Muscle sympathetic nerve activity (MSNA) increases during isometric exercise via increased firing of low-threshold action potentials (AP), recruitment of larger, higher-threshold APs, and synaptic delay modifications. Recent work found that women with post-traumatic stress disorder (PTSD) demonstrate exaggerated early-onset MSNA responses to exercise; however, it is unclear how PTSD affects AP recruitment patterns during fatiguing exercise. We hypothesized that women with PTSD (n?=?11, 43 [11] [SD] years) would exhibit exaggerated sympathetic neural recruitment compared to women without PTSD (controls; n?=?13, 40 [8] years). MSNA and AP discharge patterns (via microneurography and a continuous wavelet transform) were measured during 1 min of baseline, isometric handgrip exercise (IHG) to fatigue, 2 min of post-exercise circulatory occlusion (PECO), and 3 min of recovery. Women with PTSD were unable to increase AP content per burst compared to controls throughout IHG and PECO (main effect of group: P?=?0.026). Furthermore, relative to controls, women with PTSD recruited fewer AP clusters per burst during the first (controls: ?1.3 [1.2] vs. PTSD: ??0.2 [0.8]; P?=?0.016) and second minute (controls: ?1.2 [1.1] vs. PTSD: ??0.1 [0.8]; P?=?0.022) of PECO, and fewer subpopulations of larger, previously silent axons during the first (controls: ?5 [4] vs. PTSD: ?1 [2]; P?=?0.020) and second minute (controls: ?4 [2] vs. PTSD: ?1 [2]; P?=?0.021) of PECO. Conversely, PTSD did not modify the AP cluster size–latency relationship during baseline, the end of IHG, or PECO (all P?=?0.658–0.745). Collectively, these data indicate that women with PTSD demonstrate inherent impairments in the fundamental neural coding patterns elicited by the sympathetic nervous system during IHG and exercise pressor reflex activation.
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