Abstract

The upright posture strengthens the coupling between heart period (HP) and systolic arterial pressure (SAP) consistently with a greater contribution of the arterial baroreflex to cardiac control, while paradoxically decreasing cardiac baroreflex sensitivity (cBRS). To investigate the physiological mechanisms that mediate the coupling between HP and SAP in response to different postures, we analyzed the cross-correlation functions between low-frequency HP and SAP fluctuations and estimated cBRS with the sequence technique in healthy male subjects during passive head-up tilt test (HUTT, n = 58), during supine wakefulness, supine slow-wave sleep (SWS), and in the seated and active standing positions (n = 8), and during progressive loss of 1 L blood (n = 8) to decrease central venous pressure in the supine position. HUTT, SWS, the seated, and the standing positions, but not blood loss, entailed significant increases in the positive correlation between HP and the previous SAP values, which is the expected result of arterial baroreflex control, compared with baseline recordings in the supine position during wakefulness. These increases were mirrored by increases in the low-frequency variability of SAP in each condition but SWS. cBRS decreased significantly during HUTT, in the seated and standing positions, and after blood loss compared with baseline during wakefulness. These decreases were mirrored by decreases in the RMSSD index, which reflects cardiac vagal modulation. These results support the view that the cBRS decrease associated with the upright posture is a byproduct of decreased cardiac vagal modulation, triggered by the arterial baroreflex in response to central hypovolemia. Conversely, the greater baroreflex contribution to cardiac control associated with upright posture may be explained, at least in part, by enhanced fluctuations of SAP, which elicit a more effective entrainment of HP fluctuations by the arterial baroreflex. These SAP fluctuations may result from enhanced fluctuations of vascular resistance specific to the upright posture, and not be driven by the accompanying central hypovolemia.

Highlights

  • The upright posture challenges blood pressure and results in blood pooling and increased capillary ultrafiltration below the heart

  • ANOVA: P = 0.877 for DAP, P = 0.051 for SAP, P < 0.001 for HP and central venous pressure (CVP). *, †, and ‡: P < 0.05 vs. BASELINE, vs. BL 0.33 L, and vs. BL 0.67 L, respectively (t-test). This view: with the CCF analysis, a relatively simple timedomain technique, we found that a range of passive (HUTT) and active upright postures robustly entailed a positive correlation between HP and the previous values of SAP, which is consistent with arterial baroreflex control of HP, compared to the supine position

  • In spite of its limitations, the present results demonstrate that the CCF analysis shows excellent sensitivity to the posture-related increase in the contribution of the arterial baroreflex to cardiac control: this increase was detected in 91.4% of subjects during HUTT, significantly discriminated HUTT from the lying supine position (Figure 2), and occurred in a graded fashion from the lying supine position to the seated and active standing positions (Figure 4), which are known to elicit different cardiovascular responses (Eckberg, 1980)

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Summary

Introduction

The upright posture challenges blood pressure and results in blood pooling and increased capillary ultrafiltration below the heart. The analysis of spontaneous cardiovascular fluctuations, performed with a range of techniques designed to detect causality based on information theory, indicates that the upright posture increases the contribution of the arterial baroreflex to cardiac control (Nollo et al, 2005; Porta et al, 2011, 2014, 2015; Faes et al, 2013; Zamunér et al, 2015). The cardiac baroreflex sensitivity (cBRS) estimated based on spontaneous fluctuations decreases in the upright position (Steptoe and Vögele, 1990; O’Leary et al, 2003; Nollo et al, 2005; Faes et al, 2013; Schwartz et al, 2013; Zamunér et al, 2015). The physiological mechanisms underlying these posture-related changes in cardiovascular coupling still remain unclear

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