First‐night effect on cardiac autonomic function in different female reproductive states

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Heart rate variability (HRV), i.e. the multidimensional changes in heart rate in time (Task Force, 1996), is mediated by the changes in the heart's autonomic innervation. Sympathetic output increases heart rate and decreases short‐term HRV (Task Force, 1996), while high vagal output results in bradycardia and increased respiratory sinus arrhythmia (Task Force, 1996). Several highly intercorrelated parameters based on both linear and non‐linear mathematical methods are used to measure HRV (Task Force, 1996; Yeragani et al., 1998). The evaluation of the triggers connected with decreased HRV is essential, as the risk of lethal and potentially lethal cardiovascular events and even overall mortality are increased with decreasing HRV (Huikuri and Stein, 2013).
Heart rate variability is strongly modulated by sleep and further by various sleep stages. From wake to stable non‐rapid eye movement (NREM) sleep, sympathetic activity decreases and vagal influence gradually increases, being at its highest in slow‐wave sleep (SWS; Ako et al., 2003; Versace et al., 2003; Virtanen et al., 2007). In rapid eye movement (REM) sleep, HRV closely resembles that seen awake, with rapid vagal to sympathetic fluctuations (Ako et al., 2003; Versace et al., 2003; Virtanen et al., 2007). Sleep architecture is deteriorated in an unknown environment, with less SWS and more light sleep (the so‐called ‘first‐night effect’; Agnew et al., 1966). Therefore, it can be assumed that during a first night in a sleep laboratory there is a decrease in parasympathetic and an increase in sympathetic activity. In young adults, selective SWS deprivation attenuates the nocturnal decrease in arterial blood pressure attributed to increased parasympathetic tone (Sayk et al., 2010), and similar findings together with a higher nocturnal heart rate are seen in young adults with low sleep efficiency measured by actigraphy (Ross et al., 2014). In self‐reported insomnia, short‐term HRV during light NREM sleep and REM sleep is decreased as compared with good sleepers, and sympathetic activity is increased during pre‐sleep wakefulness (Spiegelhalder et al., 2011; de Zambotti et al., 2014).
In aging, overall and especially vagally mediated HRV is decreased both in women and in men (Laitinen et al., 1998; Vigo et al., 2005). In premenopausal women, vagally mediated HRV indexes are higher than in same‐age men but, after menopause, this favourable effect vanishes and both sexes show similar HRV (Huikuri et al., 1996; Ryan et al., 1994). Changes in hormonal levels across the menstrual cycle influence autonomic function, with increased heart rate and decreased vagal function during progesterone peaks (de Zambotti et al., 2013b, 2017). Further, menopausal hot flushes are associated with an increased heart rate and a decreased vagal tone (de Zambotti et al., 2013a). In perimenopausal or recently postmenopausal women, hormone therapy (HT) used for climacteric symptom relief increases cardiac vagal output (Gökce et al., 2005; Huikuri et al., 1996; Mercuro et al., 2000; Rosa Brito‐Zurita et al., 2003; Rosano et al., 1997). However, in women more than 10 years postmenopausal either no effect (Niskanen et al., 2002; Virtanen et al., 2000) or even a decrease in vagal activity and non‐linear complexity of heart rate has been observed (Christ et al., 1999; Lantto et al., 2012; Virtanen et al., 2008). Therefore, it can be assumed that HT may promote cardiovascular risk in older postmenopausal women (Christ et al., 1999; Grodstein et al., 2006; Hodis and Mack, 2014; Virtanen et al., 2008).
Based on the above rationale, we set out to study nocturnal HRV during two consecutive nights in a sleep laboratory in study‐naïve young, perimenopausal and postmenopausal women.
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