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Sleep Apnea Syndrome and Diastolic Blood Pressure Elevation during Exercise

Sleep Apnea Syndrome and Diastolic Blood Pressure Elevation during Exercise IntroductionThe strong association between obstructive sleep apnea syndrome (OSAS) and hypertension has attracted considerable attention in recent years [1, 2]. Several studies assessing the role of OSAS as an independent risk factor for hypertension have produced conflicting results [3, 4]. In a large number of patients attending sleep clinics, Lavie et al. [5]examined the relation between blood pressure, severity of apnea, and various confounding factors and found that sleep apnea is an independent risk factor for hypertension. Another case-control study showed that the severity of OSAS is an independent factor correlated to diurnal hypertension [6].During an incremental exercise test, there is normally a gradual rise in systolic arterial blood pressure, while diastolic blood pressure (DBP) seldom exceeds 100 mm Hg. A hypertensive blood pressure response may be evident during exercise in subjects with a normal resting blood pressure and this has been proved to be a risk factor for new onset hypertension in subsequent years [7]. Although the sleep apnea syndrome is associated with hypertension, there are no references regarding the blood pressure response of normotensive OSAS patients during exercise. The aim of this study was to investigate the relationship between blood pressure response during exercise and the severity of sleep apnea syndrome in normotensive OSAS patients.Materials and MethodsSubjectsThe study group consisted of 17 male adult nonsmokers (median age 35 and range 22–45 years), who were referred to the sleep laboratory of the G. Papanikolaou Hospital with suspected sleep apnea, because the severity of their snoring was viewed by family members as either unusual or of new onset and because of daytime somnolence. They were nonrandomized and subsequently referred for diagnostic sleep recordings. All of them were nonsymptomatic as regards cardiovascular signs or symptoms during daytime – including arterial blood pressure. Also, all were diagnosed as having OSAS after having been evaluated in our sleep laboratory.The control group consisted of 10 normal nonsmokers who were from the same families, and who had no history of any medical condition that needed treatment. All of them were evaluated by the Epworth Sleepines Scale (ESS) test and completed a quality of life questionnaire; they were 6 brothers and 4 partners (median age 35 and range 28–54 years).The ethics committee of G. Papanikolaou Hospital approved the study and all subjects signed an informed consent form prior to participation.Study ProtocolAnthropometric Measurements. Anthropometric data included height, weight, body mass index (weight/height2), and age (table 1).Table 1Anthropometric characteristics and polysomnography data for OSAS patients and normal subjectsNocturnal Polysomnography. Nocturnal polysomnography was performed at the hospital. This included monitoring of both respiration, with inductanceplethysmography and oronasal temperature as substitute measurements of respiratory effort and flow, and oxygen saturation (Flaga HS Somnologica, Reykjavik, Iceland). From thesemeasurements we obtained the apnea-hypopnea index (AHI, total numberof apneic events plus hypopneic events divided by hours of sleep), and the lowest (LoO2) and mean (MnO2) nocturnal oxygen saturation; we also recordedthe percentage of time spent asleep with oxygen saturation below 90% (TST90%) (table 1). Apnea was defined as a cessation in airflow for at least10 s [8], and hypopnea as a >30% reduction of airflow or thoracoabdominal excursion accompanied by a 4% drop in oxyhemoglobin saturation [9, 10].Blood Pressure. Blood pressure measurements at rest were taken 4 times under standard conditions, with the patients standing, supine, and just before beginning the exercise test. Hypertension was defined as having a systolic blood pressure (SBP) >140 mm Hg or a DBP >90 mm Hg [6]. Hypertensive OSAS patients were excluded from our study.Cardiopulmonary Exercise Test (CPXT). All subjects were familiarized with a bicycle ergometer (Lode BV, Groningen, The Netherlands) 1 h before testing. Each subject underwent an incremental exercise test, with a step protocol of 10, 15 or 20 W/min, depending on the subject’s presumed level of physical activity. The heart rate was monitored on a 12-lead electrocardiogram and oxygen saturation was continuously recorded throughout the test. The oxygen consumption (VO2) and carbon dioxide production (VCO2) were analyzed breath by breath (CPX-D Medgraphics, St. Paul, Minn., USA). Blood pressure measurements were taken using a cuff manometer with a stethoscope on the brachial artery at the end of each minute throughout the exercise test by an experienced physician. The physician was blinded to patients or normal subjects. In order to normalize for VO2, we divided it by body weight (VO2/kg). CPXT parameters including VO2/kg, VCO2, minute ventilation (VE), heart rate per minute (HR), oxygen pulse (VO2/HR), SBP, and DBP were recorded at rest and at peak exercise. Additionally, VO2/kg, VCO2, VE, HR, and VO2/HR were recorded at a DBP of 100 mm Hg, and at a DBP of 110 mm Hg.The subjects exercised until exhaustion. Criteria to terminate the test were a SBP over 240 mm Hg or a DBP over 120 mm Hg, electrocardiographic signs of ischemia, chest pain, and disorientation during exercise. The predicted maximumventilation capacity was calculated using the equation(37.5 × FEV1) [11]. The predicted heart rate capacitywas calculated using the equation (210–0.65 × age) [12].ESS. Normal subjects and patients were asked about their likelihood of falling asleep in eight different situations based on the ESS questionnaire [13]. An ESS score of 12/24 or more was considered as abnormally sleepy [14].Quality of Life. All participants completed a quality of life questionnaire (Nottingham Health Profile Part 1, NHP 1). The NHP evaluates patients’ perception of their own health in terms of quality of life [15]. The NHP has been widely used, and a number of different national versions have been reproduced. The questions were translated into Greek and validated in Greece [16]. The NHP 1 measures the subjective health status by asking for responses (yes or no) to a test of 38 simple statements relating to six dimensions of social functioning: emotional reactions, energy, pain, physical mobility, sleep, and social isolation. All statements are related to limitations of activity or aspects of distress. The answers are weighted with specific values, which make a score from 0 to 100 for each dimension possible. A high score indicates a high degree of limitation. The scores are usually presented as a profile and they are not added to an overall score.Statistical AnalysisValues are expressed as mean ± standard deviation (SD), unless otherwise indicated. Comparison of the values for the two groups were made using the Student unpaired t test (SPPS 10.0 for Windows, 1999, Ill., USA). In order to determine any correlation between polysomnography and exercise measurements, the multivariate correlation significance (SPPS 10.0 for Windows, 1999, Ill., USA) was used. Differences between values with p ≤ 0.05 were characterized as statistically significant.ResultsDemographic data were similar for the two groups (table 1). ESS test values were statistically significantly higher in OSAS patients than normals (median value 18, range 14–20 and median value 8, range 5–11; p < 0.01, respectively) (table 1). All dimensions of quality of life, according to NHP 1, had a mean score of <50 for both groups and there were no statistically significant differences (table 2).Table 2Estimation of different dimensions of quality of life according to the NHP 1 questionnaire in OSAS patients and normal subjectsThere were no differences in both SBP and DBP at rest between OSAS patients and normal subjects (table 3). There were no significant differences in SBP between the two groups at all stages of exercise. At peak exercise, DBP in OSAS patients was significantly higher than in normal subjects (115.3 ± 9.2 vs. 101 ± 8.4 mm Hg, p = 0.04) (table 3).Table 3Exercise parameters measured and calculated at rest and at peak exercise for OSAS patients and normal subjectsAll OSAS patients reached a DBP of 100 mm Hg during exercise in comparison to 5 of the 10 normal subjects. OSAS patients reached a DBP of 100 mm Hg at the same VO2 as normal subjects (1,211.2 ± 371.7 vs. 1,536.6 ± 267.2 ml/min, respectively, p = 0.089) (table 4), but they had a significantly lower heart rate than normals (111.2 ± 13 vs. 118.6 ± 27.6, p = 0.009). A DBP of 110 mm Hg was reached by 14 of 17 OSAS patients during exercise in comparison to 3 of the normal subjects. OSAS patients reached a DBP of 110 mm Hg at lower VO2 compared to normal subjects (1,881.5 ± 703.4 vs.1,972.3 ± 108.6 ml/min, p = 0.045, respectively) (table 4).Table 4Exercise parameters measured and calculated when DBP reached values of 100 and 110 mm Hg during exercise in OSAS patients and normal subjectsPearson’s correlation analysis for OSAS patients showed the following: (1) There was no correlation between AHI, MnO2, LoO2, TST90% and DBP response during exercise. (2) There was no correlation between AHI and VO2/kg at peak exercise. (3) There was a statistically significant correlation between AHI and VE (r = –0.538, p = 0.026; fig. 1) and respiratory rate (RR) at peak exercise (r = –0.534, p = 0.027). (4) There was a statistically significant correlation between HR at peak exercise and LoO2 (r = –0.744, p = 0.001; fig. 2).Fig. 1Negative correlation between the AHI and the VE at peak exercise in OSAS patients.Fig. 2Negative correlation between LoO2 and the HR at peak exercise in OSAS patients.The dimension ‘sleep’ according to the NHP 1 was not significantly correlated at rest and at peak exercise with VO2, HR, SBP, and DBP.DiscussionThe main finding of our study was that normotensive OSAS patients develop DBP elevation at an earlier stage during exercise compared with normal subjects. This hypertensive response was not correlated with the severity of OSAS. Several factors are probably responsible for the hemodynamic changes seen with OSAS: hypoxemia associated with apnea, Muller maneuvers that occur repetitively, autonomic nervous system stimulation, continuous passage from awake to asleep to awake, and continuous resetting of the autonomic nervous system controls that occur during this sleep fragmentation [17].OSAS is characterized by obesity, nocturnal breathing abnormalities, arterial hypertension, and an increased number of cardiovascular events. Sympathetic activity is increased during nocturnal apneic episodes, which may mediate the cardiovascular complications of sleep apnea. Tonic activation of excitatory chemoreflex afferents may contribute to an increased efferent sympathetic activity to muscle circulation in patients with OSA [18].Obesity alone, in the absence of OSAS, is not accompanied by increased sympathetic activity to muscle blood vessels [19]. Recent studies found overweight subjects with OSAS and hypertension had abnormal autonomic nervous tests. This could be due to autonomic withdrawal [20]or supersaturation of the end-organ receptors by excessive and prolonged sympathetic stimulation [21, 22].Compared to closely matched control subjects, patients with OSAS have increased ambulatory DBP both during day and night and increased SBP at night [8]. The magnitude of these differences is sufficient to carry an increased risk of cardiovascular morbidity [23]. In our study, the OSAS patients had the same values of diastolic pressure at rest compared to the normal subjects, who were from the same families. A recent population study showed that sleep apnea contributed significantly to hypertension independently of all relevant confounding variables [7]. Sleep fragmentation was independently associated with significantly higher levels of awake SBP. This effect was not discernible in adults with an AHI >1 [24]. Each apneic event per hour of sleep added about 1% to the risk of having hypertension. Moreover, a dose-response association between sleep-disordered breathing at baseline and the presence of hypertension 4 years later was found to be an independent confounding factor [25]. In our group of OSAS patients, we found no statistically significant correlation between sleep parameters and blood pressure (systolic and diastolic) at rest.A study of OSAS patients during exercise showed an impairment of the glycolytic metabolism (maximum blood lactate concentration) and oxidative metabolism (lactate elimination), which was correlated with the severity of OSAS [26]. These patients had a higher DBP than normal at peak exercise, as was the case in our study. We found that there was no correlation between AHI (and all other polysomnography parameters) and DBP elevation. However, sleep disorders may affect the normal ventilation response in OSAS patients, due to metabolic impairment during exercise as in our study, where we found a high correlation between both VEmax and respiratory rate with AHI. However, the VO2/weight and VE at peak exercise, for the equal maximum work level, were the same between patients and normal subjects.Multivariate analysis of mortality data in patients with sleep apnea has recently shown that hypertension is an independent predictor of cardiopulmonary deaths in these patients [27]. These findings have clinical implications concerning early diagnosis and treatment of sleep apnea and the associated hypertension. In a study of normotensive men and women, an exaggerated DBP response to exercise was predictive of the risk of new-onset hypertension, which may reflect a preclinical stage of hypertension [28]. Our study group, consisting of OSAS patients with normal resting DBP, increasing only at exercise, seems to be at the same risk.A well-designed study [29]and a recent review article [30]showed that normotensive patients with OSAS have a selective impairment of the sympathetic response to baroreceptor deactivation but not to baroreceptor activation or to the cold pressor test. The impairment of baroreflex sympathetic modulation in patients with OSAS is not accompanied by any impairment of baroreflex control of HR. In agreement, in our study, OSAS patients showed a statistically significant increase in HR when DBP reached a value of 100 mm Hg compared with controls. HRmax was negatively correlated with LoO2. This finding indicates that the degree of hypoxemia during sleep affects the cardiac response during stress.Until recently, most patients were referred for diagnosis only when their symptoms were severe enough to affect their quality of life. Snorers, even with obvious daytime sleepiness, were reported to be passive in seeking medical help for their symptoms [31]. Our OSAS patients were slightly symptomatic during the daytime; they were referred to our laboratory mainly because the rhythm of their snores was viewed by family members as either unusual or of new onset. Indeed, the analysis of the NHP 1 questionnaire showed that the dimensions ‘emotional reactions’ and ‘energy’ had the higher – but normal – values, which can be explained by the fact that these fields are heavily affected by OSAS. However, the score of the dimensions ‘pain’, ‘physical mobility’, and ‘social isolation’ were not elevated above baseline. The same applies to the dimension ‘sleep’, which may be unexpected at first sight; however, OSAS patients only rarely complain of sleep impairment but rather of an impaired daytime performance [32].In conclusion, our results indicate that even in the absence of daytime symptoms, normotensive OSAS patients demonstrate an early elevation of DBP during exercise. This response did not correlate with the severity of OSAS in this group of normotensive patients. Our findings may have important clinical implications, since it has been shown that diastolic hypertension during exercise is a risk factor for developing hypertension in the future. Furthermore, DBP elevation could be a limiting factor of physical performance in this group of patients [19]. Larger scale studies, including patient follow-up, are needed to further define the importance of these findings as well as to determine the role of treatment, weight reduction and regular exercise in diminishing or even reversing the abnormal blood pressure response during physical stress along with its long-term consequences. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Respiration Karger

Sleep Apnea Syndrome and Diastolic Blood Pressure Elevation during Exercise

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Publisher
Karger
Copyright
© 2004 S. Karger AG, Basel
ISSN
0025-7931
eISSN
1423-0356
DOI
10.1159/000080635
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Abstract

IntroductionThe strong association between obstructive sleep apnea syndrome (OSAS) and hypertension has attracted considerable attention in recent years [1, 2]. Several studies assessing the role of OSAS as an independent risk factor for hypertension have produced conflicting results [3, 4]. In a large number of patients attending sleep clinics, Lavie et al. [5]examined the relation between blood pressure, severity of apnea, and various confounding factors and found that sleep apnea is an independent risk factor for hypertension. Another case-control study showed that the severity of OSAS is an independent factor correlated to diurnal hypertension [6].During an incremental exercise test, there is normally a gradual rise in systolic arterial blood pressure, while diastolic blood pressure (DBP) seldom exceeds 100 mm Hg. A hypertensive blood pressure response may be evident during exercise in subjects with a normal resting blood pressure and this has been proved to be a risk factor for new onset hypertension in subsequent years [7]. Although the sleep apnea syndrome is associated with hypertension, there are no references regarding the blood pressure response of normotensive OSAS patients during exercise. The aim of this study was to investigate the relationship between blood pressure response during exercise and the severity of sleep apnea syndrome in normotensive OSAS patients.Materials and MethodsSubjectsThe study group consisted of 17 male adult nonsmokers (median age 35 and range 22–45 years), who were referred to the sleep laboratory of the G. Papanikolaou Hospital with suspected sleep apnea, because the severity of their snoring was viewed by family members as either unusual or of new onset and because of daytime somnolence. They were nonrandomized and subsequently referred for diagnostic sleep recordings. All of them were nonsymptomatic as regards cardiovascular signs or symptoms during daytime – including arterial blood pressure. Also, all were diagnosed as having OSAS after having been evaluated in our sleep laboratory.The control group consisted of 10 normal nonsmokers who were from the same families, and who had no history of any medical condition that needed treatment. All of them were evaluated by the Epworth Sleepines Scale (ESS) test and completed a quality of life questionnaire; they were 6 brothers and 4 partners (median age 35 and range 28–54 years).The ethics committee of G. Papanikolaou Hospital approved the study and all subjects signed an informed consent form prior to participation.Study ProtocolAnthropometric Measurements. Anthropometric data included height, weight, body mass index (weight/height2), and age (table 1).Table 1Anthropometric characteristics and polysomnography data for OSAS patients and normal subjectsNocturnal Polysomnography. Nocturnal polysomnography was performed at the hospital. This included monitoring of both respiration, with inductanceplethysmography and oronasal temperature as substitute measurements of respiratory effort and flow, and oxygen saturation (Flaga HS Somnologica, Reykjavik, Iceland). From thesemeasurements we obtained the apnea-hypopnea index (AHI, total numberof apneic events plus hypopneic events divided by hours of sleep), and the lowest (LoO2) and mean (MnO2) nocturnal oxygen saturation; we also recordedthe percentage of time spent asleep with oxygen saturation below 90% (TST90%) (table 1). Apnea was defined as a cessation in airflow for at least10 s [8], and hypopnea as a >30% reduction of airflow or thoracoabdominal excursion accompanied by a 4% drop in oxyhemoglobin saturation [9, 10].Blood Pressure. Blood pressure measurements at rest were taken 4 times under standard conditions, with the patients standing, supine, and just before beginning the exercise test. Hypertension was defined as having a systolic blood pressure (SBP) >140 mm Hg or a DBP >90 mm Hg [6]. Hypertensive OSAS patients were excluded from our study.Cardiopulmonary Exercise Test (CPXT). All subjects were familiarized with a bicycle ergometer (Lode BV, Groningen, The Netherlands) 1 h before testing. Each subject underwent an incremental exercise test, with a step protocol of 10, 15 or 20 W/min, depending on the subject’s presumed level of physical activity. The heart rate was monitored on a 12-lead electrocardiogram and oxygen saturation was continuously recorded throughout the test. The oxygen consumption (VO2) and carbon dioxide production (VCO2) were analyzed breath by breath (CPX-D Medgraphics, St. Paul, Minn., USA). Blood pressure measurements were taken using a cuff manometer with a stethoscope on the brachial artery at the end of each minute throughout the exercise test by an experienced physician. The physician was blinded to patients or normal subjects. In order to normalize for VO2, we divided it by body weight (VO2/kg). CPXT parameters including VO2/kg, VCO2, minute ventilation (VE), heart rate per minute (HR), oxygen pulse (VO2/HR), SBP, and DBP were recorded at rest and at peak exercise. Additionally, VO2/kg, VCO2, VE, HR, and VO2/HR were recorded at a DBP of 100 mm Hg, and at a DBP of 110 mm Hg.The subjects exercised until exhaustion. Criteria to terminate the test were a SBP over 240 mm Hg or a DBP over 120 mm Hg, electrocardiographic signs of ischemia, chest pain, and disorientation during exercise. The predicted maximumventilation capacity was calculated using the equation(37.5 × FEV1) [11]. The predicted heart rate capacitywas calculated using the equation (210–0.65 × age) [12].ESS. Normal subjects and patients were asked about their likelihood of falling asleep in eight different situations based on the ESS questionnaire [13]. An ESS score of 12/24 or more was considered as abnormally sleepy [14].Quality of Life. All participants completed a quality of life questionnaire (Nottingham Health Profile Part 1, NHP 1). The NHP evaluates patients’ perception of their own health in terms of quality of life [15]. The NHP has been widely used, and a number of different national versions have been reproduced. The questions were translated into Greek and validated in Greece [16]. The NHP 1 measures the subjective health status by asking for responses (yes or no) to a test of 38 simple statements relating to six dimensions of social functioning: emotional reactions, energy, pain, physical mobility, sleep, and social isolation. All statements are related to limitations of activity or aspects of distress. The answers are weighted with specific values, which make a score from 0 to 100 for each dimension possible. A high score indicates a high degree of limitation. The scores are usually presented as a profile and they are not added to an overall score.Statistical AnalysisValues are expressed as mean ± standard deviation (SD), unless otherwise indicated. Comparison of the values for the two groups were made using the Student unpaired t test (SPPS 10.0 for Windows, 1999, Ill., USA). In order to determine any correlation between polysomnography and exercise measurements, the multivariate correlation significance (SPPS 10.0 for Windows, 1999, Ill., USA) was used. Differences between values with p ≤ 0.05 were characterized as statistically significant.ResultsDemographic data were similar for the two groups (table 1). ESS test values were statistically significantly higher in OSAS patients than normals (median value 18, range 14–20 and median value 8, range 5–11; p < 0.01, respectively) (table 1). All dimensions of quality of life, according to NHP 1, had a mean score of <50 for both groups and there were no statistically significant differences (table 2).Table 2Estimation of different dimensions of quality of life according to the NHP 1 questionnaire in OSAS patients and normal subjectsThere were no differences in both SBP and DBP at rest between OSAS patients and normal subjects (table 3). There were no significant differences in SBP between the two groups at all stages of exercise. At peak exercise, DBP in OSAS patients was significantly higher than in normal subjects (115.3 ± 9.2 vs. 101 ± 8.4 mm Hg, p = 0.04) (table 3).Table 3Exercise parameters measured and calculated at rest and at peak exercise for OSAS patients and normal subjectsAll OSAS patients reached a DBP of 100 mm Hg during exercise in comparison to 5 of the 10 normal subjects. OSAS patients reached a DBP of 100 mm Hg at the same VO2 as normal subjects (1,211.2 ± 371.7 vs. 1,536.6 ± 267.2 ml/min, respectively, p = 0.089) (table 4), but they had a significantly lower heart rate than normals (111.2 ± 13 vs. 118.6 ± 27.6, p = 0.009). A DBP of 110 mm Hg was reached by 14 of 17 OSAS patients during exercise in comparison to 3 of the normal subjects. OSAS patients reached a DBP of 110 mm Hg at lower VO2 compared to normal subjects (1,881.5 ± 703.4 vs.1,972.3 ± 108.6 ml/min, p = 0.045, respectively) (table 4).Table 4Exercise parameters measured and calculated when DBP reached values of 100 and 110 mm Hg during exercise in OSAS patients and normal subjectsPearson’s correlation analysis for OSAS patients showed the following: (1) There was no correlation between AHI, MnO2, LoO2, TST90% and DBP response during exercise. (2) There was no correlation between AHI and VO2/kg at peak exercise. (3) There was a statistically significant correlation between AHI and VE (r = –0.538, p = 0.026; fig. 1) and respiratory rate (RR) at peak exercise (r = –0.534, p = 0.027). (4) There was a statistically significant correlation between HR at peak exercise and LoO2 (r = –0.744, p = 0.001; fig. 2).Fig. 1Negative correlation between the AHI and the VE at peak exercise in OSAS patients.Fig. 2Negative correlation between LoO2 and the HR at peak exercise in OSAS patients.The dimension ‘sleep’ according to the NHP 1 was not significantly correlated at rest and at peak exercise with VO2, HR, SBP, and DBP.DiscussionThe main finding of our study was that normotensive OSAS patients develop DBP elevation at an earlier stage during exercise compared with normal subjects. This hypertensive response was not correlated with the severity of OSAS. Several factors are probably responsible for the hemodynamic changes seen with OSAS: hypoxemia associated with apnea, Muller maneuvers that occur repetitively, autonomic nervous system stimulation, continuous passage from awake to asleep to awake, and continuous resetting of the autonomic nervous system controls that occur during this sleep fragmentation [17].OSAS is characterized by obesity, nocturnal breathing abnormalities, arterial hypertension, and an increased number of cardiovascular events. Sympathetic activity is increased during nocturnal apneic episodes, which may mediate the cardiovascular complications of sleep apnea. Tonic activation of excitatory chemoreflex afferents may contribute to an increased efferent sympathetic activity to muscle circulation in patients with OSA [18].Obesity alone, in the absence of OSAS, is not accompanied by increased sympathetic activity to muscle blood vessels [19]. Recent studies found overweight subjects with OSAS and hypertension had abnormal autonomic nervous tests. This could be due to autonomic withdrawal [20]or supersaturation of the end-organ receptors by excessive and prolonged sympathetic stimulation [21, 22].Compared to closely matched control subjects, patients with OSAS have increased ambulatory DBP both during day and night and increased SBP at night [8]. The magnitude of these differences is sufficient to carry an increased risk of cardiovascular morbidity [23]. In our study, the OSAS patients had the same values of diastolic pressure at rest compared to the normal subjects, who were from the same families. A recent population study showed that sleep apnea contributed significantly to hypertension independently of all relevant confounding variables [7]. Sleep fragmentation was independently associated with significantly higher levels of awake SBP. This effect was not discernible in adults with an AHI >1 [24]. Each apneic event per hour of sleep added about 1% to the risk of having hypertension. Moreover, a dose-response association between sleep-disordered breathing at baseline and the presence of hypertension 4 years later was found to be an independent confounding factor [25]. In our group of OSAS patients, we found no statistically significant correlation between sleep parameters and blood pressure (systolic and diastolic) at rest.A study of OSAS patients during exercise showed an impairment of the glycolytic metabolism (maximum blood lactate concentration) and oxidative metabolism (lactate elimination), which was correlated with the severity of OSAS [26]. These patients had a higher DBP than normal at peak exercise, as was the case in our study. We found that there was no correlation between AHI (and all other polysomnography parameters) and DBP elevation. However, sleep disorders may affect the normal ventilation response in OSAS patients, due to metabolic impairment during exercise as in our study, where we found a high correlation between both VEmax and respiratory rate with AHI. However, the VO2/weight and VE at peak exercise, for the equal maximum work level, were the same between patients and normal subjects.Multivariate analysis of mortality data in patients with sleep apnea has recently shown that hypertension is an independent predictor of cardiopulmonary deaths in these patients [27]. These findings have clinical implications concerning early diagnosis and treatment of sleep apnea and the associated hypertension. In a study of normotensive men and women, an exaggerated DBP response to exercise was predictive of the risk of new-onset hypertension, which may reflect a preclinical stage of hypertension [28]. Our study group, consisting of OSAS patients with normal resting DBP, increasing only at exercise, seems to be at the same risk.A well-designed study [29]and a recent review article [30]showed that normotensive patients with OSAS have a selective impairment of the sympathetic response to baroreceptor deactivation but not to baroreceptor activation or to the cold pressor test. The impairment of baroreflex sympathetic modulation in patients with OSAS is not accompanied by any impairment of baroreflex control of HR. In agreement, in our study, OSAS patients showed a statistically significant increase in HR when DBP reached a value of 100 mm Hg compared with controls. HRmax was negatively correlated with LoO2. This finding indicates that the degree of hypoxemia during sleep affects the cardiac response during stress.Until recently, most patients were referred for diagnosis only when their symptoms were severe enough to affect their quality of life. Snorers, even with obvious daytime sleepiness, were reported to be passive in seeking medical help for their symptoms [31]. Our OSAS patients were slightly symptomatic during the daytime; they were referred to our laboratory mainly because the rhythm of their snores was viewed by family members as either unusual or of new onset. Indeed, the analysis of the NHP 1 questionnaire showed that the dimensions ‘emotional reactions’ and ‘energy’ had the higher – but normal – values, which can be explained by the fact that these fields are heavily affected by OSAS. However, the score of the dimensions ‘pain’, ‘physical mobility’, and ‘social isolation’ were not elevated above baseline. The same applies to the dimension ‘sleep’, which may be unexpected at first sight; however, OSAS patients only rarely complain of sleep impairment but rather of an impaired daytime performance [32].In conclusion, our results indicate that even in the absence of daytime symptoms, normotensive OSAS patients demonstrate an early elevation of DBP during exercise. This response did not correlate with the severity of OSAS in this group of normotensive patients. Our findings may have important clinical implications, since it has been shown that diastolic hypertension during exercise is a risk factor for developing hypertension in the future. Furthermore, DBP elevation could be a limiting factor of physical performance in this group of patients [19]. Larger scale studies, including patient follow-up, are needed to further define the importance of these findings as well as to determine the role of treatment, weight reduction and regular exercise in diminishing or even reversing the abnormal blood pressure response during physical stress along with its long-term consequences.

Journal

Respiration – Karger

Published: Oct 1, 2004

Keywords: Bicycle ergometry; Cardiopulmonary exercisetest; Diastolic blood pressure; Diastolic hypertension; Sleep apnea syndrome

There are no references for this article.