Reducing Oxidative Stress Fails to Improve Blood Pressure Dysregulation in Young Adults with Posttraumatic Stress Disorder

Posttraumatic stress disorder (PTSD) is a debilitating psychiatric condition linked to an increased risk of cardiovascular disease (CVD). Impaired cardiovagal baroreflex sensitivity (cBRS)—the ability of heart rate (HR) to inversely respond to changes in systolic blood pressure (SBP)—is often lower in individuals with PTSD compared to non-PTSD controls and is linked to elevated CVD risk. Elevated oxidative stress in PTSD may impair cBRS by damaging autonomic pathways or reducing nitric oxide bioavailability, disrupting heart rate regulation. We hypothesize that acute antioxidant (AO) supplementation, aimed at reducing oxidative stress, can improve acute blood pressure control in young individuals with PTSD. METHODS: Twelve young adults with PTSD (24 ± 5 years; 12 females/0 males; PTSD Checklist-5: 43 ± 14) and twelve without PTSD (25 ± 5 years; 12 females/0 males; PCL-5: 9 ± 7) participated in this study. Acute blood pressure control was evaluated by measuring cardiovagal baroreflex sensitivity (cBRS) during Phase II and Phase IV of a 15-second Valsalva maneuver (mouth pressure = 40 millimeters of mercury (mmHg). cBRS slopes were calculated as the relationship between changes in systolic blood pressure (SBP) and inverse changes in heart rate (R-R intervals) during (Phase II) and after (Phase IV) the maneuver, with a correlation threshold (r > 0.7). To explore the role of oxidative stress in modulating cBRS, whole blood superoxide production was measured following acute antioxidant (AO) supplementation (1000 milligrams (mg) of Vitamin C, 800 international units of Vitamin E, 600 mg Alpha-Lipoic Acid) or placebo (microcrystalline cellulose). RESULTS: The PTSD group exhibited significantly higher oxidative stress (PTSD: 28853 ± 8138 arbitrary units (AU); non-PTSD: 18008 ± 7728 AU; p < 0.01) and lower Phase IV cBRS (PTSD: 6.1 ± 3.7 mmHG per millisecond (mmHg·ms - 1 ); non-PTSD: 10.1 ± 3.7 mmHg·ms - 1 ; p < 0.01) compared to the non-PTSD group. However, no significant difference was observed in Phase II cBRS (PTSD: 6.1 ± 2.0 mmHg·ms - 1 ; non-PTSD: 8.0 ± 3.9 mmHg·ms - 1 ; p = 0.15). Acute antioxidant (AO) supplementation reduced oxidative stress, eliminating group differences (PTSD: 21031 ± 13114 AU; non-PTSD: 24678 ± 17417 AU; p = 0.57). Despite this, AO supplementation did not improve Phase IV cBRS, as no significant group x condition interaction effect was observed (AO condition: PTSD: 7.0 ± 3.3 mmHg·ms - 1 ; non-PTSD: 11.9 ± 4.2 mmHg·ms - 1 ). CONCLUSION: This study demonstrated that reducing oxidative stress through acute antioxidant supplementation did not significantly improve acute blood pressure control, as indicated by the lack of change in heart rate responses to rising systolic blood pressure (Phase IV cBRS). These findings suggest that impaired blood pressure regulation in individuals with PTSD may stem from non-redox mechanisms or require a more sustained intervention to effectively lower oxidative stress and enhance cardiovascular function. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.