Abstract

Post‐traumatic stress disorder (PTSD) is a psychiatric illness that is more prevalent in women than men, and there is growing evidence suggesting a clear link between PTSD and future development of cardiovascular disease. The underlying mechanisms are unclear, but enhanced sympatheticreactivity to daily stressors may be involved. We hypothesized that PTSD women would have an augmented vasomotor sympathetic response to static exercise. We measured heart rate (HR), blood pressure (BP), and muscle sympathetic nerve activity (MSNA) in 12 female patients with PTSD and 8 healthy women (controls) during static handgrip (SHG) exercise to fatigue at 40% of maximal voluntary contraction (MVC) force followed by 2 min of postexercise circulatory arrest (PECA) and 3 min of recovery. The total SHG time was divided evenly into five stages. Age, body mass index, and body surface area were not different between groups. MVC and the time to fatigue during SHG did not differ between patients and controls (P>0.05). MSNA burst frequency (BF) in response to SHG was greater in patients than controls (timexgroup interaction P=0.03, time P=0.0001, group P=0.04), but not during PECA. During the early stages of SHG, PTSD patients showed greater MSNA BF compared to controls [stage 1: 40±5 (SE) vs.19±7 bursts/min; P=0.02, stage 2: 45±6 vs.25±7; P=0.03, stage 3: 55±6 vs.30±7; P=0.02). MSNA BF responses during stage 4 and 5 were not different between groups (P=0.09 and P=0.1, respectively). Similarly, PTSD patients showed greater systolic blood pressure (SBP) compared to controls during early stages of SHG (stage 1: 144±4 vs.129±5 mmHg; P=0.02, stage 2: 149±4 vs.132±5; P=0.03, stage 3: 159±6 vs.138±7; P=0.03, stage 4: 166±6 vs.143±7; P=0.04) but not in the last stage (at fatigue; P=0.2). SBP was not different between groups during PECA and recovery. Diastolic BP and HR were progressively increased during SHG, reached peak at the last stage, and were comparable between groups. These results suggest that women with PTSD have an augmented exercise pressor response, which may be attributed to enhanced mechano‐ rather than metabo‐reflexes. However, the actual role of the muscle reflex in cardiovascular risk in PTSD remains to be elucidated.Support or Funding InformationThis study is supported by Harry S. Moss Heart Trust research funding STU 082016‐057This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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