Sleep Deprivation Increases Blood Pressure in Healthy Normotensive Elderly and Attenuates the Blood Pressure Response to Orthostatic Challenge

Abstract

Study Objectives:

To determine how aging affects the impact of sleep deprivation on blood pressure at rest and under orthostatic challenge.

Design:

Subjects underwent a night of sleep and 24.5 h of sleep deprivation in a crossover counterbalanced design.

Setting:

Sleep laboratory.

Participants:

Sixteen healthy normotensive men and women: 8 young adults (mean 24 years [SD 3.1], range 20-28 years) and 8 elderly adults (mean 64.1 years [SD 3.4], range 60-69 years).

Interventions:

Sleep deprivation.

Measurements and Results:

Brachial cuff arterial blood pressure and heart rate were measured in semi-recumbent and upright positions. These measurements were compared across homeostatic sleep pressure conditions and age groups. Sleep deprivation induced a significant increase in systolic and diastolic blood pressure in elderly but not young adults. Moreover, sleep deprivation attenuated the systolic blood pressure orthostatic response in both age groups.

Conclusions:

Our results suggest that sleep deprivation alters the regulatory mechanisms of blood pressure and might increase the risk of hypertension in healthy normotensive elderly.

Citation:

Robillard R; Lanfranchi PA; Prince F; Filipini D; Carrier J. Sleep deprivation increases blood pressure in healthy normotensive elderly and attenuates the blood pressure response to orthostatic challenge. SLEEP 2011;34(3):335-339.

INTRODUCTION

With age, important physiological changes take place in the cardiovascular system that can at least partly explain the high prevalence of cardiovascular diseases in elderly populations. Throughout senescence, the circulatory system undergoes a decrease in arterial distensibility as well as venous and arterial compliance, leading to an increase in both systolic and diastolic blood pressure (SBP, DBP).¹ Additional modifications occurring with ageing may also affect the response of blood pressure following postural changes, translating into to two distinct disorders such orthostatic hypotension (i.e., a decrease in blood pressure upon standing up) and the more recently described orthostatic hypertension (i.e., an increase in BP upon standing). These two conditions significantly affect cardiovascular health.^2–4

With aging, sleep also undergoes important changes, going beyond the range of clinically significant sleep disorders. Polysomnographic studies of the healthy elderly reveal shorter and lighter sleep episodes fragmented with more awakenings.⁵ In the healthy elderly, daytime sleepiness has been associated with higher systolic and diastolic blood pressure and hypertension diagnosis 5 years later,⁶ suggesting that underlying sleep difficulties might affect cardiovascular health. Accordingly, in the elderly population, short and long sleepers have shown a higher prevalence of hypertension.^7,8 This suggests that variations in the homeostatic sleep process, the accumulation of sleep pressure during the day and its dissipation across the night, may be associated with cardiovascular abnormalities. However, because these associations do not allow establishing causal links, it remains unclear whether sleep problems in the elderly are a symptom secondary to cardiovascular difficulties or whether sleep problems may actually cause cardiovascular irregularities.

It was recently observed in a sample of 331 young adults that blood pressure in the waking state negatively correlated with sleep duration.⁹ Importantly, in young adults, sleep deprivation has been shown to elevate heart rate (HR), SBP, and to a lesser extent DBP.^10–13 These experimental results suggest that sleep debt can play a causal role in cardiovascular dysfunctions such as hypertension. Yet it is not understood how aging influences the cardiovascular response to sleep loss. Moreover, to our knowledge, the impacts of sleep deprivation on the cardiovascular orthostatic response have not been studied to date in either young or elderly subjects.

This study aimed to determine how age affects the impact of sleep deprivation on SBP, DBP, and HR at rest and in response to an orthostatic challenge.

METHODS

Subjects

Sixteen healthy subjects were divided into 2 age groups: 8 young adults between 20 and 28 years of age and 8 elderly adults between 60 and 69 years of age (characteristics presented in Table 1). All subjects were normotensive (BP < 140/90 mm Hg), as verified by baseline measurements in semi-recumbent position. Exclusion criteria included sleep complaints, history of psychiatric or neurological disorder, use of medication known to influence sleep or blood pressure, night work, or transmeridian travel 3 months prior to the study, and a score > 10 on the Beck Depression Scale (long version¹⁴). Exclusion criteria also included body mass index > 30 kg/m². Blood sample analysis (complete blood count, serum chemistry including hepatic and renal functions, prolactin level) and urinalysis results were checked for significant medical conditions by a certified physician. Prior to data acquisition, subjects underwent a polysomnographic (PSG) adaptation and screening night, including nasal/oral thermistor and electromyogram (EMG) leg electrode recordings to screen for poor sleep efficiency, sleep apnea, and periodic leg movements. The presence of sleep disturbances such as sleep apnea (apnea/hypopnea index > 10/h), periodic leg movements (index per hour > 10), prolonged sleep latency (> 30 min), or low sleep efficiency (< 75%) resulted in the participant's exclusion. All subjects signed an informed consent form and received monetary compensation. This study was approved by the hospital's ethics committee.

Table 1.

Subject characteristics

	Age years	Gender distribution	SBP/DBP mm Hg	BMI kg/m2
Young	24.0 (3.1)	4 F, 4 M	119.1 (11.2) / 73.1 (5.7)	23.6 (1.5)
Elderly	64.1 (3.4)	5 F, 3 M	122.9 (13.8) / 73.4 (7.0)	24.6 (3.8)

Mean (SD). F, females; M, males; SBP, systolic blood pressure; DBP, diastolic blood pressure; BMI, body mass index. Blood pressure measured during the baseline homeostatic sleep condition in semi-recumbent position.

Procedure

Each subject underwent two counterbalanced homeostatic sleep pressure conditions: a night of sleep and a night of sleep deprivation. In each age group, half the subjects undertook the sleep condition first and the sleep deprivation condition last, and half subjects undertook the sleep deprivation condition first and the sleep condition last. The two conditions were separated by > 2 weeks. In both conditions, subjects were asked to refrain from consuming caffeinated food or beverages starting at noon on the day of their arrival in the laboratory, and they were not allowed to consume caffeine, alcohol, or medication while in the laboratory. Seven days prior to recording, subjects were asked to maintain a regular sleep schedule within 30 minutes of their self-selected bedtime and wake time and to fill out sleep diaries.

In the sleep condition, subjects slept one night in the laboratory according to their habitual sleep-wake schedule. BP and HR measures were started 30 min after wake time (mean test time: 7:56 [SD 0:55]). In the sleep deprivation condition, subjects were sleep deprived for 24.5 h, and BP and HR measures were subsequently taken 30 min after their habitual wake time (mean test time: 7:55 [SD 0:55]). During the sleep deprivation night, a research assistant ensured that subjects remained awake.

Measurements

In both homeostatic sleep pressure conditions, measurements were performed on the non-dominant arm in two postural positions: semi-recumbent and upright. Subjects first remained semi-recumbent ≥ 10 min prior to BP and HR measurements. Subjects then stood up and remained upright for 1 min while leaning against a wall prior to BP and HR measurements. Although the American Academy of Neurology recommends measuring orthostatic changes 3 min after standing up, a 1-min delay period was chosen to better highlight age effects. A study comparing blood pressure modulation in healthy elderly at 1 and 3 min after standing found that the most prominent orthostatic effects occurred 1 min after the positional change.¹⁵ Importantly, a study comparing different methodologies to assess blood pressure and HR response to orthostatic changes in various age groups concluded that a delay period of 1 min is sufficient to detect autonomic dysfunction and BP dysregulation.¹⁶ For each measurement, BP and HR were measured twice, 1 min apart, by an automatic monitor (Omron, HEM-907XL, Omron Healthcare INC. IL, USA). Statistical analyses were performed on the means of the two measures.

Analyses

SBP, DBP, and HR were submitted to 2 × 2 × 2 mixed factorial ANOVAs with two repeated measures (two homeostatic sleep pressure conditions [sleep and sleep deprivation] and two positions [semi-recumbent and upright]) and one independent factor (two age groups [young adults and elderly adults]). HR measures were log-transformed before analysis to improve normality. For all ANOVAs, simple effect analyses were performed to decompose significant interaction effects. These tests were designed to contrast (a) homeostatic sleep pressure effects in each age group separately and (b) position effects in each homeostatic sleep pressure condition separately. Only effects or interactions involving sleep are presented.

RESULTS

Table 2 presents SBR, DBP, and HR data in each age group in both postural conditions after sleep and sleep deprivation. No significant age by position by homeostatic sleep pressure interaction was found for SBP, DBP, or HR.

Table 2.

Cardiovascular measures in both sleep conditions

	Sleep		Sleep Deprivation
	SR	UR	SR	UR
SBP
Young	119.1 (11.2)	113.8 (13.2)	118.4 (11.3)	118.9 (12.3)
Elderly	123.8 (13.0)	120.6 (13.2)	135.5 (20.1)	139.4 (17.5)
DBP
Young	73.1 (5.7)	77.0 (6.9)	69.8 (2.9)	77.9 (8.0)
Elderly	74.0 (6.7)	75.8 (5.7)	79.9 (13.3)	83.6 (10.7)
HR
Young	57.9 (7.2)	83.3 (16.2)	58.5 (9.5)	81.6 (9.0)
Elderly	60.3 (6.6)	71.8 (8.7)	62.9 (9.4)	71.3 (8.5)

Mean (SD). SBP, systolic blood pressure; DBP, diastolic blood pressure; HR, heart rate; SR, semi-recumbent; UR, upright (df = 1, 14).

Figure 1 illustrates SBP, DRP and HR for each age group in both sleep conditions. SBP and DRP showed a significant age by homeostatic sleep pressure interaction (F_1,14 = 22.4, P < 0.01 and F_1,14 = 7.9, P = 0.01, respectively). Sleep deprivation significantly increased SBP and DBP compared to sleep condition in elderly (both P < 0.01) but not young adults. To describe the clinical implications of this effect, Figure 2 presents the proportions of older individuals whose blood pressure was raised at the prehypertensive and hypertensive levels following sleep deprivation in the semi-recumbent condition. No significant interaction between age and sleep condition was found for HR.

Figure 1.

Interaction between age and homeostatic sleep pressure. Sleep deprivation induced a significant increase in blood pressure for elderly, but not younger adults. Data from both position conditions were pooled because the age by sleep condition interaction bears no significant interaction with the position factor.

Figure 2.

Older adults after sleep deprivation. Proportions of older individuals whose systolic blood pressure remained at the normotensive level (white), was raised at the prehypertensive level (lighter gray) or at the hypertensive level (darker gray) following sleep deprivation in the semi-recumbent condition.

Figure 3 presents SBP, DBP, and HR measured in the semi-recumbent and upright position under both homeostatic sleep pressure conditions for all subjects. A significant homeostatic sleep pressure by position interaction was found for SBP (F_1,1 = 15.5, P < 0.01) but not for DBP and HR. While SBP decreased from semi-recumbent to upright position in the sleep condition (P < 0.05), there was no significant difference between the two positions after sleep deprivation. Figure 4 shows the individual responses to position changes in the two groups. After sleep deprivation, the physiological SBP reduction with postural changes was, in most of the subjects, either attenuated or even reversed (i.e., replaced by an increase following positional change).

Figure 3.

Interaction between position and homeostatic sleep pressure. The orthostatic response of systolic pressure was significant in the sleep condition but not in the sleep deprivation condition. Data of the two age groups were pooled because the position and sleep deprivation bear no interaction with the age factor. SBP, systolic blood pressure; DBP, diastolic blood pressure; HR, heart rate; SR, semi-recumbent; UR, upright.

Figure 4.

Individual changes in SBP following the transition from the semi-recumbent to the upright position for young and elderly subjects. The sleep condition is shown in gray and the sleep deprivation in black.

DISCUSSION

These results indicate that sleep deprivation substantially raises SBP and DBP close to, and in some subject even above, the clinical threshold for hypertension (≥ 140/90 mm Hg) in healthy elderly subjects whose blood pressure at baseline was normal and comparable to that of young adults. In addition we found that sleep deprivation attenuates, and in some cases even reverses, the SBP orthostatic response in both young and elderly subjects.

In contrast to previous studies,^10,17–21 we found no significant effect of sleep deprivation on semi-recumbent position measures in young adults. Previous studies covered a wide age range, including middle-aged subjects. According to the present results, older adults may be more likely to show blood pressure raises in reaction to sleep deprivation. Hence, this methodological difference may explain the discrepancies in results.

In the semi-recumbent position, although the mean SBP, DBP, and HR of elderly subjects were slightly higher than those of young adults, there was no significant difference between the two age groups at baseline. However, we found a drastic increase in both SBP and DBP in the elderly after sleep deprivation, which reached pathological values of frank hypertension for half of the elderly subjects.

Systemic catecholamine and cortisol levels have been shown to increase in conditions of high sleep pressure.²² Studies have shown that with age some changes occur in the cardiovascular response to sympathetic excitation, with enhanced BP responses and blunted HR responses in older as compared to younger subjects. ^23–25 Therefore, we can speculate that a greater sympathetic drive after sleep deprivation and/or enhanced vascular responsiveness to heightened adrenergic excitation in elderly could be factors implicated in the higher cardiovascular sensitivity of elderly subjects to sleep loss in our study.

It has been proposed that frequent rises in blood pressure maintained over long periods of time induce permanent BP elevation.²⁶ Hence, our results imply that by inducing repeated blood pressure elevation, chronic sleep loss in the elderly can lead to hypertension. Considering the widespread sleep problems in the elderly population, this highlights poor sleep as a potential contributor to cardiovascular problems in senescence.

A second aim of our study was to assess the impact of sleep deprivation on cardiovascular response to postural changes. Transition from the sitting to the standing position forces the cardiovascular system to adapt to gravity and the subsequent hemodynamic downward shift, translating in lowering of SBP. Consequently, standing triggers an increase in sympathetic activity with cardio-acceleration (increased HR) and vasoconstriction to counteract the reduction in blood pressure and maintain adequate blood flow to vital organs.²⁷ BP responses during orthostatic position are widely used to assess the integrity of autonomic cardiovascular regulation, which can be altered in older subjects, leading to either orthostatic hypotension or hypertension.²⁸

As expected, our results showed that in the sleep condition the transition from semi-recumbent to upright position induced a slight decrease in SBP and an increase in both DBP and HR. Compared to young adults, our elderly subjects showed similar BP responses but a lower increase in HR after transition from semi-recumbent to upright position, in agreement with previous studies showing that HR responsiveness to heightened sympathetic excitation decreases with age.¹⁹ Conversely, sleep deprivation in both groups of subjects did not affect HR and DBP responses to position change, but had a significant impact on SBP's orthostatic response which was globally attenuated. A closer look at individual data revealed that, while in half of the subjects, the decrease in SBP following positional change was significantly reduced, for the other half, it was replaced by a considerable increase in SBP (ranging between +2 and +24 mm Hg, with older individuals showing the most pronounced increases). These altered responses to orthostatic stress following sleep deprivation (i.e., lower sensitivity or changes towards orthostatic hypertension) suggest alterations in circulatory and autonomic regulation that may contribute to maintain high blood pressure.

DISCLOSURE STATEMENT

This was not an industry supported study. Dr. Filipini has participated in a speaking engagement for Valeant Canada. The other authors have indicated no financial conflicts of interest.