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(Chest. 2004;126:801-807.)
© 2004 American College of Chest Physicians

Baroreflex Sensitivity in Nonapneic Snorers and Control Subjects Before and After Nasal Continuous Positive Airway Pressure*

Gregory J. Gates, MA; Susan E. Mateika, BSc; Robert C. Basner, MD and Jason H. Mateika, PhD

* From the Department of Biobehavioral Sciences (Mr. Gates and Ms. S.E. Mateika), Teachers College, and the Department of Medicine (Dr. Basner), College of Physicians, and Surgeons, Columbia University, New York, NY; and the Department of Internal Medicine (Dr. J.H. Mateika), Wayne State University School of Medicine, Detroit, MI.

Correspondence to: Jason H. Mateika, PhD, John D. Dingell VA Medical Center, 4646 John R (11R), Room 4308, Detroit, MI, 48201; e-mail: jmateika{at}intmed.wayne.edu


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Hypothesis: We hypothesized that baroreflex sensitivity is decreased during wakefulness and non-rapid eye movement sleep in normotensive, nonapneic snorers who are otherwise healthy. Moreover, we hypothesized that nocturnal alterations in baroreflex sensitivity are abolished during the application of nasal continuous positive airway pressure (nCPAP).

Design: The sequencing technique was used to measure baroreflex sensitivity in 16 normotensive nonapneic snorers and 16 control subjects matched for age, height, weight, gender, and race. Subsequently, baroreflex sensitivity was measured in 12 of 16 snorers and 14 of 16 control subjects during the application of nCPAP.

Results: Mean (± SE) baroreflex sensitivity was reduced during sleep in the nonapneic snoring group (wakefulness, 20.99 ± 1.46 ms/mm Hg; sleep, 15.85 ± 1.49 ms/mm Hg), but not in the control group (wakefulness, 21.82 ± 2.48 ms/mm Hg; sleep, 23.54 ± 2.18 ms/mm Hg). This reduction was abolished by the application of nCPAP in the snoring group (before nCPAP therapy, 16.30 ± 2.17 ms/mm Hg; during nCPAP therapy, 20.63 ± 2.40 ms/mm Hg). The application of nCPAP did not alter baroreflex sensitivity in the control group (before nCPAP therapy, 23.54 ± 2.18 ms/mm Hg; during nCPAP therapy, 22.56 ± 1.73 ms/mm Hg). BP was not significantly different between the snoring and control groups either before or during nCPAP application.

Conclusions: Our findings suggest that nocturnal alterations in baroreflex sensitivity may exist in nonapneic snoring subjects prior to alterations in other cardiovascular variables.

Key Words: baroreflex sensitivity • non-rapid eye movement sleep • wakefulness


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Studies completed in individuals experiencing obstructive sleep apnea have provided evidence that nocturnal decreases in baroreflex sensitivity and increases in sympathetic nervous system activity persist during wakefulness in normotensive individuals.12 These alterations may be responsible for the association between obstructive sleep apnea and hypertension,3 and thus might provide early warning that hypertension may develop. Given that snoring, independent of nocturnal hypoxemia, may be an independent risk factor for the development of daytime hypertension,345 it is possible that decreases in baroreflex sensitivity may exist during wakefulness and sleep in nonapneic snorers who are otherwise healthy. To test this hypothesis, we employed the spontaneous baroreflex sequencing technique6 to quantify baroreflex sensitivity during wakefulness and sleep in nonapneic snorers and control subjects who were matched for race, age, gender, and body mass index. Moreover, we obtained these measures before and after the application of nasal continuous positive airway pressure (nCPAP) to examine whether nocturnal baroreflex sensitivity measures are normalized after the elimination of snoring.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 Conclusion
 References
 
Sixteen self-reported snoring subjects with no known medical conditions were recruited from the community. The snoring group was composed of 14 men (Asian, 1 man; African American, 1 man; Hispanic, 3 men; and white, 9 men) and 2 white women. The subjects were selected from a group of 45 individuals who had completed a preliminary sleep study in response to an advertisement. The remaining subjects were excluded from participating in the study because they experienced another sleep disorder (eg, periodic leg movement syndrome and obstructive sleep apnea), consumed alcohol prior to the completion of the study, or were unable to tolerate the experimental conditions. Each of the 16 nonapneic snorers recruited for the study was matched for race, age, height, weight, and gender with a nonsnoring subject who had been recruited from the community. All subjects gave their informed consent to participate in the study, which was approved by the institutional review boards of New-York Presbyterian Medical Center and Teachers College, Columbia University.

The snoring subjects and their matched control subjects visited the sleep laboratory on either two or three occasions. Twenty-four hours prior to each visit, the subjects were advised to avoid alcohol and caffeine. The first occasion was used to familiarize the subjects with the laboratory environment and to confirm that the subjects were nonapneic snoring individuals or nonsnoring individuals. The second study was completed in order to measure the cardiovascular and autonomic variables outlined below during non-rapid eye movement (NREM) sleep. This second study will be referred to as trial 1 from this point forward. Subsequent to the completion of trial 1, 12 of the 16 snoring subjects and 14 of 16 control subjects adapted to nCPAP therapy at 5 cm H2O for 7 to 10 days at home. The selection of the nCPAP pressure was based on the results from our pilot data, which showed that this level of pressure effectively eliminated snoring in nonapneic individuals. The purpose of the adaptation period was to ensure that the subjects were able to tolerate nCPAP for a minimum of 4 h during the completion of a third sleep study (ie, trial 2). nCPAP was employed initially for 1 h during the first night at home. Thereafter, the duration of treatment was increased by an additional hour each night until 4 h of nCPAP therapy was tolerated. During the adaptation period, subjects received a phone call on days 3 and 6 to ensure that the protocol was being followed. All but two subjects were able to tolerate nCPAP at 5 cm H2O by day 4 of the 7-day adaptation period. The two subjects who could not tolerate a pressure of 5 cm H2O by day 4 were able to tolerate the prescribed pressure after 7 days. Consequently, the adaptation period was extended to 10 days. During all sleep studies, subjects were required to sleep in the supine position to ensure that alterations in the recorded BP were not due to variations in body position. The subjects were monitored via an infrared camera to ensure that this position was maintained throughout the sleep period.

Nocturnal Polysomnography
The sleep-monitoring montage included an EEG (C3/A2, C4/A1, O1/A2, and O2/A1), an electrooculogram, a submental and tibialis anterior electromyogram, and an ECG. Abdominal movements were monitored using a piezoelectric band (Pro-tech; Woodinville, WA), and nasal pressure was measured using a pressure transducer/airflow sensor (Pro-tech). Thus, breathing frequency (Bf) was monitored breath-by-breath. Oxygen saturation was measured using a pulse oximeter (Biox 3700; Ohmeda; Boulder, CO). Snoring was measured using a microphone that was mounted on the wall located adjacent to the subject’s head. Arterial pressure was monitored continuously and noninvasively from the middle phalanx of the ring or middle fingers using a digital infrared photoplethysmograph (Finapres 2300; Ohmeda; Madison, WI). The accuracy of the BP monitor was verified during presleep wakefulness and nocturnal awakenings by comparing its values to measurements made with a standard mercury sphygmomanometer. To ensure that the monitoring site of the digital infrared photoplethysmograph was adequately perfused with blood throughout the evening, its operation was discontinued consistently during rapid eye movement (REM) sleep and at times during NREM sleep, if necessary. We consistently selected to discontinue the operation of the digital infrared photoplethysmograph during REM sleep because snoring was recorded more frequently during NREM sleep in the preliminary studies. Moreover, we were primarily interested in studying the impact of snoring on cardiovascular function during NREM sleep.

For a minimum of 30 min prior to the onset of sleep and during sleep, all physiologic variables underwent analog-to-digital conversion at a sampling frequency of 100 Hz per channel and input into a microcomputer using a commercially available software package (CODAS; Dataq Instruments; Akron OH).

Data Analysis
Sleep Variables:
Sleep was staged in 30-s epochs according to standard criteria.78 For each subject, the total sleep period time as well as the percentage of total sleep time spent in a given sleep stage were calculated. The total number of arousals, apneas, hypopneas, and snores, and the mean, minimal, and maximal oxygen saturation measured were calculated for the total sleep time. An apnea was defined as the absence of inspiratory airflow for a minimum of 10 s. The apnea index was defined as the total number of apneas occurring per hour of sleep. A hypopnea was defined as a > 50% reduction in the flow signal, lasting > 10 s. The hypopnea index was defined as the total number of hypopneas per hour of sleep time. A breath that was characterized by respiratory noises that registered as an obvious deflection from the baseline of the snoring channel was counted as a snore. In addition, the respiratory noises were subjectively determined to be snores by a polysomnographic technologist monitoring an audiovisual 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 during wakefulness was detected.

After staging a given sleep study, snoring segments that were 5 min in length were identified from the stage II sleep and slow-wave sleep (SWS) of each NREM sleep cycle. The segments selected were devoid of apneas, hypopneas, and arousals, and were identified as snoring segments if 67 to 100% of the breaths in a given segment were associated with snoring. Note, in the presentation of our results we did not differentiate between stage II sleep and SWS. Although the data were originally analyzed in this fashion, we found that our findings were not stage-dependent, and thus the data recorded from each NREM sleep cycle were combined. The total number of segments analyzed for each subject represented on average 2.2 h of data obtained from stage II sleep and SWS recorded over the entire sleep period.

Respiratory, Cardiovascular, and Autonomic Variables:
The number of snores and breaths was calculated for each segment. Subsequently, the values calculated were divided by the total segment time and were reported as snoring frequency (ie, the number of snores per minute) and Bf (ie, the number of breaths per minute). The R waves of the ECG, and the systolic BP (SBP) and diastolic BP (DBP) of each pulse wave were identified using a threshold detection program. The time interval between the detected R waves (ie, the interbeat interval), and the SBP and DBP values were imported as an ASCII file into a commercially available spreadsheet program. Subsequently, the beat-to-beat mean arterial pressure (MAP) was calculated from the SBP and DBP values. The mean interbeat interval, SBP, DBP, and MAP values were calculated for each segment.

After calculating the mean values for each segment, the corresponding beat-to-beat R-R interval and SBP values were imported into a software program that was custom designed and written to measure spontaneous baroreflex sensitivity using the sequencing technique.6 The program was designed to detect sequences in which the SBP either increased or decreased by at least 1 mm Hg during each of three or more BP waves. In addition, the program required that the change in SBP be accompanied by a concomitant lengthening or shortening of at least 4 ms/mm Hg for each R-R interval of the sequence. The program was designed to detect sequences in which the R-R interval lagged the change in SBP by 0, 1, or 2 beats. After a sequence was identified, linear regression analysis was performed on the SBP and R-R interval values. The slope of the regression line was considered to be a measure of baroreflex sensitivity. 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 of > 0.85 were included. In addition, if sequence overlap occurred (eg, it is possible that a 4-beat sequence of lag 1 could also be detected as a 3-beat sequence of lag 0), the lag with the largest number of beats was selected. Last, 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.

Statistical Analysis
Unpaired t tests were used to compare the anthropometric and sleep data between groups. A two-way analysis of variance in conjunction with the Student-Newman-Keuls post hoc test was employed to compare the physiologic variables measured during wakefulness and NREM sleep in the 16 snoring and 16 nonsnoring subjects before treatment with nCPAP (GB-STAT, version 8.0; Dynamic Microsystems; Silver Spring, MD). The two factors in the design were arousal state (ie, wakefulness vs NREM sleep) and subject population (ie, snorers vs nonsnorers). A similar analysis was used to compare the physiologic variables within each group before and after treatment with nCPAP. The two factors in the design were wakefulness vs NREM sleep, and before vs after nCPAP treatment. This analysis was completed using the 14 control subjects and 12 snoring subjects who were able to adapt to nCPAP. All values are presented as the mean ± SE, and the level of significance chosen was p ≤ 0.05.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Conclusion
 References
 
Anthropometric and Sleep Measurements
Race, age, body mass index, apnea index, hypopnea index, arousal index, and mean nocturnal oxygen saturation were not different between the snoring and control groups (Table 1 ). Similarly, sleep efficiency and the percentage of time (relative to the total sleep period time) spent in a given stage of sleep did not vary significantly between groups during the completion of trial 1 (Table 1). Snoring episodes measured from the nonapneic snorers were characterized by a mean snoring frequency of 11.60 ± 0.43 snores per minute. In contrast, no snoring was detected from the control group. The sleep architecture during trial 2 did not differ significantly from that reported during trial 1. Additionally, the application of nCPAP effectively eliminated snoring in all subjects.


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  		Table 1. Anthropometric and Sleep Data*

 
Autonomic and Cardiovascular Measures During Wakefulness and Sleep With and Without nCPAP
During trial 1, BP, heart rate, Bf, and baroreflex sensitivity were similar throughout wakefulness in the snoring and control groups. During sleep, BP and Bf were similar between groups (Table 2 ). In contrast, heart rate was significantly greater (p = 0.03), while baroreflex sensitivity (p = 0.01) was significantly less in the snoring group compared to the control group (Table 2). The decrease in baroreflex sensitivity was not accompanied by a resetting of the baroreflex, since the x-intercept of the regression line (mean, 8.54 ± 0.27 mm Hg) that defined the SBP vs R-R interval relationship for the snorers was not significantly different compared to that of control subjects (mean, 7.93 ± 0.22 mm Hg).


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  		Table 2. Cardiovascular, Respiratory, and Baroreflex Sensitivity Measures Obtained From Control Subjects and Nonapneic Snorers*

 
After the period of adaptation to nCPAP (trial 2), there was no change in any of the physiologic measures during wakefulness in the snoring and control groups. Likewise, compared to trial 1 (ie, without nCPAP), the physiologic measures recorded from the control group were not altered during sleep by the application of nCPAP (Table 3 ). This was also the case for the snoring group, with the exception that the application of nCPAP during sleep resulted in an increase in baroreflex sensitivity (p = 0.03) [Table 3] compared to the values recorded during sleep in trial 1. The increase in baroreflex sensitivity after treatment with nCPAP was not accompanied by a resetting of the baroreflex, since the x-intercept of the SBP vs R-R interval relationship (mean, 8.39 ± 0.34 mm Hg) before nCPAP treatment was not significantly different compared to the x-intercept of the regression line after treatment with nCPAP (mean, 7.62 ± 0.36 mm Hg).


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  		Table 3. Cardiovascular, Respiratory, and Baroreflex Sensitivity Measures in Control Subjects and Nonapneic Snorers With and Without nCPAP*

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
Conclusion
 References
 
Summary of Findings
Our major findings were that baroreflex sensitivity was decreased in the snoring group compared to that of control subjects. Moreover, baroreflex sensitivity increased during NREM sleep in the nonapneic snorers in response to the application of nCPAP.

Critique of the Methods
Our subjects were exposed to nCPAP for an adaptation period of 7 to 10 days prior to completing trial 2. This adaptation period occurred after a baseline study had been completed. Consequently, the order of baseline and treatment studies was not randomized. Nevertheless, if the order of the trials impacted on our measures, we would expect that the response to nCPAP application would have been similar between groups, since both groups were comparable (eg, healthy with no complaint of daytime sleepiness) in all aspects with the exception of snoring. This was not the case.

It is also unlikely that any differences observed between groups during trial 2 were a consequence of discrepancies in nCPAP compliance because, based on subject self-report, this measure was similar between groups. Although it is possible that some subjects did not truthfully report their compliance, we believe that it is unlikely that healthy nonsnorers and nonapneic snorers would have tolerated nCPAP for 4 h during trial 2 if they had not adhered to the protocol during the adaptation period.

The spontaneous baroreflex-sequencing technique was used in the present study to obtain noninvasive measures of baroreflex sensitivity. The spontaneous baroreflex-sequencing technique has been critiqued extensively.9 In short, results obtained using the sequencing technique have been found to be similar to measurements obtained simultaneously using other noninvasive techniques, the injection of a vasoactive drug101112 or the Valsalva maneuver.13 Additionally, this method has been assessed using surrogate data analysis,6 and the results indicated that spontaneous baroreflex sequences represent physiologic rather than chance interaction.

Baroreflex Sensitivity During Wakefulness and Sleep
Baroreflex sensitivity was similar during wakefulness and NREM sleep both before and after the application of nCPAP in control subjects. This result is consistent with some previous studies.214 However, our results differ from those of other studies that have reported that baroreflex sensitivity increases during sleep compared to wakefulness.1516 Our results may differ from those of Conway et al15 because of dissimilarities in experimental methodology. Conway et al15 utilized bolus injections of phenylephrine to measure baroreflex sensitivity, while we employed the sequencing technique. The sequencing method is noninvasive and as a result does not interrupt sleep. Consequently, multiple measures of baroreflex sensitivity can be obtained throughout the entire sleep period. In contrast, although the number of trials performed to measure baroreflex sensitivity was not detailed by Conway et al,15 baroreflex sensitivity was likely measured infrequently throughout the sleep period, given the invasiveness of the procedure employed and its propensity toward inducing arousal from sleep. Thus, a limited number of measures confined to a small portion of the sleep cycle may not accurately reflect changes in baroreflex sensitivity throughout the entire sleep period.

If this suggestion is correct, then our results should be similar to those of Parati and colleagues,16 because these investigators measured baroreflex sensitivity in subjects without obstructive sleep apnea using the baroreflex-sequencing technique. However, this was not the case since baroreflex sensitivity was increased during sleep in the study by Parati et al.16 This discrepancy may have occurred because the measures of baroreflex sensitivity that were reported for our control subjects were obtained solely from NREM sleep, while measures of baroreflex sensitivity in the investigation by Parati et al16 were obtained during NREM and REM sleep.16 Whether or not the measures during REM sleep were principally responsible for the increase in baroreflex sensitivity observed by Parati et al16 was not reported. Moreover, we cannot substantiate this postulation with results from the present study because BP was not monitored during REM sleep. Nevertheless, our premise is supported by a publication from the same group,2 which showed that baroreflex sensitivity during wakefulness and NREM sleep was similar in control subjects. Furthermore, our postulation is similar to that previously put forth by Bristow and colleagues14 to explain their findings showing that, despite similar experimental methodology (ie, bolus injections of angiotensin), baroreflex sensitivity measures did not increase during sleep, which is contrary to the findings of Smyth and colleagues.17

In contrast to the findings obtained in the control group, we showed that baroreflex sensitivity was reduced in the nonapneic snorers during NREM sleep and that this reduction was reversed after the application of nCPAP during sleep. Given that we controlled for a number of confounding variables (ie, age, race, gender, sleep architecture, hypoxemia, and Bf) that might independently affect baroreflex sensitivity, we speculate that the decrease was a consequence of snoring. However, the spontaneous baroreflex-sequencing technique reflects the integrated response to multiple inputs to the cardiovascular control centers. Thus, we can only speculate on the mechanisms responsible for the reduction in baroreflex sensitivity.

One possibility is that even though Bf was similar between groups, snoring altered the pattern of breathing during sleep (ie, inspiratory time/expiratory time ratio), which subsequently resulted in a reduction in baroreflex sensitivity compared to the control group. This possibility is supported by the results of a previous study,18 which showed that the inspiratory time/expiratory time ratio is increased in snoring subjects. Moreover, it is well-established that the gain of baroreflex activation is not absolute but depends on the phase of breathing.1920 The cardioinhibitory response to baroreflex stimulation is smaller during inspiration compared to expiration. The diminution of the response during inspiration is likely due to a reduction in vagal-cardiac motoneuron responsiveness, which is a consequence of inhibition originating from inspiratory motoneurons and lung stretch receptors.21 Thus, the prolongation of inspiratory time in snoring subjects could lead to a reduction in baroreflex sensitivity. Unfortunately, inspiratory and expiratory time could not be accurately measured using the airflow sensor that was employed in our study, and thus this possibility requires further study.

Another possibility is that changes in intrathoracic pressure associated with snoring may ultimately lead to a reduction in baroreflex sensitivity222 as a consequence of the concomitant activation of the Bainbridge reflex.23 The Bainbridge reflex is elicited by activation of atrial stretch receptors and leads to tachycardia because of reductions in vagal activity and increases in sympathetic activity.24 This reflex could be strongly activated during snoring as a consequence of increased venous return to the heart, which might occur as consequence of the increased negative thoracic pressure25 that is known to accompany snoring.26 If this is the case, then the reduction in vagal motoneuron activity induced by the Bainbridge reflex may lead to a reduction in baroreflex gain. This postulation is supported by the findings of Barbieri and colleagues,27 who provided evidence in humans that the arterial baroreflex gain was reduced in response to volume loading. Moreover, they provided evidence that under this condition vagal activity is reduced due to the predominance of the Bainbridge reflex. Although increased activation of low-pressure receptors might have a role in the reduction of baroreflex gain in snoring individuals, this suggestion is speculative and requires experimental support.

We think that the increase in baroreflex sensitivity in the snorers was likely an acute effect induced by the application of nCPAP during trial 2 and was not a consequence of exposure to nCPAP during the adaptation period for the following reasons. First, adaptations in baroreflex sensitivity were not observed in either the control or snoring group during wakefulness after adaptation to nCPAP. Second, we previously have shown in nonapneic snorers that baroreflex sensitivity during nonsnoring episodes was greater compared to snoring for a given stage of sleep (ie, stage II sleep).22 The difference in baroreflex sensitivity between the nonsnoring and snoring periods in our previous study was similar to the difference in nocturnal baroreflex sensitivity that was measured before and after nCPAP in the present investigation.

Given our findings, it is possible that decreases in baroreflex sensitivity previously reported in NREM sleep for individuals experiencing obstructive sleep apnea2 might in some cases be an acute response to snoring or apnea rather than a chronic alteration in the response of this receptor. This suggestion is supported by the findings of Parati et al,16 which showed that baroreflex sensitivity in patients with obstructive sleep apnea was similar to that of control subjects during wakefulness but was reduced during sleep. Moreover, Bonsignore et al2 have shown that the increase in baroreflex sensitivity that occurred after treatment with nCPAP in subjects with obstructive sleep apnea was accompanied by decreases in the apnea/hypopnea index and in the severity of oxygen desaturation.2 Thus, findings to date do not definitively support the notion that baroreflex sensitivity is chronically reduced during sleep in individuals with obstructive sleep apnea. Nonetheless, independent of whether or not baroreflex sensitivity might be altered in the long term, short-term reductions might be significant inasmuch as they could lead to a decreased sensitivity to nocturnal BP surges that might ultimately result in an increased risk of experiencing a nocturnal cardiovascular event.


   Conclusion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
References
 
Our results have shown that baroreflex sensitivity is reduced during snoring in otherwise healthy humans, and that this reduction is reversed after the application of nCPAP. This reduction could ultimately lead to an increased risk of experiencing a nocturnal cardiovascular event in snorers. Nevertheless, whether the alterations that we observed in our relatively young, healthy, and predominantly male snoring population would benefit from long-term treatment with nCPAP or become more severe with age and/or the presence of other comorbid diseases requires further investigation.


   Acknowledgements
 
The American Heart Association supported this study. The continuous positive airway pressure machines used in this study were supplied by ResMed.


   Footnotes
 
Abbreviations: Bf = breathing frequency; DBP = diastolic BP; MAP = mean arterial pressure; nCPAP = nasal continuous positive airway pressure; NREM = non-rapid eye movement; REM = rapid eye movement; SBP = systolic BP; SWS = slow-wave sleep

Received for publication November 14, 2003. Accepted for publication April 19, 2004.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 

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Eur. Respir. J., January 1, 2006; 27(1): 128 - 135.
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Nonapneic and apneic snorers during sleep.
Bing Tang, et al.
Chest Online, 5 Apr 2006 [Full text]
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