Electronic Thesis and Dissertation Repository


Doctor of Philosophy




Dr. J. Kevin Shoemaker


The overall objectives of the current dissertation were to 1) establish the neural coding principles employed by the sympathetic nervous system (SNS) in response to acute physiological stress; and 2) to determine the various mechanisms of control underlying these sympathetic neural recruitment strategies. This research tested the working hypothesis that efferent post-ganglionic muscle sympathetic nerve activity exhibits neural coding patterns reflecting increased firing of lower-threshold axons, recruitment of latent sub-populations of higher-threshold axons, as well as malleable synaptic delays, and further, that these strategies are governed by factors such as reflex-specificity, stress severity, perception of effort or stress, age, and cardiovascular disease. Specifically, we utilized a novel signal processing approach to study sympathetic action potential discharge patterning during periods of acute reflex-mediated sympathoexcitation. Overall, these studies support the working hypothesis and confirm that neural coding principles operate within the SNS. Specifically, in response to acute homeostatic perturbation, the SNS has options to increase the firing rate of already-active, lower-threshold axons, recruit sub-populations of previously silent (i.e., not present at baseline), larger-sized and faster conducting sympathetic axons, as well as modify acutely synaptic delays. Study 1 demonstrated that the ability to recruit latent neural sub-populations represents a fixed, reflex-independent recruitment strategy, as this pattern was observed during chemoreflex- and baroreflex-mediated sympathoexcitation. In turn, this option appears reserved for severe stress scenarios. Furthermore, study 2 suggests that central, perceptual features may play a specific role in modifying the synaptic delay aspect of efferent discharge timing, whereas peripheral-reflex mechanisms mediate the recruitment of latent axons. Study 3 demonstrates that, while the ability to acutely modify synaptic delays appears preserved, the ability to increase firing frequency of already-active axons, and importantly, the capacity of the SNS to recruit latent sub-populations of higher-threshold axons are reduced with healthy aging and perhaps lost altogether with cardiovascular disease. Finally, study 4 suggests that the lack of ventilation itself, rather than the ever-increasing chemical drive, mediates the robust sympathetic neural recruitment observed during apnea. In conclusion, the series of studies contained herein confirm the presence of neural coding patterns in human efferent post-ganglionic sympathetic nerve activity.