Salivary α-Amylase Reactivity to Laboratory Social Stress With and Without Acute Sleep Restriction

Abstract

A growing literature suggests that salivary α-amylase (sAA) may serve as a minimally invasive marker of psychophysiological stress-induced activity of the sympathetic-adrenal-medullary system (SAM). Previous inconsistencies in the experimental literature relating sAA response to short sleep duration may be as a result of poor reliability of self-reported sleep time, suggesting that further examination of sAA response following verified sleep loss is required. With regard to the potential usefulness of sAA as a biomarker of psychosocial stress in the laboratory, previous research has also relied primarily on traditional psychosocial stress protocols, including physically present evaluative observers. The present study aimed to examine sAA response following a period of verified acute sleep restriction compared to a rested condition, in addition to examining the sensitivity of sAA response to a laboratory stress protocol that exposed participants to negative social evaluation presented by video relay. One hundred and eight healthy young adults (age 17–22 years; M = 18.39 years, SD = 0.87) completed a laboratory social stress task and provided saliva samples pre- and post-stressor presentation, after a night of partial sleep restriction or a full night’s rest. Marked increases in sAA activity to the video-relayed stressor were observed in both rested and sleep restricted groups. Further, sleep restricted participants exhibited significantly increased basal levels of sAA activity. The data corroborate previous limited data indicating a general upregulation of sAA activity following poor sleep and support previous findings concerning the efficacy of an experimental paradigm that presents laboratory social stress by means of video recording.

Shortened sleep fuels inflammatory responses to marital conflict: Emotion regulation matters

“…These results suggest that recent nights without sufficient sleep may promote a person’s inflammatory responses to interpersonal conflict and perhaps other stressors. Previous studies have demonstrated the effects of sleep-loss-related stressor reactivity (i.e., via the sympathetic nervous system, SNS) to challenging computer-based cognitive tasks after extreme sleep deprivation (Liu et al, 2015; O’Leary et al, 2015). Furthermore, examining responsiveness to marital conflict around a preexisting disagreement, a personally meaningful stressor, enhanced the external validity of the sleep-reactivity association.…”

“…Experimentally sleep-deprived people mount exaggerated sympathetic responses to stressful tasks compared to well-rested people (Liu et al, 2015; O’Leary et al, 2015). Because sympathetic activation heightens inflammation (Pongratz and Straub, 2014), increased inflammatory responsiveness may follow short sleep in daily life as well.…”

Sleep Duration and Quality in Relation to Autonomic Nervous System Measures: The Multi-Ethnic Study of Atherosclerosis (MESA)

“…cortisol, amylase) responses to stressors has been examined in animals 58 and in restricted human population samples, only children 38,59 or only women. 60 In a more recent study 39 with 108 young adults ages 17 to 22 y, sleep restriction was imposed on the participants before a social stressor task. The study found differences in sAA at baseline but no differences in the response to the stress task in the two groups (with sleep restriction versus without).…”

“…34 A few studies have examined the association of sleep with sAA responses to mental stress, but these have been restricted to children 38 or healthy young adults. 39 No reported study to our knowledge has evaluated the association of habitual sleep characteristics with sAA responses to mental stress in a population-based sample.…”

Decreased salivary alpha-amylase levels are associated with performance deficits during sleep loss

“…Interestingly, it has been reported that sAA measures also exhibit a similar diurnal profile, with levels peaking in the afternoon and declining towards the evening (Nater et al, 2004;Nater et al, 2007). Additionally, increased sAA activity has also been reported following acute sleep restriction (O'Leary et al, 2015) and total sleep deprivation (Seugnet et al, 2006), suggesting sAA may be a measure of increased sleep pressure. Based on these findings, it is conceivable that changes in sAA may reflect deviations in performance during extended wakefulness.…”