http://uhbs-international.net/fileadmin/unispitalbaselch/Bereiche/Medizin/Psychosomatik/Publikationen/Grossmann_Paul/grossman_understanding_respiratory_sinus_2007.pdf

Toward understanding respiratory sinus arrhythmia: relations to cardiac vagal tone, evolution and biobehavioral functions.

Mayer waves are oscillations of arterial pressure occurring spontaneously in conscious subjects at a frequency lower than respiration (∼0.1 Hz in humans). Mayer waves are tightly coupled with synchronous oscillations of efferent sympathetic nervous activity and are almost invariably enhanced during states of sympathetic activation. For this reason, the amplitude of these oscillations has been proposed as a surrogate measure of sympathetic activity, although in the absence of a clear knowledge of their underlying physiology. Some studies have suggested that Mayer waves result from the activity of an endogenous oscillator located either in the brainstem or in the spinal cord. Other studies, mainly based on the effects of sinoaortic baroreceptor denervation, have challenged this view. Several models of dynamic arterial pressure control have been developed to predict Mayer waves. In these models, it was anticipated that the numerous dynamic components and fixed time delays present in the baroreflex loop would result in the production of a resonant, self-sustained oscillation of arterial pressure. Recent analysis of the various transfer functions of the rat baroreceptor reflex suggests that Mayer waves are transient oscillatory responses to hemodynamic perturbations rather than true feedback oscillations. Within this frame, the amplitude of Mayer waves would be determined both by the strength of the triggering perturbations and the sensitivity of the sympathetic component of the baroreceptor reflex.

http://www.nat.vu.nl/~ivo/PSM/lit/2006THMwaves.pdf

The enigma of Mayer waves: Facts and models.

In recent years there has been substantial support for heart rate variability biofeedback (HRVB) as a treatment for a variety of disorders and for performance enhancement (Gevirtz, 2013). Since conditions as widely varied as asthma and depression seem to respond to this form of cardiorespiratory feedback training, the issue of possible mechanisms becomes more salient. The most supported possible mechanism is the strengthening of homeostasis in the baroreceptor (Vaschillo et al., 2002; Lehrer et al., 2003). Recently, the effect on the vagal afferent pathway to the frontal cortical areas has been proposed. In this article, we review these and other possible mechanisms that might explain the positive effects of HRVB.

http://bio-medical.com/resources/wp-content/uploads/2015/11/fpsyg-05-00756.pdf

Heart rate variability biofeedback: how and why does it work?

Objective We evaluated heart rate variability biofeedback as a method for increasing vagal baroreflex gain and improving pulmonary function among 54 healthy adults. Methods We compared 10 sessions of biofeedback training with an uninstructed control. Cognitive and physiological effects were measured in four of the sessions. Results We found acute increases in low-frequency and total spectrum heart rate variability, and in vagal baroreflex gain, correlated with slow breathing during biofeedback periods. Increased baseline baroreflex gain also occurred across sessions in the biofeedback group, independent of respiratory changes, and peak expiratory flow increased in this group, independently of cardiovascular changes. Biofeedback was accompanied by fewer adverse relaxation side effects than the control condition. Conclusions 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.

Heart rate variability biofeedback increases baroreflex gain and peak expiratory flow.

Altered variability in the cardiovascular system is associated with a range of cardiovascular diseases and increased mortality. Because blood pressure and heart rate show distinct low-frequency oscillations that appear to be affected by either vagal or sympathetic activity, it has been hoped that measurement of the strength of these oscillations could be used as an index of autonomic tone and thus form the basis of a diagnostic test. This review focuses on recent research that has examined the fundamental origin of variability associated with respiration and a slow oscillation at 0.1 Hz in the human. A new hypothesis is proposed to account for the slow oscillation in heart rate and blood pressure that incorporates components of the central nervous system, other reflex pathways regulating sympathetic activity, and resonance in the baroreflex control of blood pressure. Whereas it is clear that sympathetic activity and arterial baroreflexes are critical elements in producing cardiovascular variability, there is also evidence that other factors, including the ability of the vasculature to respond to sympathetic activity, appear to play a role in determining the strength of oscillations. Given the potential impact of other nonbaroreflex or nonautonomic pathways in affecting cardiovascular variability, it is proposed that one must use care in relating changes in the strength of an oscillation in blood pressure and heart rate as definitively due to a change in autonomic control.

Neural influences on cardiovascular variability: possibilities and pitfalls

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-1 (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 necessary for maximal respiratory gating to occur.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1469-7793.1999.0617t.x

Human responses to upright tilt: a window on central autonomic integration

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.

https://www.physiology.org/doi/pdf/10.1152/ajpheart.2001.280.6.H2674

Respiratory modulation of human autonomic rhythms

We studied three Russian cosmonauts to better understand how long-term exposure to microgravity affects autonomic cardiovascular control. We recorded the electrocardiogram, finger photoplethysmogra...

Nine months in space: effects on human autonomic cardiovascular regulation.

Because it is likely that, in healthy human subjects, baroreflex mechanisms operate continuously, independent of experimental interventions, we asked the question, In what ways might study of unprovoked, very infrequent muscle sympathetic bursts inform baroreflex physiology? We closely examined arterial pressure and R-R interval responses of 11 supine healthy young subjects to arterial pressure ramps triggered by large isolated muscle sympathetic bursts. We triggered data collection sweeps on the beginnings of sympathetic bursts and plotted changes of arterial pressure (finger volume clamp or intra-arterial) and R-R intervals occurring before as well as after the sympathetic triggers. We estimated baroreflex gain from regression of R-R intervals on systolic pressures after sympathetic bursts and from the transfer function between cross-spectra of systolic pressure and R-R intervals at low frequencies. Isolated muscle sympathetic bursts were preceded by arterial pressure reductions. Baroreflex gain, calculated with linear regression of R-R intervals on systolic pressures after bursts, was virtually identical to baroreflex gain, calculated with the cross-spectral modulus [mean and (range): 24 (7-43) vs. 24 (8-45) ms/mmHg], and highly significant, according to linear regression (r(2) = 0.91, P = 0.001). Our results indicate that 1) since infrequent human muscle sympathetic bursts are almost deterministically preceded by arterial pressure reductions, their occurrence likely reflects simple baroreflex physiology, and 2) the noninvasive low-frequency modulus reliably reproduces gains derived from R-R interval responses to arterial pressure ramps triggered by infrequent muscle sympathetic bursts.

Alexandra A. Crossman

Papers

Human responses to upright tilt: a window on central autonomic integration

Respiratory modulation of human autonomic rhythms

Nine months in space: effects on human autonomic cardiovascular regulation.

Baroreflex physiology studied in healthy subjects with very infrequent muscle sympathetic bursts.