Spontaneous ‘baroreflex sequences’ occur as deterministic functions of breathing phase

Abstract

Parallel increases or decreases of systolic pressures and R-R intervals occur spontaneously in healthy resting humans, and are thought to be expressions of vagal baroreflex physiology. We studied ten healthy supine young adults, and tested the null hypothesis that spontaneous baroreflex sequences are distributed uniformly throughout the breathing cycle. We recorded the electrocardiogram, photoplethysmographic arterial pressure, respiration (pneumobelt), and peroneal nerve muscle sympathetic activity in supine subjects who breathed spontaneously, or held their breaths in inspiration after 2 min of hyperventilation with 100% oxygen. We analysed pairs of three or more increasing or decreasing systolic pressures and R-R intervals with linear regression, and related the gain and timing of the onset of such sequences to the phase of respiration, and to preceding muscle sympathetic nerve activity. We found that baroreflex sequences occur erratically, at a frequency about one-third that of breathing. However, when baroreflex sequences do occur, the timing of their onset is dictated by the phase of respiration. Parallel increases of systolic pressures and R-R intervals ('up' sequences) begin just before and after the beginning of expiration, and parallel decreases of systolic pressures and R-R intervals ('down' sequences) begin during late expiration and inspiration. Average gains of up and down baroreflex sequences triggered by muscle sympathetic bursts are comparable during breathing and apnoea. However, the latencies between sympathetic bursts and baroreflex sequences are less during breathing than during apnoea. We propose that parallel systolic pressure--R-R interval sequences are expressions of arterial baroreflex physiology, and that the nearly fixed timing of such sequences within breaths reflects simply respiratory gating of muscle sympathetic bursts.

Conditional symbolic analysis detects nonlinear influences of respiration on cardiovascular control in humans

“…Respiratoryrelated nonlinear influences were detected over both SAP-HP and MSNA-SAP joint behaviours. The nonlinear effect of respiration on the SAP-HP interactions might be the result of the nonlinear effect of respiration on cardiac baroreflex [8,9] and on venous return leading to modulations of the relation from HP to SAP [26,40]. The nonlinear effect of respiration on the MSNA-SAP interactions might be the result of the nonlinear effect of respiration on the baroreflex control of MSNA [41].…”

“…Indeed, stimulation of carotid baroreceptors via brief neck suction pulses elicits a greater HP lengthening during late inspiratory and early expiratory phases [8], thus proving that respiration can modulate the baroreflex. The influence of respiration on baroreflex was also detected by the analysis of spontaneous variations of HP and systolic arterial pressure (SAP): indeed, a different distribution of spontaneous cardiac baroreflex sequences in expiratory and inspiratory phases was observed [9] with more frequent up baroreflex sequences with gain significantly different from 0 in expiration than inspiration, whereas the reverse situation holds for down baroreflex sequences. A brief neck pressure pulse compressing the carotid sinuses increases MSNA more remarkably during expiration than inspiration [10], thus demonstrating that respiration can modulate the baroreflex control of MSNA.…”

Autonomic mechanisms associated with heart rate and vasoconstrictor reserves

“…Vagal baroreflex sensitivity (BRS) was assessed via the sequence method [37]. The WinCPRS software was used to automatically detect potential sequences between the RRI and SAP signals.…”

“…The WinCPRS software was used to automatically detect potential sequences between the RRI and SAP signals. A valid sequence was defined as at least three sequentially decreasing SAPs with at least a 1 mmHg change per beat and associated RRIs with at least a 4 ms change per beat [37]. Baroreflex gain was then estimated via linear regression [37].…”

Strength training does not affect vagal?cardiac control or cardiovagal baroreflex sensitivity in young healthy subjects

“…Within this same time range, we analyzed sequences of three or more increasing systolic pressures (increasing by at least 1 mmHg) and R-R intervals (increasing by at least 4 ms) with linear regression analysis. Only sequences with correlation coefficients of at least 0.8 were included for statistical comparison (Rothlisberger et al 2003).…”