Background The early hours of the morning after awakening areassociated with an increased frequency of events such as myocardialinfarction and ischemic stroke. The triggering mechanisms forthese events are not clear. We investigated whether autonomicchanges occurring during sleep, particularly rapid-eye-movement(REM) sleep, contribute to the initiation of such events.
Methods We measured blood pressure, heart rate, and sympathetic-nerveactivity (using microneurography, which provides direct measurementsof efferent sympathetic-nerve activity related to muscle bloodvessels) in eight normal subjects while they were awake andwhile in the five stages of sleep.
Results The mean (±SE) amplitude of bursts of sympathetic-nerveactivity and levels of blood pressure and heart rate declinedsignificantly (P<0.001), from 100 ±9 percent, 90 ±4mm Hg, and 64 ±2 beats per minute, respectively, duringwakefulness to 41 ±9 percent, 80 ±4 mm Hg, and59 ±2 beats per minute, respectively, during stage 4of non-REM sleep. Arousal stimuli during stage 2 sleep elicitedhigh-amplitude deflections on the electroencephalogram (called"K complexes"), which were frequently associated with burstsof sympathetic-nerve activity and transient increases in bloodpressure. During REM sleep, sympathetic-nerve activity increasedsignificantly (to 215 ±11 percent; P<0.001) and theblood pressure and heart rate returned to levels similar tothose during wakefulness. Momentary restorations of muscle toneduring REM sleep (REM twitches) were associated with cessationof sympathetic-nerve discharge and surges in blood pressure.
Conclusions REM sleep is associated with profound sympatheticactivation in normal subjects, possibly linked to changes inmuscle tone. The hemodynamic and sympathetic changes duringREM sleep could play a part in triggering ischemic events inpatients with vascular disease.
The early morning hours after awakening (approximately 6 to11 a.m.) are associated with a higher-than-expected incidenceof cardiovascular events, such as myocardial infarction andischemic stroke1,2,3. The relation between sleep and these eventsis not clear. Ischemic events can occur during sleep, especiallyin patients with severe coronary artery disease4 and vasospasticangina5. REM, or rapid-eye-movement, sleep is especially associatedwith myocardial ischemia4,5. In animals with coronary-arterystenosis, REM sleep causes further decreases in coronary-arteryblood flow,6 possibly due to sympathetic activation during thissleep stage. Surprisingly, although there have been extensiveinvestigations in animals, there have been few studies of autonomiccontrol of the circulation during sleep in humans7,8. Microneurographyallows direct recording of peripheral sympathetic-nerve trafficto the skeletal-muscle vascular bed9,10. We therefore studiedsympathetic-nerve activity and hemodynamic changes occurringduring the different stages of sleep in normal subjects.
Methods
We studied 14 normal subjects (10 men and 4 women) after obtainingtheir informed written consent. These studies were approvedby our institution's committee on experimentation in human subjects.
We obtained technically excellent recordings of sympathetic-nerveactivity during quiet wakefulness and non-REM sleep (stages1 through 4) in eight subjects (seven men and one woman, whosemean [±SD] age was 25 ±5 years). Sympathetic-nerveactivity was also recorded during REM sleep in six of theseeight subjects. We were unable to measure nerve activity intwo of the remaining six subjects. In three subjects, electrodeswere shifted repeatedly, with loss of nerve recording, whilethe subjects were awake or in stage 1 or early stage 2 sleep;studies were therefore abandoned in these subjects. One additionalsubject was excluded from the analysis because inadequate timemarkings on separate microneurographic and polysomnographicrecords precluded precise synchronization of the microneurographicwith the polysomnographic recordings.
We obtained direct multiunit (involving multiple nerve fibers)intraneural recordings of efferent sympathetic-nerve activityinvolving muscle blood vessels, using tungsten microelectrodes(shaft diameter, 200 microm; tip length, 1 to 5 microm). Oneelectrode was inserted into the sympathetic-nerve fasciclesof the peroneal nerve posterior to the fibular head (for microneurographicrecording)9,10. A reference electrode was inserted subcutaneouslyabout 3 cm away. The neural electrical signals were amplified,filtered, rectified, and integrated to produce a display ofsympathetic-nerve activity at a mean voltage.
Sympathetic bursts were identified by inspecting the mean-voltageneurogram, and sympathetic activity was calculated by countingthe number of bursts per minute, as well as by measuring thetotal amplitude of the burst per minute, which is expressedin arbitrary units9. In the present study, burst amplitude isexpressed as a percentage of the activity during wakefulness.
For measurements of sympathetic-nerve activity, the data werenormalized so that the mean value recorded during wakefulnesswas 100 percent. The mean of the absolute values for sympathetic-nerveactivity during three four-minute segments of wakefulness wasused as a denominator for all measures of sympathetic activity(including the wakefulness segments), thus expressing all measuresof nerve activity within each subject as a percentage of averagevalues recorded during wakefulness. In comparisons of multiunitnerve recordings in subjects, when differences between subjectsin gain can greatly affect absolute values for nerve activity,this percentage is a more appropriate measure of changes innerve activity.
The heart rate was measured by electrocardiography, and bloodpressure by the FINAPRES (FINger Arterial PRESsure) system,allowing continuous indirect, noninvasive measurements of beat-by-beatblood pressure11. FINAPRES measurements of blood pressure correspondclosely to intraarterial measurements, both at rest and duringphysiologic rapid changes in blood pressure12; we did not comparethese two types of measurements, and we therefore cannot confirmthe accuracy of FINAPRES measurements of absolute levels ofblood pressure in our study group. Each subject was fitted witha FINAPRES cuff appropriate for the size of the finger tested.The FINAPRES system was switched off for 5 to 10 minutes approximatelyevery 2 hours, for the subject's comfort. Blood-pressure measurementsobtained before and after temporary cessation of FINAPRES recordingwere similar. To ensure consistency among these recordings,the position of the recording arm was fixed with the aid ofsandbags and an arm board. Complete polysomnographic monitoringwas carried out, including measurements of oxygen saturation,air flow, and chest movement and electromyography, electroencephalography,and electro-oculography. All variables were measured continuously.
The stages of sleep were scored according to the recommendationsof Rechtstaffen and Kales13. In brief, the stages of sleep havebeen characterized electroencephalographically as slow-wave(non-REM) sleep or desynchronized (REM) sleep14,15,16. Non-REMsleep consists of stages 1 to 4, characterized by a progressivelyslower frequency and increased voltage activity on the electroencephalogram;these changes correspond to progressive increases in the depthof sleep. Muscle relaxation occurs, with preservation of muscletone. REM sleep is characterized by sudden, low voltage andfast activity on the electroencephalogram, which are associatedwith loss of muscle tone. Slow, rolling eye movements occurduring this phase, with intermittent discrete episodes of rapideye movement. REM sleep is associated with irregular respirationand increases in blood pressure and heart rate, and is the stageof sleep when dreaming is likely to occur14,15,16.
Because of the extended periods of sleep recordings in eachsubject (averaging approximately five hours per subject), alldata were initially visually analyzed to establish trends orassociations between autonomic, hemodynamic, and polysomnographicfindings (qualitative analysis). Representative four-minuteperiods of wakefulness, stage 2 sleep, stage 4 sleep, and REMsleep were examined by quantitative analysis. Three randomlyselected four-minute segments were analyzed from each of thesestages. In one subject, only two 4-minute segments from theREM stage could be analyzed, because this stage persisted foronly 10 minutes. For each subject, the longest duration of continuousrecording of REM sleep obtained during this study ranged from10 to 23 minutes (mean [±SE], 17.7 ±2.0). Onlytwo-minute periods of stage 2 and stage 3 sleep were analyzedbecause of the relatively short duration of these transitionalstages.
Initial studies indicated that non-REM sleep (especially stage4 sleep) was associated with reductions in blood pressure, aswell as in heart rate and sympathetic-nerve activity. This wassurprising, since baroreceptor-reflex mechanisms would be expectedto counter the fall in the blood pressure by increasing theheart rate and sympathetic-nerve discharge. We therefore attemptedto simulate the hypotension observed during stage 4 sleep insix subjects (in three of whom sleep recordings were obtainedas described above) while they were awake. Hypotension was inducedby the infusion of sodium nitroprusside, initially at a rateof 0.5 µg per kilogram of body weight per minute. Therate was increased by 0.5 µg per kilogram per minute everyfour minutes until the mean blood pressure fell by approximately15 mm Hg. The blood pressure, heart rate, and sympathetic-nerveactivity were measured for three minutes before and during thenitroprusside infusion.
Two-way analysis of variance was used to evaluate two factors,subject and sleep stage, with more than one observation perstage for each subject. Comparisons of interest between thestages were tested by defining contrasts between stage means.These were then tested with the t-test statistic; standard errorsfor the test were computed from variance estimates derived fromthe analysis of variance17. P values reported are based on atwo-tailed test; a P value below 0.05 was assumed to indicatestatistical significance. Results are expressed as means ±SE.
Results
Qualitative analysis revealed a decline in heart rate and sympathetic-nerveactivity during non-REM sleep, most marked during stage 4, ascompared with measurements obtained during quiet wakefulness.Associated with this was a decrease in the level and variabilityof arterial pressure. During REM sleep, however, there was amarked increase in both the frequency and height of sympatheticbursts (Figure 1 and Figure 2), associated with intermittentincreases in blood pressure (Figure 1). The increase in sympathetic-nerveactivity during REM sleep was more striking during periods ofrapid eye movement.
Figure 1. Recordings of Sympathetic-Nerve Activity (SNA) and Mean Blood Pressure (BP) in a Single Subject while Awake and while in Stages 2, 3, 4, and REM Sleep.
As non-REM sleep deepens (stages 2 through 4), sympathetic-nerve activity gradually decreases and blood pressure (measured in millimeters of mercury) and variability in blood pressure are gradually reduced. Arousal stimuli elicited K complexes on the electroencephalogram (not shown), which were accompanied by increases in sympathetic-nerve activity and blood pressure (indicated by the arrows, stage 2 sleep). In contrast to the changes during non-REM sleep, heart rate, blood pressure, and blood-pressure variability increased during REM sleep, together with a profound increase in both the frequency and the amplitude of sympathetic-nerve activity. There was a frequent association between REM twitches (momentary periods of restoration of muscle tone, denoted by T on the tracing) and abrupt inhibition of sympathetic-nerve discharge and increases in blood pressure.
Figure 2. Sympathetic-Nerve Activity during Sleep Stages.
Changes in discharge frequency and amplitude are shown during the transition from stage 2 sleep to REM sleep (upper tracing) and the transition from REM sleep to stage 1 sleep with frequent "microarousals" and then to established stage 1 sleep (lower tracing).
An analysis of consistent associations between polysomnographicand autonomic measurements and hemodynamic measurements showedthat during non-REM sleep, arousal stimuli such as a knock onthe door frequently elicited K complexes (which are sharp deflectionsof high amplitude on the electroencephalogram during stage 2sleep associated with arousal from sleep). These were associatedwith momentary increases in sympathetic-nerve activity and increasesin blood pressure (Figure 1, stage 2 sleep). No clear associationwas observed between sleep spindles (which are synchronizedwaves of frequency between 7 and 14 Hz, occurring during stages2 and 3 of non-REM sleep) and sympathetic-nerve activity. Withmomentary restoration of muscle tone during periods of REM sleep(REM twitches), there were often surges in blood pressure andabrupt cessations of sympathetic-nerve discharge (Figure 1).
The heart rate fell slightly, from 64 ±2 beats per minuteduring wakefulness to 59 ±2 beats per minute during stage4 sleep (P<0.001). During REM sleep, the heart rate was 63±2 beats per minute, similar to the rates recorded duringconsciousness (Figure 3). Both systolic and diastolic bloodpressure fell during non-REM sleep. The mean blood pressurefell from 90 ±4 mm Hg during wakefulness to 80 ±4mm Hg during stage 4 (P<0.001), but averaged 91 ±4mm Hg during REM sleep (Figure 3). The frequency of sympatheticbursts averaged 25 ±3 per minute during wakefulness,then decreased between stage 1 and stage 4, reaching 13 ±3bursts per minute in stage 4 sleep (P<0.001) (Figure 3).During REM sleep, however, burst frequency increased markedly,to 34 ±3 bursts per minute (P<0.001, as compared withwakefulness). Like burst frequency, the amplitude of sympatheticbursts was influenced by sleep stages; the total amplitude fellfrom 100 ±9 percent during wakefulness to 41 ±9percent during stage 4 (P<0.001) and increased to 215 ±11percent during REM sleep (P<0.001) (Figure 3). The bloodpressure and sympathetic-burst amplitude and frequency (butnot the heart rate) were lower in stage 3 and stage 4 sleepthan in stage 2 sleep (P 0.005).
Figure 3. Heart Rate, Mean Blood Pressure, Sympathetic-Burst Frequency, and Burst Amplitude during Wakefulness and Non-REM Sleep (Eight Subjects) and REM Sleep (Six Subjects).
Heart rate and blood pressure were significantly lower during all stages of non-REM sleep than during wakefulness, and sympathetic activity was significantly lower during stages 3 and 4 (the asterisk denotes P<0.001). During REM sleep, sympathetic activity increased significantly (P<0.001), but the values for blood pressure and heart rate were similar to those recorded during wakefulness. Values are means ±SE.
Nitroprusside Studies
Infusion of nitroprusside when the subjects were awake reducedthe mean blood pressure and elicited profound increases in sympathetic-nerveactivity and heart rate in all subjects. In the three subjectsin whom complete sleep recordings were obtained, nitroprussidereduced the mean blood pressure from 85 ±3 to 78 ±3mm Hg and increased the heart rate from 61 ±7 to 75 ±7beats per minute, the sympathetic-burst frequency from 22 ±2to 47 ±7 bursts per minute, and the total amplitude to239 ±88 percent. In these three subjects stage 4 sleepwas associated with a greater fall in the mean blood pressure,from 84 ±6 to 71 ±7 mm Hg, than the fall inducedby nitroprusside. In contrast, however, during the period fromwakefulness to stage 4 sleep, the heart rate decreased from61 ±4 to 57 ±3 beats per minute, the sympathetic-burstfrequency from 28 ±4 to 11 ±3 bursts per minute,and the total amplitude to 35 ±14 percent of levels recordedduring wakefulness.
Discussion
Our data indicate that sympathetic-nerve activity, blood pressure,and heart rate are lower in normal subjects while they are indeep non-REM sleep than while they are awake. Arousal stimuliduring non-REM sleep elicit K complexes, which are accompaniedby bursts of sympathetic-nerve activity and transient increasesin blood pressure. During REM sleep, sympathetic-nerve activityincreases above the levels recorded during wakefulness, andthe values for blood pressure and heart rate return to thoserecorded during wakefulness. Momentary restoration of muscletone during REM sleep (REM twitch) is frequently associatedwith cessation of sympathetic-nerve discharge and increasesin blood pressure.
Studies in animals have shown that the mechanisms underlyingthe fall in blood pressure during non-REM sleep include a reductionin cardiac output and a decrease in total peripheral resistance18.During REM sleep, distinct and profound mesenteric and renalvasodilation and skeletal-muscle vasoconstriction occur. Reiset al.19 demonstrated that vasoconstriction during REM sleepinvolved only the red, tonic muscles (which are involved inpostural support). Interestingly, REM sleep is associated witha complete loss of postural muscle tone. Furthermore, this musclevasoconstriction appears to depend on an intact sympatheticinnervation as well as intact afferent impulses from the skeletalmuscles,20 suggesting that the loss of muscle tone during REMsleep is a disinhibitory (or excitatory) stimulus to sympathetic-nerveactivation of muscle, but not mesenteric or renal blood vessels.REM-sleep "twitches," or brief periods of return of muscle tone,induce surges in blood pressure that are due to even greatervasoconstriction of skeletal muscle16.
Our data provide some mechanistic explanations for the abovefindings in animals. REM sleep (and loss of muscle tone) triggersmarked increases in sympathetic-nerve activity involving muscleblood vessels. REM-sleep twitches result in surges in bloodpressure, and despite evidence of increased vasoconstrictionin animals, we found a suppression of sympathetic-nerve activityin our subjects. The abrupt cessation of sympathetic activityduring the REM-sleep twitches is probably due to the restorationof muscle tone, possibly augmented by baroreceptor-reflex-mediatedinhibition of sympathetic activity in response to the increasein blood pressure.
The finding of lower blood pressure, heart rate, and sympathetic-nerveactivity during non-REM sleep suggests a dramatic modulationof the baroreceptor reflex during sleep, as reflected by themarked tachycardia and sympathetic excitation, with comparativelymilder hypotension during wakefulness (as evidenced by the nitroprussidestudies). These data do not indicate whether this modulationinvolves resetting, a change in sensitivity, or both. Otherinvestigators, however, have shown that baroreceptor-reflexgain increases during sleep21,22. Power spectral analysis ofsimultaneous frequencies of variation of the heart rate andblood pressure supports the notion of such an increase duringsleep23.
Power spectral analysis of blood pressure and heart rate hasalso suggested that sleep is associated with increased vagalactivation and decreased sympathetic activation24,25. By directmeasurement of sympathetic activity in sleep-deprived subjects,Hornyak et al.7 found changes in sympathetic activation duringsleep that were qualitatively similar to those in our study.The effects were less pronounced than in our study, possiblybecause of sleep deprivation, which affects both sleep patternand blood-pressure regulation during sleep26. Furthermore, mostof their subjects were studied during daytime sleep, and theirvalues for sympathetic-nerve activity during wakefulness alsoincluded data recorded during stage 1 sleep. The duration ofREM sleep (2 to 13.5 minutes; mean, 7.4) in their study7 wassubstantially less than in ours (10 to 23 minutes; mean, 17.7).Simultaneous recording of blood pressure and sympathetic-nerveactivity was obtained during all sleep stages in only two subjects.
More recently, Okada et al.8 have studied changes in the frequencyof sympathetic bursts during sleep stages. It is not known whethertheir volunteers underwent sleep deprivation. Although bloodpressure was measured in some subjects, data were not reportedfor the group. There was no apparent increase in nerve activitybetween wakefulness and REM sleep, perhaps because total nerveactivity was not measured, although the authors described qualitativeincreases in burst amplitude during REM sleep.
The association of arousal stimuli and K complexes with increasedsympathetic activation and blood pressure has also been notedby Hornyak et al.7 and Okada et al.,8 and appears to constitutepart of the fight-or-flight response of sleep. Remarkably, arousalstimuli during wakefulness do not increase sympathetic-nerveactivity involving muscle, but do increase sympathetic-nerveactivity involving skin27. Arousal stimuli do, however, increasesympathetic activity in muscle after spinal cord injury28 oranesthesia of the vagal and glossopharyngeal nerves (which carrybaroreceptor-reflex afferent impulses)29. Therefore, it appearsthat during sleep, there is a change in the neural processingof auditory and possibly other arousal stimuli. This would bea logical alteration since, because of the hypotension duringnon-REM sleep, acute increases in blood pressure would be requiredto allow adequate cerebral and cardiac perfusion during arousal,postural change, or confrontation.
Changes in heart rate and blood pressure during sleep are small,in keeping with findings in earlier studies of sleep in humansubjects30,31,32,33. The increases in sympathetic activity duringREM sleep are more pronounced than the changes in heart rateand blood pressure (relative to stage 4 sleep and wakefulness).Thus, measurements of heart rate and blood pressure may underestimatethe magnitude of the autonomic cardiovascular adjustments duringREM sleep. The less marked change in heart rate may be explainedby a dissociation of muscle and cardiac sympathetic activityor alternatively by simultaneous cardiac parasympathetic activationoffsetting cardiac sympathetic activation.
REM sleep is most manifest toward the end of sleep, before arousal.Sympathetic and hemodynamic alterations during REM sleep couldconceivably initiate increased platelet aggregability, plaquerupture, or coronary vasospasm,4,5,6,34,35 thus acting as atriggering mechanism for thrombotic events that may presentclinically only after arousal.
Supported by grants (HL-14388 and HL-24962) from the NationalHeart, Lung, and Blood Institute.
We are indebted to Nancy Stamp for assistance in the preparationof the manuscript, to Mary Clary, R.N., for technical assistance,and to Bridget Zimmerman, Ph.D., for statistical advice.
Source Information
From the Department of Medicine, the Department of Physiology and Biophysics, and the Cardiovascular Center (V.K.S., A.L.M., F.M.A.) and the Department of Neurology (M.E.D.), University of Iowa College of Medicine, Iowa City.
Address reprint requests to Dr. Somers at the Department of Internal Medicine, College of Medicine, University of Iowa, Iowa City, IA 52242.
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0.005). 
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