The Impact of Acute Psychological Stress on Heart Rate Variability and Myocardial Oxygen Demand in Healthy Adults

Original Research | 2026 | Volume 2 | Issue 1 | Page 89-98

Dr. Shahan Layek, Independent Researcher, West Bengal, India, Email: layekcallmeshahan@gmail.com

The Impact of Acute Psychological Stress on Heart Rate Variability and Myocardial Oxygen D.

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Abstract

Background: Acute psychological stress triggers immediate autonomic and cardiovascular shifts, increasing the risk of transient cardiac events even in healthy populations. This study evaluates the impact of acute laboratory-induced stress on autonomic regulation, measured via Heart Rate Variability (HRV), and myocardial oxygen demand, quantified by the Rate Pressure Product (RPP).

Methods: Data were analyzed from a cohort of 50 healthy adults (mean age: 28.4 \pm 4.2 years; 50% female) who underwent the Trier Social Stress Test (TSST). Continuous electrocardiogram (ECG) and beat-to-beat blood pressure monitoring were conducted across three phases: a 10-minute baseline, a 10-minute acute stress task, and a 15-minute recovery period. HRV time-domain parameters, specifically the Root Mean Square of Successive Differences (RMSSD), and the RPP Heart Rate} \Systolic Blood Pressur were calculated for each phase.

Results: Acute psychological stress induced a profound suppression of vagal tone, with RMSSD decreasing significantly from a baseline of 42.6 \pm 5.1\ to 18.3 \pm 3.4\ms during the stress task (p < 0.001). Concurrently, myocardial oxygen demand escalated sharply; RPP increased from a resting value of 7,850 \pm 620\ mmHg}\bpm to a peak of 14,200 \pm 1,150 mm Hg}\bpm during stress (p < 0.001). During the 15-minute recovery phase, RPP values returned near baseline (8,100 \pm 580\ mmHg}bpm, whereas RMSSD remained slightly suppressed (34.1 \pm 4.8\ ms}), indicating delayed parasympathetic reactivation.

Conclusion: Acute psychological stress abruptly disrupts autonomic homeostasis by suppressing parasympathetic activity and simultaneously multiplying myocardial oxygen workload. These findings highlight that even in healthy cardiovascular systems, brief psychological stressors demand substantial cardiac reserve, underscoring the physiological cost of mental stress.