Heart rate reactivity to acute mental stress is associated with adiposity, carotid distensibility, sleep efficiency, and autonomic modulation in young men.

Acute mental stress (AMS) increases heart rate (HR) and blood pressure. Since obesity can impair the cardiovascular reactivity to AMS, a better understanding of the mechanisms involved in this response is needed. We aimed to evaluate the cardiovascular reactivity to AMS in young men with normal or excess body fat. We also assessed the association between cardiovascular reactivity to AMS and cardiovascular risk factors, including autonomic modulation, carotid artery distensibility, physical activity levels, and sleep efficiency. Sixty-six young men (26.1 ± 4.1 years old) underwent anthropometric and body fat assessment (dual-energy X-ray absorptiometry) and had right-carotid artery ultrasonography. Accelerometers assessed physical activity levels and sleep efficiency. AMS was induced through the Stroop color-word test while blood pressure, HR, and cardiac interval were measured. Analyses were performed in Normal and Excess fat groups divided by fat mass index (FMI). Continuous data was used for multiple linear regression analyses. An interaction between FMI and time for HR reactivity was observed. Cardiac interval variability analysis showed that only participants with normal fat displayed parasympathetic withdrawal during AMS (P < 0.05). Multiple linear regression analysis supported the role of adiposity and autonomic modulation in the HR reactivity to AMS and showed involvement of carotid distensibility and sleep efficiency (P < 0.05). Carotid distensibility was the only predictor for blood pressure reactivity (P < 0.05). Physical activity was not associated with AMS's cardiovascular reactivity. We conclude that increased adiposity is associated with reduced HR reactivity to AMS, which is possibly linked to an impaired parasympathetic withdrawal. Carotid distension and sleep efficiency seem to contribute to this response.