Mov Sport Sci/Sci Mot
Number 115, 2022
Page(s) 25 - 32
Published online 11 January 2022

© ACAPS, 2022

1 Introduction

Melatonin (N-acetyl-5 methoxytryptamine) is mainly secreted in the pineal gland and plays an important role in the regulation of circadian rhythms, contributing to the temporal organization of human behavior and physiology (Escames et al., 2012). Indeed, it has been reported that melatonin administration reduced heart rate (HR) and blood pressure in humans at rest, implying that melatonin increases cardiac vagal tone in awake men in the supine position (Escames et al., 2012). However, it is unclear how melatonin affects the HR response to exercise. One study reported no significant difference in HR during intermittent activity between both the melatonin and the placebo groups (Atkinson et al., 2005a), while another highlighted a significant “slight” decrease in HR of 6 to 9 bpm (Atkinson, Jones, Edwards, & Waterhouse, 2005b). Melatonin lowers HR by suppressing sympathetic tone (Viswanathan, Hissa, & George, 1986; Wang et al., 1999) and decreasing catecholamine levels (Laflamme, Wu, Foucart, & de Champlain, 1998).Melatonin was noted to be safe and effective in protecting the infected heart from reactive oxygen species, regardless of the cause (Dominguez-Rodriguez & Abreu-Gonzalez, 2010; Dominguez-Rodriguez, Abreu-Gonzalez, Piccolo, Galasso, & Reiter, 2016; Dominguez-Rodriguez, Abreu-Gonzalez, & Reiter, 2012). Adults’ pro- and antioxidant mechanisms are both upregulated in response to acute exercise (Avloniti et al., 2017). Superoxide dismutase (SOD), an antioxidant free-radical chain-breaking enzyme, catalyzes the dismutation of superoxide into oxygen and hydrogen peroxide and it may accelerate healing after oxidative damage (Halliwell & Gutteridge, 2015). In aerobic organisms, SOD is an essential antioxidant defense mechanism that may be impacted by greater body temperature (Öztürk & Gümüşlü, 2004). In the case of acute oxidative stress, SOD may play a role in biological response. Endogenous melatonin levels have been shown to have a positive relationship with antioxidant capacity (Benot et al., 1999). Although it appears to be a reasonable idea to use melatonin to boost serum antioxidant activities and protect the heart from free radicals during exercise, there have been a few reports of adverse effect of melatonin, such as down-regulation of nitric oxide synthase (NOS) (Geary, Duckles, & Krause, 1998; Okatani, Wakatsuki, Watanabe, Taniguchi, & Fukaya, 2001; Pozo, Reiter, Calvo, & Guerrero, 1994; Silva et al., 2007; Tamura, Silva, & Markus, 2006). Indeed, a low concentration of free radicals appears to be effective in the regulation of hyperaemia during physical exercise in perfectly functioning hearts (Trinity, Broxterman, & Richardson, 2016). There is a scarcity of data on the effects of antioxidants on healthy hearts in normal redox balance.

The aims of this research were to look into the effect of melatonin on the evolution of HR during submaximal exercise in healthy men, as well as to determine if melatonin could be used to improve cardiovascular function.

2 Population and methods

2.1 Participants

Eight healthy physical education students volunteered to take part in the study [age: 21.8 ± 0.9 years; BMI: 21.0 ± 0.8 kg/m2]. All participants were non-smokers, have abstained from exercising and consuming alcohol or caffeine-containing beverages for at least 24 hours prior to the assessments. Participants were chosen based on their chronotype using Horne and Ostberg’s questionnaire (Horne & Östberg, 1976). The study was approved also by the Farhat HACHED ethical committee, Sousse, Tunisia (FH/1609021). The study protocol was in accordance with current national laws and regulations. After receiving both a verbal and written explanation of the experimental protocol, as well as its potential risks and benefits, the participants gave their written informed consent.

2.2 Study design

The participants were requested to visit the research laboratory three times (Fig. 1). On the very first visit, the participants completed the VAMEVAL test to determine their maximum aerobic speed (MAS). Participants were asked to complete the two visits of the protocol in a randomized and counterbalanced order on the second and third occasions (placebo or melatonin). All the three visits were performed indoors at a relative humidity of 60% ± 3% and a temperature of 23 °C ± 0.1 °C and at the same time of the day (i.e., between 8.00 and 10.35 A.M.) to minimize the effects of diurnal variations in the measured variables (Souissi, Yousfi, Souissi, Haddad, & Driss, 2020).

thumbnail Figure 1

Flowchart of the study’s methodology.

2.3 Experimental protocol

Participants sat in a supine position, then each participant had a rectal thermistor implanted (inserted 10 cm beyond the anal sphincter). At 09:00 A.M., the participants ingested whether the 6-mg of quick-release vegetable melatonin (Jamieson Laboratories Toronto, Montreal, Canada) or placebo capsule with 500 mL of water before resting for 40 minutes in the supine position. The HR and rectal temperature (Tre) were continuously recorded using a HR monitor (Polar RS800, Finland) and a rectal probe (Universal YSI400, China), respectively. Then, a blood sample was taken from the right antecubital vein. At 09:50 A.M. participants ran for 45 minutes at a submaximal intensity fixed at 60% of their MAS on a treadmill (Finnlo, Germany). HR and Tre were measured simultaneously, and data were selected every five minutes. At the end of the exercise, blood samples were taken from the left antecubital vein, triglycerides, cholesterol, HDL-c, lactate, SOD and protein concentrations were measured.

2.4 Blood variables analysis

Biochemical assays were carried out at the Laboratory of the Hospital of Children in Tunis (Tunisia), using standard methods and the COBAS 6000. As per Beauchamp & Fridovich (1971), SOD concentrations was measured spectrophotometrically by monitoring the inhibition of photochemical reduction of nitro blue tetrazolium (NBT) at 560 nm.

2.5 Statistical analyses

The data were presented as the mean and standard deviation (±SD). The Kolmogorov-Smirnov test for normality indicated that all data-sets were normally distributed. The data were analyzed using repeated measures analysis of variance (ANOVA). The Bonferroni’s test was used to determine significant differences. Effect sizes were calculated as partial eta-squared (ηp2) to determine the practical significance of the results. Magnitudes of effect sizes were classified as trivial (0–0.19), small (0.20–0.49), medium (0.50–0.79), and large (≥0.80) (Cohen, 1992). An independent samples t-test was performed for Tre and HR to compare the difference between conditions. The level of significance was predetermined to be P < 0.05 for all statistical analyses. The Statistical Software Version 10.0 for Windows (StatSoft, Maisons-Alfort, France) was used for data analysis.

3 Results

All the participants undergoing submaximal exercise successfully completed the exercise. None of the participants achieved a thermal steady state during exercise and the mean lactate values for both conditions were less than 2.50 mmol/L.

The changes in HR during the rest period and exercise under both conditions are presented in Figure 2A. HR was significantly higher at the end of exercise under the placebo condition (P < 0.01). HR increased progressively during exercise, but it did not reach its maximum in the two conditions. At 10 minutes, we observed the most important difference between the two conditions (Fig. 3A). HR increased considerably during exercise from 5 to 10 minutes, only under the placebo condition. In brief, the results show that melatonin exerts an effect on HR at 10 minutes of exercise, reducing HR by 6.6% (9 bpm; P < 0.001), and this effect decreased to 3.6% at the end of exercise (6 bpm; P < 0.01).

The changes in Tre during the rest period and exercise under both conditions are presented in Figure 2B. The results showed that melatonin has hypothermic effect only at rest. The Student’s t-test revealed that the total increase of Tre during exercise was more important in melatonin condition compared to placebo condition (P < 0.01) (Fig. 3B).

No significant (condition × exercise) interaction was obtained for triglycerides [F = 1.6; P = 0.24; ηp2 = 0.9]. A significant exercise effect was indicated for the triglycerides [F = 50.6; P = 0.0001; ηp2 = 0.8]. No significant (condition × exercise) interaction was obtained for cholesterol [F = 4; P = 0.08; ηp2 = 0.3]. A significant exercise effect was indicated for the cholesterol [F = 7.9; P = 0.02; ηp2 = 0.5]. No significant (condition × exercise) interaction was obtained for HDL-C [F = 0.06; P = 0.8; ηp2 = 0.009] (Tab. 1).

No significant (condition × exercise) interaction was obtained for protein [F =&#9617 P = 0.33; ηp2 = 0.1]. A significant condition was obtained for SOD [F = 9.8; P = 0.01; ηp2 = 0.58]. Post-hoc analysis revealed that SOD was significantly higher under placebo than melatonin condition at rest (P < 0.01) (Tab. 1).

thumbnail Figure 2

Changes in physiological parameters during the test (n = 8 men). A 6-mg of melatonin or a placebo capsule was ingested just before the rest period. (A) Changes in heart rate during the rest period and exercise at 23 °C and 60% relative humidity. (B) Changes in rectal temperature during the rest period and exercise at 23 °C and 60% relative humidity. Significant differences between placebo condition and melatonin condition are indicated by a dashed line in the diagrams (P < 0.05). Data in (A and B) were analyzed with Student’s t-test. The values are presented as the mean ± SD.

thumbnail Figure 3

Heart rate response at 10 min of exercise and total temperature elevation during exercise in placebo and melatonin conditions (n = 8 men). (A) Heart rate recorded at 10 min after melatonin or placebo ingestion. (B) The total increase of rectal temperature during exercise after melatonin or placebo ingestion. Data in (A and B) were analyzed with Student’s t-test. *Significant difference between melatonin and placebo (P < 0.05). The values are presented as the mean and ± SD.

Table 1

The pre- and post-exercise results of biochemical variables for both conditions (n = 8 healthy men).

4 Discussion

In agreement with Marrin, Drust, Gregson, & Atkinson (2013) who confirmed that melatonin decreased the body temperature at rest. However, melatonin has no hypothermic effect during exercise. In agreement with the results of Brandenberger, Ingalls, Rupp, & Doyle (2018) and McLellan, Smith, Gannon, & Zamecnik (2000), which indicated that melatonin has no hypothermic effect during submaximal exercise. The main finding of the present study revealed that melatonin reduced HR by 6.6% after 10 minutes of exercise, and this effect fades to 3.6% at the end of the exercise. To the best of the author’s knowledge, this is the first study that looked at the impact of a single high dose of melatonin on the HR response to continuous, submaximal exercise.

The findings of the present study are in agreement with Atkinson et al. (2005b) who reported that melatonin may reduce HR by 6 to 9 bpm. The authors suggested that melatonin lowers HR by suppressing sympathetic tone (Viswanathan et al., 1986; Wang et al., 1999) and decreasing catecholamine levels (Laflamme et al., 1998). It has been shown that melatonin administration (in a dose of 1-mg) greatly influences artery blood flow, decreases blood pressure, and blunts noradrenergic activation in young, healthy subjects (Cagnacci et al., 1997). However, it was reported that 2.5-mg of melatonin did not influence HR during intermittent exercise (Atkinson et al., 2005a). This contradiction might be due to the difference in methodology (protocol, intensity, and duration). The current results showed that melatonin reduced rectal temperature only at rest. The present study confirms that melatonin has no hypothermic effect during exercise (Brandenberger et al., 2018; McLellan et al., 2000). Therefore, we wonder why melatonin has an hypothermic effect only at rest. The effect of melatonin on cardiovascular response during exercise could explain perhaps the absence of hypothermic effect. In fact, it is well known that the increase in HR induced an elevation in cardiac output to enhance thermoregulatory control and heat dissipation by increasing skin blood flow (Johnson & Proppe, 2010; Taylor, Johnson, O’Leary, & Park, 1984; Souissi, Haddad, Dergaa, Saad, & Chamari, 2021). Indeed, the HR increase during exercise could be related to exercise induced-vasodilation (Horiuchi & Fukuoka, 2019; Rowell, 1974; Souissi et al., 2021). Since the results of the present study indicated an important increase of HR at 10 minutes in the placebo condition associated with appropriate thermoregulatory response, one could speculate that the HR raise at 10 minutes is partially due to the involvement of free radical (nitric oxide) to the active vasodilator response. Furthermore, previous findings revealed that performing 10-minutes submaximal exercise increases circulating nitric oxide levels (Franco, Doria, & Mattiucci, 2001; Rowell, 1974). It is possible that the rise in HR at 10 minutes, which is usually accompanied by an increase in skin blood flow and cardiac output (Rowell, 1974), is connected to the effects of nitric oxide-induced vasodilation. It would be possible to suggest that melatonin may exert antioxidants and anti-adrenergic effects at 10 minutes of exercise reducing the extent of HR elevation and limiting the ability of thermoregulatory control. On the other hand, we highlight that the important effect of melatonin exerted on heart rate at 10 minutes could be simply due to the fact that the half-life of melatonin is 40–60 minutes and the time required to reach the maximum concentration of the drug in the blood after oral administration is ≈41 minutes (Andersen et al., 2016).

The present results revealed different findings from our hypothesis. A high dose of antioxidant has no beneficial effect in healthy men at rest and could decrease SOD concentration. In agreement with previous studies demonstrating that high-dose of antioxidants may have pro-oxidant activities by disrupting the redox balance (Kruk, Aboul-Enein, & Duchnik, 2021; Trinity et al., 2016). The present study is also in agreement with several investigations observing an alteration of blood flow (vascular control) during dynamic exercise in healthy young adults following the inhibition of free radical accumulation/production with oral antioxidant administration (Donato, Uberoi, Bailey, Walter Wray, & Richardson, 2010; Richardson et al., 2007). Moreover, a large dose of melatonin provided during the day (at bedtime) can cause mild narcotic effects, drowsiness, and other side effects, so it is not advised (Hardeland, Coto-Montes, & Poeggeler, 2003). When taken during the day, melatonin can disrupt the internal time system, resulting in an elevation of oxidative stress (Hardeland et al., 2003). The present results revealed, however, that melatonin did not affect triglycerides, HDL-C, and cholesterol levels.

In short, this study supports the research results that suggest that the dose of antioxidants must be carefully selected and based on expert knowledge (Meagher & Rader, 2001). The current finding could enable physicians, coaches, and practitioners to take action (by using antioxidants) in order to comply with the humans’ bodies needs in order to enhance cardiovascular function during exercise or other stressful situations.

Amongst the limitations of the present study are:

  • the post-exercise analytical values were expressed without a correction for plasma volume changes:

  • the assessed blood parameters were limited, further research is needed to measure catecholamine and free radical concentrations to assess the effect of exogenous melatonin on cardiovascular response during submaximal exercise:

  • the study was conducted exclusively in men students with a small sample size; replication studies on a larger number of participants is warranted.

Additionally, the thermoregulatory outcome measures were limited to rectal temperature.

5 Conclusions

Acute melatonin administration (50 min prior to the start of exercise) did not enhance cardiovascular function during prolonged exercise in healthy men. Melatonin supplementation at high doses caused bradycardia during exercise and may have a negative impact on cardiovascular function and thermoregulatory control by lowering free radicals (by exerting antioxidants effects) and catecholamine production. Based on previous studies, the authors of the present study believe that the key to improving cardiovascular function during exercise is to restore or maintain an "optimal" redox balance. Interestingly, the present study showed that the significant increase in HR during the first 5–10 minutes of submaximal exercise is a cardiovascular response that may be partly due to free radicals’ role in thermoregulatory control.

Conflicts of interest

The authors declare that they have no conflicts of interest in relation to this article.

Authors’ contributions

Dr. Amine Souissi contributed to the conception, management of the study and original draft.

Professor Helmi Ben Saad contributed to the conception, management of the study, writing, review and editing.

Dr. Ismail Dergaa analyzed the data and contributed to the preparation (writing) of the manuscript.

Professor Nizar Souissi contributed to the writing, review and editing.

Dr. Sarah Musa added the flowchart of the study’s methodology.

All authors read and approved the final version of the manuscript.


ANOVA: analysis of variance

HR: heart rate

MAS: maximum aerobic speed

NBT: nitro blue tetrazolium

NOS: nitric oxide synthase

SD: standard deviation

SOD: superoxide dismutase

Tre: srectal temperature


The authors would like to thank the students who assisted in the project, as well as each of the subjects for their selfless participation.


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Cite this article as: Souissi A, Dergaa I, Musa S, Ben Saad H, & Souissi N (2022) Effects of daytime ingestion of melatonin on heart rate response during prolonged exercise. Mov Sport Sci/Sci Mot, 115, 25–32

All Tables

Table 1

The pre- and post-exercise results of biochemical variables for both conditions (n = 8 healthy men).

All Figures

thumbnail Figure 1

Flowchart of the study’s methodology.

In the text
thumbnail Figure 2

Changes in physiological parameters during the test (n = 8 men). A 6-mg of melatonin or a placebo capsule was ingested just before the rest period. (A) Changes in heart rate during the rest period and exercise at 23 °C and 60% relative humidity. (B) Changes in rectal temperature during the rest period and exercise at 23 °C and 60% relative humidity. Significant differences between placebo condition and melatonin condition are indicated by a dashed line in the diagrams (P < 0.05). Data in (A and B) were analyzed with Student’s t-test. The values are presented as the mean ± SD.

In the text
thumbnail Figure 3

Heart rate response at 10 min of exercise and total temperature elevation during exercise in placebo and melatonin conditions (n = 8 men). (A) Heart rate recorded at 10 min after melatonin or placebo ingestion. (B) The total increase of rectal temperature during exercise after melatonin or placebo ingestion. Data in (A and B) were analyzed with Student’s t-test. *Significant difference between melatonin and placebo (P < 0.05). The values are presented as the mean and ± SD.

In the text

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