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Effects of Melatonin Supplementation on Cardiovascular Reactivity to Acute Psychosocial Stress
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Introduction: Elevated blood pressure responses to acute mental stress are associated with cardiovascular risk. Prior studies demonstrate that melatonin supplementation reduces sympathetic nerve activity, which raises the possibility that it may lessen cardiovascular responses during psychosocial stress. However, the influence of melatonin on the cardiovascular response to social evaluative stress has not been investigated. The present study examined whether acute melatonin supplementation reduces stress-induced increases in blood pressure (BP) and heart rate (HR) during a standardized social evaluative stress task (i.e., Trier Social Stress Test). We hypothesized that melatonin ingestion would reduce cardiovascular reactivity to acute stress. Methods: 10 healthy adults (5 males, 5 females; age 20 ± 1 years; BMI 23 ± 4 kg/m
2
) completed two afternoon laboratory visits in a randomized, placebo-controlled, crossover design. On each visit, participants ingested either 3 mg melatonin or a placebo pill. After a 45-minute absorption period, participants completed a standardized Trier Social Stress Test (TSST), which consisted of a resting baseline (10 min), nonverbal speech preparation phase (5 min), verbal stress phase consisting of a judged speech (5 min) and mental arithmetic (5 min), followed by a recovery (5 min) phase. All sessions included continuous recordings of HR (electrocardiography), beat-to-beat BP (finger plethysmography), respiration (thoracic respiratory belt), and subjective assessment of perceived stress. The full protocol was repeated one month later with the opposite condition (i.e., placebo or melatonin). Cardiovascular responses were analyzed using repeated-measures ANOVA to assess the effects of time, condition, and their interaction on acute stress reactivity. Results: Stress significantly increased systolic blood pressure (SBP), diastolic blood pressure (DBP), and HR across nonverbal and verbal task phases in both experimental conditions (all p < 0.001). Average SBP did not differ between conditions (Placebo: 128 ± 8 mmHg; Melatonin: 125 ± 13 mmHg; p = 0.409), and SBP stress reactivity was similar (interaction p = 0.993). DBP was lower on average following acute melatonin supplementation compared to placebo (Placebo: 76 ± 5 mmHg; Melatonin: 70 ± 9 mmHg; p = 0.035), although melatonin did not change the DBP response to the TSST (interaction p = 0.326). Mean HR tended to be lower following melatonin supplementation (Placebo: 81 ± 13 BPM; Melatonin: 73 ± 8 BPM; p = 0.085), but melatonin did not alter heart rate reactivity across nonverbal or verbal stress tasks (interaction p = 0.379). Conclusion: Oral melatonin supplementation lowered resting DBP and showed a trend toward reduced HR, but it did not impact BP or HR responsiveness to acute psychosocial stress. Stress related increases in systolic and diastolic pressure and heart rate were similar between melatonin and placebo, suggesting that the acute effects of psychological stress supersede the beneficial cardiovascular effects of melatonin.
Funding: Sleep Research Society Foundation (02-SRG-23)
This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
American Physiological Society
Title: Effects of Melatonin Supplementation on Cardiovascular Reactivity to Acute Psychosocial Stress
Description:
Introduction: Elevated blood pressure responses to acute mental stress are associated with cardiovascular risk.
Prior studies demonstrate that melatonin supplementation reduces sympathetic nerve activity, which raises the possibility that it may lessen cardiovascular responses during psychosocial stress.
However, the influence of melatonin on the cardiovascular response to social evaluative stress has not been investigated.
The present study examined whether acute melatonin supplementation reduces stress-induced increases in blood pressure (BP) and heart rate (HR) during a standardized social evaluative stress task (i.
e.
, Trier Social Stress Test).
We hypothesized that melatonin ingestion would reduce cardiovascular reactivity to acute stress.
Methods: 10 healthy adults (5 males, 5 females; age 20 ± 1 years; BMI 23 ± 4 kg/m
2
) completed two afternoon laboratory visits in a randomized, placebo-controlled, crossover design.
On each visit, participants ingested either 3 mg melatonin or a placebo pill.
After a 45-minute absorption period, participants completed a standardized Trier Social Stress Test (TSST), which consisted of a resting baseline (10 min), nonverbal speech preparation phase (5 min), verbal stress phase consisting of a judged speech (5 min) and mental arithmetic (5 min), followed by a recovery (5 min) phase.
All sessions included continuous recordings of HR (electrocardiography), beat-to-beat BP (finger plethysmography), respiration (thoracic respiratory belt), and subjective assessment of perceived stress.
The full protocol was repeated one month later with the opposite condition (i.
e.
, placebo or melatonin).
Cardiovascular responses were analyzed using repeated-measures ANOVA to assess the effects of time, condition, and their interaction on acute stress reactivity.
Results: Stress significantly increased systolic blood pressure (SBP), diastolic blood pressure (DBP), and HR across nonverbal and verbal task phases in both experimental conditions (all p < 0.
001).
Average SBP did not differ between conditions (Placebo: 128 ± 8 mmHg; Melatonin: 125 ± 13 mmHg; p = 0.
409), and SBP stress reactivity was similar (interaction p = 0.
993).
DBP was lower on average following acute melatonin supplementation compared to placebo (Placebo: 76 ± 5 mmHg; Melatonin: 70 ± 9 mmHg; p = 0.
035), although melatonin did not change the DBP response to the TSST (interaction p = 0.
326).
Mean HR tended to be lower following melatonin supplementation (Placebo: 81 ± 13 BPM; Melatonin: 73 ± 8 BPM; p = 0.
085), but melatonin did not alter heart rate reactivity across nonverbal or verbal stress tasks (interaction p = 0.
379).
Conclusion: Oral melatonin supplementation lowered resting DBP and showed a trend toward reduced HR, but it did not impact BP or HR responsiveness to acute psychosocial stress.
Stress related increases in systolic and diastolic pressure and heart rate were similar between melatonin and placebo, suggesting that the acute effects of psychological stress supersede the beneficial cardiovascular effects of melatonin.
Funding: Sleep Research Society Foundation (02-SRG-23)
This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format.
There is no downloadable file or PDF version.
The Physiology editorial board was not involved in the peer review process.
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