SPONTANEOUS BAROREFLEX ANALYSIS IN NON–APNEIC SNORING INDIVIDUALS
Spontaneous Baroreflex Analysis in Non–apneic Snoring
Individuals during NREM sleep
Jason H. Mateika (PhD)1, 2, Neil B. Kavey (MD)3 and George Mitru (MS)1
of Biobehavioral Sciences, Teachers College, Columbia University, New York, NY, 10027; 2Department of
Rehabilitation Medicine, Columbia Presbyterian Medical Center, New York, NY, 10032; 3The Sleep Disorders Center,
Columbia Presbyterian Medical Center, New York, NY, 10032
1Department
Summary: The primary purpose of this study was to measure baroreceptor sensitivity (BS) during wakefulness and non–rapid eye
movement (NREM) sleep in non–apneic snoring individuals. To achieve this purpose continuous and simultaneous measurements
of snoring, oxygen saturation, sleep stages, arterial blood pressure and heart rate were obtained from seven non–apneic snoring
subjects. After obtaining these measures, a computer program was employed to detect concomitant increases or decreases in systolic blood pressure and R–R interval duration during sequences of three or more consecutive beats that occurred during stage II
and slow wave sleep (SWS). The values recorded from a given sequence were plotted and the slope of the regression line fit to the
data was used as a measure of BS. The results showed that mean arterial pressure and heart rate during stage II and SWS of
NREM sleep were not significantly different from wakefulness. In contrast, the BS measured during NREM sleep was significantly
lower than values recorded during wakefulness. In addition, linear regression analysis showed that an inverse and significant correlation existed between snoring frequency and the decrease in BS during sleep. We conclude that the decrease in blood pressure
and heart rate normally observed during NREM sleep in healthy non–snoring individuals is attenuated or abolished in non–apneic
snoring individuals and that these cardiovascular alterations may be partially mediated by a decrease in BS.
INTRODUCTION
viduals was significantly greater than values measured
from control subjects. In addition, Mateika et al.3 showed
that the non–apneic snorers in their investigation did not
experience a fall in blood pressure during sleep.
Attenuation of the decrease in blood pressure during sleep
in non–apneic snorers is likely mediated by increases in
SNS activity, since this system has been shown to play a
significant role in altering blood pressure during sleep in
healthy individuals4–7 and those that suffer from obstructive
sleep apnea.12–14 If this is correct, then the alterations in cardiovascular function that exist in non–apneic snorers may
be accompanied and partially mediated by a concomitant
reduction in BS. However, baroreceptor function in
non–apneic snoring individuals during sleep has not been
examined. Therefore, the primary purpose of the present
investigation was to utilize the method of spontaneous
baroreflex analysis in order to determine if a reduction in
BS occurs during NREM sleep in non–apneic snoring subjects.
A NOTABLE DECREASE in mean arterial pressure
(MAP) (20–30 mmHg) and heart rate occurs during the
transition from wakefulness to stage 2 and slow wave sleep
(SWS) of non–rapid eye movement (NREM) sleep in
non–snoring healthy humans.1–3 The cumulative results
obtained from many investigations suggest that these modifications are the consequence of a decrease in sympathetic
nervous system (SNS) activity4–7 which is elicited, in part,
by an increase in baroreceptor sensitivity (BS).8–10
In contrast to non–snoring healthy humans, Mateika et
al.3 and Young et al.11 showed that the average MAP
recorded during NREM sleep in non–apneic snoring indi-
Accepted for publication January 1999
Correspondence: Jason H. Mateika Ph.D., Teachers College, Columbia
University, 525 West 120th Street, Box 199, New York, NY, 10027, Phone:
(212) - 678 - 3226, Fax: (212) - 678 - 3322, e-mail: [email protected]
SLEEP, Vol. 22, No. 4, 1999
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Spontaneous Baroreflex Analysis—Mateika et al.
METHODS
Data Analysis (sleep variables)
Subjects
Sleep was staged in 30–second epochs according to standard criteria.15 For each subject the total sleep period time
as well as the percent of total sleep time spent in a given
sleep stage was calculated. The total number of arousals,
apneas, hypopneas, snores, and the mean, minimal, and
maximal oxygen saturation measured was calculated for
the total sleep time. An arousal was identified according to
criteria that has been published previously.16 An apnea was
defined as the absence of inspiratory airflow for a minimum of 10 seconds. The apnea index was defined as the
total number of apneas per hour of sleep. An hypopnea was
defined as greater than a 50% reduction in the flow signal
lasting more than 10 seconds. The hypopnea index was
defined as the total number of hypopneas per hour of sleep
time. Snoring was identified as respiratory noises that registered as an obvious deflection from the baseline of the
snoring channel. In addition, the respiratory noises were
subjectively determined to be snores by a polysomnographic technologist monitoring an audio–visual system.
We are confident that the sounds recorded were associated
with snoring since normal and heavy breathing during
wakefulness did not register on the sound system while
simulated snoring was detected. The snoring index was
defined as the total number of snores per hour of sleep time.
After staging a given sleep study, stage 2 and SWS of
NREM were divided into segments that were 8–10 minutes
in duration. The segment duration selected was constant for
a given subject but in some cases varied by one or two
minutes between subjects. This slight variation in segment
duration between subjects was allowed to maximize the
amount of data that could be obtained from each subject.
Each segment was defined by sleep that was not accompanied by arousals associated with a change in sleep stage.
The number of arousals per minute (arousal frequency) and
snores per minute (snoring frequency) were calculated for
each segment. The total number of segments analyzed for
each subject represented on average two hours of data
obtained from stage 2 and SWS throughout the total sleep
period.
Seven self–confessed snoring males that were otherwise
healthy gave their informed consent to participate in the
study which was approved by the Institutional Review
Board of Columbia Presbyterian Medical Center. All subjects reported regular sleep–wake schedules without any
difficulties in initiating or maintaining sleep. Twenty–four
hours prior to the onset of the study the subjects were
advised to avoid alcohol and caffeine. Each subject visited
the sleep laboratory on two occasions. The first occasion
was used to familiarize the subjects with the laboratory
environment and to confirm that the subjects were
non–apneic snoring individuals. The second investigation
was completed in order to measure spontaneous BS during
NREM sleep. On both occasions the subjects were
required to sleep in the supine position to ensure that alterations in recorded blood pressure were not due to variations
in body position. The subjects were monitored via an
infrared camera to ensure that the supine position was
maintained throughout the entire sleep period.
Nocturnal Polysomnography
The sleep monitoring montage included an electroencephalogram (C3/A2 or C4/A1), electrooculogram, submental electromyogram, and an electrocardiogram to measure heart rate. Abdominal movements were monitored
using a piezoelectric band (Pro–tech., Woodinville, WA)
and oronasal airflow was measured using a thermocouple
(Rochester Medical, Tampa, FL). Oxygen saturation was
measured using a pulse oximeter (Biox 3700, Ohmeda
Corp., Boulder, CO). Snoring was measured using a microphone that was mounted on the wall located adjacent to the
subjects head. Arterial pressure was monitored continuously and non–invasively from the middle phalanx of the
index finger using a Finapres blood pressure monitor
(Finapres 2300, Ohmeda Corp., Madison, WI). The accuracy of the blood pressure monitor was verified during
pre–sleep wakefulness and nocturnal awakenings by comparing its values to measurements made with a standard
mercury sphygmomanometer. To ensure that the monitoring site of the Finapres was accurately perfused with blood
throughout the evening, we discontinued the operation of
the Finapres for 10 minutes after each 60 minutes of monitoring.
For a minimum of 20 minutes prior to the onset of sleep
and during sleep all physiological variables were analogue
to digitally converted at a sampling frequency of 200
Hz/channel and input into a microcomputer using a commercially available software package (CODAS, Dataq
Instruments, Akron OH).
SLEEP, Vol. 22, No. 4, 1999
Data Analysis (spontaneous baroreflex analysis)
After the segments were identified, the R waves of the
electrocardiogram, and the systolic and diastolic blood
pressure of each pulse wave were identified using a threshold detection program. The time interval between the
detected R waves (interbeat interval – IBI), and the systolic
and diastolic blood pressure values were imported as an
ASCII file into a commercially available spreadsheet program. Subsequently, beat–to–beat mean arterial pressure
(MAP) was calculated from the systolic (SBP) and diastolic blood pressure (DBP) values. The mean IBI, SBP,
DBP, and MAP values were calculated for each segment.
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Spontaneous Baroreflex Analysis—Mateika et al.
critique of methods). Figure 1 (left) shows a sequence in
which the R–R interval lagged the change in blood pressure
by one beat. After a sequence was identified linear regression analysis was performed on the systolic blood pressure
and R–R interval values. The slope of the regression line
was considered to be a measure of BS. To minimize the
possibility of counting a sequence in which random variations in SBP and R–R interval appeared as a sequence, only
regressions with linear r2 values >0.85 were included (Fig.
1– right). In addition, if sequence overlap occurred (e.g., it
is possible that a four–beat sequence of lag 1 could also be
detected as a three–beat sequence of lag zero) the lag with
the largest number of beats was selected. Lastly, if overlapping sequences were of the same length, the first
sequence observed was selected since we were interested in
the lag at the initiation of the baroreflex response
The mean BS, IBI, and mean arterial pressure values calculated for each segment (see Data Analysis: sleep variables) recorded from a given subject were determined and
a mean value was then calculated for wakefulness, stage 2
and SWS. A group mean was then calculated for these
stages. A one–way analysis of variance with repeated measures in conjunction with Student–Newman–Keuls post
hoc test was employed to determine if a significant difference in MAP, heart rate, and BS existed between wakefulness and stage 2 and SWS of NREM sleep. Subsequently,
an average value for snoring frequency, for a given subject
and stage of sleep (stage 2 and SWS), was calculated and a
t–test was employed to determine if the average snoring
frequency values recorded during stage 2 and SWS were
significantly different. The mean change in BS relative to
wakefulness was then determined for a given subject and
stage of sleep. Subsequently, the relationship between snoring and BS was examined by plotting the average BS values against the average snoring frequency for each stage
Fig. 1–—Example of a four beat sequence during which systolic blood pressure (lower left) and R–R interval (upper left) decreased. Note that the change
in duration of the R–R interval lagged the decrease in blood pressure by one
beat (lag 1). In addition, a scatterplot (right) showing the change in R–R interval as a function of systolic blood pressure. Solid line represents the regression line calculated by method of least squares (y = 8.17x –156.6; r2 = 0.85).
Slope of the line represents baroreceptor sensitivity recorded for this
sequence.
After calculating the mean values for each segment, the
corresponding beat–to–beat R–R interval and systolic
blood pressure values were imported into a software program that was designed to measure spontaneous baroreflex
sensitivity.17 The program was designed to detect
sequences in which the systolic blood pressure either
increased or decreased by at least 1 mmHg during each of
three or more blood pressure waves (Fig. 1 lower left). In
addition, the program required that the change in systolic
blood pressure was accompanied by a concomitant lengthening or shortening of at least 4 ms/mmHg for each R–R
interval of the sequence (Fig. 1 upper left). The program
was designed to detect sequences in which the R–R interval lagged the change in systolic blood pressure by zero,
one or two beats (for further discussion of the method see
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Spontaneous Baroreflex Analysis—Mateika et al.
Student–Newman–Keuls post hoc test was employed to
determine if a significant difference in BS existed between
wakefulness and the snoring and non–snoring segments
recorded during stage 2. In addition, a t–test was employed
to determine if the arousal frequency and snoring frequency for the non–snoring and snoring segments were significantly different. Data recorded during SWS was not included in this analysis since non–snoring segments during SWS
did not exist for four of seven subjects. The level of statistical significance was set at p ≤ 0.05.
and subject. A linear regression analysis was employed to
determine the correlation between snoring frequency and
BS during NREM sleep. To further examine whether or not
snoring, independent of other confounding factors (i.e.,
oxygen saturation and sleep architecture), altered BS we
divided the segments recorded during stage II into snoring
and non–snoring segments. Snoring segments were defined
by a snoring frequency of greater than five snores per
minute. On average the snoring segments recorded outnumbered the non–snoring segments by a ratio of 2:1. Once
the segments were divided a mean value for BS was calculated for wakefulness and the non–snoring and snoring segments obtained from each subject. A one–way analysis of
variance with repeated measures in conjunction with
RESULTS
The age, body mass index (BMI), apnea, hypopnea,
arousal, and snoring index recorded for each subject is
shown in Table 1. The results in Table 1 show that the snoring subjects were non–apneic since the average
apnea/hypopnea index for the group was less than three.
This finding is supported by the average oxygen saturation
values recorded during sleep which did not deviate significantly from the value of 97.4 ± 0.4% recorded during
wakefulness. In addition, Table 1 shows that the arousal
index recorded for each subject was within normal limits.18,19
Table 2 shows the sleep architecture recorded for each
subject. On average the percentage of total sleep period
time spent in stage 2 and SWS were within the range of
normal predicted values for this population. In contrast the
percentage time spent in REM and the total sleep period
was less than normal (see discussion for explanation of this
result). Sleep efficiency was reduced in subjects two, six
and seven however a prolonged awakening associated with
a trip to the bathroom was primarily responsible for the
reduced sleep efficiency recorded for subjects two and six.
Figure 2 shows that MAP recorded during stage 2 and
Fig. 2—Histograms and a line plot showing the average mean arterial pressure (hatched bars), heart rate (open bars) and baroreceptor sensitivity
recorded from non–apneic snoring subjects during wakefulness, stage 2 and
slow wave sleep (SWS). * – significantly different from wakefulness, p <
0.005; ** – significantly different from stage 2, p < 0.05.
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1.2 and 12.7 ± 1.1 for wakefulness, stage 2 and SWS,
respectively. On average, the R–R intervals lagged blood
pressure by 0 beats in 85% of the sequences detected during wakefulness and sleep (see critique of methods for a
discussion on the importance of this value).
Figure 3 shows for each subject the average change in
BS, relative to wakefulness, plotted against the average
snoring frequency calculated for the segments obtained
from stage 2 and SWS. The figure demonstrates that on
average snoring frequency was significantly greater
(p=0.01) during SWS (11.2 ± 1.6 snores/min) as compared
to stage 2 (7.5 ± 0.9 snores/min). In addition, the plot
shows that an inverse and significant (p<0.001) correlation
(r=–0.9) existed between snoring frequency and baroreceptor sensitivity. This relationship may be independent of
stage of sleep since individuals with higher snoring frequencies during stage 2 (subjects 4,5,6) tended to have a
greater decrease in BS compared to values recorded from
subjects with a lower snoring frequency during SWS (subjects 2,3,7).
Figure 4 shows that the average BS recorded for stage 2
snoring segments was significantly less than the BS calculated for the non–snoring segments and wakefulness
(p=0.004). In contrast, baroreceptor sensitivity calculated
for wakefulness and the non–snoring segments were not
significantly different. The average arousal frequency was
not significantly different between the snoring (0.09 ±
0.04) and non–snoring segments (0.19 ± 0.04). In contrast,
the average snoring frequency was significantly different
(p=0.001) between the snoring (10.57 ± 2.5) and non–snoring (1.43 ± 0.4) segments.
Fig. 3—Scatterplot showing the change in baroreceptor sensitivity as a function of snoring frequency in each subject for both stage 2 (closed symbols)
and slow wave sleep (open symbols). Solid line represents the regression line
calculated by method of least squares (y = –0.74x + 2.09; r2 = 0.81).
SWS was not significantly different from the values recorded during wakefulness. Similarly, neither awake supine
SBP (115 ± 5.7 mmHg) nor DBP (66 ± 3.2) differed from
the average values recorded during stage 2 (SBP=112 ±
2.8; DBP=64 ± 2.8) and SWS (SBP=109 ± 3.9; DBP=64 ±
4.1). Figure 2 also reveals that heart rate recorded during
stage 2 and SWS was not significantly different from wakefulness. In contrast, Fig. 2 demonstrates that BS was significantly less during stage 2 (p=0.004) and SWS
(p=0.005) compared to wakefulness and that the BS measured during SWS (p=0.05) was less than the average value
recorded during stage 2. The average number of sequences
detected per minute of segment time was 10.0 ± 0.8, 12.1 ±
DISCUSSION
Critique of the methods
Much of the present knowledge of baroreflex function in
humans during sleep has been determined by measuring the
heart rate response to the injection of vasoactive drugs.8–10
However, this procedure does have its limitations since it
cannot be used to monitor the dynamic modulation of BS
in individuals during sleep. Furthermore, the applied stimulations may disrupt sleep thereby interfering with the
mechanisms under evaluation. Fortunately, the sequence
analysis method employed in the present investigation does
not disrupt sleep and allows for the dynamic modulation of
BS. The sequencing technique is a valid and reliable
method since measurements of BS using the technique
were similar to results obtained simultaneously using the
injection of a vasoactive drug20–22 or the Valsalva maneuver.23 Furthermore, this method has been assessed using
surrogate data analysis and the results indicated that spontaneous baroreflex sequences represent physiological
rather than chance interaction.17 However, the technique
does have its limitations. First, the method does not take
Fig. 4—Histograms showing the average baroreceptor sensitivity recorded
from non–apneic subjects during wakefulness and, non–snoring and snoring
segments obtained from stage 2 of NREM sleep. * – significantly different
from wakefulness and stage 2 non–snoring segments, p<0.004.
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Spontaneous Baroreflex Analysis—Mateika et al.
Baroreceptor Sensitivity in non–apneic snorers
into account the closed–loop nature of blood pressure –
heart rate interactions. In the intact system blood pressure
acts on heart rate via the baroreflex but heart rate simultaneously acts on blood pressure mainly through changes in
cardiac output. This reciprocal and simultaneous interaction is not taken into account by the method employed in
this investigation. Second, the sequence analysis only
quantifies the relationship between blood pressure and
heart rate variations. The findings do not necessarily imply
the existence of a causal relationship between the changes
in these two variables.
The method employed in the present investigation
detected sequences in which the change in R–R interval
lagged the change in systolic blood pressure by zero, one,
or two beats. The validity of selecting sequences with lag
zero must be considered because a minimum time is
required for the baroreflex to respond to a change in arterial pressure. It has been demonstrated in man that a pharmacologically induced increase in SBP alters the R–R
interval within the same beat if the interval is greater than
775 ms prior to initiation of the perturbation.24
Furthermore, Balber et al. showed, using real and surrogate
data that the baroreflex response in seated awake subjects
can occur within the same beat if the R–R interval is greater
than 900 ms.17 Blaber et al. provided further support for
this hypothesis by demonstrating that shortening of the
R–R interval from 1,038 ms to 804 ms via lower body negative pressure was accompanied by a change in the functional relationship between SBP and R–R interval.25 A significant increase in the number of sequences with a lag of
two was measured since the effect of the baroreflex at the
lower R–R interval could not manifest itself within the
same beat at the increased heart rate. Given that the R–R
intervals of our subjects ranged between 950 – 1152 ms it
is reasonable to suggest that the baroreflex response affected the R–R interval within the same beat. This suggestion
is supported by the results of the present investigation
which showed that the largest percentage of sequences
were of lag zero and did not vary between wakefulness and
sleep. This latter finding was expected since the average
heart rate was similar during wakefulness and sleep.
Non–apneic snoring males that were otherwise healthy
participated in the present investigation. However, the
anthropometric results showed that the BMI of six subjects
was greater than 25 which is a value used recently as a indicator of obesity.26 However, these subjects were characterized by a muscular build and a mesomorphic body type that
likely accounted for the BMI values. This suggestion is
supported by the results of body impedance analysis completed on six subjects which showed that the percentage of
body fat was equal to or less than the predicted normal values for the subjects height and weight.
SLEEP, Vol. 22, No. 4, 1999
The results from many experimental investigations have
been unequivocal in demonstrating that blood pressure and
heart rate decrease while baroreceptor sensitivity increases
during the transition from wakefulness to SWS in
non–snoring healthy individuals.8–10 These findings have
lead a number of investigators to suggest that the increase
in baroreceptor sensitivity may be partly responsible for the
reduction in blood pressure observed during NREM
sleep.8–10 Furthermore, these findings have lead to the suggestion that attenuation of the normal decrease in blood
pressure observed in individuals with sleep disordered
breathing may be mediated partially by a decrease in
baroreceptor sensitivity. This hypothesis has received support recently by the results obtained by Carlson et al. and
Parati et al. which showed that baroreceptor sensitivity was
reduced in individuals with obstructive sleep apnea.12,27
The alterations in cardiovascular and baroreceptor function in individuals with sleep disordered breathing have
often been linked to increases in sympathetic activity that
are elicited in response to hypoxemia that occurs concomitantly with obstructive sleep apnea.12–13,27 However, a number of studies have implied that these same alterations may
occur in individuals who snore but do not suffer from
obstructive sleep apnea (see 28 for review). Unfortunately,
few studies have examined this proposal by obtaining continuous and simultaneous measurements of snoring, cardiovascular function, and sleep stages. Although Young et al.11
did not obtain continuous measurements of these variables,
they did show that blood pressure in non–apneic snoring
individuals during sleep was significantly greater than values obtained from non–snoring individuals. These results
supported the earlier findings of Mateika et al.3 who
demonstrated that blood pressure did not decrease in
non–apneic snoring individuals during NREM sleep and
that the values were significantly greater then measurements recorded from non–snoring individuals. These earlier findings were replicated in the present investigation
since average blood pressure and heart rate measurements
recorded during stage 2 and SWS were not significantly
different than the values recorded during wakefulness.
A decrease in BS may have contributed wholly or in part
to an increase in sympathetic activity leading to the cardiovascular dysfunction that was observed during sleep in the
non–apneic snoring subjects. This proposal is supported by
the results that demonstrated how BS decreased significantly during stage 2 and SWS of NREM sleep compared
to wakefulness despite the maintenance of awake heart rate
and blood pressure values during these sleep stages.
Furthermore, MAP and HR were not significantly different
between stage 2 and SWS while BS sensitivity decreased
during SWS. Hence, the reduction in BS may have contributed to the maintenance of MAP and HR during SWS,
even though the subjects entered what is considered tradi466
Spontaneous Baroreflex Analysis—Mateika et al.
tionally to be a "deeper" stage of sleep that is normally
accompanied by reduced sympathetic activity compared to
stage 2 in non–snoring individuals.4,29
nificant role in reducing BS then it would be expected that
the subjects with the greatest change in baroreceptor sensitivity and snoring frequency also experienced the poorest
sleep architecture (see Table 2). This was not the case.
Similarly, if alterations in sleep architecture were principally responsible for the observed changes in BS then it
might be expected that BS during snoring and non–snoring
periods would be similar. However, the results showed that
the lowest BS was recorded during snoring segments as
compared to non–snoring segments. This difference
occurred even though the average arousal frequency was
similar between the snoring and non–snoring segments.
Therefore, the results obtained from the present investigation suggest that snoring may be capable of altering BS
independent of other well–established confounding factors
such as oxygen saturation and sleep architecture.
Possible mechanisms responsible for baroreceptor
response in non–apneic snorers
Although the mechanism responsible for the alteration in
BS was not examined in the present investigation, the alterations that were observed may have been linked directly or
indirectly to changes in upper airway resistance and/or
intrathoracic pressure that occurred during snoring. Three
lines of evidence suggest that this proposal may be correct.
First, although it is not known whether increases in snoring
frequency were accompanied by changes in airway resistance in the present investigation, previous studies have
reported that snoring (snoring frequency and/or intensity)
in a given individual is accompanied by an increase in
inspiratory resistance as compared to non–snoring periods.30 Second, the results from the present investigation
showed a significant correlation between snoring frequency and change in BS during sleep. Third, other confounding factors, such as oxygen saturation and sleep architecture that might contribute to alterations in BS and blood
pressure seemingly did not play a significant role in this
investigation.
The results showed that the average oxygen saturation
did not deviate from awake values during sleep and the
average apnea/hypopnea index recorded for the group was
2.54 ± 0.48. Furthermore, although it might be argued that
the sleep architecture, which was not normal, might have
contributed to the change in BS that was observed this case
is unlikely for the following reasons. The reduced sleep
efficiency, total sleep period time and the percentage time
spent in REM sleep was not due to an increased number of
arousals associated with snoring, since the arousal index
for each subject was within the normal range.18,19 Rather
the alteration in total sleep period time and the percentage
time spent in REM sleep was due primarily to the termination of the sleep studies after an adequate amount of NREM
sleep had been recorded. Most of the sleep studies were terminated early to minimize discomfort. Discomfort
occurred because the subjects, who were recruited solely
for the purpose of completing this investigation, were
required to sleep in the supine position for the entire sleep
period time in order to control rigorously for the effect of
position on blood pressure. As a result the total sleep period time was reduced and this was accompanied by a
decrease in the percentage of time spent in REM sleep
since this stage of sleep comprises a larger percentage of
the NREM/REM cycle in the early morning. The probable
reason for the reduced sleep efficiency was outlined in the
results section. The minimal impact of sleep architecture
on our results is further supported by the data that was presented in Figures 3 and 4. If sleep architecture played a sigSLEEP, Vol. 22, No. 4, 1999
Summary
Previous investigations showed that the decrease in
blood pressure that is normally observed during sleep may
be attenuated in non–apneic snoring individuals that are
otherwise healthy.3,11 This finding was supported by the
results of the present investigation which showed that MAP
recorded during NREM sleep was not significantly different from wakefulness. More importantly, the present investigation revealed that a reduction in BS, which was negatively correlated to snoring frequency, may be partially
responsible for the cardiovascular dysfunction that has
been observed in snoring individuals. Given these findings
we suggest that over time the nighttime alterations in cardiovascular function could lead to nocturnal cardiovascular
complications or to daytime hypertension, thereby providing support for the hypothesis that snoring and cardiovascular disease are linked directly.28 In addition, we propose
that the findings from this study may be the first step
towards providing a rationale for clinicians to treat
non–apneic snoring individuals in order to prevent the
development of cardiovascular dysfunction.
ACKNOWLEDGEMENTS
This study was supported by the VIDDA foundation.
REFERENCES
(1) Bixler EO, Kales A, Vela–Bueno A, Niklaus DE, Shubert DD and
Soldatos CR. Nocturnal sleep and blood pressure in essential hypertension. Intern. J. Neuroscience. 1988;40:1–11.
(2) Littler WA, Honour AJ, Carter RD and Sleight P. Sleep and blood
pressure. British Medical Journal. 1975;3:346–348.
(3) Mateika JH, Mateika S, AS Slutsky and Hoffstein V. The effect of
snoring on mean arterial blood pressure during non–rem sleep. Am. Rev.
Respir. Dis. 1992;145:141–146.
(4) Baharav A, Kotagal S, Gibbons V, Rubin BK, Pratt G, Karin J and
Akselrod S. Fluctuations in autonomic nervous activity during sleep displayed by power spectrum analysis of heart rate variability. Neurology.
1995;45 (6):1183–1187.
467
Spontaneous Baroreflex Analysis—Mateika et al.
(5) Bonnet MH and Arand DL. Heart rate variability: sleep stage, time
of night and arousal influences.
Electroencephalogr. Clin.
Neurophysiol. 1997;102(5):390–396.
(6) Somers VK, Phil D, Dyken M and Abboud FM. Sympathetic nerve
activity during sleep in normal subjects. N. Engl. J. Med. 1993;328:
303–307.
(7) Vanoli E, Adamson PB, Pinna GD, Lazzara R and Orr WC. Heart rate
variability during specific sleep stages. A comparison of healthy subjects
with
patients
after
myocardial
infarction.
Circulation.
1995;91(7):1918–1922.
(8) Conway J, Boon N, Vann Jones J and Sleight P. Involvement of the
baroreceptor reflexes in the changes in blood pressure with sleep and
mental arousal. Hypertension 1983;5:746–748.
(9) Sleight P. The relevance of baroreflex mechanisms to the control of
ambulatory and exercise blood pressure in humans. Clin. and Exp.
Pharm. and Physiol. 1989;Suppl.15:65–69.
(10) Smyth HS, Sleight P and Pickering GW. Reflex regulation of arterial pressure during sleep in man. Circ. Res. 1969;24:109–121.
(11) Young T, Finn L, Hla M, Morgan B and Palta M. Snoring as a part
of the dose–response relationship between sleep disordered breathing
and blood pressure. Sleep. 1996;19:S202–205.
(12) Carlson JT, Hedner JA, Sellgren J, Elam M and Wallin BG.
Depressed baroreflex sensitivity in patients with obstructive sleep apnea.
Am. J. Respir. Crit. Care Med. 1996;154(5):1490–1496.
(13) Somers VK, Dyken ME, Clary MP and Abboud FM. Sympathetic
neural mechanisms in obstructive sleep apnea. J. Clin. Invest.
96(4):1897–1904.
(14) Waradekar NV, Sinoway LI, Zwillich CW and Leuenberger UA.
Influence of treatment on muscle sympathetic nerve activity in sleep
apnea. Am. J. Resp. Crit. Care Med. 1996;153(4):1333–1338.
(15) Rechtschaffen A, Kales A. A manual of standardized terminology,
techniques and scoring for sleep stages of human subjects. Department
of Health, Education and Welfare, Washington DC, (NIH publication),
1968.
(16) Anonymous. EEG arousals–scoring rules and examples– A preliminary report from the sleep disorders atlas task force of the American
Sleep Disorders Association. 1992;Sleep 15(2):174–184.
(17) Blaber A, Yamamoto Y and Hughson RL. Methodology of spontaneous baroreflex relationship assessed by surrogate data analysis. Am. J.
Physiol. 1995;268:H1682–H1687.
(18) Boselli M, Parrino L, Smerieri A and Terzano MG. Effect of age
on EEG arousals in normal sleep. 1998;Sleep 21(4):351–357.
(19) Marthur R and Douglas NJ. Frequency of EEG arousals from nocturnal sleep in normal subjects. 1995;Sleep 18(5):330–333.
(20) James MA, Panerai RB and Potter JF. Applicability of new techniques in the assessment of arterial baroreflex sensitivity in the elderly:
a comparison with established pharmacological methods. Clin Sci.
1998;94(3):245–253.
(21) Parlow J, Viale JP, Annat G, Hughson R and Quintin L. Spontaneous
cardiac baroreflex in humans. Comparison with drug induced responses.
Hypertension. 1995;25(5):1058–1068.
(22) Watkins LL, Grossman P and Sherwood A. Noninvasive assessment of baroreflex control in borderline hypertension. Comparison with
the phenylephrine method. Hypertension 1996;28 (2):238–243.
(23) Kardos A; Rudas L; Simon J; Gingl Z; Csan´ady M. Effect of postural changes on arterial baroreflex sensitivity assessed by the spontaneous sequence method and Valsalva manoeuvre in healthy subjects.
Clin. Auton. Res. 1997;7(3):143–148.
(24) Pickering TG and Davies J. Estimation of the conduction time of
the baroreceptor–cardiac reflex in man. Cardiovasc. Res.
1973;7:213–219.
(25) Blaber AP, Yamamoto Y and Hughson RL. Change in the phase
relationship between SBP and R–R interval during lower body negative
pressure. Am. J. Physiol. 1995;268:H1688–H1693.
(26) Flegal KM, Carroll MD, Kuczmarski RJ and Johnson CL.
Overweight and obesity in the United States: prevalence and trends,
SLEEP, Vol. 22, No. 4, 1999
1960–1994. Int. J. Obes. Relat. Metab. Disord. 1998;22(1):39–47.
(27) Parati G, Di Rienzo M, Bonsignore MS, Insalaco G, Marrone O,
Castiglioni P, Bonsignore, G and Mancia G. Autonomic cardiac regulation in obstructive sleep apnea syndrome: evidence from spontaneous
baroreflex analysis during sleep.J. of Hypertension.1997;15:1621–1626.
(28) Silverberg DS and Oksenberg A. Essential hypertension and
abnormal upper airway resistance during sleep.
1997;Sleep
20(9):794–806.
(29) Oken BS and Salinsky M. Alertness and attention – Basic science
and electrophysiologic correlates. J. of
Clin. Neurophysiol.
1992;9:(4)480–494.
(30) Dawson A, Bigby BG, Poceta JS and Miller MM. Effect of sleep
stage on inspiratory resistance of male snorers. 1998;Sleep 21
(Supplement):156.
468
Spontaneous Baroreflex Analysis—Mateika et al.