Effects of Acute Sleep Restriction on Laboratory and Ambulatory Physiological Reactivity in Young Adults

Abstract

Introduction. Reduced sleep duration has been associated with adverse health outcomes, in particular negative cardiovascular health. The mechanisms by which sleep loss may influence cardiovascular health are unclear but may be related to alterations in physiological stress responding. The current project sought to assess the association between sleep duration and cardiovascular response to laboratory social stress in addition to examining ambulant cardiovascular functioning using experimental partial restriction of sleep duration in a sample of healthy young adults. To objectively monitor adherence to the sleep manipulation, participants were provided with a wrist activity monitor. Associated physiological processes, including salivary markers of neuroendocrine stress functioning and inflammation were additionally monitored to further explore the effects of acute sleep restriction on stress system functioning across both laboratory and ambulatory contexts. Methods. Resulting from pooled data collected from 128 college students, five empirical studies are reported, incorporating successive methodological refinements to help advance understanding of the effects of sleep loss on physiological responding. In a sample of 93 college students, Study 1 examined laboratory cardiovascular reactivity (i.e., systolic and diastolic blood pressure [SBP and DBP, respectively], and heart rate [HR]) during evaluative social stress, including assessments of hemodynamic determinants of blood pressure, to determine if cardiovascular reactivity to laboratory stress (CVR) was altered under conditions of experimental sleep restriction relative to a rested group. The primary aim of Study 1 was to examine laboratory CVR as a possible mechanism through which sleep restriction may be related to increased cardiovascular risk. In Study 2, in order to assess possible additional physiological effects of laboratory stress that may exist across stress systems, salivary alpha-amylase response (sAA) to social stress, as a measure of sympatho-adrenal-medullary system (SAM) activity, was examined in 113 college students following acute sleep restriction, compared to a rested group. The SAM axis releases the hormones epinephrine and norepinephrine and denotes the instantaneous sympathetic response to stress. However, as only two previous examinations of sAA response following sleep loss exposure obtained objective assessment of sleep duration (using actigraphy), further examinations of sAA response following verified short sleep durations were required. A secondary aim sought to shed light on the sensitivity of the sAA response to a laboratory stress protocol (as used in Study 1), exposing participants to negative social evaluation, presented by video relay. Study 3 extended the traditional CVR laboratory protocol, testing the potential for the findings of the previous laboratory based CVR observations in Study 1, to generalise to conditions outside of the laboratory setting. Further, few studies have measured how sleep loss affects cardiovascular response to naturalistic stressors, while periods of interpersonal contact have been suggested as a useful task for investigating CVR in the field. One hundred and six participants underwent ambulatory blood pressure and HR monitoring while engaging in everyday activities, comparing cardiovascular arousal during periods of high and low stress and interpersonal contact, whilst rested and sleep restricted. Examination of nocturnal blood pressure dipping was also conducted to explore if the habitual nocturnal reduction in blood pressure is associated with reduced sleep duration. In Study 4, in order to establish whether reduced sleep duration influences ambulant measures of hypothalamic-pituitary-adrenal (HPA; i.e., cortisol) activity, advancing the previous limited and incomplete research of such effects, the awakening response of cortisol was examined. Relative to SAM axis activation (Study 2), the HPA axis controls the longer-term neuroendocrine stress response. One hundred and twenty college students were requested to provide four waking saliva samples, in their own homes, over the first 45 mins post-awakening, for the assessment of the awakening response in cortisol. The previous studies (1 and 3) examined the influence of sleep restriction, social stress, and interpersonal contact, on measures of laboratory and ambulatory CVR. Study 2 examined levels of sAA, while Study 4 assessed measures of HPA activity, investigating sleep loss related change in cortisol awakening response and SAM related activation. However, failure to obtain adequate amounts of sleep has also been suggested to promote low-level systemic inflammation, itself associated with cardiovascular risk. In Study 5, a brief exploratory investigation into the effects of sleep restriction on levels of a novel marker of low level systemic inflammation, C-reactive protein (CRP) detectable in saliva, was examined in 120 college students, offering a preliminary examination of both the validity of the marker and its ability to detect change associated with reduced sleep duration. Results. Study 1 confirmed that relative to a rested group, acute sleep restriction was associated with alterations in the hemodynamic determinants of blood pressure in response to social stress (vascular response evident), while overall blood pressure response (SBP, DBP, and HR) remained unchanged between rested and sleep restricted groups. In Study 2, marked increases in basal sAA activity following one night of partial sleep restriction were identified. The data additionally corroborated previous findings regarding the sensitivity of [alpha]-amylase to laboratory social stress exposure, while further demonstrating a significant increase in sAA in response to an acute social stress protocol where the primary social evaluative element was presented by virtual (i.e., video-relayed) observers. Study 3 suggested the potential role that sleep restriction may have in negatively affecting both nocturnal ambulatory cardiovascular indices and reactivity to naturally occurring interpersonal contact (i.e., increased SBP and DBP), in ways that have been implicated in the etiology of heightened risk for cardiovascular disease. In Study 4, acute sleep loss was related to morning stimulation of the HPA-axis and, in particular, dampening of morning cortisol levels. Finally, in Study 5, while CRP, assessed in saliva, remained statistically unchanged following sleep restriction, increased CRP level in conjunction with greater body mass index, a known correlate of systemic inflammation, suggested an association between sleep restriction and augmented salivary CRP response. Conclusions. The findings provide evidence of alterations to both overall measures of cardiovascular function and underlying hemodynamic determinants, in addition to associative (neuroendocrine and inflammatory) physiological changes related to cardiovascular functioning, following acute sleep restriction, in both laboratory and ambulant conditions. Such data highlight lines of research leading to pathway clarification, though which reduced sleep duration may, over time, influence cardiovascular health.