Elsevier

Psychoneuroendocrinology

Volume 81, July 2017, Pages 151-156
Psychoneuroendocrinology

Poor habitual sleep efficiency is associated with increased cardiovascular and cortisol stress reactivity in men

https://doi.org/10.1016/j.psyneuen.2017.04.013Get rights and content

Highlights

  • Poor habitual sleep is associated with exaggerated stress reactivity.

  • Sleep predicted blood pressure and cortisol levels during stress and recovery.

  • Objective sleep efficiency but not duration was significantly related to reactivity.

Abstract

Inadequate sleep and psychological stress can both elevate physiological stress markers, such as cortisol. Prior studies that have applied induced psychosocial stress after a night of experimental sleep deprivation have found these effects to be compounded. We examined whether the relationship between stress reactivity and poor sleep also extends to habitual sleep patterns. Fifty-nine adult male participants were recruited. Habitual sleep patterns were monitored with actigraphy for a week. Participants subsequently underwent the Trier Social Stress Test. Cardiovascular responses and salivary cortisol were measured at baseline, during stress, and during recovery. Subjects who showed poor habitual sleep efficiency during the week before stress induction responded with higher stress-related elevations of blood pressure and cortisol levels as compared to subjects with high sleep efficiency. This relationship between poor sleep efficiency and elevated blood pressure persisted during the post-stress recovery period. Similar associations between total sleep time in the week prior to the stress induction and physiological reactivity did not reach significance. Our findings indicate that habitual low sleep efficiency exaggerates cardiovascular and neuroendocrine effects of psychosocial stress, in a male population.

Introduction

Inadequate sleep and stress both have negative impact on health, increasing the risk for negative outcomes such as cardiovascular disease, diabetes and depression (Cappuccio et al., 2011, Cappuccio et al., 2010, Hamer et al., 2010, Hamer and Steptoe, 2012, Maglione et al., 2014, Susman et al., 1997). Moreover, the effects of inadequate sleep are known to potentiate the physiological effects of stress. Laboratory studies on the acute effects of total sleep deprivation (TSD) have found that TSD affects physiological markers of stress, elevating blood pressure (BP; Kato et al., 2000), bringing about immune suppression, and altered neuroendocrine function (Dinges et al., 1995, Spiegel et al., 1999, Wright et al., 2015). TSD also elevates evening cortisol levels, reflecting altered regulation of the hypothalamus-pituitary-adrenal (HPA) axis (Spiegel et al., 1999, Vgontzas et al., 1999). Over and above these effects on baseline physiology, sleep deprivation also exaggerates physiological responses to particular stressors. When exposed to stress induction, sleep deprived participants show greater physiological reactivity (i.e. increased BP, increased skin conductance levels and elevated cortisol responses) than those who had a night of normal sleep (Franzen et al., 2011, Liu et al., 2015, Minkel et al., 2014).

While experiments involving a night of total sleep deprivation on stress reactivity are important in uncovering the causal relationship of these effects, most persons are not regularly exposed to this type of sleep loss. Moreover, the impact of poor sleep on stress physiology may be particularly detrimental when patterns of inadequate sleep are experienced for longer periods of time. Long-term laboratory studies on the effects of short sleep are logistically difficult and expensive to undertake but studies examining the consequences of adverse habitual sleep patterns can be informative.

Several studies have investigated the association between habitual sleep patterns and stress reactivity in developmental contexts. In these studies, children and adolescents who report poor habitual sleep or have actigraphically verified low sleep efficiency, show higher cortisol elevations following stress induction (Mrug et al., 2016, Pesonen et al., 2012, Räikkönen et al., 2010), with some exceptions (Capaldi et al., 2005). As developmental changes occur both in sleep patterns and stress physiology during adolescence (Carskadon et al., 1998, Gunnar et al., 2009), it is important to investigate if these findings generalize to adults. The few studies of this type performed in adults have yielded inconclusive findings (Bassett et al., 2015, Mezick et al., 2014, Wright et al., 2007). Possible reasons for this include the use of non-optimal stress induction procedures (Wright et al., 2007), the use of different physiological outcome measures (BP, cortisol, etc.; Mezick et al., 2014) or not objectively measuring habitual sleep (Bassett et al., 2015).

In the current study we examined the association between habitual sleep, as measured by one week of actigraphy, and stress reactivity, induced by a strong stress procedure (Trier Social Stress Test; Kirschbaum et al., 1993). In order to examine the consistency between different physiological outcome measures, we measured both cardiovascular (BP, heart rate) and HPA reactivity (salivary cortisol). In light of prior total sleep deprivation studies, and studies on habitual sleep in adolescents and children, we hypothesized that indices of poor sleep (i.e. short sleep duration, low sleep efficiency) would be associated with exaggerated reactivity to stress (Mezick et al., 2014).

Section snippets

Participants & procedure

Fifty-nine male volunteers were recruited from the university population (mean age [sd] = 22.83 [2.49]). Initial selection based on a web-based questionnaire. In order to obtain a sufficient numbers of persons with short and longer habitual sleep durations, approximately equal numbers of persons who slept 7–8 h and less than 6 h per night, were enrolled from a larger sample of screened participants (Mezick et al., 2014). Habitual sleeping patterns were then objectively measured using wrist

Sample characteristics

By design, participants were exclusively males of Chinese ethnicity. They aged between 20–33 years. Resting physiological measurements taken during the baseline before the start of the stress induction indicated no clinically significant elevation of blood pressure and normal levels of salivary cortisol (Table 1). Furthermore, physiological measures at baseline were not correlated with habitual sleep metrics total sleep time (TST: all p's > 0.05) and sleep efficiency (SE: all p's > 0.05).

Sleep metrics

Discussion

The current findings demonstrate that poor sleep efficiency is associated with exaggerated reactivity to acute psychosocial stress. In our sample of young adult male participants, cortisol reactivity was inversely correlated with habitual sleep efficiency, objectively measured through seven days of actigraphy. This finding concurs with data from a sample of children (Räikkönen et al., 2010), in which individuals with poor actigraphically recorded sleep efficiency showed increased HPA-axis

Funding sources

This work was supported by a grant awarded to Michael Chee from the National Medical Research Council Singapore (NMRC/STaR/0015/2013) and the Far East Organization. The authors have not received any financial support from other sources.

Author contribution

SAAM, JCJL and MWLC have designed the study. SAAM, NBM and JCJL have conducted the study. SAAM has analyzed the data. SAAM, JCJL and MWLC have written the manuscript.

Acknowledgments

The authors would like to thank Vinod Khanna for assistance with data collection and analysis. This work was supported by a by a grant awarded to Michael Chee from the National Medical Research Council Singapore (NMRC/STaR/0015/2013) and the Far East Organization.

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    This work was performed at Duke-NUS Medical School Singapore.

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