Sympathetic Neural Outflow and Chemoreflex Sensitivity Are Related to Spontaneous Breathing Rate in Normal Men

Abstract

Abstract-Respiration contributes importantly to short-term modulation of sympathetic nerve activity. However, the relationship between spontaneous breathing rate, chemoreflex function, and direct measures of sympathetic traffic in healthy humans has not been studied previously. We tested the hypothesis that muscle sympathetic nerve activity and chemoreflex sensitivity are linked independently to respiratory rate in normal subjects. We studied 69 normal male subjects aged 29.6Ϯ8.1 years. Subjects were subdivided according to the tertiles of respiratory rate distributions. Mean respiration rate was 10.6 breaths/min in the first tertile, 14.8 breaths/min in the second tertile, and 18.0 breaths/min in the third tertile. Subjects from the third tertile (faster respiratory rate) had greater sympathetic activity than subjects from the first tertile (slower respiratory rate; 29Ϯ3 versus 17Ϯ2 bursts/min; PϽ0.001).Stepwise multiple linear regression analysis revealed that only respiratory rate was linked independently to sympathetic activity (rϭ0.42; PϽ0.001). In comparison to subjects with slow respiratory rate, subjects with fast respiratory rate had greater increases in minute ventilation during both hypercapnia (7.3Ϯ0.8 versus 3.2Ϯ1.0 L/min; Pϭ0.005) and hypoxia (5.7Ϯ0.8 versus 2.4Ϯ0.7 L/min; Pϭ0.007). Muscle sympathetic nerve activity and chemoreflex sensitivity are linked to spontaneous respiratory rate in normal humans. Faster respiratory rate is associated with higher levels of sympathetic traffic and potentiated responses to hypoxia and hypercapnia. Spontaneous breathing frequency, central sympathetic outflow, and chemoreflex sensitivity exhibit significant and hitherto unrecognized interactions in the modulation of neural circulatory control. Key Words: autonomic nervous system Ⅲ sympathetic nervous system Ⅲ blood pressure Ⅲ heart rate T he sympathetic nervous system plays a central role in cardiovascular regulation in both health and disease. Sympathetic activation has been implicated in the pathogenesis of hypertension, obstructive sleep apnea, and congestive heart failure. [1][2][3][4] In healthy humans, muscle sympathetic nervous activity (MSNA) varies widely across subjects but is relatively reproducible within the same individual. 5,6 The substantial between-subject variance in sympathetic traffic can be only partially explained by age, body mass index, blood pressure, reflex mechanisms, and genetic factors. [7][8][9][10] Several studies have shown that respiration contributes importantly to short-term modulation of sympathetic nerve traffic. 11-15 MSNA increases at end expiration and decreases to minimum levels at end inspiration. 11 Little is known about the contribution of spontaneous respiratory rate to baseline MSNA burst frequency. It has been proposed that respiration affects timing but not tonic levels of sympathetic nervous activity. 12 However, in congestive heart failure, MSNA is related to spontaneous respiratory rate. Patients with rapid breathing, a pattern commonly observed in heart failure,...

Dynamic time-varying analysis of heart rate and blood pressure variability in cats exposed to short-term chronic intermittent hypoxia

“…It is worthwhile to mention that recent reports show that reduced overall HRV and increased LF spectral power are associated with increased mortality (53), hypertension (36), and sympathetic overactivity (12,36). Moreover, studies performed in humans with OSA detected an increased peripheral chemoreflex drive (31,32) and reduced HRV with LF predominance (29). Interestingly, Narkiewicz et al (29) reported that patients with mild OSA presented decreased overall HRV without changes in BPV, while patients with moderate to severe OSA showed increased BPV.…”

Reduction of Sympathetic Nervous Activity With Device‐Guided Breathing

“…One of the hypotheses raised would be the reduction of nervous sympathetic activity: reductions in respiratory frequency of about 6 to 10 breaths per minute, as they increase tidal volume, would stimulate cardiopulmonary stretch receptors, which conversely would reduce the discharge of efferent sympathetic fibers, resulting in decreased systemic vascular resistance and consequent reduction of arterial pressure. 9 However, such a hypothesis has not yet been fully confirmed in hypertensive patients who regularly perform this type of intervention. …”

Correlations between the Poincaré Plot and Conventional Heart Rate Variability Parameters Assessed during Paced Breathing

“…The change in RR intervals caused by breathing is known as respiratory sinus arrhythmia, which is regulated by breathing phase, depth, and rate [14][15][16]. The variation of RR intervals with respiration was suggested as a measure of the autonomic nervous system function in the 1970s, and it has been evaluated by different methods with particular focus on the spectral approach to HRV, but never with an analysis of Poincaré plots [14,[17][18][19] …”