Influence of ventilation and hypocapnia on sympathetic nerve responses to hypoxia in normal humans

Abstract

The sympathetic response to hypoxia depends on the interaction between chemoreceptor stimulation (CRS) and the associated hyperventilation. We studied this interaction by measuring sympathetic nerve activity (SNA) to muscle in 13 normal subjects, while breathing room air, 14% O2, 10% O2, and 10% O2 with added CO2 to maintain isocapnia. Minute ventilation (VE) and blood pressure (BP) increased significantly more during isocapnic hypoxia (IHO) than hypocapnic hypoxia (HHO). In contrast, SNA increased more during HHO [40 +/- 10% (SE)] than during IHO (25 +/- 19%, P less than 0.05). To determine the reason for the lesser increase in SNA with IHO, 11 subjects underwent voluntary apnea during HHO and IHO. Apnea potentiated the SNA responses to IHO more than to HHO. SNA responses to IHO were 17 +/- 7% during breathing and 173 +/- 47% during apnea whereas SNA responses to HHO were 35 +/- 8% during breathing and 126 +/- 28% during apnea. During ventilation, the sympathoexcitation of IHO (compared with HHO) is suppressed, possibly for two reasons: 1) because of the inhibitory influence of activation of pulmonary afferents as a result of a greater increase in VE, and 2) because of the inhibitory influence of baroreceptor activation due to a greater rise in BP. Thus in humans, the ventilatory response to chemoreceptor stimulation predominates and restrains the sympathetic response. The SNA response to chemoreceptor stimulation represents the net effect of the excitatory influence of the chemoreflex and the inhibitory influence of pulmonary afferents and baroreceptor afferents.

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

“…Increased ventilation acts as a powerful restraint on the sympathetic response to chemoreflex stimulation. 14 Nevertheless, the increase in sympathetic activity in subjects with faster breathing rate was still comparable to that seen in subjects with slower breathing rate, despite the higher ventilation. Thus, potentiation of the chemoreflex response in subjects with faster breathing rates appears to affect both the ventilatory and sympathetic efferent limbs of the reflex.…”

“…The protocol used to determine chemoreflex responses to isocapnic hypoxia and hyperoxic hypercapnia was identical to that used in previous studies. 14,15 Subjects were exposed to a hypoxic gas mixture to induce peripheral chemoreflex activation (10% oxygen in nitrogen with carbon dioxide titrated to maintain isocapnia) and a hypercapnic gas mixture to induce central chemoreflex activation (7% oxygen/93% carbon dioxide). During hypoxic stimulation of peripheral chemoreceptors, perturbation of central chemoreceptors was minimized by the maintenance of isocapnia.…”

“…[7][8][9][10] Several studies have shown that respiration contributes importantly to short-term modulation of sympathetic nerve traffic. [11][12][13][14][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.…”

Carotid body function in heart failure

“…In fact, the augmented sympathetic drive occurs in the face of a potentiated ventilatory response that might be expected to attenuate the sympathetic response due to negative feedback from pulmonary afferents (Somers et al 1989). In addition, central input from the CB provides a tonic excitatory influence on sympathetic outflow in rabbits with established CHF since hyperoxia reduces resting sympathetic nerve activity in CHF but not sham animals (Sun et al 1999a), and selective CB denervation attenuates the elevated resting sympathetic nerve activity and plasma norepinephrine normally observed in CHF rabbits (Fig.…”

Obstructive sleep apnea syndrome: effect of respiratory events and arousal on pulse wave amplitude measured by photoplethysmography in NREM sleep

“…In previous studies, changes in PWA were measured by photoplethysmography in relation to arousals induced by acoustical stimulus in healthy subjects [6,10]. In sleeprelated breathing disorders, blood gas disturbances and other factors potentially further modulate activation-related autonomic activity [16,17] and could modify this cardiovascular response. If reliable changes in PWA could be detected in relation to obstructive sleep respiratory events, the photoplethysmography could become an interesting screening method for detecting respiratory events and for assessing sleep fragmentation in obstructive sleep apnea patients.…”