Output vs. outcome: neurovascular transduction at rest

Abstract

Microneurography techniques that allow the direct recording of sympathetic nerve activity (SNA) in humans have been used to examine the neural control of cardiovascular regulation in a wide variety of populations. In the context of vascular control, SNA directed at the vasculature within skeletal muscle (muscle SNA; MSNA) occurs in a ‘bursting’ pattern, which is typically quantified as burst frequency (in bursts per minute), burst incidence (in bursts per 100 heart beats), burst amplitude (in arbitrary units) and total activity (frequency × amplitude). Each burst of activity represents the summation of multiple action potentials from multiple neurons, resulting in the downstream release of vasoactive neurotransmitters. However, due to the irregular bursting pattern and relatively low frequency of basal MSNA typically observed in in young, healthy individuals (e.g. 20–30 bursts (100 heart beats)−1; Steinback et al. 2010; Vianna et al. 2012; Fairfax et al. 2013a,b2013b; Tan et al. 2013), the standard metrics of activity are typically averaged over time (minutes) at rest or during the steady state following an initiating stimulus. Due to this limitation, little information is currently available regarding the specific vascular effects of ongoing MSNA (i.e. on a burst-by-burst basis) or the time course of activation in response to various stimuli. A related series of publications, including the recent work published in The Journal of Physiology by Fairfax et al. (2013a), have attempted to address these issues using an adapted approach to measure neurovascular ‘transduction’. The authors have built upon an earlier description of transduction by Wallin & Nerhed (1982) to describe the functional effect of a given burst (or group of bursts) of MSNA on the cardiovascular system. They achieved this by using burst-triggered averaging to define the time course and magnitude of cardiovascular responses (i.e. mean arterial pressure, vascular conductance and cardiac output) over 15 cardiac cycles immediately following a spontaneous sympathetic burst. Categorization of bursts by size and frequency (clusters) was used to evaluate the influence of variations in total MSNA. Furthermore, analysis of the time course of responses following cardiac cycles without bursts and sampling of white noise during random cardiac cycles (with and without bursts) acted as a control analysis. Similar to previous accounts (Wallin & Nerhed, 1982; Vianna et al. 2012; Fairfax et al. 2013b), the authors describe a peak vascular response graded in proportion to the total activity, which occurs approximately five to eight cardiac cycles following a given burst or group of bursts (Fairfax et al. 2013a). In the most recent publication in this series, appearing in The Journal of Physiology, the authors expand upon their previous findings to evaluate the direct contribution of α-receptor-mediated pathways to basal transduction and regional differentiation between upper and lower limbs (Fairfax et al. 2013a).