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The Influence Of Post-traumatic Stress Disorder On The Exercise Pressor Response: 2161
Abstract   Peer reviewed

The Influence Of Post-traumatic Stress Disorder On The Exercise Pressor Response: 2161

Jeremy K. Alpenglow, Jarred J. Iacovelli, Kanokwan Bunsawat and D. Walter Wray
Medicine and science in sports and exercise, Vol.58(10S), 2161
10/2026
DOI: 10.1249/01.mss.0001265616.39598.c2

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Abstract

INTRODUCTION: Patients with post-traumatic stress disorder (PTSD) have increased cardiovascular disease (CVD) risk, which may be underpinned by exaggerated cardiovascular responses during stress, including exercise. PTSD-mediated neurological changes may contribute to an exaggerated exercise pressor response (EPR), a characteristic of other populations with CVD. Some data suggests elevated EPR during static handgrip exercise (SHG) in PTSD, but evidence is limited and the relationship between EPR and PTSD symptom severity has not been explored. PURPOSE: To determine the influence of PTSD on EPR and investigate the relationship between EPR and PTSD symptom severity. METHODS: In PTSD (n = 10, 5M/5F, 32±8 yrs) and CON subjects (n = 10, 5M/5F, 32±1 yrs) systolic blood pressure (SBP, Finapres) was determined at rest and in 30-second bins during static SHG (3 min, 40% MVC), followed by post-exercise-circulatory-occlusion (PECO, 2 min). PTSD symptom severity was measured via PTSD checklist (PCL-5). 2-way repeated measures analysis of variance was used to compare SBP responses (ΔSBP) between groups. Spearman’s ranked correlation coefficient was used to assess relationships between ΔSBP and PCL-5 scores. SUMMARY OF RESULTS: Resting SBP was not statistically different between PTSD vs. CON (119±10 vs.113±12 mmHg; P=0.208). There was a significant group effect for ΔSBP across SHG and PECO (P=0.005), specifically at the onset (13±7 vs. 5±4 mmHg; P=0.008) and end (42±11 vs.30±10 mmHg; P=0.012) of SHG and the end of PECO (37±12 vs. 26±18 mmHg; P=0.028). There were significant and positive relationships between ΔSBP and PCL-5 scores at the onset (r=0.547, P=0.013) and end of SHG (r=0.522, P=0.018), and the end of PECO (r=0.498. P=0.025). CONCLUSION: These data demonstrate elevated EPR in PTSD throughout SHG and PECO and may be related to PTSD-mediated neurological changes, reflected by PCL-5 scores. Exaggerated EPR may be an important factor contributing to increased CVD risk in these patients and the relationship between PTSD symptom severity and EPR suggests the possibility of reducing CVD risk by interventions aimed at reducing PTSD symptom severity.

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