Abstract
Depression is associated with altered cerebrovascular hemodynamics, including lower cerebral blood flow, higher cerebral pulsatility, and greater arterial stiffness. There is evidence that perceived stress may contribute to depressive symptomology, but it is unknown if stress may directly impact cerebrovascular hemodynamics. The purpose of this investigation was to examine associations among middle cerebral artery (MCA) hemodynamics, arterial stiffness, and perceived stress in young and middle-aged adults. It was hypothesized that individuals with higher reported social stress would have lower MCA mean velocity and higher MCA pulsatility and arterial stiffness. Methods: 168 adults (range 18-64 years; 40 ± 16 years; BMI 26.6 ± 4.6 kg/m2; n=88 females) underwent resting cerebrovascular measures and completed the self-reported perceived stress scale (PSS-10). Brachial blood pressure and carotid pulse pressure were assessed via oscillometric cuff and tonometry, respectively. Arterial stiffness was assessed as carotid-femoral pulse wave velocity (cfPWV) via tonometry and MCA mean velocity and pulsatility index were assessed via Transcranial Doppler. Results: The sample contained 4 adults with high (PSS score ≥27; mean, 28 ± 1), 38 adults with moderate (PSS score 14-26; mean, 17 ± 2), and 126 adults with low stress (PSS score <13; mean, 8 ± 3). Self-reported perceived stress was not significantly linearly associated with MCA mean velocity (r=-0.10), MCA Pulsatility Index (r=-0.08), or arterial stiffness (r=0.05). A secondary analysis comparing adults with moderate/high stress (n=42) to adults with low stress (n=126) revealed a significantly lower MCA mean velocity among moderate/high stress adults (p<0.05), however this difference was attenuated and no longer statistically significant after covarying for age. Conclusions: This data suggests that perceived stress 1) is not associated with altered cerebrovascular hemodynamics or arterial stiffness in our sample of generally healthy young and middle-aged adults, and 2) may not play a major role in altering cerebrovascular hemodynamics in the context of stress-related disorders (e.g., depression), however future research is required to directly test this hypothesis. Iowa State University College of Human Sciences Faculty Seed Grant. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
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