Dwain L. Eckberg
Virginia Commonwealth University
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Featured researches published by Dwain L. Eckberg.
Psychosomatic Medicine | 2003
Paul M. Lehrer; Evgeny G. Vaschillo; Bronya Vaschillo; Shou En Lu; Dwain L. Eckberg; Robert Edelberg; Weichung Joe Shih; Yong Lin; Tom Kuusela; Kari U. O. Tahvanainen; Robert M. Hamer
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.
American Journal of Physiology-heart and Circulatory Physiology | 1998
William H. Cooke; James F. Cox; André Diedrich; J. Andrew Taylor; Larry A. Beightol; James E. Ames; Jeffrey B. Hoag; Henrik Seidel; Dwain L. Eckberg
The purpose of this study was to determine how breathing protocols requiring varying degrees of control affect cardiovascular dynamics. We measured inspiratory volume, end-tidal CO2, R-R interval, and arterial pressure spectral power in 10 volunteers who followed the following 5 breathing protocols: 1) uncontrolled breathing for 5 min; 2) stepwise frequency breathing (at 0.3, 0.25, 0.2, 0.15, 0.1, and 0.05 Hz for 2 min each); 3) stepwise frequency breathing as above, but with prescribed tidal volumes; 4) random-frequency breathing (∼0.5-0.05 Hz) for 6 min; and 5) fixed-frequency breathing (0.25 Hz) for 5 min. During stepwise breathing, R-R interval and arterial pressure spectral power increased as breathing frequency decreased. Control of inspired volume reduced R-R interval spectral power during 0.1 Hz breathing ( P < 0.05). Stepwise and random-breathing protocols yielded comparable coherence and transfer functions between respiration and R-R intervals and systolic pressure and R-R intervals. Random- and fixed-frequency breathing reduced end-tidal CO2modestly ( P < 0.05). Our data suggest that stringent tidal volume control attenuates low-frequency R-R interval oscillations and that fixed- and random-rate breathing may decrease CO2 chemoreceptor stimulation. We conclude that autonomic rhythms measured during different breathing protocols have much in common but that a stepwise protocol without stringent control of inspired volume may allow for the most efficient assessment of short-term respiratory-mediated autonomic oscillations.
The Journal of Physiology | 2007
Ken-ichi Iwasaki; Benjamin D. Levine; Rong Zhang; Julie H. Zuckerman; James A. Pawelczyk; André Diedrich; Andrew C. Ertl; James F. Cox; William H. Cooke; Cole A. Giller; Chester A. Ray; Lynda D. Lane; Jay C. Buckey; Friedhelm J. Baisch; Dwain L. Eckberg; David Robertson; Italo Biaggioni; C. Gunnar Blomqvist
Exposure to microgravity alters the distribution of body fluids and the degree of distension of cranial blood vessels, and these changes in turn may provoke structural remodelling and altered cerebral autoregulation. Impaired cerebral autoregulation has been documented following weightlessness simulated by head‐down bed rest in humans, and is proposed as a mechanism responsible for postspaceflight orthostatic intolerance. In this study, we tested the hypothesis that spaceflight impairs cerebral autoregulation. We studied six astronauts ∼72 and 23 days before, after 1 and 2 weeks in space (n= 4), on landing day, and 1 day after the 16 day Neurolab space shuttle mission. Beat‐by‐beat changes of photoplethysmographic mean arterial pressure and transcranial Doppler middle cerebral artery blood flow velocity were measured during 5 min of spontaneous breathing, 30 mmHg lower body suction to simulate standing in space, and 10 min of 60 deg passive upright tilt on Earth. Dynamic cerebral autoregulation was quantified by analysis of the transfer function between spontaneous changes of mean arterial pressure and cerebral artery blood flow velocity, in the very low‐ (0.02–0.07 Hz), low‐ (0.07–0.20 Hz) and high‐frequency (0.20–0.35 Hz) ranges. Resting middle cerebral artery blood flow velocity did not change significantly from preflight values during or after spaceflight. Reductions of cerebral blood flow velocity during lower body suction were significant before spaceflight (P < 0.05, repeated measures ANOVA), but not during or after spaceflight. Absolute and percentage reductions of mean (±s.e.m.) cerebral blood flow velocity after 10 min upright tilt were smaller after than before spaceflight (absolute, −4 ± 3 cm s−1 after versus−14 ± 3 cm s−1 before, P= 0.001; and percentage, −8.0 ± 4.8% after versus−24.8 ± 4.4% before, P < 0.05), consistent with improved rather than impaired cerebral blood flow regulation. Low‐frequency gain decreased significantly (P < 0.05) by 26, 23 and 27% after 1 and 2 weeks in space and on landing day, respectively, compared with preflight values, which is also consistent with improved autoregulation. We conclude that human cerebral autoregulation is preserved, and possibly even improved, by short‐duration spaceflight.
Journal of Applied Physiology | 2013
Tomislav Stankovski; William H. Cooke; László Rudas; Aneta Stefanovska; Dwain L. Eckberg
We experimentally altered the timing of respiratory motoneuron activity as a means to modulate and better understand otherwise hidden human central neural and hemodynamic oscillatory mechanisms. We recorded the electrocardiogram, finger photoplethysmographic arterial pressure, tidal carbon dioxide concentrations, and muscle sympathetic nerve activity in 13 healthy supine young men who gradually increased or decreased their breathing frequencies between 0.05 and 0.25 Hz over 9-min periods. We analyzed results with traditional time- and frequency-domain methods, and also with time-frequency methods (wavelet transform, wavelet phase coherence, and directional coupling). We determined statistical significance and identified frequency boundaries by comparing measurements with randomly generated surrogates. Our results support several major conclusions. First, respiration causally modulates both sympathetic (weakly) and vagal motoneuron (strongly) oscillations over a wide frequency range-one that extends well below the frequency of actual breaths. Second, breathing frequency broadly modulates vagal baroreflex gain, with peak gains registered in the low frequency range. Third, breathing frequency does not influence median levels of sympathetic or vagal activity over time. Fourth, phase relations between arterial pressure and sympathetic and vagal motoneurons are unaffected by breathing, and are therefore likely secondary to intrinsic responsiveness of these motoneurons to other synaptic inputs. Finally, breathing frequency does not affect phase coherence between diastolic pressure and muscle sympathetic oscillations, but it augments phase coherence between systolic pressure and R-R interval oscillations over a limited portion of the usual breathing frequency range. These results refine understanding of autonomic oscillatory processes and those physiological mechanisms known as the human respiratory gate.
The Journal of Physiology | 2016
Dwain L. Eckberg; William H. Cooke; André Diedrich; Italo Biaggioni; Jay C. Buckey; James A. Pawelczyk; Andrew C. Ertl; James F. Cox; Tom Kuusela; Kari U. O. Tahvanainen; Tadaaki Mano; Satoshi Iwase; Friedhelm J. Baisch; Benjamin D. Levine; Beverley Adams-Huet; David Robertson; C. Gunnar Blomqvist
We studied healthy supine astronauts on Earth with electrocardiogram, non‐invasive arterial pressure, respiratory carbon dioxide concentrations, breathing depth and sympathetic nerve recordings. The null hypotheses were that heart beat interval fluctuations at usual breathing frequencies are baroreflex mediated, that they persist during apnoea, and that autonomic responses to apnoea result from changes of chemoreceptor, baroreceptor or lung stretch receptor inputs. R‐R interval fluctuations at usual breathing frequencies are unlikely to be baroreflex mediated, and disappear during apnoea. The subjects’ responses to apnoea could not be attributed to changes of central chemoreceptor activity (hypocapnia prevailed); altered arterial baroreceptor input (vagal baroreflex gain declined and muscle sympathetic nerve burst areas, frequencies and probabilities increased, even as arterial pressure climbed to new levels); or altered pulmonary stretch receptor activity (major breathing frequency and tidal volume changes did not alter vagal tone or sympathetic activity). Apnoea responses of healthy subjects may result from changes of central respiratory motoneurone activity.
The Journal of Physiology | 2016
Dwain L. Eckberg; André Diedrich; William H. Cooke; Italo Biaggioni; Jay C. Buckey; James A. Pawelczyk; Andrew C. Ertl; James F. Cox; Tom Kuusela; Kari U. O. Tahvanainen; Tadaaki Mano; Satoshi Iwase; Friedhelm J. Baisch; Benjamin D. Levine; Beverley Adams-Huet; David Robertson; C. Gunnar Blomqvist
We studied healthy astronauts before, during and after the Neurolab Space Shuttle mission with controlled breathing and apnoea, to identify autonomic changes that might contribute to postflight orthostatic intolerance. Measurements included the electrocardiogram, finger photoplethysmographic arterial pressure, respiratory carbon dioxide levels, tidal volume and peroneal nerve muscle sympathetic activity. Arterial pressure fell and then rose in space, and drifted back to preflight levels after return to Earth. Vagal metrics changed in opposite directions: vagal baroreflex gain and two indices of vagal fluctuations rose and then fell in space, and descended to preflight levels upon return to Earth. Sympathetic burst frequencies (but not areas) were greater than preflight in space and on landing day, and astronauts’ abilities to modulate both burst areas and frequencies during apnoea were sharply diminished. Spaceflight triggers long‐term neuroplastic changes reflected by reciptocal sympathetic and vagal motoneurone responsiveness to breathing changes.
The Journal of Physiology | 2017
Dwain L. Eckberg
My Neurolab colleagues and I studied autonomic mechanisms of healthy subjects on Earth and in space, and in two articles (Eckberg et al. 2016a,b) drew several conclusions, including this one: that at usual breathing frequencies ( 0.25 Hz), R-R interval changes occur too soon after systolic pressure changes to be mediated by vagal baroreflex mechanisms. Karemaker & DeBoer (2017) challenged this conclusion on three bases. (1) They simulated blood pressure fluctuations with a 0.25 Hz sinusoid and calculated latencies between the peaks of the waveforms and the intervals between waveforms (presumably) offset by 0.6 s. Their calculated phase angles were −54 deg (latency of 1.35 s) for 0.1 Hz oscillations, and 0 deg (latency of 0 s) for 0.25 Hz oscillations. (2) They cited evidence that baroreflex slopes calculated after pressor injections yield higher correlation coefficients when each systolic pressure is correlated with the R-R interval in which it occurs, rather than the next. (3) They speculated that the longer latencies calculated at 0.1 Hz reflect sympathetic stimulation, which shifts pressure pulse to P wave intervals. We thank Karemaker and DeBoer for their careful reading of our article, and for their thoughtful comments. Their challenge focuses on several interrelated aspects of the physiology we studied: respiratory sinus arrhythmia; sinoatrial node responses to individual, or trains of successive, experimental or spontaneous baroreceptor stimuli; and the kinetics of sinoatrial node responses to noradrenaline and acetylcholine. Data derived from animal research indicate that about 72% of the total baroreflex latency reflects the kinetics of sinoatrial node responses to released acetylcholine (Eckberg & Sleight, 1992). A human study published 40 years ago (Eckberg, 1976) delineates the time course of sinoatrial node responses to baroreflex inhibition. Carotid baroreceptors were stimulated by precise, highly reproducible 60 mmHg, 0.58 s neck suction pulses, timed to sweep entire R-R intervals. Figure 1 shows the responses of one subject to 73 individual applications of neck suction. The author assumed that each stimulus provokes equal releases of acetylcholine and that, therefore, the variability of responses reflects changing sinoatrial membrane properties. Since during brief held expiration R-R intervals are nearly constant, responses to baroreceptor stimuli can be plotted as functions of their timing before the next P waves. These data document an absolute latency between the onset of stimulation and P waves of 0.54 s, and QRS complexes of 0.7 s, and illustrate the time course of sinoatrial responses to released acetylcholine. Phase angles are functions of the kinetics of sinoatrial node responses; it is unclear how
Cardiovascular Oscillations (ESGCO), 2014 8th Conference of the European Study Group on | 2014
Tomislav Stankovski; Dwain L. Eckberg; Aneta Stefanovska
We varied the timing of respiration as a means to modulate and better understand otherwise hidden human central neural and cardiovascular mechanisms. Time-frequency methods (wavelet transform, wavelet phase coherence, and directional coupling) were applied to analyze these time-varying signals. We found that respiration causally modulates both sympathetic (weakly) and vagal motoneuron (strongly) oscillations over a wide frequency range - one that extends well below the frequency of actual breaths. Breathing frequency does not affect phase coherence between diastolic pressure and muscle sympathetic oscillations, but it augments phase coherence between systolic pressure and R-R interval oscillations over a limited portion of the usual breathing frequency range.
Cardiovascular Oscillations (ESGCO), 2014 8th Conference of the European Study Group on | 2014
Philip T. Clemson; Jeffrey B. Hoag; Aneta Stefanovska; Dwain L. Eckberg
The effect of the drugs atropine (a parasympathetic blocker) and propranolol (a sympathetic blocker) is investigated. In the experiment, the subjects were measured under an experimental protocol that used saline controls, with both spontaneous and paced breathing as well as apnea. The recorded data included an electrocardiogram, end tidal CO2, blood pressure and a direct measurement of the muscle sympathetic nerve activity. The signals were analysed using time-frequency methods and an information theory approach, revealing information about the change in coupling and coherence that has not previously been studied. The results show that atropine strongly reduces the power in the signals and also removes the coupling and coherence between cardiovascular oscillations. The effects occur across a wide range of frequencies and provide insight into the neurophysiological mechanisms involved in the regulation of the cardiovascular system.
American Journal of Physiology-heart and Circulatory Physiology | 1996
Michael L. Smith; Larry A. Beightol; Janice M. Fritsch-Yelle; Kenneth A. Ellenbogen; Thomas R. Porter; Dwain L. Eckberg