Sympathetic drive is modulated by central chemoreceptor activation.

To determine the effects of central chemoreceptor stimulation upon sympathetic modulation while minimizing baroreceptor influences, we performed a single-blind, counter-balanced, placebo-controlled trial of a modified hypercapnic/hyperoxic rebreathe protocol stimulus to activate the central chemoreflex. Muscle sympathetic nerve activity (MSNA), heart rate, blood pressure, and ventilation were recorded dynamically as subjects transitioned from a hypocapnia to hypercapnia state. The stages of data recording were defined as hyperventilation (HyV), pre-threshold (PreT) and post-threshold (PostT), with threshold being defined as the point of non-linear deviation in ventilation. The changes in MSNA (-4.2+/-52.4 arbitrary units (AU) vs. 245.0+/-84.0AU) and burst count (-0.1+/-0.7 bursts/segment vs. 2.5+/-1.7 bursts/segment) were significantly different between control and rebreathe for the HyV to PreT step. There was also a significant difference for PreT to PostT for total MSNA (3.9+/-65.4AU vs. 183.7+/-104.2AU). In a hypercapnic/hyperoxic state, the central chemoreceptors modulate sympathetic activity below the chemoreflex threshold independently of the baroreceptors, possibly contributing to basal autonomic/sympathetic tone. Central chemoreceptors also appear to play a significant role in sympathetic modulation after the threshold.