Sleep Breath DOI 10.1007/s11325-014-1066-x
ORIGINAL ARTICLE
Effect of acute sleep deprivation on heart rate recovery in healthy young adults Altug Cincin & Ibrahim Sari & Mustafa Oğuz & Sena Sert & Mehmet Bozbay & Halil Ataş & Beste Ozben & Kursat Tigen & Yelda Basaran
Received: 29 May 2014 / Revised: 28 September 2014 / Accepted: 2 October 2014 # Springer-Verlag Berlin Heidelberg 2014
Abstract Background Sleep deprivation (SD) is known to be associated with increased incidence of adverse cardiovascular events, but underlying pathophysiological mechanism has not been clearly demonstrated. Autonomic nervous system plays an important role in the regulation of cardiovascular function, and impairment in this system is associated with increased cardiovascular mortality. The aim of the current study was to investigate the effect of acute SD on autonomic regulation of cardiac function by determining heart rate recovery (HRR). Methods Twenty-one healthy security officers and nine nurses (mean age 33.25±8.18) were evaluated. Treadmill exercise test was applied once after a night with regular sleep and once after a night shift in hospital. The HRR was calculated as the reduction in heart rate from peak exercise to the 30th second (HRR 30), 1st minute (HRR1), 2nd minute (HRR2), 3rd minute (HRR3), and 5th minute (HRR5). The change in blood pressure (BP) measurements was also determined. Results Exercise capacity of individuals with SD was significantly lower (10.96±1.01 vs. 11.71±1.30 metabolic equivalent task (MET)s; p=0.002), and peak systolic BP was significantly higher (173.8±16.3 vs. 166.2±9.9; p=0.019). There was a signicant difference in HRR30 (12.74±6.19 vs. 17.66± 5.46; p=0.003) and HRR1 (31±6.49 vs. 36.10±7.78; p= 0.004). The ratio of these indices to peak HR was also significantly lower with SD (HRR%30 8.04±4.26 vs. 10.19±3.21; p =0.025 and HRR%1: 18.66 ± 4.43 vs. 20.98± 4.72; p = 0.013). The difference in other indices of HRR was not significant. A. Cincin (*) : I. Sari : M. Oğuz : S. Sert : M. Bozbay : H. Ataş : B. Ozben : K. Tigen : Y. Basaran Department of Cardiology, Marmara University Faculty of Medicine, Pendik, Istanbul, Turkey e-mail: [email protected]
Conclusion Our findings suggest that SD blunts cardiovascular autonomic response, and consequences of this relation might be more pronounced in subjects who are exposed to sleeplessness regularly or in subjects with baseline cardiovascular disease. Keywords Heart rate recovery . Exercise test . Autonomic dysfunction . Sleep deprivation . Blood pressure
Introduction Sleep deficiency is associated with increased morbidity and mortality [1, 2]. Although cardiovascular effects of sleep deprivation (SD) have been demonstrated in several studies, underlying pathophysiological mechanism has not been clearly demonstrated [3–7]. Autonomic nervous system plays a major role in the regulation of cardiovascular function, and the effect of sleep deprivation on cardiovascular autonomic response is not clear [8, 9]. Heart rate recovery (HRR) is the reduction in heart rate after peak exercise during a fixed cool-down period. In addition to conventional parameters of exercise testing, HRR is known to provide a prognostic information [10]. The fall in heart rate after exercise is considered to be regulated by autonomic regulation. Heart rate recovery which is one of the index methods for demonstrating autonomic function is known to be strictly associated with parasympathetic activity [11]. Impaired HRR in early phases of recovery has been shown to be an independent predictor of increased cardiovascular mortality [12]. Theoretically, one can expect that damage of a harmful event is supposed to be greater if exposed frequently or regularly. Therefore, the effect of sleep debt in people who frequently expose it as an occupational obligation is much more important than those who expose it occasionally. Up
Sleep Breath
until now, only a limited number of studies have real-life models of cohorts who are exposed to sleeplessness [13, 14]. Several studies investigating the effect of acute and chronic SD on health workers reported augmented sympathetic tonus, parasympathetic withdrawal, and increased blood pressure (BP) measurements [8, 15]. In our current study, we hypothesized that HRR would decrease with acute SD, which indicates impaired cardiac autonomic regulation. To test this hypothesis, we evaluated HRR indices after a treadmill exercise test in healthy adults both after a night of regular sleep and sleeplessness.
Methodology Twenty-one (three females) healthy security officers and nine (eight females) nurses were evaluated. Subjects selected within the staff of Marmara University Medical Faculty Hospital in the principle of voluntariness. Exclusion criteria were pregnancy, usage of any drug affecting heart rate or autonomic nervous system, presence of chronic renal insufficiency, anemia, diabetes mellitus, or any known cardiovascular disease including hypertension. Subjects with a history of seizure disorder, with acute or chronic sleep disorders including long and short sleepers and obstructive sleep apnea (OSA), and daily ethanol users were also not included in the study. Age, gender, body mass index, smoking status, and medical history of the participants were recorded. All volunteers were evaluated with physical examination, ECG, and echocardiography before the study to be accepted as a healthy subject. Echocardiographic examinations were performed by using a commercially available ultrasound machine and fully sampled matrix array transducer (iE33 and X5-1 transducer, Philips Medical Systems, Andover, MA, USA). Participants’ medical records including basic laboratory measurements were checked for any unsuitability. Regular sleep durations of the subjects were asked and recorded. Volunteers scheduled for night shifts were postponed within minimum 15 days prior to study date. This study complied with the Declaration of Helsinki and was approved by the local ethic committee of Marmara University. Subjects underwent standard treadmill exercise test according to Bruce protocol once after a night with regular sleep and once after a night-shift in hospital. Subjects were instructed to follow a standard diet, and they were asked to sleep regularly before the test night. The sleep durations of volunteers which cover the last 24 h were questioned and recorded. If sleep duration of a volunteer after a night shift had exceeded the half of his or her regular sleep time, the test was postponed. All tests were performed in the morning hours (8:30–10:00 a.m.). The 12 lead ECG was continuously monitored during the test. Blood pressure was recorded basally, once in each stage and at peak exercise.
The predicted peak HR was calculated as (220-age) beats per minute, and the aim of the exercise was to reach at least 85 % of the age-predicted heart rate. Interruption criteria were angina, ST segment change over 2 mm, clinically significant arrhythmia, hypotension (systolic BP decreased over 20 mmHg compared with the previous measurement), hypertension (systolic BP over 240 mmHg or diastolic BP over 140 mmHg), and other potentially dangerous clinical conditions. The decision of ending the exercise was made by a physician according to related guidelines or subject’s request [16]. The recovery phase of exercise always lasted 5 min, but it was prolonged if clinically indicated. ECG recordings were printed at baseline; at the end of each stage; at peak exercise (pre-recovery); and 30th second (s), 1st, 2nd, 3rd, and 5th minute of recovery. The HRR index was calculated as the reduction in HR from peak exercise to the 30th s (HRR30), 1st minute (HRR1), 2nd minute (HRR 2 ), 3rd minute (HRR 3 ), and 5th minute (HRR5). The “HRR%” was calculated as the percentage of HRR to peak HR for each time interval. Maximal exercise capacity of the subjects was determined with exercise duration and oxygen consumption which was defined as metabolic equivalent task ((MET); 1 MET= 3.5 ml/kg per min of oxygen consumption). Any symptoms of the indivuduals were recorded during exercise. Attending physician and nurse were blinded to the study plan of the subject, either he or she is sleepless or not.
Statistical analysis Continuous variables were expressed as mean ± standard deviation, and categorical data were expressed as percentages. Statistical comparisons of quantitative data were performed by paired sample t test. Comparative analysis of the data according to gender was performed by Student’s t test. A p level of
ORIGINAL ARTICLE
Effect of acute sleep deprivation on heart rate recovery in healthy young adults Altug Cincin & Ibrahim Sari & Mustafa Oğuz & Sena Sert & Mehmet Bozbay & Halil Ataş & Beste Ozben & Kursat Tigen & Yelda Basaran
Received: 29 May 2014 / Revised: 28 September 2014 / Accepted: 2 October 2014 # Springer-Verlag Berlin Heidelberg 2014
Abstract Background Sleep deprivation (SD) is known to be associated with increased incidence of adverse cardiovascular events, but underlying pathophysiological mechanism has not been clearly demonstrated. Autonomic nervous system plays an important role in the regulation of cardiovascular function, and impairment in this system is associated with increased cardiovascular mortality. The aim of the current study was to investigate the effect of acute SD on autonomic regulation of cardiac function by determining heart rate recovery (HRR). Methods Twenty-one healthy security officers and nine nurses (mean age 33.25±8.18) were evaluated. Treadmill exercise test was applied once after a night with regular sleep and once after a night shift in hospital. The HRR was calculated as the reduction in heart rate from peak exercise to the 30th second (HRR 30), 1st minute (HRR1), 2nd minute (HRR2), 3rd minute (HRR3), and 5th minute (HRR5). The change in blood pressure (BP) measurements was also determined. Results Exercise capacity of individuals with SD was significantly lower (10.96±1.01 vs. 11.71±1.30 metabolic equivalent task (MET)s; p=0.002), and peak systolic BP was significantly higher (173.8±16.3 vs. 166.2±9.9; p=0.019). There was a signicant difference in HRR30 (12.74±6.19 vs. 17.66± 5.46; p=0.003) and HRR1 (31±6.49 vs. 36.10±7.78; p= 0.004). The ratio of these indices to peak HR was also significantly lower with SD (HRR%30 8.04±4.26 vs. 10.19±3.21; p =0.025 and HRR%1: 18.66 ± 4.43 vs. 20.98± 4.72; p = 0.013). The difference in other indices of HRR was not significant. A. Cincin (*) : I. Sari : M. Oğuz : S. Sert : M. Bozbay : H. Ataş : B. Ozben : K. Tigen : Y. Basaran Department of Cardiology, Marmara University Faculty of Medicine, Pendik, Istanbul, Turkey e-mail: [email protected]
Conclusion Our findings suggest that SD blunts cardiovascular autonomic response, and consequences of this relation might be more pronounced in subjects who are exposed to sleeplessness regularly or in subjects with baseline cardiovascular disease. Keywords Heart rate recovery . Exercise test . Autonomic dysfunction . Sleep deprivation . Blood pressure
Introduction Sleep deficiency is associated with increased morbidity and mortality [1, 2]. Although cardiovascular effects of sleep deprivation (SD) have been demonstrated in several studies, underlying pathophysiological mechanism has not been clearly demonstrated [3–7]. Autonomic nervous system plays a major role in the regulation of cardiovascular function, and the effect of sleep deprivation on cardiovascular autonomic response is not clear [8, 9]. Heart rate recovery (HRR) is the reduction in heart rate after peak exercise during a fixed cool-down period. In addition to conventional parameters of exercise testing, HRR is known to provide a prognostic information [10]. The fall in heart rate after exercise is considered to be regulated by autonomic regulation. Heart rate recovery which is one of the index methods for demonstrating autonomic function is known to be strictly associated with parasympathetic activity [11]. Impaired HRR in early phases of recovery has been shown to be an independent predictor of increased cardiovascular mortality [12]. Theoretically, one can expect that damage of a harmful event is supposed to be greater if exposed frequently or regularly. Therefore, the effect of sleep debt in people who frequently expose it as an occupational obligation is much more important than those who expose it occasionally. Up
Sleep Breath
until now, only a limited number of studies have real-life models of cohorts who are exposed to sleeplessness [13, 14]. Several studies investigating the effect of acute and chronic SD on health workers reported augmented sympathetic tonus, parasympathetic withdrawal, and increased blood pressure (BP) measurements [8, 15]. In our current study, we hypothesized that HRR would decrease with acute SD, which indicates impaired cardiac autonomic regulation. To test this hypothesis, we evaluated HRR indices after a treadmill exercise test in healthy adults both after a night of regular sleep and sleeplessness.
Methodology Twenty-one (three females) healthy security officers and nine (eight females) nurses were evaluated. Subjects selected within the staff of Marmara University Medical Faculty Hospital in the principle of voluntariness. Exclusion criteria were pregnancy, usage of any drug affecting heart rate or autonomic nervous system, presence of chronic renal insufficiency, anemia, diabetes mellitus, or any known cardiovascular disease including hypertension. Subjects with a history of seizure disorder, with acute or chronic sleep disorders including long and short sleepers and obstructive sleep apnea (OSA), and daily ethanol users were also not included in the study. Age, gender, body mass index, smoking status, and medical history of the participants were recorded. All volunteers were evaluated with physical examination, ECG, and echocardiography before the study to be accepted as a healthy subject. Echocardiographic examinations were performed by using a commercially available ultrasound machine and fully sampled matrix array transducer (iE33 and X5-1 transducer, Philips Medical Systems, Andover, MA, USA). Participants’ medical records including basic laboratory measurements were checked for any unsuitability. Regular sleep durations of the subjects were asked and recorded. Volunteers scheduled for night shifts were postponed within minimum 15 days prior to study date. This study complied with the Declaration of Helsinki and was approved by the local ethic committee of Marmara University. Subjects underwent standard treadmill exercise test according to Bruce protocol once after a night with regular sleep and once after a night-shift in hospital. Subjects were instructed to follow a standard diet, and they were asked to sleep regularly before the test night. The sleep durations of volunteers which cover the last 24 h were questioned and recorded. If sleep duration of a volunteer after a night shift had exceeded the half of his or her regular sleep time, the test was postponed. All tests were performed in the morning hours (8:30–10:00 a.m.). The 12 lead ECG was continuously monitored during the test. Blood pressure was recorded basally, once in each stage and at peak exercise.
The predicted peak HR was calculated as (220-age) beats per minute, and the aim of the exercise was to reach at least 85 % of the age-predicted heart rate. Interruption criteria were angina, ST segment change over 2 mm, clinically significant arrhythmia, hypotension (systolic BP decreased over 20 mmHg compared with the previous measurement), hypertension (systolic BP over 240 mmHg or diastolic BP over 140 mmHg), and other potentially dangerous clinical conditions. The decision of ending the exercise was made by a physician according to related guidelines or subject’s request [16]. The recovery phase of exercise always lasted 5 min, but it was prolonged if clinically indicated. ECG recordings were printed at baseline; at the end of each stage; at peak exercise (pre-recovery); and 30th second (s), 1st, 2nd, 3rd, and 5th minute of recovery. The HRR index was calculated as the reduction in HR from peak exercise to the 30th s (HRR30), 1st minute (HRR1), 2nd minute (HRR 2 ), 3rd minute (HRR 3 ), and 5th minute (HRR5). The “HRR%” was calculated as the percentage of HRR to peak HR for each time interval. Maximal exercise capacity of the subjects was determined with exercise duration and oxygen consumption which was defined as metabolic equivalent task ((MET); 1 MET= 3.5 ml/kg per min of oxygen consumption). Any symptoms of the indivuduals were recorded during exercise. Attending physician and nurse were blinded to the study plan of the subject, either he or she is sleepless or not.
Statistical analysis Continuous variables were expressed as mean ± standard deviation, and categorical data were expressed as percentages. Statistical comparisons of quantitative data were performed by paired sample t test. Comparative analysis of the data according to gender was performed by Student’s t test. A p level of
