Impaired Sympathetic Neural Recruitment During Skeletal Muscle Metaboreflex Activation in Women with Posttraumatic Stress Disorder

Abstract

Posttraumatic stress disorder (PTSD) is a debilitating psychiatric disorder that is more prevalent in women than men and has been linked to an elevated risk of developing cardiovascular disease. Although the physiological mechanisms are unclear, it is thought that exaggerated neuro‐cardiovascular reactivity is partially responsible. Indeed, women with PTSD demonstrate exaggerated muscle sympathetic nerve activity (MSNA) responses at the onset of exercise. However, it is unknown whether PTSD modifies the underlying sympathetic action potentials (AP) coding patterns that comprise the integrated MSNA signal during fatiguing exercise in women. We therefore hypothesized that women with PTSD will exhibit exaggerated MSNA and AP recruitment compared to women without PTSD during fatiguing handgrip exercise. MSNA and AP discharge patterns (via microneurography and a continuous wavelet transform) were assessed in eleven women with PTSD (43±11 [SD] years) and thirteen women without PTSD (Controls; 40±8 years) during isometric handgrip exercise (IHG) to fatigue at 40% of maximal voluntary contraction (MVC) force, followed by 2 minutes of post‐exercise circulatory occlusion (PECO), and three minutes of recovery. The IHG time was divided equally into five stages. IHG duration (P=0.867) and MVC (P=0.226) were similar between both groups. PTSD did not modify the increase in MSNA and AP frequency or incidence during IHG and PECO (all group‐by‐stage interactions: P=0.294‐0.380). Conversely, throughout IHG and PECO, AP content per burst was greater in the Controls compared to women with PTSD (main effect of group: P=0.026). Furthermore, relative to Controls, women with PTSD were unable to increase the number of AP clusters per burst during the first (Controls: ∆1.3±1.2 vs. PTSD: ∆‐0.2±0.8 clusters/burst; P=0.016) and last minute (Controls: ∆1.2±1.1 vs. PTSD: ∆‐0.1±0.8 clusters/burst; P=0.022) of PECO, and recruited fewer subpopulations of previously silent axons during the first (Controls: ∆5±4 vs. PTSD: ∆1±2 clusters; P=0.020) and last minute (Controls: ∆4±2 vs. PTSD: ∆1±2 clusters; P=0.021) of PECO. Lastly, although an interaction effect was observed for the AP cluster size‐latency relationship during IHG and PECO (P=0.042), post‐hoc analyses revealed that PTSD did not modify this relationship (all P=0.658‐0.999). These data indicate that the central features of sympathetic outflow are impaired in women with PTSD during skeletal muscle metaboreflex activation.