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. 2013 Jun 15;304(12):H1615-23.
doi: 10.1152/ajpheart.00112.2013. Epub 2013 Apr 12.

Respiratory influences on muscle sympathetic nerve activity and vascular conductance in the steady state

Jacqueline K Limberg  1 , Barbara J Morgan, William G Schrage, Jerome A Dempsey
Affiliations

Respiratory influences on muscle sympathetic nerve activity and vascular conductance in the steady state

Jacqueline K Limberg et al. Am J Physiol Heart Circ Physiol. .

Abstract

In patients with hypertension, volitional slowing of the respiratory rate has been purported to reduce arterial pressure via withdrawal of sympathetic tone. We examined the effects of paced breathing at 7, 14, and 21 breaths/min, with reciprocal changes in tidal volume, on muscle sympathetic nerve activity, forearm blood flow, forearm vascular conductance, and blood pressure in 21 men and women, 8 of whom had modest elevations in systemic arterial pressure. These alterations in breathing frequency and volume did not affect steady-state levels of sympathetic activity, blood flow, vascular conductance, or blood pressure (all P > 0.05), even though they had the expected effect on sympathetic activity within breaths (i.e., increased modulation during low-frequency/high-tidal volume breathing) (P < 0.001). These findings were consistent across subjects with widely varied baseline levels of sympathetic activity (4-fold), mean arterial pressure (78-110 mmHg), and vascular conductance (15-fold), and those who became hypocapnic during paced breathing vs. those who maintained normocapnia. These findings challenge the notion that slow, deep breathing lowers arterial pressure by suppressing steady-state sympathetic outflow.

Keywords: blood pressure; hypertension; respiration.

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Figures

Fig. 1.
Fig. 1.
Original polygraph records showing cardiorespiratory responses to a voluntary increase and decrease in breathing frequency (fB) [with corresponding decrease and increase in tidal volume (VT)] in a representative subject. In this example, steady-state values for muscle sympathetic nerve activity (MSNA) burst frequency remained unchanged over the range of fB and VT (39, 41, and 38 bursts/min for spontaneous breathing, 7 breaths/min, and 21 breaths/min). PetCO2, end-tidal CO2 tension.
Fig. 2.
Fig. 2.
A: MSNA power spectra during spontaneous breathing and voluntary decreases and increases in fB with reciprocal changes in VT in one subject. Note that power at the respiratory frequency was greatly increased by slowing fB to 7 breaths/min and diminished by increasing fB to 21 breaths/min. B: mean values for power at the respiratory frequency in subjects divided into two groups: those with relatively high baseline MSNA (burst incidence >40%; filled bars) vs. those with relatively low baseline MSNA (burst incidence <40%; hatched bars). Two-way repeated-measures ANOVA revealed a significant main effect of frequency (P < 0.001) and a significant frequency-by-group interaction (P = 0.027). Sp1, initial spontaneous breathing period; Sp2, final spontaneous breathing period.
Fig. 3.
Fig. 3.
Effects of voluntary alterations in breathing pattern on MSNA expressed as burst frequency (A), burst incidence (B), and total minute activity (%baseline) (C) in individual subjects. In A–C, subjects are partitioned into two groups: those with MSNA burst incidence >40% (group mean indicated by filled circles and individual subjects by solid lines) and those with burst incidence <40% (open circles, dashed lines). Two-way repeated-measures ANOVA revealed no frequency-by-group interaction (P = 0.605–0.936).
Fig. 4.
Fig. 4.
Effects of voluntary alterations in breathing pattern on mean arterial pressure (A), forearm blood flow (B), and forearm vascular conductance (C) in individual subjects. In A–C, subjects are partitioned into two groups: those with MSNA burst incidence >40% (group mean indicated by filled circles and individual subjects by solid lines) and those with burst incidence <40% (open circles, dashed lines). There were no frequency-by-group interactions (P = 0.100–0.274).
Fig. 5.
Fig. 5.
Effects of voluntary alterations in breathing pattern on mean arterial pressure (MAP, A), forearm blood flow (B), and forearm vascular conductance (C) in individual subjects. In A–C, subjects are partitioned into two groups: those with mean arterial pressures greater than or equal to the median for the group (group mean indicated by filled circles and individual subjects by solid lines) and those with pressures less than the group median (open circles, dashed lines). Two-way repeated-measures ANOVA revealed no frequency-by-group interactions (P = 0.710–0.866).
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