 min) also showed a significant difference as a function of Location (F3,9 = 6.40; P = 0.013) such that cortisol levels were higher following sleep in the lab compared to those collected after the baseline sleep period at home (Baseline vs Lab1; F1,11 = 9.15; P = 0.012 and Baseline vs Lab2; F1,11 = 13.80; P = 0.0034). The overall daily profile of cortisol levels appeared similar irrespective of the location of testing with the exception of the PostLab location +30 min after awakening, where the rise in cortisol typically observed at this time point was notably absent [Figure - 1].
Salivary melatonin: The mean melatonin concentration values are presented in [Figure - 2]. The overall diurnal pattern in the levels of melatonin was similar for all testing environments. Melatonin levels were highest in the early morning, decreased throughout the day and began to increase again at night. However, statistical analysis of these data yielded a significant interaction between testing location and sampling time (F9,88 = 2.35; P = 0.02 with H-F correction). Simple effects analyses revealed no difference between locations at awakening but a difference was detected at +30 min (F3,8 = 5.94; P = 0.020) and before sleep (F3,8 = 4.34; P = 0.043). Melatonin levels from samples collected in the home location (Baseline and PostLab) were significantly different from those collected in the laboratory environment (Lab1 and Lab2) such that at +30 min home levels were lower than those in the laboratory (F1,10 = 10.75; P = 0.008), while the opposite pattern was apparent for the samples taken before sleep; home vs. lab (F1,10 = 6.25; P = 0.031).
Salivary alpha-amylase: Log transformed alpha-amylase levels (original units presented in [Table - 1]) appeared to steadily increase in the morning and plateau at the later sampling times [Figure - 3]. A significant effect of sampling time was evident for these data (F3,21 = 22.46; P = 0.000002). Furthermore, this profile was consistent for all testing locations suggesting that alpha-amylase levels were not influenced by the location in which the subject slept the previous night.
Specific comparison of the two lab conditions across the sampling times did not reveal any difference in cortisol or melatonin levels. Furthermore, calculating Cohen's d, [41] a measure of effect size, yielded d ≤ 0.1. Typically, a small, medium and large effect are considered to exist when d = 0.2, 0.5 and 1.0, respectively. [41] Finally, power calculations revealed that a much larger sample size would be required to increase power levels substantially beyond that observed for cortisol and melatonin (i.e., 2.5% and 4.1%, respectively). This contrast was not performed on the alphah-amylase data given that there was no difference between location or any interaction with sampling time.
Actual sampling times. [Figure - 4] provides a plot of the variability in actual sampling times for 11 of the 12 subjects across all 4 locations. Non-parametric analyses of the actual sampling times was conducted for each location using Friedman's rank test. Analyses revealed a significant difference between locations for samples provided immediately upon awakening (χ2 F3 = 13.18, P = 0.0043); + 90 min (χ2 F3 = 15.62, P = 0.0014); noon (χ2 F3 = 8.82, P = 0.032); and 5 pm (χ2 F3 = 13.26, P = 0.0041). There were no significant variations at the + 30 min and before sleep samples. Generally, the variation in actual sampling times tended to be greater in the home environment (Base and PostLab) compared to in the lab environment. This was particularly evident for the morning sampling periods.
Subjective ratings of disturbance: T-tests were carried out to compare the effects of the presentation of the acoustic stimuli (i.e., Lab1 vs Lab2). Neither the subjective impression of the number of awakenings nor the time spent awake differed between the two nights ( P > 0.05). Subjects reported hearing the acoustic stimuli more often on the night the stimuli had actually been presented (Lab2) compared to when they had not been presented (Lab1). This difference was significant, P < 0.05. Although more subjects reported that the sounds did cause an awakening, the difference between the two nights was not significant, P > 0.05. Subjects rated their sleep to be more disturbed by the perception of the auditory stimuli following Lab2, but the difference failed to attain significance, P < 0.08.
Overall subjective sleep quality: Upon awakening from sleep at home and sleep in the lab, subjects rated their quality of sleep on the 7-point Likert scale, where 1 = extremely poor and 7 = excellent. We observed an overall difference (χ2 F3 = 11.13; P = 0.011) on these ratings. Given that Baseline ratings did not differ from PostLab and the Lab conditions did not differ from each other, we collapsed the data to represent a Home condition (sum of Baseline and PostLab) and a Lab condition (sum of Lab1 and Lab2). A Wilcoxon matched-pairs test indicated that ratings from the Home and Lab conditions were different (Wilcoxon test, P = 0.015) with slightly higher mean scores for subjective sleep quality reported upon awakening at Home (5.34) versus awakening in the Lab (4.21).
| Discussion | | |
When it comes to understanding how night-time noise exposure might disturb sleep, a crucial question remains unanswered regarding data obtained in the sleep laboratory. That is, to what extent do these results transcend the artificial nature of the laboratory and allow one to predict and/or estimate how noise exposure at home might disturb sleep? By extension, it is unknown if such data can be used to develop policies on nighttime noise guidelines. The general consensus that sleep disturbance (especially awakenings) is more apparent in the lab is based on comparing thresholds for awakenings between studies conducted in the lab, to those conducted in the field . However, such cross-study comparisons are limited by methodological variations between studies, which make it exceedingly difficult to attribute any differences solely to the sleep environment. To our knowledge, no study has directly assessed sleep disturbance as a function of the environmental setting, but there are a number of reports supporting the contention that data obtained following the first night in the lab can be very different to that obtained afterwards. [26],[42],[43],[44],[45]
Experience gained from the large-scale construction of the central artery tunnel in Boston suggests that the night-time use of backup alarms represented a significant source of complaints. By their very nature, acoustic alarms are meant to draw one's attention away from ongoing activity and it seems plausible that they could represent a significant source of sleep disturbance. This study aimed to investigate how exposure to a simulated backup alarm during sleep in a laboratory environment would alter subjective measures of sleep disturbance as well as the profile of waking salivary biomarkers the following day. In order to evaluate the impact that the laboratory itself may have had on salivary biomarkers, we also monitored these endpoints following sleep at home, before and following sleep in the lab.
In general, we found that subjects did report slightly reduced sleep quality, as reported on a 7-point Likert scale, upon awakening in the lab compared to that reported following awakening at home. For this global measure of sleep quality there were no differences between the two nights in the lab that might be related to the FNE or to noise exposure on the 2 nd night. Although no subjects indicated any discomfort associated with the insert headphone, subtle effects might have contributed to impaired subjective sleep quality in the lab. A loud-speaker set-up might be one way of circumventing this concern. It is also conceivable that the variability in actual awakening time had some influence on subjective sleep quality because scheduled awakening times in the lab may have been slightly more unpleasant than unscheduled awakening at home. The only notable difference that we observed with respect to subjective measurements of sleep disturbance derived from the SSS questionnaire was an increase in subjective sleepiness during the evening (8 pm) following the 2 nd night in the laboratory. In addition, we did observe a significant reduction in melatonin levels at this time point, but it was similarly reduced following both nights in the lab, relative to both home conditions. These somewhat contradictory findings may warrant further investigation, since lower evening melatonin levels have been linked to serious sleep disturbance, particularly insomnia.
Failure to find an effect of the acoustic stimuli with respect to subjective reports of sleep disturbance runs counter to what might be expected from the frequent complaints about the disruptive effects of backup acoustic alarms on sleep. It ought to be considered that there may be fundamental differences between our subjects (who are university students), who presumably are not disturbed by the night time use of backup alarms and those who live near a construction project and frequently complained about the use of these alarms at night. Also, it is unclear if the complaints in past studies were associated with awakenings and/or an inability to initiate/resume sleep from the wakened state. In this study, the presentation of the stimuli was stopped if subjects awakened and therefore we were unable to assess the impact these alarms may have had on returning to the sleeping state. These factors, together with the limited number of subjects, can not be expected to necessarily be representative of the personal and situational variables that characterize natural field conditions. Indeed, our sample size may have been too limited to observe the subjective sleep disturbance reported in the field.
Consistent with subjective measures of sleep disturbance, there were no observable differences in any of the salivary biomarkers following either night of sleep in the lab. This suggests that noise exposure on the 2 nd night did not have any effect on our measured endpoints. Furthermore, as noted in the results section, the low effect size and corresponding power for both cortisol and melatonin following the contrast between the two nights in the lab would suggest that any prediction of a difference in the levels of these biomarkers that might result from noise exposure on the 2 nd night would be unfounded. For the monitored salivary biomarkers, we observed the expected fluctuations in levels throughout waking hours similar to those previously reported. [46],[47] By-and-large, these patterns were essentially the same when subjects slept at home or when they slept in the laboratory the previous night. However, there were some notable exceptions to this with respect to both cortisol and melatonin levels in the morning. The expected increase in cortisol level after awakening was not observed when the subjects resumed sleeping at home (i.e., PostLab, awakening versus PostLab, +30 min). Furthermore, a clear elevation was apparent for cortisol levels 30 minutes after awakening following both nights in the sleep lab, when compared to the baseline home condition. Melatonin levels at this time were significantly elevated following sleep in the lab compared to both home sampling conditions (Baseline and PostLab).
The greater elevation in salivary cortisol levels shortly after awakening in the lab (+30 min) is suggestive of a greater activation of the HPA axis under these conditions. This would be consistent with the notion that waking in the laboratory environment may act as a mild stressor, compared to the more familiar home environment, where our subjects slept unencumbered by experimental apparatus. Certainly, it ought to be considered that sleeping in a novel environment, attached to recording electrodes, represented an atypical sleep condition that might be perceived as sufficiently novel to trigger a greater increase in cortisol following awakening. Similarly, in our study, sleep was restricted to an 8 hr period that could have instilled in our subjects an anticipatory awakening response, which has been shown to accelerate the release of plasma ACTH levels 1 hr before awakening. [2] Although this would typically evoke a further increase in cortisol, these authors failed to observe a corresponding elevation in cortisol upon awakening, which suggests that an anticipatory awakening response may actually be associated with adrenal insensitivity to circulating ACTH. Therefore, a tentative conclusion at this time could be that a greater cortisol response following awakening in the lab reflected the stressful nature of this environment.
A more striking observation with respect to cortisol levels was the complete absence of an increase in cortisol 30 minutes after awakening when subjects resumed sleeping at home (i.e. PostLab). Others have reported that the morning cortisol response is dependent upon actual awakening time. [48],[49] Indeed, awakening sample times varied widely in the PostLab setting, which may account for the apparent shift in the cortisol response at this time. Alternatively, a rapid fall in plasma cortisol has been shown to occur in spontaneously awakened subjects that quietly remain awake lying in bed, [50] which may have unknowingly occurred under the PostLab conditions in our study. Additional work will be necessary to determine the reproducibility and underlying mechanism(s) of this finding.
Melatonin was significantly elevated 30 min after awakening following sleep in the laboratory (Lab1 and Lab2), relative to that observed at home (Baseline and PostLab), while the opposite pattern was observed for the final evening sample. Since salivary melatonin levels are known to be dependent upon both light intensity and the duration of light exposure, it should be considered that our observed changes in salivary melatonin levels might reflect differences in lighting between the home and lab settings, especially given that our sleep lab was without windows. [51] Indeed, prolonged light exposure at home following the completion of the study would suppress melatonin levels as observed under the PostLab condition. Also, it has been shown that posture is related to melatonin levels in such a way that changing from a supine to a standing position showed elevated salivary and plasma melatonin levels. [52] It is conceivable that subjects arise from awakening to a standing position more quickly following an awakening in the lab than they do at home, which could account for the spike in melatonin 30 minutes after awakening. Again, actual awakening time may also influence the morning melatonin response, similar to the cortisol awakening response. The magnitude of the importance of these factors cannot be assessed because this study did not account for lighting conditions or changes in posture.
This was the first study in which changes in salivary alpha-amylase levels were assessed following nighttime noise exposure. The rationale for selecting this biomarker was based on reports that it represented the activity of the sympathetic nervous system. Some [53] but not all studies [54] have shown this system to be influenced by nighttime noise exposure. [55] We were encouraged that this marker was sensitive to stressor exposure since two trials in our lab showed that it increased in response to public speaking (1 female) and anticipating blood draw (1 male). We observed a variation in alpha-amylase levels throughout the day that was characterized by a steady increase in concentrations from the morning to late evening time period. This daily variation was remarkably similar, irrespective of where subjects slept the preceding evening. To the extent that salivary alpha-amylase activity is thought to be representative of changes in plasma catecholamines, our study suggests that this endpoint was insensitive to simulated backup alarms during sleep and not influenced by the sleeping environment. However, future research is needed to determine if transportation sources that have been shown to influence catecholamines (see above) would also alter salivary alpha-amylase levels.
| Conclusion | | |
The lack of any major differences in subjective measures or salivary biomarkers between the 1 st and 2 nd night of sleep in the laboratory suggests that our source of night time noise exposure on the 2 nd night was without effect on these endpoints. To evaluate how sleeping in the lab might influence our selected salivary biomarkers we compared levels following sleep in the lab to sleep at home. The overall daily patterns for cortisol, melatonin and alpha-amylase were quite similar when subjects slept in the lab or at home. The only exception to this was an observed increase in both cortisol and melatonin shortly after awakening from sleep in the lab. We suggest that the elevated cortisol was indicative of a mild stress response under these conditions that was not present in the more familiar home environment. Elevated melatonin at the same time may reflect differences in lighting conditions and/or postural changes in the lab, relative to the home. Alpha-amylase patterns, however, did not change between the home and the laboratory environment and therefore may prove to be useful in predicting effects in the field because it appears to be insensitive to where one sleeps. Likewise, it may prove to be a useful tool in distinguishing between stressors that selectively activate the HPA axis and those that also activate the sympathetic system. To this end, future work is needed to determine if other noise stimuli cause changes in this system.
| Acknowledgements | | |
This makes an incorrect statement that a financial grant was provided for this research. Authors D. Michaud, S. Miller, C. Ferrarotto and S. Keith were at the time of this work all employees of Health Canada, Consumer and Clinical Radiation Protection Bureau, Healthy Environments and Consumer Safety Branch. Co-author K. Campbell was given a contract for his contributions to this research.
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Correspondence Address:
David S Michaud
Acoustics Division, Consumer and Clinical Radiation Protection Bureau, Healthy Environments and Consumer Safety Branch, 775 Brookfi eld Road, Address locator 6301B Ottawa, Ontario K1A 1C1
Canada
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1463-1741.32465
[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4]
[Table - 1], [Table - 2], [Table - 3] |
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