POINT-COUNTERPOINTRebuttal from EckbergPublished Online:01 May 2009https://doi.org/10.1152/japplphysiol.91107.2008bMoreSectionsPDF (36 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat This Point:Counterpoint debate reduces very complex physiology to a single question, which (as the debate was framed) has only two possible and mutually exclusive answers. What mechanism explains respiratory frequency R-R interval fluctuations? Are they caused by central gating of vagal-cardiac motoneurons (2) or are they caused by vagal baroreflex responses to respiration-induced blood pressure changes (1)?I based my original argument primarily on the simple propositions that central gating is sufficient to explain respiratory frequency R-R interval fluctuations and that the latency between blood pressure changes and parallel R-R interval changes, as defined by cross-spectral phase, is too short for meaningful baroreflex responses to be mounted.Consider cross-spectral baroreflex gains derived at ∼0.1 Hz and the breathing frequency (assuming that both are, in fact, baroreflex mediated). First, their magnitudes may be similar because both are tied to baroreceptor activity. Low-frequency systolic pressure ramps increase baroreceptor firing and provoke R-R interval lengthening. Respiratory frequency R-R interval fluctuations are mediated centrally; however, although they are caused by respiratory motoneuron activity, their magnitude depends critically on the level of baroreceptor stimulation (3)].Second, low- and respiratory-frequency baroreflex gains may be different. First, spontaneous baroreflex sequences occur at a frequency of ∼0.1 Hz (4), but not the respiratory frequency. Second, baroreflex latencies derived from cross-spectral analyses average ∼2.0 s; however, latencies derived from time (not frequency-)-domain analyses at usual breathing frequencies are much shorter. This disparity, whatever its precise mathematical value, suggests counterintuitively, that the kinetics of sinoatrial node responses to released acetylcholine (which account for most of baroreceptor-cardiac reflex latencies) differ greatly, according to the frequency over which baroreflex mechanisms are operative.This Point:Counterpoint debate exposes a vein of rich and extraordinarily complex physiology. Respiratory frequency R-R interval fluctuations are the final expression of a host of ongoing influences, each with its own latency and time course. This large list includes breathing rate; respiration-induced arterial pressure changes; respiratory gating of vagal-cardiac motoneuron responsiveness to arterial pressure changes; baseline R-R intervals; and fluctuations of R-R intervals, which continuously alter the temporal relations between pulsatile releases of acetylcholine and sinoatrial node diastolic depolarization.In this debate, I concede a small point: respiratory frequency R-R interval fluctuations may include some unknowable admixture of baroreflex mechanisms and central gating. However, in subjects with usual R-R intervals and breathing rates, the baroreflex contribution is small. Therefore, cross-spectral estimates of baroreflex gain should exclude those occurring at respiratory frequencies.REFERENCES1 de Boer RW, Karemaker JM, Strackee J. Hemodynamic fluctuations and baroreflex sensitivity in humans: a beat-to-beat model. Am J Physiol Heart Circ Physiol 253: H680–H689, 1987.Link | ISI | Google Scholar2 Eckberg DL. The human respiratory gate. J Physiol 548: 339–352, 2003.Crossref | PubMed | ISI | Google Scholar3 Eckberg DL, Rea RF, Andersson OK, Hedner T, Pernow J, Lundberg JM, Wallin BG. Baroreflex modulation of sympathetic activity and sympathetic neurotransmitters in humans. Acta Physiol Scand 133: 221–231, 1988.Crossref | PubMed | Google Scholar4 Rothlisberger BW, Badra LJ, Hoag JB, Cooke WH, Kuusela TA, Tahvanainen KUO, Eckberg DL. Spontaneous “baroreflex sequences” occur as deterministic functions of breathing phase. Clin Physiol Funct Imag 23: 307–313, 2003.Crossref | PubMed | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 106Issue 5May 2009Pages 1744-1744 Copyright & PermissionsCopyright © 2009 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.91107.2008bHistory Published online 1 May 2009 Published in print 1 May 2009 Metrics