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