Date of Award
Master of Science (MS)
Heart rate variability (HRV) and cortisol are well-established biomarkers of the human stress response system. As such, their respective relationships with trait anxiety have been studied. As high HRV indicates healthy emotion regulation while low HRV signifies poor emotion regulation, a negative relationship between HRV and anxiety is found in the literature. Conversely, cortisol both prepares the body for stress and helps it to recover and current studies yield mixed results on its relationship with anxiety. While the link between vagal activity, which mediates HRV, and the HPA-axis, which outputs cortisol, is generally assumed, few studies have examined these biomarkers in the same study design, and specifically how this relationship, if present, manifests over time or in relation to anxiety. Importantly, studying these biomarkers together provides a clearer depiction of the stress response and may better inform treatments aimed at improving biological outcomes in clinical samples, such as highly anxious individuals. Using archival data from 438 mid-life adults, the impetus of the present study was to examine the relationship between cortisol and HRV over time (pre-, during-, post- cognitive and physical stressors) using standard, literature-defined metrics to quantify increased/decreased cortisol and HRV in response to stress. Additionally, we used latent growth mixture modeling (LGMM) to examine trajectories of cortisol and HRV over time in response to stress. Finally, we tested the relationship between all measures of cortisol and HRV to anxiety. Results revealed that in response to a cognitive stressor, higher HRV reactivity was associated with higher cortisol reactivity. LGMM analyses identified differential cortisol and HRV trajectories. Despite this and contrary to hypothesis, we did not find support for a relationship between anxiety and HRV and cortisol metrics, including differential trajectories of change, in the full sample. In exploratory analyses, we did find that individuals with greater anxiety exhibited less cortisol reactivity to the cognitive stressor when we restricted our analysis to a “clinically-detectable” anxious sub-group. Results hold clinical relevance in that targeting moment-to-moment adaption to stress via HRV may help promote more adaptive cortisol responding via changing cortisol output. However, more research is needed to better understand this relationship.