Does acute melatonin supplementation affect cerebrovascular reactivity in healthy young adults?

Melatonin receptors have been found in the cerebrovasculature in animal models, and melatonin has been shown to improve systemic vascular control. While there is a correlation between low melatonin production and cardiovascular disease, the effect of acute melatonin supplementation on the cerebrovasculature, and more specifically, cerebrovascular reactivity (CVR), is unknown. PURPOSE: To determine if acute melatonin supplementation alters CVR via CO 2 rebreathing in healthy, young adults. Methods: 14 healthy young adults (Age 23.7±4.39, 7 females tested during the first 5 days of their menstrual cycle) participated in a familiarization visit followed by 2 experimental visits separated by ≥48hrs. Participants received a sublingual dose of either a placebo (PLA, mixture of mint extract and filtered water, to mimic taste of melatonin) or 5mg of melatonin (MEL, mint flavor) in a single-blind, randomized, crossover design. After ingestion, participants rested for 30 minutes prior to the experiment to allow for melatonin levels to reach peak concentration in the blood (Bartoli et al., 2013). After which, mean arterial pressure (MAP, mmHg, finger photoplethysmography), middle cerebral artery velocity (MCA v , cm/s, Transcranial Doppler), and end-tidal CO 2 concentration (PetCO 2 , mmHg, Gas Analyzer) were measured continuously for 5 minutes of supine rest while breathing atmospheric air followed by a CO 2 rebreathing challenge (CO 2 =3%, O 2 =40%, balanced N 2 ) until the participant displayed a PetCO 2 increase of ≥10mmHg. Cerebrovascular conductance index was calculated as CVCi = MCA v /MAP (cm/s/mmHg). CVR was calculated in absolute ΔMCA v /ΔPetCO 2 , ΔCVCi/ΔPetCO 2 , and percent change from resting values. Results: Data presented as change (Δ) from rest to CO 2 rebreathing, as mean ± SD. All values were not different between treatments during rest. No value was significantly different between treatments when comparing Δ from rest to CO 2 rebreathing (MCA v PLA Δ13.35±5.1 vs. MEL Δ11.62±6.03, p = 0.31, d = 0.28, MAP PLA Δ1.75±3.91 vs. MEL Δ-0.55±4.49, p = 0.20, d = 0.34, CVCi PLA Δ0.11±0.04 vs. MEL Δ0.11±0.05, p = 0.55, r = 0.16, CVR MCAv PLA Δ2.75±1.30 vs. MEL Δ3.54±2.57, p = 0.92, r = 0.03, %CVR MCAv PLA Δ18.41±7.07 vs. MEL Δ16.12±10.00, p = 0.36, r = 0.24, CVR CVCi PLA Δ0.02±0.03 vs. MEL Δ0.02±0.02, d = 0.28, p = 0.31, %CVR CVCi PLA Δ2.32±2.58 vs. MEL Δ1.52±1.83, d = 0.28, p = 0.31). CONCLUSION: Our results indicate that melatonin does not affect MCA v , CVCi, MAP, or CVR during rest or CO 2 rebreathing. Reactivity was variable individually and did not trend in any direction when comparing PLA treatment to MEL treatment. Thus, melatonin supplementation does not improve cerebrovascular function indicating melatonin supplementation may have differential responses between the cerebral and peripheral vasculature in humans. This work was supported by a Robberson Research Grant provided by the University of Oklahoma graduate college. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.