Human cardiovascular function can be characterized by steady-state measures of muscle sympathetic nerve activity, arterial pressure, R-R intervals and respiration. Additional information can be obtained from the study of the oscillations of these parameters, as they exist individually, and in relation to each other. The magnitude of oscillations can be gauged with frequency domain methods, including fast Fourier transformation and autoregressive modelling, and the coherence between these measures and their phase relations can be gauged with cross-spectral analysis. We closely examined haemodynamic and autonomic neural periodicities in a group of healthy young volunteers in order Journal of Physiology (1999) 1. We examined interactions between haemodynamic and autonomic neural oscillations during passive upright tilt, to gain better insight into human autonomic regulatory mechanisms. 2. We recorded the electrocardiogram, finger photoplethysmographic arterial pressure, respiration and peroneal nerve muscle sympathetic activity in nine healthy young adults. Subjects breathed in time with a metronome at 12 breaths min¢ (0·2 Hz) for 5 min each, in supine, and 20, 40, 60, 70 and 80 deg head-up positions. We performed fast Fourier transform (and autoregressive) power spectral analyses and integrated low-frequency (0·05-0·15 Hz) and respiratory-frequency (0·15-0·5 Hz) spectral powers. 3. Integrated areas of muscle sympathetic bursts and their low-and respiratory-frequency spectral powers increased directly and significantly with the tilt angle. The centre frequency of low-frequency sympathetic oscillations was constant before and during tilt. Sympathetic bursts occurred more commonly during expiration than inspiration at low tilt angles, but occurred equally in expiration and inspiration at high tilt angles. 4. Systolic and diastolic pressures and their low-and respiratory-frequency spectral powers increased, and R-R intervals and their respiratory-frequency spectral power decreased progressively with the tilt angle. Low-frequency R-R interval spectral power did not change. 5. The cross-spectral phase angle between systolic pressures and R-R intervals remained constant and consistently negative at the low frequency, but shifted progressively from positive to negative at the respiratory frequency during tilt. The arterial baroreflex modulus, calculated from low-frequency cross-spectra, decreased at high tilt angles. 6. Our results document changes of baroreflex responses during upright tilt, which may reflect leftward movement of subjects on their arterial pressure sympathetic and vagal response relations. The intensity, but not the centre frequency of low-frequency cardiovascular rhythms, is modulated by the level of arterial baroreceptor input. Tilt reduces respiratory gating of sympathetic and vagal motoneurone responsiveness to stimulatory inputs for different reasons; during tilt, sympathetic stimulation increases to a level that overwhelms the respiratory gate, and vagal stimulation decreases to a level below that ...

Heart rate variability biofeedback had strong long-term influences on resting baroreflex gain and pulmonary function. It should be examined as a method for treating cardiovascular and pulmonary diseases. Also, this study demonstrates neuroplasticity of the baroreflex.

We evaluated a method of baroreflex testing involving sequential intravenous bolus injections of nitroprusside followed by phenylephrine and phenylephrine followed by nitroprusside in 18 healthy men and women, and we drew inferences regarding human sympathetic and vagal baroreflex mechanisms. We recorded the electrocardiogram, photoplethysmographic finger arterial pressure, and peroneal nerve muscle sympathetic activity. We then contrasted least squares linear regression slopes derived from the depressor (nitroprusside) and pressor (phenylephrine) phases with 1) slopes derived from spontaneous fluctuations of systolic arterial pressures and R-R intervals, and 2) baroreflex gain derived from cross-spectral analyses of systolic pressures and R-R intervals. We calculated sympathetic baroreflex gain from integrated muscle sympathetic nerve activity and diastolic pressures. We found that vagal baroreflex slopes are less when arterial pressures are falling than when they are rising and that this hysteresis exists over pressure ranges both below and above baseline levels. Although pharmacological and spontaneous vagal baroreflex responses correlate closely, pharmacological baroreflex slopes tend to be lower than those derived from spontaneous fluctuations. Sympathetic baroreflex slopes are similar when arterial pressure is falling and rising; however, small pressure elevations above baseline silence sympathetic motoneurons. Vagal, but not sympathetic baroreflex gains vary inversely with subjects’ ages and their baseline arterial pressures. There is no correlation between sympathetic and vagal baroreflex gains. We recommend repeated sequential nitroprusside followed by phenylephrine doses as a simple, efficientmeans to provoke and characterize human vagal and sympathetic baroreflex responses.

Patients with orthostatic vasovagal reactions have impaired vagal baroreflex responses to arterial pressure changes below resting levels but normal initial responses to upright tilt. Subtle vasovagal physiology begins before overt presyncope. The final trigger of human orthostatic vasovagal reactions appears to be the abrupt disappearance of muscle sympathetic nerve activity.

We studied the influence of three types of breathing [spontaneous, frequency controlled (0.25 Hz), and hyperventilation with 100% oxygen] and apnea on R-R interval, photoplethysmographic arterial pressure, and muscle sympathetic rhythms in nine healthy young adults. We integrated fast Fourier transform power spectra over low (0.05-0.15 Hz) and respiratory (0.15-0.3 Hz) frequencies; estimated vagal baroreceptor-cardiac reflex gain at low frequencies with cross-spectral techniques; and used partial coherence analysis to remove the influence of breathing from the R-R interval, systolic pressure, and muscle sympathetic nerve spectra. Coherence among signals varied as functions of both frequency and time. Partialization abolished the coherence among these signals at respiratory but not at low frequencies. The mode of breathing did not influence low-frequency oscillations, and they persisted during apnea. Our study documents the independence of low-frequency rhythms from respiratory activity and suggests that the close correlations that may exist among arterial pressures, R-R intervals, and muscle sympathetic nerve activity at respiratory frequencies result from the influence of respiration on these measures rather than from arterial baroreflex physiology. Most importantly, our results indicate that correlations among autonomic and hemodynamic rhythms vary over time and frequency, and, thus, are facultative rather than fixed.

of biosignal analysis in assessing terbutaline-induced heart rate and blood pressure changes. Am J Physiol Heart Circ Physiol 282: H773-H781, 2002; 10.1152/ajpheart. 00559.2001.-The aim of this study was to characterize how different nonlinear methods characterize heart rate and blood pressure dynamics in healthy subjects at rest. The randomized, placebo-controlled crossover study with intravenous terbutaline was designed to induce four different stationary states of cardiovascular regulation system. The R-R interval, systolic arterial blood pressure, and heart rate time series were analyzed with a set of methods including approximate entropy, sample entropy, Lempel-Ziv entropy, symbol dynamic entropy, cross-entropy, correlation dimension, fractal dimensions, and stationarity test. Results indicate that R-R interval and systolic arterial pressure subsystems are mutually connected but have different dynamic properties. In the drug-free state the subsystems share many common features. When the strength of the baroreflex feedback loop is modified with terbutaline, R-R interval and systolic blood pressure lose mutual synchrony and drift toward their inherent state of operation. In this state the R-R interval system is rather complex and irregular, but the blood pressure system is much simpler than in the drug-free state. nonlinear dynamics; complexity; dimensionality; entropy TRADITIONAL LINEAR ANALYSIS methods of heart rate and blood pressure time series data, such as the time-and frequency-domain methods, measure the strength of oscillations in heart rate and blood pressure within a specific frequency range, for example, in the low-frequency (0.04-0.15 Hz) and high-frequency (0.15-0.4 Hz) bands. The spectral powers obtained can be used, for example, to estimate sympathetic and parasympathetic nervous activity and, with cross-spectral approaches, to characterize arterial baroreflex functions. Generally, the linear methods (time-and frequencydomain methods) are useful and have been widely adopted in studies of health and disease because results from linear methods are quite easy to interpret in physiological terms. But they also have limitations, and criticisms have been raised against their use (5).Multiple feedback loops in cardiovascular regulation systems make rapid adaptations possible under a large variety of physiological and environmental conditions. In analyzing heart rate and blood pressure time series with traditional linear methods, we lose a lot of information on the dynamic patterns used by the cardiovascular regulation systems to adjust heart rate and blood pressure. Linear methods have not been designed to yield information on the systems' inherent dynamic properties. Nonlinear methods of signal analysis can be more useful when characterizing complex dynamics. Thus the idea of using nonlinear statistics in the analysis of heart rate and blood pressure time series data is theoretically very sound and is a challenging objective for both cardiovascular physiologists and system theoreticians. Nonlinear ...

When astronauts return to Earth and stand, their heart rates may speed inordinately, their blood pressures may fall, and some may experience frank syncope. We studied brief autonomic and haemodynamic transients provoked by graded Valsalva manoeuvres in astronauts on Earth and in space, and tested the hypothesis that exposure to microgravity impairs sympathetic as well as vagal baroreflex responses. We recorded the electrocardiogram, finger photoplethysmographic arterial pressure, respiration and peroneal nerve muscle sympathetic activity in four healthy male astronauts (aged 38–44 years) before, during and after the 16 day Neurolab space shuttle mission. Astronauts performed two 15 s Valsalva manoeuvres at each pressure, 15 and 30 mmHg, in random order. Although no astronaut experienced presyncope after the mission, microgravity provoked major changes. For example, the average systolic pressure reduction during 30 mmHg straining was 27 mmHg pre‐flight and 49 mmHg in flight. Increases in muscle sympathetic nerve activity during straining were also much greater in space than on Earth. For example, mean normalized sympathetic activity increased 445 % during 30 mmHg straining on earth and 792 % in space. However, sympathetic baroreflex gain, taken as the integrated sympathetic response divided by the maximum diastolic pressure reduction during straining, was the same in space and on Earth. In contrast, vagal baroreflex gain, particularly during arterial pressure reductions, was diminished in space. This and earlier research suggest that exposure of healthy humans to microgravity augments arterial pressure and sympathetic responses to Valsalva straining and differentially reduces vagal, but not sympathetic baroreflex gain.

This study was designed to evaluate the effect of modulating cardiac parasympathetic input on the high frequency component of heart rate variability. We stimulated the right vagus nerve with three different stimulation patterns in anaesthetized, vagotomized and spinal anaesthetized dogs. We kept the mean stimulation frequency constant; controlled the amplitude of modulation with programmed stimulation patterns, and analysed the resulting heart rate variability by power spectral analysis. Constant frequency vagal stimulation increased the cardiac interval, but did not change heart rate variability markedly. There was a slight increase, from 11 +/- 2 to 27 +/- 11 ms2, in the high frequency component. However, when the instantaneous stimulation frequency oscillated between 4 and 17 Hz during 5 s period, we could produce a marked heart rate variation, with 91 +/- 9% of the variation corresponding to the frequency of the modulation (0.20 Hz). The high frequency component was 12932 +/- 7701 ms2. With an increased magnitude of modulation, i.e. the difference between minimum and maximum instantaneous frequency, the high frequency component increased to 32711 +/- 17943 ms2. Thus, the high frequency component of heart rate variability reflects the magnitude of fluctuation in the cardiac parasympathetic input rather than parasympathetic 'tone'.