Date Published: February 2, 2017
Publisher: Public Library of Science
Author(s): Daniel S. Quintana, Torbjørn Elvsåshagen, Nathalia Zak, Linn B. Norbom, Per Ø. Pedersen, Sophia H. Quraishi, Atle Bjørnerud, Ulrik F. Malt, Inge R. Groote, Tobias Kaufmann, Ole A. Andreassen, Lars T. Westlye, Henrik Oster.
Heart rate variability (HRV) has become an increasingly popular index of cardiac autonomic control in the biobehavioral sciences due to its relationship with mental illness and cognitive traits. However, the intraindividual stability of HRV in response to sleep and diurnal disturbances, which are commonly reported in mental illness, and its relationship with executive function are not well understood. Here, in 40 healthy adult males we calculated high frequency HRV—an index of parasympathetic nervous system (PNS) activity—using pulse oximetry during brain imaging, and assessed attentional and executive function performance in a subsequent behavioral test session at three time points: morning, evening, and the following morning. Twenty participants were randomly selected for total sleep deprivation whereas the other 20 participants slept as normal. Sleep deprivation and morning-to-night variation did not influence high frequency HRV at either a group or individual level; however, sleep deprivation abolished the relationship between orienting attention performance and HRV. We conclude that a day of wake and a night of laboratory-induced sleep deprivation do not alter supine high frequency HRV in young healthy male adults.
Heart rate variability (HRV) provides a non-invasive measure of cardiac parasympathetic nervous system (PNS) control [1, 2]. Meta-analyses have established a relationship between poor cardiac autonomic regulation and a range of psychiatric disorders [3–6]. HRV has also been associated to specific psychiatric illness symptoms, such as social cognition [7, 8], executive function , and self-regulation . Given the association with psychiatric symptoms across diagnoses, researchers have proposed that HRV may be a transdiagnostic symptom biomarker . HRV is also fundamental to leading biobehavioral frameworks used to understand social behavior and psychiatric illness, the polyvagal theory  and the neurovisceral integration model . However, to become a viable biomarker in studies of psychopathology, its intraindividual stability and variables that can modulate HRV need to be established.
Demographics, sleep, and heart rate variables are summarized in Table 2. There were no significant differences in age, sleep habits, or mood variables between the sleep and sleep deprivation groups (Table 2). While participants had less hours of sleep the night previous to testing (mean = 6.75, SD = 1.2) compared to the average hours of sleep over the previous month (mean = 7.61, SD = 0.8; t(39) = -4.37, p < 0.001), there was no difference in hours of sleep the previous night between groups (Table 2). Between-subjects ANOVA revealed a main effect for group on HRV, with the data providing substantial support that the sleep-deprived group had higher HRV compared to the sleep group (Table 3, Fig 1A). There was no main effect of time or time by group interaction, with the BFs providing substantial evidence for the null hypotheses that HRV was not different across time and that there were no group by time interaction effects on HRV. As the BF for the time by group interaction was 0.19, this indicates that the data were appropriately powered and the null hypothesis was 5.3 more likely than the alternative hypothesis. Between-subjects ANOVA revealed no significant main effect for group on HR–with data providing anecdotal support that the sleep-deprived group had a decreased HR overall compared to the sleep group–and no main effect of time (Table 3, Fig 1B). Finally, there was no significant time by group interaction, with data providing substantial evidence for the null hypothesis that there was no group by time interaction effects on HR (Table 3, Fig 1B). Utilizing a repeated-measures design, we have demonstrated that supine HRV is robust against 24-hour sleep deprivation and diurnal variation in healthy male young adults. As well as providing substantial evidence for no significant group by time interaction on HRV, the data also indicate strong reproducibility of HRV measures on an individual level across both sleep deprived and non-sleep-deprived participants. Consistent with the neurovisceral integration model , the data suggest that HRV is related to orienting attention at baseline; however, this relationship was not evident after sleep deprivation. The present research is also congruous with evidence suggesting that PNS, which is closely approximated by HRV, is not influenced by diurnal factors  or sleep disturbances , at least for a 24-hour period. It has been previously suggested that the effect of sleep deprivation on the ANS may only manifest in those who are more susceptible to the psychological stressors associated with sleep deprivation . Thus, the low likelihood of either trait or state anxiety in the study participants may have contributed to the non-significant effect of sleep deprivation on HRV. Reductions in HRV observed in longer periods of sleep deprivation [21–25] indicate that the PNS may only be robust against shorter periods of deprivation. Moreover, circadian influences on HRV have been reported [20, 67–69], however, in these instances HRV was recorded more regularly throughout the day. Regular assessment provides a much more nuanced view of circadian rhythms than the comparison of morning-to-night diurnal differences, thus the divergence of present result with other research may be due to having only one time point comparison. Moreover, studies investigating circadian changes tend to report increased HRV during the day , whereas the current study only recorded data at morning and night. Thus, researchers should still be particularly vigilant when comparing HRV collected during the afternoon to morning and night HRV data. Source: http://doi.org/10.1371/journal.pone.0170921