Sympathetic neurovascular transduction following acute hypoxia.

Abstract

Following an acute exposure to hypoxia, sympathetic nerve activity remains elevated. However, this elevated sympathetic nerve activity does not elicit a parallel increase in vascular resistance suggesting a blunted sympathetic signaling [i.e. blunted sympathetic neurovascular transduction (sNVT)]. Therefore, we sought to quantify spontaneous sympathetic bursts and related changes in total peripheral resistance following hypoxic exposure. We hypothesized that following hypoxia sNVT would be blunted. Nine healthy participants (n = 6 men; mean age 25 ± 2years) were recruited. We collected data on muscle sympathetic nerve activity (MSNA) using microneurography and beat-by-beat total peripheral resistance (TPR) via finger photoplethysmography at baseline, during acute hypoxia and during two periods of recovery (recovery period 1, 0-10min post hypoxia; recovery period 2, 10-20min post hypoxia). MSNA burst sequences (i.e. singlets, doublets, triplets and quads+) were identified and coupled to changes in TPR over 15 cardiac cycles as an index of sNVT for burst sequences. A sNVT slope for each participant was calculated from the slope of the relationship between TPR plotted against normalized burst amplitude. The sNVT slope was blunted during hypoxia [Δ 0.0044 ± 0.0014 (mmHg/L/min)/(a.u.)], but unchanged following termination of hypoxia [recovery 1, Δ 0.031 ± 0.0019 (mmHg/L/min)/(a.u.); recovery 2, Δ 0.0038 ± 0.0014 (mmHg/L/min)/(a.u.) compared to baseline (Δ 0.038 ± 0.0015 (L/min/mmHg)/(a.u.)] (main effect of group p = 0.012). Contrary to our hypothesis, we have demonstrated that systemic sNVT is unchanged following hypoxia in young healthy adults.