STUDY OBJECTIVES: Recent work indicates that cardiac sympathetic activity is not influenced by the circadian system and instead decreases after sleep onset. However, little is known about the pattern of change in cardiac sympathetic activity during NREM/REM sleep cycles and whether this is associated with alterations in slow-wave activity (SWA). To address these questions, we examined SWA, cardiac sympathetic activity, heart rate and rectal and foot temperatures during the first three NREM/REM sleep cycles and during transitions between NREM and REM sleep.
DESIGN: Subjects were required to maintain a constant sleep-wake cycle for at least a week and have at least one adaptation night, before their night of recording.
SETTING: Individual temperature controlled bedrooms.
PARTICIPANTS: 10 young healthy males and females.
INTERVENTIONS: NA.
MEASUREMENTS AND RESULTS: All variables showed the greatest change in the first NREM cycle. Specifically, SWA, sympathetic activity, heart rate and foot temperature increased while rectal temperature decreased. After the initial increase, cardiac sympathetic activity decreased across the sleep phase, in association with a decrease in heart rate. Cardiac sympathetic activity did not significantly alter across NREM-REM cycles.
CONCLUSIONS: The results suggest that increases in heart rate and cardiac sympathetic activity early in the sleep period are, in part, a compensatory reaction to the concomitant thermoregulatory changes observed. These results also indicate that the effect of time asleep on cardiac sympathetic activity may be greater than the influence of sleep cycles. These results are discussed with reference to the recuperative value of naps.

In a longitudinal study of Dutch adolescent and young adult twins, their parents and their siblings, questionnaire data were collected on depression, anxiety and correlated personality traits, such as neuroticism. Data were collected by mailed surveys in 1991, 1993, 1995 and 1997. A total of 13,717 individuals from 3344 families were included in the study. To localise quantitative trait loci (QTLs) involved in anxiety and depression, the survey data were used to select the most informative families for a genome-wide search. For each individual a genetic factor score was computed, based on a genetic multivariate analysis of anxiety, depression, neuroticism and somatic anxiety. A family was selected if at least two siblings (or DZ twins) had extreme factor scores. Both discordant (high-low) and concordant (high-high and low-low) pairs were included in the selected sample. Once an extreme sibling pair was selected, all family members (parents and additional siblings of the selected pair) who had at least once returned a questionnaire booklet were asked to provide a DNA sample. In total, 2724 individuals from 563 families (1007 parents and 1717 offspring) were approached and 1975 individuals from 479 families (643 patients and 1332 offspring) complied by returning a buccal swab for DNA isolation. All offspring from selected families were asked to participate in a psychiatric interview and in a 24-hour ambulatory assessment of cardiovascular parameters and cortisol. The interview consisted of the WHO-Composite International Diagnostic Interview and was administered to 1253 offspring. In this paper we describe the genetic-epidemiological analyses of the survey data on anxiety, somatic anxiety, neuroticism and depression. We detail how these data were used to select families for the QTL study and discuss strategies that may help elucidate the molecular pathways leading from genes to anxious depression.

This study examined the acute immunological effects of two laboratory stressors, expected to evoke distinct patterns of cardiac autonomic activity; namely an “active coping” time-paced memory test, and a “passive coping” stressful video showing surgical operations. We measured salivary S-IgA, IgA-subclasses (IgA1, IgA2), and secretory component (SC). SC is responsible for the transport of S-IgA across the epithelium, and thus a rate-determining step in S-IgA secretion. Thirty-two male undergraduates were subjected to both stressors and a control video (a didactic television program). The memory test induced a typical “fight-flight” response, characterized by increases in heart rate and blood pressure in association with a decrease in cardiac preejection period (PEP) and vagal tone. The surgical video produced a “conservation-withdrawal”-like response, characterized by an enhanced vagal tone, a decrease in heart rate, and a moderate sympathetic coactivation (as indicated by a shortened PEP and an increased systolic pressure). The memory test induced an increase in the concentration and, to a lesser extent, in the output of S-IgA, IgA], and SC. The output of IgA2 was not significantly affected. For the surgical video, a different pattern emerged: During stressor exposure S-IgA remained unaffected, against the background of a small increase in SC output. However, 10 min after the surgical video S-IgA levels had decreased. This decrease in S-IgA was paralleled by a decrease in IgA1, but not IgA2. We conclude that acute stress can have both enhancing and suppressive effects on secretory immunity, the IgA1 subclass in particular. The mechanisms that underlie these divergent responses may include stressor-specific patterns of autonomic activation.

Impedance cardiography has been used increasingly to measure human physiological responses to emotional and mentally engaging stimuli. The validity of large-scale ensemble averaging of ambulatory impedance cardiograms was evaluated for preejection period (PEP), interbeat interval, and dZ/dt(min) amplitude. We tested whether the average of “classical” 60-sec ensemble averages across periods with fixed activity, posture, physical load, social situation, and location could be accurately estimated from a single large-scale ensemble average spanning these entire periods. Impedance and electrocardiograms were recorded for about 24-h from 21 subjects. Recordings were scored by seven raters, using both methods for each subject. Good agreement (average intraclass correlation coefficient was .91) between both ensemble averaging methods was found for all three cardiac function measures. The results indicate that for unambiguous ambulatory impedance cardiograms, large-scale ensemble averaging is valid, which makes measuring prolonged changes in cardiac sympathetic activity by measuring ambulatory PEP feasible even in large epidemiological samples.

Shift workers encounter an increased risk of cardiovascular disease compared to their day working counterparts. To explore this phenomenon, the effects of one week of simulated night shift on cardiac sympathetic (SNS) and parasympathetic (PNS) activity were assessed. Ten (5m; 5f) healthy subjects aged 18-29 years attended an adaptation and baseline night before commencing one week of night shift (2300-0700 h). Sleep was recorded using a standard polysomnogram and circadian phase was tracked using salivary melatonin data. During sleep, heart rate (HR), cardiac PNS activity (RMSSD) and cardiac SNS activity (pre-ejection period) were recorded. Night shift did not influence seep quality, but reduced sleep duration by a mean of 52 +/- 29 min. One week of night shift evoked a small chronic sleep debt of 5 h 14 +/- 56 min and a cumulative circadian phase delay of 5 h +/- 14 min. Night shift had no significant effect on mean HR, but mean cardiac SNS activity during sleep was consistently higher and mean cardiac PNS activity during sleep declined gradually across the week. These results suggest that shiftwork has direct and unfavourable effects on cardiac autonomic activity and that this might be one mechanism via which shiftwork increases the risk of cardiovascular disease. It is postulated that sleep loss could be one mediator of the association between shiftwork and cardiovascular health.

Melatonin has a functional role in the nocturnal regulation of sleep and thermoregulation. In addition to its action on peripheral receptors, melatonin may act by altering autonomic activity. To determine the effect of melatonin on cardiac autonomic activity, 5 mg of melatonin or placebo was orally administered to 12 young subjects at 14:00 hr, in a repeated measures design. Melatonin decreased sleep onset latency to Stage 2 sleep by 4.92+/-1.81 min (measured by Multiple Sleep Latency Tests), rectal temperature by 0.19+/-0.05 degrees C, and increased foot temperature by 0.74+/-0.45 degrees C (all P<0.05). Melatonin decreased heart rate by 3.66+/-1.68 beats/min (P<0.05) and pre-ejection period (measure of cardiac sympathetic activity) by 16.48+/-4.28 ms (P<0.05), but had no effect on respiratory sinus arrhythmia (measure of cardiac parasympathetic activity) (P>0.05). As the decrease in pre-ejection period is likely to have resulted from a decrease in blood pressure, these results do not confirm an effect of melatonin on cardiac sympathetic activity. However, the results do clearly indicate that melatonin is unlikely to drive the previously observed presleep increase in cardiac parasympathetic activity.

This study assessed the heritability of ambulatory heart period, respiratory sinus arrhythmia (RSA), and respiration rate and tested the hypothesis that the well-established correlation between these variables is determined by common genetic factors. In 780 healthy twins and siblings, 24-h ambulatory recordings of ECG and thorax impedance were made. Genetic analyses showed considerable heritability for heart period (37%-48%), RSA (40%-55%), and respiration rate (27%-81%) at all daily periods. Significant genetic correlations were found throughout. Common genes explained large portions of the covariance between heart period and RSA and between respiration rate and RSA. During the afternoon and night, the covariance between respiration rate and RSA was completely determined by common genes. This overlap in genes can be exploited to increase the power of linkage studies to detect genetic variation influencing cardiovascular disease risk.

OBJECTIVE: This study examined the effects of exposure to job strain on independent predictors of cardiovascular disease (ambulatory blood pressure, heart rate, and heart rate variability).
METHODS: The participants comprised a homogeneous group of 159 healthy female nurses [mean age 35.9 (SD 8.5) years]. The choice of this population minimized variance attributable to gender, socioeconomic status, and work characteristics. Job demands, decision latitude, and social support were measured with the Karasek job content questionnaire, which was administered twice with an average interval of 12.2 months. The nurses’ scores for job demands and decision latitude on both occasions were used to define their job-strain category. Ambulatory blood pressure, heart rate, and heart rate variability were assessed on a workday and a day of leisure.
RESULTS: No effect on the ambulatory levels of blood pressure, heart rate, or heart rate variability was found for job strain by itself or in interaction with social support. In addition, job strain was not associated with differences in short-term or long-term physiological recovery during sleep after a workday or a day of leisure. High job demand was associated with higher systolic blood pressure at work and with higher diastolic blood pressure at work, but the latter association was found only when decision latitude was concurrently high, rather than low.
CONCLUSIONS: High job strain among young female nurses is not associated with an unfavorable ambulatory cardiovascular profile. The robust effect of job strain on male health appears to be less apparent for women.

Theorists have staked out two ostensibly opposing views of human crying as either an arousing behavior that signals distress or a soothing behavior that reduces arousal after distress. The present study examined whether these views of crying might be reconciled by attending to physiological changes that unfold over crying episodes. Sixty female students watched neutral and cry-eliciting films while autonomic physiology, including respiratory sinus arrhythmia and pre-ejection period, was assessed. Crying participants exhibited heart rate increases that rapidly subsided after crying onset. Crying onset was also associated with increases in respiratory sinus arrhythmia and slowed breathing. All crying effects subsided by 4 minutes after onset. It is possible that crying is both an arousing distress signal and a means to restore psychological and physiological balance, depending on how and when this complex behavior is interrogated.

Chewing has been shown to alleviate feelings of sleepiness and improve cognitive performance during the day. This study investigated the effect of chewing on alertness and cognitive performance across one night without sleep as well as the possible mediating role of cardiac autonomic activity. Fourteen adults participated in a randomized, counterbalanced protocol employing a chewing, placebo and caffeine condition. Participants completed tasks assessing psychomotor vigilance, tracking, grammatical reasoning, alertness and sleepiness each hour across the night. All participants received either placebo or caffeine (200 mg), while the chewing condition also chewed on a tasteless and odorless substance for 15 min each hour. Heart rate (HR), root mean square of the successive differences in R-R intervals on the ECG (RMSSD), and preejection period (PEP) were simultaneously recorded. Alertness and cognitive performance amongst the chewing condition did not differ or were in fact worse when compared with placebo. Similarly, measures of HR and RMSSD remained the same between these two conditions; however, PEP was reduced in the later part of the night in the chewing condition compared with a relative increase for placebo. Caffeine led to improved speed and accuracy on cognitive tasks and increased alertness when compared with chewing. Relative increases in RMSSD and reductions in HR were demonstrated following caffeine; however, no change in PEP was seen. Strong associations between cardiac parasympathetic activity and complex cognitive tasks, as well as between subjective alertness and simpler cognitive tasks, suggest a differential process mediating complex versus simple cognitive performance during sleep deprivation.