Role of Respiratory Motor Output in Within-Breath Modulation of Muscle Sympathetic Nerve Activity in Humans

Abstract

Abstract-We measured muscle sympathetic nerve activity (MSNA, peroneal microneurography) in 5 healthy humans under conditions of matched tidal volume, breathing frequency, and end-tidal CO 2 , but varying respiratory motor output as follows: (1) passive positive pressure mechanical ventilation, (2) voluntary hyperventilation, (3) assisted mechanical ventilation that required the subject to generate -2.5 cm H 2 O to trigger each positive pressure breath, and (4) added inspiratory resistance. Spectral analyses showed marked respiratory periodicities in MSNA; however, the amplitude of the peak power was not changed with changing inspiratory effort. Time domain analyses showed that maximum MSNA always occurred at end expiration (25% to 30% of total activity) and minimum activity at end inspiration (2% to 3% of total activity), and the amplitude of the variation was not different among conditions despite marked changes in respiratory motor output. Furthermore, qualitative changes in intrathoracic pressure were without influence on the respiratory modulation of MSNA. In all conditions, within-breath changes in MSNA were inversely related to small changes in diastolic pressure (1 to 3 mm Hg), suggesting that respiratory rhythmicity in MSNA was secondary to loading/unloading of carotid sinus baroreceptors. Furthermore, at any given diastolic pressure, within-breath MSNA varied inversely with lung volume, demonstrating an additional influence of lung inflation feedback on sympathetic discharge. Our data provide evidence against a significant effect of respiratory motor output on the within-breath modulation of MSNA and suggest that feedback from baroreceptors and pulmonary stretch receptors are the dominant determinants of the respiratory modulation of MSNA in the intact human. (Circ Res. 1999;85:457-469.)Key Words: autonomic nervous system Ⅲ cardiorespiratory interaction Ⅲ positive pressure ventilation T he independent influence of the respiratory rhythm generator on the timing of sympathetic outflow has been studied using reduced preparations in which peripheral reflex mechanisms were eliminated by vagotomy and/or sinoaortic denervation. In these deafferented animal preparations, sympathetic neurons fire mainly during inspiration (ie, in synchrony with phrenic discharge), with their minimum activity occurring during expiration. 1,2 The close temporal relationship between phrenic discharge and sympathetic activity recorded in anesthetized, paralyzed, and vagotomized animals has led to the hypothesis that the 2 neural outputs either arise from the same brain stem neurons or are driven by a common oscillator. 1,3 However, in the intact human, sympathetic outflow to skeletal muscle (muscle sympathetic nerve activity; MSNA) declines during inspiration, reaching its nadir at end inspiration/early expiration, and then rises, reaching its peak at end expiration. 4,5 The influence of central respiratory motor output on the within-breath modulation of MSNA has not been studied in humans.The purpose of the present study was to ex...

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

“…Therefore, even though it was recently shown that indexes describing HP variability time asymmetry provide non-redundant information compared with symbolic indexes [39], a certain degree of correlation can be expected between time asymmetry and symbolic indexes when symbolic analysis is gated by respiration. In addition, during PRESY, the presence of 0V patterns in HP variability increased and that of patterns more variable than the 0V ones decreased more evidently during EXP period ( figure 4a,d,g) than during INSP one ( figure 3a,d,g), thus suggesting that the increase of sympathetic modulation and the inhibition of vagal activity was facilitated during the EXP phase [1][2][3]. Similarly, during PRESY, the increase of 2UV% in MSNA variability was significant only during the EXP phase ( figure 4l versus figure 3l).…”

Self-Regulation of Breathing as a Primary Treatment for Anxiety

“…It has been established that during respiration, inspiration inhibits sympathetic nervous system activity (CzyzykKrzeska and Trzebski 1990; Dempsey et al 2002;Seals et al 1990;St Croix et al 1999). In fact, slow-deep breathing has been shown to cause near-complete sympathoinhibition (Seals et al 1990).…”

“…In fact, slow-deep breathing has been shown to cause near-complete sympathoinhibition (Seals et al 1990). This sympathoinhibition varies inversely with lung volume, with high lung volumes leading to the most inhibition (St. Croix et al 1999). Most of this sympathoinhibition also occurs in the second half of inspiration.…”

Estrogen Replacement Therapy Improves Baroreflex Regulation of Vascular Sympathetic Outflow in Postmenopausal Women

“…Arterial pressures, R-R intervals, and sympathetic activity were averaged for each 3-mm Hg increment in pressure, and linear relations between variables were determined. Moment-to-moment changes in resting arterial pressure and auto-nomic outflow are influenced by a number of physiological inputs, including beat-to-beat changes in stroke volume, 13 ventilation, 14 central respiratory drive, 15 neuronal function, 16 and cardiopulmonary and arterial baroreflexes. 14 Thus, our index encompasses all inputs to autonomic activity and arterial pressure under resting conditions, providing broad insight into resting arterial pressure regulation.…”