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The present study was designed to examine the effect of voluntarily slowed respiration on the cardiac parasympathetic response to a threat: the anticipation of an electric shock. Thirty healthy college students were randomly assigned to the slow, fast, and nonpaced breathing groups (10 subjects each). Subjects in the slow and fast paced breathing groups regulated their breathing rate to 8 and 30 cpm, respectively, and those in the nonpaced breathing group breathed spontaneously. Immediately after the period of paced or nonpaced breathing for 5 minutes, the subjects were exposed for 2 minutes to the anticipation of an electric shock during breathing paced at 15 cpm. The amplitude of the high frequency (HF) component of the heart rate variability, an index of cardiac parasympathetic tone, significantly decreased during the threat in the fast and nonpaced breathing groups, whereas it was unchanged in the slow paced breathing group. No significant difference was observed among the three groups in the amplitude of respiration during the threat. Results suggest that a slowed respiration decreases the cardiac parasympathetic withdrawal response to the threat. This study provides a rationale for the therapeutic uses of the slowed respiration maneuver in attenuating the cardiac autonomic responses in patients with anxiety disorder.

We analyzed by means of autoregressive spectral analysis the spontaneous beat-to-beat heart-rate variability (HRV) of 10 myotonic dystrophy (MD) patients (4 men and 6 women, aged 37-53 years) and 10 age- and sex-matched healthy, sedentary humans (control) at rest in the supine position. All MD patients had no cardiac conduction disturbances (i.e., atrioventricular or intraventricular conduction defects) on 12-lead electrocardiogram and were able to walk and perform daily activities. In the MD group, the total power, the power of the low-frequency component (a marker of sympathetic and vagal modulation of heart rate) and that of the high-frequency component (a marker of vagal modulation of heart rate) were smaller than those in the control group (P < 0.01, P < 0.05 and P < 0.05, respectively). The results of this study suggest that the cardiovascular autonomic nervous system contributing to the HRV may be disturbed even in the MD patients who can walk and perform daily activities. Therefore, one must give careful consideration to the cardiovascular autonomic dysfunction, as well as the cardiac conduction disturbance in the MD patients.

We analyzed by means of autoregressive spectral analysis the spontaneous beat-to-beat heart rate variability (HRV) of quadriplegic and paraplegic male subjects at rest in the supine position. In agreement with our previous study, in nine of 15 quadriplegic patients only the high-frequency (HF: center frequency = respiratory frequency) component (a marker of vagal modulation of heart rate) was observed. In contrast, in six of the quadriplegic patients both the HF component and the low-frequency (LF: center frequency at approx. 0.1 Hz, 0.03-0.15 Hz in this study) component (a marker of sympathetic and vagal modulation of heart rate) were observed. However, in six quadriplegic patients who presented the LF component, (i) the center frequency of the LF component was lower than that in 10 healthy, sedentary, age-matched males (control I) (P < 0.01), (ii) the power of the HF component was smaller than that in the control-I group (P < 0.01) and (iii) the LF/HF power ratio (an index of sympathovagal balance) was larger than that in the control-I group (P < 0.05). On the other hand, in nine paraplegic patients with an intact 1st-4th thoracic spinal cord, from which the cardiac sympathetic nerves originate, the total power, the power of the LF component and that of the HF component were smaller than those in nine healthy, sedentary, age-matched males (control II) (P < 0.05, P < 0.01 and P < 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

The tachycardia that accompanies isometric exercise decreases with age in humans; however, the mechanism of this decline is unknown. To determine whether less cardiac vagal withdrawal is associated with the age-related decrease in this response, we assessed high-frequency R-R interval variability (0.15-0.40 Hz), an index of cardiac vagal tone, before (control) and during isometric exercise to exhaustion in healthy young (21-29 yr; n = 12) and older (61-72 yr; n = 11) men. During control, the two groups did not differ in respiratory rate, mean arterial pressure, or heart rate, although the older subjects had a lower high-frequency amplitude (12.2 +/- 1.1 vs. 29.4 +/- 4.6 ms/Hz; P < 0.05). During isometric exercise, the respiratory rate and arterial pressure responses did not differ; however, the older men had a lower absolute heart rate and a smaller increase in heart rate, and only the young men demonstrated a significant decline in high-frequency amplitude. The heart rate responses to exercise were correlated with the declines in high-frequency amplitude (initial, r = -0.808; midpoint, r = -0.714; peak, r = -0.632; all P < 0.005), which were, in turn, correlated with the control high-frequency amplitude (initial, r = -0.727; midpoint, r = -0.643; peak, r = -0.610; all P < 0.01). Thus smaller declines in high-frequency amplitude, related to lower baseline amplitude, corresponded to smaller increases in heart rate throughout isometric exercise. Therefore, we conclude that the smaller tachycardiac response to isometric exercise in older humans is associated with an inability to decrease cardiac vagal tone below an already reduced baseline level.

1. The notion that small, 'non-hypotensive' reductions of effective blood volume alter neither arterial pressure nor arterial baroreceptor activity is pervasive in the experimental literature. We tested two hypotheses: (a) that minute arterial pressure and cardiac autonomic outflow changes during hypovolaemia induced by lower body suction in humans are masked by alterations in breathing, and (b) that evidence for arterial baroreflex engagement might be obtained from measurements of thoracic aorta dimensions. 2. In two studies, responses to graded lower body suction at 0 (control), 5, 10, 15, 20 and 40 mmHg were examined in twelve and ten healthy young men, respectively. In the first, arterial pressure (photoplethysmograph), R-R interval, and respiratory sinus arrhythmia amplitude (complex demodulation) were measured during uncontrolled and controlled breathing (constant breathing frequency and tidal volume). In the second, cross-sectional areas of the ascending thoracic aorta were calculated from nuclear magnetic resonance images. 3. Lower body suction with controlled breathing resulted in an increased arterial pulse pressure at mild levels (5-20 mmHg; ANOVA, P < 0.05) and a decreased arterial pulse pressure at moderate levels (40 mmHg; ANOVA, P < 0.05). Both R-R intervals and respiratory sinus arrhythmia were negatively related to lower body suction level, whether group averages (general linear regression, r > 0.92) or individual subjects (orthogonal polynomials, 12 of 12 subjects) were assessed. 4. Aortic pulse area decreased progressively and significantly during mild lower body suction, with 47% of the total decline occurring by 5 mmHg. 5. These results suggest that small reductions of effective blood volume reduce aortic baroreceptive areas and trigger haemodynamic adjustments which are so efficient that alterations in arterial pressure escape detection by conventional means.

We investigated the responses of the frequency components of heart rate (HR) and blood pressure (BP) variabilities to progressive changes in autonomic activity induced by the graded head-up tilt technique in 12 normal subjects (age 19-27 yr) under the condition of frequency-controlled respiration (0.25 Hz). During low-level tilt (0-30 degrees), the R-R interval was unchanged and the amplitude of the high-frequency (HF; 0.25 Hz) component of HR variability showed only a slight insignificant decrease. The amplitude of the low-frequency (LF; 0.04-0.15 Hz) component of HR variability increased progressively as the angle increased (P < 0.05). During high-level tilt (30-90 degrees), the R-R interval and the HF amplitude of HR variability decreased progressively with tilt angle (P < 0.001 for both). The LF amplitude of HR variability peaked at a tilt angle of 30 degrees. The LF-to-HF ratio of HR variability and the LF amplitude of systolic and diastolic BP variabilities increased progressively as the tilt angle increased from 0 to 60 degrees (P < 0.001), although systolic and diastolic BPs were unchanged. These results suggest that mixed autonomic responses to orthostatic stress, which are thought to be mediated by both cardiopulmonary and arterial baroreflex mechanisms, can be distinguished by changes in the frequency components of HR and BP variabilities.

A complex demodulation (CDM) method for continuous assessment of frequency shifts and time-dependent changes in amplitude in the rhythmic components existing in predefined frequency bands was proposed and applied to the analysis of high-frequency (HF) and low-frequency (LF) components of the R-R interval and to the analysis of respiration via impedance spirogram. Simulation studies revealed that this CDM technique furnishes mathematical features well suited to the investigation of non-stationary R-R interval signals and can delineate time-dependent fluctuations in both amplitude and frequency, accurately differentiating between HF and LF components. Analysis of data during paced breathing at different respiratory frequencies revealed that the estimated frequency of the HF component and respiration faithfully reflected the frequency of paced breathing. Analysis of data during dynamic exercise with increasing workload (20 W/min) showed that the frequency of the HF component was elevated with exercise and that both HF and LF amplitudes were reduced progressively with advancing load. CDM-derived frequency and amplitude of respiration were highly correlated to direct breath-by-breath respiratory frequency and tidal volume measurements. We conclude that this method could provide a powerful means for continuously assessing time-dependent changes in both cardiovascular and respiratory variations.

We studied the effects of cervicothoracic epidural anesthesia or intravenous phentolamine on periodical blood pressure variation during cardiopulmonary bypass in 12 adult patients undergoing open heart surgery under fentanyl anesthesia. Spontaneous periodical fluctuation of the blood pressure was analyzed by means of autoregressive power spectrum method. Amplitudes of the low frequency (0.02-0.15 Hz) component of the blood pressure variation amplitudes were calculated. The amplitudes decreased significantly 10 minutes after cervicothoracic epidural block with 15 ml of 2% lidocaine solution (P < 0.05), and after infusion of 0.4 mg.kg-1 of phentolamine (P < 0.05). Since amplitudes of the blood pressure variation were reduced by adequate epidural block or phentolamine, they are likely to reflect sympathetic vasomotor activity.

To determine whether paced breathing (PB) and respiratory interval of PB modify the relationship between spectral components of heart rate variability (HRV) and cardiac vagal tone, we studied seven healthy young males under the condition of beta-adrenergic blockade by intravenous propranolol (0.2 mg/kg). Compared with spontaneous breathing, PB at the same respiratory interval as that of individual spontaneous breathing showed no significant effect on the amplitude of the high-frequency (HF) component or the mean R-R interval in either the supine or tilt position, whereas the PB decreased the amplitude of the low-frequency (LF; 0.04-0.15 Hz) component in both positions (P = 0.004 and 0.042, respectively). When the respiratory interval was increased from 3 to 6 s, the HF amplitude showed a progressive increase in both positions (P = 0.001 and 0.035, respectively), while the LF amplitude and mean R-R interval remained unchanged. These results indicate that the effects of PB and respiratory interval on the spectral components of HRV are not mediated by the changes in mean cardiac vagal tone and support the hypothesis that increased respiratory interval amplifies the respiratory-related vagal modulation of heart rate.

To examine the hypothesis that the relaxation response is associated with an increase in cardiac parasympathetic tone, the frequency components of heart rate variability during relaxation training were investigated in 16 college students. Electrocardiograms and pneumograms were recorded during a 5-min baseline period followed by three successive 5-min sessions of the autogenic training (relaxation) or by the same periods of quiet rest (control), while subjects breathed synchronously with a visual pacemaker (0.25 Hz). Although neither the magnitude nor the frequency of respiration showed a significant difference between relaxation and control, the amplitude of the high-frequency component of heart rate variability increased only during relaxation (p = .008). There was no significant difference in the ratio of the low-frequency (0.04-0.15 Hz) to the high-frequency amplitudes. The increased high-frequency amplitude without changes in the respiratory parameters indicates enhanced cardiac parasympathetic tone. Thus, our results support the initial hypothesis of this study. Enhanced cardiac parasympathetic tone may explain an important mechanism underlying the beneficial effect of the relaxation response.

Forty-six patients with documented coronary artery disease were studied to examine the relation of cardiovascular reactivity to mental stress and cardiac vagal activity. Cardiac vagal activity was measured by means of frequency-domain analysis of heart rate variability with 48-hour out-of-hospital Holter monitoring. The amplitude of the high-frequency component (0.16 to 0.40 Hz) of heart rate variability is considered to be an index of cardiac vagal activity. Cardiovascular reactivity was measured in the laboratory during a 3-minute public speaking task. Results revealed that (1) the amplitude of the high-frequency component was significantly higher during sleep (24.6 +/- 11.3 ms) than during waking (18.2 +/- 8.0 ms) (p = 0.002); (2) compared to subjects with low diastolic blood pressure reactivity, those who displayed high diastolic blood pressure reactivity exhibited a significantly lower amplitude of the high-frequency component (19.2 +/- 6.9 vs 23.4 +/- 9.6 ms, p = 0.03). These results indicate that decreased cardiac vagal activity may contribute to the exaggerated diastolic blood pressure reactivity to mental stress in patients with coronary artery disease.

Usefulness of complex demodulation (CDM) in assessing the frequency components of cardiovascular variability was assessed and, subsequently, this technique was utilized to determine the time-dependent responses of the low-frequency (LF) and high-frequency (HF) amplitudes of heart rate and blood pressure variabilities during postural tilt. CDM provides the time-dependent changes in amplitude of a particular frequency component on a continuous basis. Analysis of simulated data showed that CDM has sufficient frequency resolution to separately measure LF and HF amplitudes with a time resolution < 15 s and that CDM is robust to alterations in the frequency of the components. Analysis of actual data during postural tilt test in 23 young healthy subjects demonstrated that the HF amplitude of heart rate, an index of cardiac parasympathetic tone, rapidly decayed with head-up tilt (P < 0.01) and increased quickly showing an overshoot with tilt back to the supine position (P < 0.01). The LF amplitude of blood pressure, an index of vasomotor sympathetic activity, showed marked rhythmic fluctuation at an interval of 48-100 s during head-up tilt (P < 0.01), synchronizing with similar fluctuation in the LF amplitude of heart rate (P < 0.01). These results suggest that CDM can be used to provide a continuous assessment of cardiovascular variability components and that the dynamic responses of autonomic circulatory control to upright posture result in a phasic modulation of LF amplitude.

Thirty-four patients with essential hypertension at WHO stage I or II were divided into three groups. Group I consisted of 22 cases who displayed normal renin activity (NR) or low renin activity (LR) and who received a single administration of captopril. Group II consisted of 6 cases given beta-blockers after administration of captopril. Group III consisted of 6 cases in whom beta-blocker was replaced with thiazide diuretics after administration of captopril alone. Blood pressure decreased significantly by captopril treatment alone in group I of the NR and LR subgroups (except for the diastolic blood pressure [DBP] of the NR subgroup) and fell below the target blood pressure (SBP of 165 mmHg and DBP of 95 mmHg) in 86% of the NR subgroup and 73% of the LR subgroup. Combined treatment with captopril and beta-blocker in Group II did not decrease blood pressure any lower than with captopril alone treatment and achieved the target blood pressure in only 50% of the patients. In group III, combined treatment with captopril and thiazide achieved the target blood pressure in 100% of the patients. Plasma renin activity (PRA) was increased by captopril but reduced by captopril in combination with beta-blocker. However, when beta-blocker was replaced with thiazide, PRA increased. The serum sodium concentration was significantly reduced in the LR subgroup after a single administration of captopril, but there was no other variation.

Left ventricular performance was evaluated in 51 patients with acute myocardial infarction and angina pectoris using parameters derived from the flow velocity waveform at the ascending aorta. Flow velocity waveforms were obtained from the suprasternal notch by continuous-wave Doppler echocardiography and were recorded on a line-scan recorder at a paper speed of 100 mm/sec with lead II ECG. The peak flow velocity and the systolic time interval from the beginning of ECG Q wave to the peak flow velocity (Q-V peak interval) were measured. Relationships were investigated between these parameters and the left ventricular ejection fraction (LVEF) obtained from multigated equilibrium blood pool imaging with 99mTc-pertechnetate. The peak flow velocity did not correlate with LVEF (r = 0.27). However, a highly significant negative correlation was observed between the systolic time interval Q-V peak and LVEF (r = -0.84, p less than 0.001). The regression equation was LVEF = -0.46 X (Q-V peak) + 142. We conclude that left ventricular performance can be evaluated in patients with coronary artery disease at the bedside using the Q-V peak interval measured from simultaneous recording of the velocity waveform at the ascending aorta and the ECG.

Decreased vagal activity is frequently observed in coronary artery disease, but the mechanism of this association is unknown. We investigated cardiac autonomic function by relating heart rate spectral components to clinical and angiographic findings in 80 patients who were undergoing coronary angiography. The age- and sex-adjusted magnitude of the respiratory spectral component, which is an index of cardiac vagal tone, showed a significant negative correlation with the extent of coronary atheromatosis (r = -0.43, p less than 0.0001) and a less significant negative correlation with the severity of coronary stenosis (r = -0.30, p = 0.0070). These relationships were independent of previous myocardial infarction and of left ventricular function. Stepwise regression analysis showed that the respiratory spectral component contributed to atheromatosis independently of established coronary risk factors (partial R2 = 9.4%, p = 0.002), but not to stenosis. Our results support the hypothesis that decreased cardiac vagal activity is associated with an increased risk of coronary atherosclerosis.

The correlations of 11 indexes of heart rate variability were examined with pharmacologically determined cardiac vagal tone in 15 normal subjects at supine rest. After sympathetic influences by intravenous propranolol were eliminated, RR interval variability was measured for 10 minutes under controlled respiration (0.25 Hz), and cardiac vagal tone was determined as the decrease in mean RR interval following complete vagal blockade with atropine. Time domain indexes (standard deviation, coefficient of variance and mean successive difference) correlated strongly with vagal tone (r = 0.87, 0.81 and 0.92, respectively; p less than 0.001 for all). The same was true for frequency domain indexes for the high-frequency (0.25 Hz) component calculated both by autoregressive spectrum analysis (square root of power and coefficient of component variance) and by fast Fourier transform (mean amplitude) (r = 0.91, 0.85 and 0.86, respectively; p less than 0.0001 for all). However, frequency domain indexes for the low-frequency spectral component (0.03 to 0.15 Hz) correlated less strongly (r = 0.69, 0.55 and 0.70, respectively), and the fraction of power [power/(total power greater than 0.03 Hz)] of both components showed no correlation. Principal component analysis showed that the first 6 indexes with strong correlations contained solely the first principal component closely related to vagal tone, whereas the remaining 5 indexes also contained the second component unrelated to vagal tone. These results indicate that most of the time and frequency domain analyses in use provides an accurate and common measure of cardiac vagal tone at rest.

Coronary risk factors were assessed in 186 consecutive patients who received coronary angiography. The severity of coronary luminal narrowing was scored as the coronary sclerosis index (CSI). Patients were divided into normal coronary arteries (N, n = 72), coronary sclerosis without infarction (C, n = 73) and previous myocardial infarction (MI, n = 41). The CSI increased with age. A significant difference in serum triglycerides, HDL cholesterol and atherogenic index was observed between Groups C or MI and N. Multivariate analysis revealed that CSI had correlated with total- and HDL-cholesterol, uric acid and age in subjects under 55 years; and with age, blood sugar, factor H and HDL cholesterol in those of 55 years or over. When patients were classified by their total and LDL cholesterol level, a significantly different CSI was found between the desirable and high cholesterol levels in subjects under the age of 55, but it was not significant in those over 55. Therefore, disorders in lipid metabolism should be corrected in early middle age.

We analyzed the spectral components of RR interval variability under controlled respiration (15 breaths/min) in 56 patients (age range, 35-73 years) referred for coronary angiography; 14 patients had multivessel disease (group M), 21 had one-vessel disease (group S), and 21 had nonsignificant disease or normal coronary artery (group N). There were 43 healthy controls (age range, 36-71 years) (group C). The patients had no clinical evidence of heart failure, hypertension, diabetes mellitus, or acute stage of infarction and had taken no medication for 3 days. The autoregressive power spectral density of RR interval variability contains two major components, respiratory sinus arrhythmia (RSA) (0.25 Hz) and Mayer wave-like sinus arrhythmia (MWSA) (0.04-0.15 Hz), which have magnitudes that are quantitative markers of cardiac vagal activity and sympathetic activity with vagal modulation, respectively. We represented the magnitudes by the coefficient of component variance (CCV), which provided the amplitude relative to the mean RR interval. The age- and sex-adjusted mean of CCVRSA significantly decreased with advancing angiographic severity (1.64 +/- 0.09%, 1.66 +/- 0.12%, 1.22 +/- 0.13%, and 0.81 +/- 0.16% for groups C, N, S, and M, respectively) (p = 0.0001). The CCVRSA was unrelated to left ventricular function, previous myocardial infarction, or stenosis of any specific artery including the sinoatrial and atrioventricular node arteries. The CCVMWSA decreased only in group M (p = 0.0462). These results indicate that coronary artery disease is associated with vagal dominant impairment in autonomic cardiac function and that reduction in the vagal cardiac function correlates with the angiographic severity.

To investigate the diurnal variation in autonomic cardiac control, the magnitudes of the power spectral components of supine and standing heart rate variability were measured during controlled respiration (15 breaths/min). Examination was performed hourly between 0700 and 2300 h in eight male subjects whose activities and food intake were controlled for 24 h in the laboratory. The respiratory component (0.25 Hz) was greater in the morning than in the late afternoon (P less than 0.05) and decreased 30 min after food intake (P less than 0.01) in the supine position, but it was unaffected by the time of day or food intake while in the standing position. The Mayer wave component (0.03-0.15 Hz) did not change with the time of day, but it increased 90 min after food intake in both supine and standing positions (P less than 0.01 and P less than 0.05, respectively). These data suggest that supine vagal cardiac control during the waking period increases in the morning and decreases 30 min after food intake and that sympathetic cardiac control increases 90 min after food intake.

The short- and long-term effects of cigarette smoking on autonomic cardiac regulation were investigated by power spectral analysis of heart rate variability under controlled respiration (15/min). The short-term effects were examined in 9 smokers without evidence of cardiopulmonary disorders after an overnight abstinence from smoking. The heart rate spectral component reflecting the respiratory sinus arrhythmia (0.25 Hz), a quantitative index of vagal cardiac control, decreased 3 minutes after smoking 1 cigarette (p = 0.0061) and the component reflecting Mayer wave sinus arrhythmia (0.04 to 0.15 Hz), which includes sympathetically mediated activity, increased after 10 to 17 minutes (p = 0.0124). The long-term effects were examined in 81 normal subjects comprising 25 nonsmokers, 31 moderate (1 to 24 cigarettes/day) smokers and 25 heavy (greater than 25 cigarettes/day) smokers after an overnight abstinence. Although the magnitude of the Mayer wave component was unaffected by the smoking status, the respiratory component in the supine position was smaller in the young (less than or equal to 30 years) heavy smokers than in the young nonsmokers or moderate smokers (p = 0.0078). Also, postural changes in the components, a decrease in the respiratory component and an increase in the Mayer wave component with standing, were observed in the nonsmokers but not in the heavy smokers. These results suggest that smoking causes an acute and transient decrease in vagal cardiac control, and that heavy smoking causes long-term reduction in vagal cardiac control in young people and blunted postural responses in autonomic cardiac regulation.

The responses to the Japanese edition of the Jenkins Activity Survey (JAS) (Form C) were analyzed in 1682 male employees of a Japanese enterprise to investigate the characteristics of the Type A behavior pattern (TABP) in Japan. When the occupational level was controlled, the mean values of the Type A score were found to be quite similar to those of the Western Collaborative Group Study (WCGS), although those of factor H scores were considerably lower than those of the WCGS. Additionally, the results of a factor analysis conducted on the responses to JAS questions showed that the factor structure of the responses was basically equal to that found in the WCGS. In contrast to factor J of the WCGS, however, Japanese factor J did not comprise the items which signaled rises in positions or incomes in recent years. The results of this study indicate that the JAS is able to measure the TABP in Japan, at least concerning its three component factors. Furthermore, they suggest that the TAPB is not necessarily reinforced in Japanese occupational environments.