Key result
Exposure to acute stress immediately increased heart rate and caused a delayed decrease in heart rate variability, with latent class modeling identifying a subgroup exhibiting an atypical increase in HRV associated with elevated anxiety.
Why the study?
Most studies have treated physiological acute stress responses as static entities, overlooking inter-individual variability in how physiological stress response trajectories unfold over time.
Does a laboratory acute stress induction manipulation alter dynamic heart rate and heart rate variability trajectories in healthy adult females?
Observational (n=78)
No
Does a laboratory acute stress induction manipulation alter dynamic heart rate and heart rate variability trajectories in healthy adult females?
Analyzing physiological stress responses as dynamic trajectories rather than static entities reveals latent subgroups, such as individuals with atypical HRV increases during stress who also exhibit higher baseline anxiety.
Atypical HRV rises during stress associate with higher anxiety; hypothesis-generating for dynamic trajectories as anxiety markers.
BACKGROUND: Acute stressors trigger an immediate physiological response, involving multiple intricating pathways. These adaptive physiological responses include, among other processes, an increase in heart rate (HR) and a decrease in heart rate variability (HRV). Despite substantial efforts, linking individual variability in physiological acute stress response patterns with related psychological constructs such as anxiety and depression remains challenging. Notably, the majority of studies to date treated physiological stress responses as static entities, overlooking putative inter-individual variability in the dynamics at which physiological acute stress response trajectories unfold over-time. METHODS: To address this gap, physiological responses (HR and HRV) were continuously recorded from 78 healthy adult female participants during an established 10-min-long laboratory acute stress induction manipulation. These physiological responses were separately quantified for three consecutive 3.3-min-long segments that together encompass the entire acute stress procedure, as well as for the 3.3-min-long segments immediately before and after stress. RESULTS: At the whole group level stress was found to immediately increase HR, while HRV showed a delayed decrease with a post-stress overshoot effect. Latent class modeling revealed subgroups with unique physiological response trajectories, including a subset of participants that exhibited an atypical increase in HRV during stress. These individuals also exhibited elevated anxiety levels. CONCLUSIONS: Results underscore the complexity of physiological responses to acute stress and suggest that a dynamic approach could contribute to our understanding of the interplay between physiological stress responses and related psychological constructs. Further research is needed to replicate these findings and explore putative implications for stress-related mental health conditions.
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Rosenblum et al. (2025) conducted an observational in Healthy adults (n=78). Maastricht Acute Stress Test (MAST) vs. Pre-stress baseline was evaluated on Heart rate (HR) and heart rate variability (HRV) dynamics across time points (p=<0.001). Exposure to acute stress immediately increased heart rate and caused a delayed decrease in heart rate variability, with latent class modeling identifying a subgroup exhibiting an atypical increase in HRV associated with elevated anxiety.
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