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. Author manuscript; available in PMC: 2026 Mar 9.
Published in final edited form as: Chronobiol Int. 2025 Sep 8;42(11):1536–1546. doi: 10.1080/07420528.2025.2556841

Light exposure impact on cardiac autonomic control before and following exercise

Thais C Marin a,b, Gustavo F Oliveira a,b, Luan M Azevêdo a, Tiago Peçanha c, Saurabh S Thosar d, José Cipolla-Neto e, Cláudia L M Forjaz a, Leandro C Brito a,b,d
PMCID: PMC12967282  NIHMSID: NIHMS2145697  PMID: 40916939

Abstract

We aimed to investigate whether bright light (BL) exposure affects sympathovagal activity in controlling heart rate (HR) before and after exercise. Eighteen healthy men (28 ± 4 years) underwent two experimental conditions: one under BL (5000 lux) and another under dim light (DL < 8 lux). In both conditions, subjects performed an aerobic exercise bout (cycle ergometer, 30 min at 50–60% of HRreserve). HR (electrocardiography) and respiratory rate (piezoelectric belt) were initially assessed at baseline light (500 lux). Measurements were repeated before and 10 min after the exercise in both light conditions, BL and DL. Cardiac autonomic modulation was evaluated using spectral analysis of HR variability. Before exercise, DL did not change HR but decreased low- to high-frequency ratio of HR variability (LF/HFRR, DL = −0.35 ± 0.43 vs. BL = +0.00 ± 0.55, p < 0.01). From pre- to post-exercise, HR increased similarly, while LF/HFRR increase was greater in DL than BL (+1.12 ± 0.87 vs. +0.60 ± 0.98, p = 0.04). Contrary to our hypothesis, in healthy men, BL did not exacerbate HR and cardiac sympathovagal balance. However, DL exposure decreased pre-exercise cardiac sympathovagal balance, a difference that no longer persisted postexercise.

Keywords: Autonomic nervous system, heart rate variability, aerobic exercise, light, heart rate

Introduction

The dynamic process of reestablishing the basal resting state causes cardiac instability, elevating up to 2.3-fold the risk of adverse events for up to 1 h following exercise (Smyth et al. 2016). Part of this instability results from cardiac autonomic imbalance. For instance, recovery from exercise shows elevated heart rate (HR) mainly due to increased cardiac sympathovagal balance, which reflects an increase in sympathetic and a reduction in parasympathetic modulation of the heart (Pecanha et al. 2017).

The magnitude of increase in postexercise cardiac sympathovagal balance varies in the literature due to different factors. For instance, cardiac sympathovagal balance is higher following aerobic exercise when the exercise is performed at higher than moderate intensity (Pecanha et al. 2014) or when subjects are hydrated versus dehydrated (Porto et al. 2023). Not only can exercise or subject characteristics influence cardiac sympathovagal balance postexercise, but environmental changes also can, such as temperature (Pecanha et al. 2020) and time of day (Brito, Pecanha et al. 2015; Brito, Rezende et al. 2015).

Recent studies suggest that changes in the intensity of environmental light can affect cardiac autonomic modulation (Saito et al. 1996; Sakakibara et al. 2000; Scheer et al. 2004). For instance, previous studies with animal models demonstrated that exposure to bright light (BL) changes cardiac autonomic control, increasing HR via the suprachiasmatic nuclei on a neuroanatomical basis, by increasing HR only if this pathway is preserved (Kalsbeek et al. 2006; Meijer et al. 1996; Scheer et al. 2001). Similarly, in humans, exposure to BL (5000 lux) increased cardiac sympathovagal modulation, HR, and muscle sympathetic nerve activity (Saito et al. 1996; Sakakibara et al. 2000; Scheer et al. 2004). When investigated separately, aerobic exercise (Pecanha et al. 2017) and BL exposure (Sakakibara et al. 2000; Scheer et al. 2004) have been identified as triggers for increasing cardiac sympathovagal balance. Thus, it is reasonable to suggest that performing an aerobic exercise bout under BL may delay postexercise autonomic restoration, leading to an additional risk of an adverse cardiovascular event inherent to the first hour postexercise (Albert et al. 2000). However, the combined effects of BL exposure and aerobic exercise on cardiac autonomic modulation have not been investigated, and the current study aimed to fill this knowledge gap.

Therefore, this study aimed to compare the effect of BL (5000 lux) versus dim light (DL < 8 lux) exposure on HR and its cardiac autonomic control before and following a single aerobic exercise session.

Materials and Methods

This study is an ancillary aim of a randomized crossover study approved by the Research Ethics Committee of the School of Physical Education and Sport of the University of São Paulo (n° 3.742.479) and registered at the Brazilian Clinical Trials (http://ensaiosclinicos.gov.br/rg/RBR-4vcfjmm). The primary aims of the current study were published elsewhere (Oliveira et al. 2024). All subjects provided written consent before participation.

Subjects

Healthy young adult men took part in this study if they were between 20 and 39 y old, had a body mass index <30 kg/m2, were recreationally active, non-smokers, without a diagnosis of any chronic disease, and not taking any over-the-counter medications, supplements, or vitamin supplements. Eligibility was confirmed via self-report and the following procedures. Subjects were only included if they responded “NO” to all questions of the Physical Activity Readiness Questionnaire (Shephard et al. 1981). Physical activity levels were determined using the short version of the International Physical Activity Questionnaire, and subjects were excluded if identified as very physically active with >300 min/week of moderate-intensity physical activity or >60 min/week of vigorous-intensity (Craig et al. 2003). Auscultatory blood pressure was assessed using an aneroid sphygmomanometer (Missouri, Mikato Ltda, São Paulo, Brazil) after five min of seated rest in two visits, when measurements were performed in triplicate on both arms in accordance with the national guidelines (Feitosa et al. 2024). Subjects were excluded when the average values of systolic and/or diastolic blood pressures were ≥140 and/or ≥90 mmHg, respectively (Feitosa et al. 2024). Body weight and height were measured using a calibrated scale (Welmy, W200a Led, Brazil) to calculate the body mass index. Chronotype status was confirmed by using the morningness-eveningness questionnaire of Horne and Ostberg (Horne and Ostberg 1976). Subjects were excluded if they were classified as morning types (score >65) or evening types (score <45).

Experimental Protocol

Subjects who met the study criteria underwent, in random order, two experimental conditions, BL and DL. The experimental conditions were conducted on the same day of the week, with an interval of seven days between them. They started at 13:30 h to avoid any effect of the diurnal variation on the cardiac autonomic response (Brito, Pecanha et al. 2015; Brito, Rezende et al. 2015) and were in a temperature-controlled laboratory (20–22°C). Before both experimental conditions, subjects were instructed to abstain from strenuous physical effort for 48 h, alcohol consumption for 24 h, and caffeine ingestion for 12 h. They also had to be fastened for at least 2 h. Adherence to these instructions was confirmed by self-report at the beginning of each in-lab visit.

The experimental condition is shown in Figure 1. Subjects arrived at the laboratory at 13:30 h, received a standardized meal (2 cereal bars and 100 ml of water), and were encouraged to use the bathroom. These are standard procedures used in our studies (Brito, Rezende et al. 2015, 2018; Oliveira et al. 2024). After returning to the laboratory, subjects removed their glasses or contact lenses, if worn, and their body mass was measured (Welmy, W200a Led, Brasil). Then, they lay on the bed in supine position, and the environmental light was adjusted to our wash-out light condition of 500 lux. This approach was adopted to minimize differences in light exposure before the in-lab visit and ensure that every subject started with the same amount of light exposure in the experiment. After 20 min of resting, R-R interval and respiratory signals were recorded for 10 min to assess cardiac autonomic modulation. Afterward, the environmental light was adjusted according to the experimental condition, BL – 5000 lux or DL - < 8 lux, and maintained until the end of the visit. Measurements were performed 20 min after the experimental light was turned on (pre-exercise). During subjects’ transition to the cycle ergometer, the lamps were moved, and light levels were reassessed to ensure the desired lux level. After completing the exercise, subjects returned to bed, and R-R interval and respiratory signals were registered between 10 and 20 min of the postexercise period.

Figure 1.

Figure 1.

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Experimental protocol. Heart rate (HR).

Aerobic Exercise

The aerobic exercise protocol used in both experimental conditions consisted of 5 min warm-up at 30 watts, followed by 30 min of pedaling at 50–60% of the HR reserve, which represents a moderate intensity and was calculated according to Karvonen’s formula as follows: [(220−age)−restingHR)∗(Intensity%+restingHR)] (Karvonen et al. 1957). We employed this exercise protocol because it fits the current recommendations for inducing overall cardiovascular benefits in untrained individuals (ACSM and Cemal 2025; McEvoy et al. 2024; Whelton et al. 2018). In addition, previous studies employing similar protocols have identified significant changes in postexercise cardiac autonomic modulation (Brito, Rezende et al. 2015; Pecanha et al. 2014). During the exercise, HR was continuously measured using an HR monitor (Polar, CRX800, Kempele, Finland), and workload was adjusted when appropriate to maintain the desired intensity.

Light Protocol

We designed our light protocol based on previous studies that found an increase in cardiovascular sympathetic activity after a short exposure to BL (Saito et al. 1996; Sakakibara et al. 2000). Customized polychromatic LED lamps were used to control light intensity, positioned around the subjects and directed towards their eyes to regulate the experimental light intensities (Figure 2). We placed the lamps around subject’s head, and there were marks on the floor to maintain them in the same position. The lamps were inclined at a 60° angle. Subjects were exposed to 500 lux during the baseline period for 30 min, with measurements starting at the 20 min mark. Light intervention commenced immediately after baseline in both experimental conditions (DL = ≤ 8 lux, and BL = 5000 lux) and continued until the end of the experiment (Figure 1). Light intensity was verified at eye level using a lux meter (Instrutherm 920T, São Paulo, Brazil) whenever the light intensity was changed in the experimental conditions or subjects changed their body posture (i.e. from bed to cycle ergometer and then back to bed). To ensure the same levels of light in both visits, the laboratory’s regular lights were turned off, and blackout curtains were used to block the entrance of any external light. Light exposure was not measured before the in-lab visit. We used customized lamps as previously published by our group (Oliveira et al. 2024), the customized LED lamps adjusted for BL condition exhibited: 5000 lux; correlated color temperature (CCT) = 5022 K; and an average irradiance level and wavelength for blue = 10.4 μW/cm2 and 450 nm, green = 6.7 μW/cm2 and 550 nm, yellow = 7.8 μW/cm2 and 580 nm, orange = 7.1 μW/cm2 and 600 nm, and red = 2.3 μW/cm2 and 700 nm. Lamps were turned off to conduct DL (≤8 lux).

Figure 2.

Figure 2.

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Demonstrative figure of the customized lamps and the laboratory setup during the experiment.

Measurements

Electrocardiogram (ECG – EMG System do Brazil, EMG 030 110/00B, São Paulo, Brazil) and breath-to-breath respiratory signal (Piezoelectric thoracic belt – UFI, Pneumotrace2, Morro Bay, CA) were continuously obtained for 10 min through a multichannel acquisition system (Windaq, DI-720, Akron, USA) with a sampling frequency of 500 Hz per channel. This allowed the ECG and respiratory signals to be exported to a specific software for analysis (Heart Scope II, v. 1.3.0.1; A.M.P.S. LLC, New York, NY).

Cardiac autonomic modulation was assessed by spectral analysis of HR variability using stationary segments of 300 beats in accordance with the recommendations of the Task Force developed by the European Society of Cardiology and the North American Society of Pacing and Electrophysiology (Task Force 1996). The variability of these signals was analyzed in the frequency domain using the autoregressive method, which enables the calculation of the total spectral power and quantifies the central frequency and power of each relevant spectrum band. The oscillatory components of the time series were modeled by the Levinson – Durbin recursion, and the model order was chosen according to Akaike’s criterion (Malliani et al. 1991). Low-frequency (LFRR: 0.04–0.15 Hz) and high-frequency (HFRR: 0.15–0.4 Hz) components of HR variability were expressed as normalized units (n.u). To interpret the results: total variance of R-R interval (TVRR) and the normalized values of HFRR represent the cardiac parasympathetic modulation; the normalized values of LFRR were interpreted as predominantly representing the cardiac sympathetic modulation, and the ratio between LF and HF (LF/HFRR) represents the cardiac sympathovagal balance (Task Force 1996).

Statistical Analysis

The minimum sample size of 18 subjects was calculated a priori to detect significant differences in LF/HFRR, which was a secondary outcome from a larger study. This calculation considered a moderate effect size with Cohen’s f = 0.30 based on results of a previous publication of our group (Brito, Rezende et al. 2015), a power of 0.80, and an alpha error of 0.05 for a two-way ANOVA for repeated measures (G*Power v. 3.1.9.2, Universität Kiel, Germany). The primary outcome of the larger study was systolic blood pressure postexercise, and the results were published elsewhere (Oliveira et al. 2024).

Data distribution was checked using the Shapiro-Wilk test (SPSS for Windows, IBM Corp., Armonk, NY, USA). HR variability indices that did not show a normal distribution were log-transformed. A two-way ANOVA for repeated measures was used with light conditions (BL vs. DL) and time (Baseline vs. pre-exercise) as the main factors to test the effect of light at pre-exercise. A two-way ANOVA for repeated measures was used with light condition (BL vs. DL) and time (pre-exercise vs. postexercise) as the main factors to test the effect of light on cardiac autonomic modulation postexercise. When necessary, the Newman Keuls test was conducted for post-hoc analyses. HFRR n.u., LFRR n.u., and LF/HFRR were significantly different between BL and DL pre-exercise. ANCOVAs were performed for these variables using their pre-exercise values as covariates to test whether these differences were influencing their respective postexercise responses. Because there was no difference in ANCOVAs’ compared to ANOVAs’ results, ANOVAs’ results were shown. Analyses were performed using a statistical software package (Statistica v.10, StatSoft Inc., Tulsa, OK, USA). All data were shown as mean ± standard deviation, and values of p ≤0.05 were considered significant. Cohen’s d effect sizes (ES) for repeated measures (e.g. Cohen’s drm) were calculated as a complementary analysis for variables that have statistically significant interaction with ANOVA. Cohen’s drm was classified as small (ES ≤ 0.49), medium (ES 0.50–0.79), or large (ES ≥ 0.80) (Lakens 2013).

Results

Twenty-three subjects who signed the consent form underwent the preliminary procedures. Two subjects were excluded, one due to diastolic blood pressure values exceeding 90 mmHg and another due to body mass index above 30 kg/m2. Thus, 21 subjects initiated the experimental protocol. One did not complete it due to personal reasons, and the data of two others were not analyzed due to poor ECG signal quality. The characteristics of the 18 subjects included in the analysis are shown in Table 1.

Table 1.

Characteristics of subjects.

Variable Value
N 18
Age (y) 28 ± 4
Chronotype (scores) 49 ± 10
Anthropometrics
Height (m) 1.78 ± 0.05
Weight (Kg) 78.1 ± 13.7
Body mass index (kg/m2) 24.6 ± 3.7
Hemodynamics
Systolic blood pressure (mmHg) 116 ± 8
Diastolic blood pressure (mmHg) 77 ± 6
Heart rate (bpm) 72 ± 14
Physical activity levels
Inactive, n (%) 3 (17)
Insufficient active, n (%) 7 (39)
Active, n (%) 8 (44)
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Data are shown as mean±standard deviation.

Effect of Light Condition on Pre-Exercise Cardiac Autonomic Modulation

From baseline to pre-exercise (Figure 3), HR decreased significantly and similarly under both DL and BL conditions (−3 ± 4 and −2 ± 4 bpm, ptime < 0.01, respectively). A statistically significant interaction revealed a decrease only after DL compared to BL in lnLF/HFRR (−0.35 ± 0.43 vs. +0.00 ± 0.55, a.u., plight ×time < 0.01) and LFRR (−8.24 ± 10.67 vs. −0.72 ± 12.32 n.u., plight ×time = 0.02), respectively. The ES for lnLF/HFRR and LFRR pre-exercise values for DL versus BL were small (0.42, 95%CI = 0.31–0.54) and (0.39, 95% CI = 0.27–0.51), respectively. A significant interaction also showed an increase only after DL versus BL in HFRR (+7.07 ± 9.36 vs. −0.52 ± 13.64 n.u., plight ×time = 0.01), respectively. The ES for HFRR pre-exercise values for DL versus BL was small (0.42, 95%CI = 0.32–0.51). lnTVRR did not change in both light conditions.

Figure 3.

Figure 3.

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Variables measured at the baseline period (500 lux) and at the pre-exercise period during bright light condition (5000 lux, represented by dashed line with squares) and dim light condition ( <8 lux, represented by continuous line with triangles). Panel A: heart rate; panel B: natural logarithm of the total variance of R-R intervals (lnTVRR); panel C: natural logarithm of the low- to high-frequency ratio of R-R interval variability (lnLF/HFRR); panel D: normalized HF component of R-R interval variability (HFRRn.u); panel E: normalized LF component of R-R interval variability (LFRRn.u). Data is shown as mean±standard deviation. * Different from baseline (p ≤ 0.05); # different from BL at the same time (p ≤ 05).

Effect of Light Condition on Cardiovascular Parameters During Exercise

In BL and DL light conditions, subjects achieved similar workloads (104 ± 21 vs. 104 ± 23 watts, p = 0.90), relative intensity (57 ± 5 vs. 55 ± 8% of the HR reserve, p = 0.72), and increase in HR during exercise (+65 ± 2 vs. +66 ± 1 bpm, p = 0.63), respectively.

Effect of Light Condition on Postexercise Cardiac Autonomic Modulation

From pre- to postexercise (Figure 4). HR increased significantly and similarly in DL and BL (+11 ± 7 and + 8 ± 5 bpm, ptime < 0.01), respectively. lnLF/HFRR and LFRR had lower absolute values pre-exercise under DL than BL, which were compensated for a greater increase under DL versus BL (+1.12 ± 0.87 vs. +0.60 ± 0.98 a.u., plight ×time = 0.04 and + 22.68 ± 16.84 vs. +10.85 ± 19.32 n.u., plight ×time = 0.02), respectively, resulting in similar absolute values postexercise (Figure 4C,E). The ES for lnLF/HFRR and LFRR postexercise comparing DL and BL were small (0.14, 95%CI = 0.00–0.27 and 0.31, 95% CI = 0.15–0.48), respectively. HFRR had higher absolute values pre-exercise under DL compared to BL, which were compensated for a more pronounced decrease postexercise under DL than BL (−22.67 ± 18.60 vs. −13.64 ± 16.88 n.u., plight ×time = 0.05), respectively, resulting in similar absolute values (Figure 4D). The ES for HFRR postexercise values comparing DL and BL was small (0.06, 95%CI = 0.00–0.19). lnTVRR decreased significantly and similarly in both DL and BL (−0.77 ± 0.97 and −0.61 ± 0.98 ms2, ptime = 0.01), respectively.

Figure 4.

Figure 4.

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Variables measured at the pre- and postexercise periods during bright light condition (5000 lux, represented by dashed line with squares) and dim light condition ( <8 lux, represented by continuous line with triangles). Panel A: heart rate; panel B: natural logarithm of the total variance of R-R intervals (lnTVRR); panel C: natural logarithm of the low- to high-frequency ratio of R-R interval variability (lnLF/HFRR); panel D: normalized HF component of R-R interval variability (HFRRn.u); panel E: normalized LF component of R-R interval variability (LFRRn.u). Data is shown as mean±standard deviation. * Different from baseline (p ≤ 0.05); # different from BL at the same time (p ≤ 05).

Discussion

This investigation focused on testing whether BL exposure (5000 lux) would exacerbate the postexercise cardiac sympathovagal balance observed after an aerobic exercise session compared to DL (< 8 lux) exposure. The main finding of the study did not confirm our hypothesis. The cardiac sympathovagal balance from pre- to postexercise was blunted and did not exacerbate under BL compared to DL. Interestingly, unlike our hypothesis, the main changes induced by light exposure were observed with DL and not with BL. Indeed, DL decreased cardiac sympathovagal balance from baseline to pre-exercise and exacerbated its increase from pre- to postexercise.

Previous studies with rodents showed that the bright light effect on autonomic control of HR occurs through multisynaptic projections from the suprachiasmatic nucleus to the paraventricular nucleus and nucleus of the solitary tract (Buijs et al. 1999, 2014; Niijima et al. 1992; Scheer et al. 2001). Additionally, in one of these studies, Scheer and colleagues demonstrated that changes in HR promoted by bright light depend on intact suprachiasmatic nuclei in rats (Scheer et al. 2001). Along this line, studies conducted with humans also reported an increase in HR and sympathetic indices of cardiac autonomic modulation, and in muscle sympathetic nerve activity after BL exposure (Saito et al. 1996; Sakakibara et al. 2000; Scheer et al. 1999, 2004). Surprisingly, the current study did not observe an increase in HR or cardiac autonomic modulation with BL exposure at the pre-exercise period.

Among the possible variations of the BL protocol, neither light intensity nor duration seems to explain the absence of effect on cardiac autonomic modulation primarily and HR observed in this experimental condition. For instance, a previous study found an increase in HR and cardiac sympathetic activity after BL exposure at 800 lux for 10 min (Scheer et al. 1999, 2004). Thus, the light intensity and duration imposed in this study generated a significantly lower stimulus than the 5000 lux for 20 min exposure applied at the first assessment of the current study. Notably, once BL was turned on, it was maintained, and postexercise assessments were taken after approximately 60 min of exposure, i.e. even a longer stimulus than the pre-exercise one.

On the other hand, the time of day at which BL exposure was applied appears promising in explaining the absence of change in cardiac autonomic modulation in our findings. Supporting this theory, Scheer and colleagues found that BL exposure (800 lux) increased HR and cardiac sympathetic activity only in the early morning or at night, but not in the afternoon (Scheer et al. 2004). In addition, previous studies reporting autonomic changes with BL were performed in the morning (Saito et al. 1996) or the evening (Sakakibara et al. 2000). Nevertheless, the current study was conducted in the afternoon and did not present an effect of BL, similar to what Scheer and colleagues found at this same time of the day (Scheer et al. 2004). In humans, the most sensitive mechanism involved in light input through the retinohypothalamic tract to the suprachiasmatic nucleus is mediated by melanopsins, a photopigment expressed in the retinal ganglion cells (Schmidt et al. 2011). Noteworthy, melanopsins are less sensitive to light during daytime (Markwell et al. 2010). This reduced sensitivity in the afternoon may have mitigated the light input pathway and contributed to the absence of change in HR and cardiac autonomic modulation with BL in the current study. In addition, the suprachiasmatic nucleus’s response to light exposure also depends on the time of day. A previous study found that a light pulse caused no change in the suprachiasmatic nucleus’s neuron activity around midday. In contrast, its activity increased significantly in the middle of the night in freely moving rats (Meijer et al. 1996). Meijer and colleagues attributed this to differences in suprachiasmatic nucleus baseline activity, which is high during the daytime and low during the nighttime (Meijer et al. 1996). Notably, a similar finding was observed in young healthy adults using state-of-the-art imaging techniques (e.g. functional MRI) (Vimal et al. 2009). It has been demonstrated that light input to the autonomic control of HR occurs through the suprachiasmatic nucleus (Scheer et al. 2001). Thus, it is reasonable to suggest that the absence of change in cardiac autonomic modulation with BL in the present study could be related to an attenuated response of melanopsins and an increased baseline activity of the suprachiasmatic nucleus in the afternoon.

A new finding of the present study was that, at least in the afternoon, exposure to DL increased cardiac parasympathetic modulation (assessed by TVRR and HFRR), decreased sympathetic modulation, and sympathovagal balance (assessed by LFRR and LF/HFRR, respectively), as measured at rest between baseline and pre-exercise measurements. Although understanding how DL impacts cardiac autonomic modulation is out of the scope of the present study, a reduction in alertness can lead to a shift in cardiac sympathovagal balance, which should not be disregarded (Barber et al. 2020). Previous studies demonstrated that dim light reduces alertness during the daytime (i.e. morning and afternoon) (de Zeeuw et al. 2019; Lok et al. 2022). Despite a researcher guaranteeing that the subjects were awake throughout the experiments, alertness was not assessed in the current study, and its influence should be investigated in the future. Mechanistically, an increase in melatonin should not explain the decrease in cardiac sympathovagal balance observed after DL in the current study. Exposure to darkness, even when it offers sleep opportunities during the daytime, is insufficient to produce melatonin in humans (Buxton et al. 2000). Previous studies have shown that the suprachiasmatic nucleus does not project dark information to the pineal gland to produce melatonin during the daytime in rats (Fukuhara 2004; Simonneaux and Ribelayga 2003). A possibility is that DL exposure approximates HR control to its endogenous circadian rhythm (Scheer, Hu et al. 2010), in which values are typically lower than diurnal rhythms (Degaute, van de Borne et al. 1991; Jones, Atkinson et al. 2006). However, this hypothesis needs to be adequately tested in the future.

The increase in HR observed at 10 min of the post-exercise period in the current study was around 10 bpm in both sessions, which is similar to a previous study also performed with young adult males that reported an increase of around 12 bpm in HR at the same period of 10 min postexercise (Pecanha et al. 2014). This increase in HR was followed by a reduction in cardiac parasympathetic and an increase in cardiac sympathetic modulation in both experimental conditions in the current study. This is expected and has been previously reported in studies conducted with the same population and similar experimental protocol (Casonatto et al. 2011; Pecanha et al. 2014). Therefore, the aerobic exercise protocol used in this study elicited the expected responses in postexercise cardiac autonomic modulation.

The increase in cardiac sympathovagal balance from pre- to postexercise was greater in DL than BL, compensating for the lower pre-exercise values observed under DL and generating similar postexercise values. Thus, it is reasonable to suppose that moderate aerobic exercise had a larger effect on cardiac autonomic control than environmental light. In other words, the exercise stimuli may have overcome the effects of light exposure on cardiac autonomic modulation. During exercise, cardiac parasympathetic withdrawal and sympathetic activation are necessary adjustments to increase HR and cardiac output as part of the multi-mechanistic control necessary to adequately match the oxygen demands of the contracting skeletal muscles (Fisher et al. 2015; Saltin et al. 1998; Seals et al. 1988). Our findings suggest that the absolute demand promoted by exercise overcame the stimulus generated by DL for regulating cardiac autonomic modulation. In support of this theory, the present study found that HR increased similarly in both light conditions during the exercise. Additionally, HR and all cardiac autonomic indices evaluated were similar postexercise in BL and DL, indicating that light did not have an impact on postexercise cardiac autonomic modulation. However, the current findings could have been affected if exercise was conducted at different intensities. For instance, it is well-known that postexercise cardiac sympathovagal recovery is slower as exercise intensity increases (Pecanha et al. 2017; Seiler et al. 2007). Additionally, cardiac autonomic modulation usually returns to baseline within 10 min after an aerobic exercise conducted below the anaerobic threshold in healthy individuals (Seiler et al. 2007). Aerobic exercise performed below the anaerobic threshold is considered low-intensity (ACSM and Cemal 2025). Considering exercise duration, postexercise HRV was not affected when duration increased 100% (Casonatto et al. 2011; Kaikkonen et al. 2007; Seiler et al. 2007), but was impacted by increases of 400% (Kaikkonen et al. 2010). Thus, the possibility that DL could affect cardiac autonomic regulation after exercise bouts of lower intensities conducted for short durations cannot be discarded and needs to be tested in the future.

Although not being the focus of this study, the implications of our findings for future studies can focus on two topics: 1) the decrease of resting cardiac sympathovagal balance with DL, and 2) the effect of moderate aerobic exercise overcoming the DL impact on cardiac sympathovagal balance. Future studies confirming that DL has the potential to decrease resting cardiac sympathovagal balance could be of great interest to clinical populations with sympathetic overdrive. For instance, cardiac patients with heart failure or arrhythmia, for whom reducing cardiac sympathetic activity is part of the treatment to reduce the chances of adverse cardiac events (Heidenreich et al. 2023). However, before studying the clinical relevance of this finding, it is necessary to investigate its replication, if there is a dose-response relationship between DL and cardiac autonomic modulation, as well as the duration of this effect. Considering topic two, a moderate aerobic exercise session overcame the effects of light exposure on cardiac sympathovagal balance. However, we cannot disregard the possibility that cardiac autonomic modulation after aerobic exercises performed at lower intensities may be influenced by light exposure, which warrants further investigation in the future. For instance, it is well-known that cardiac sympathovagal balance recovery following exercise has a positive correlation with exercise intensity (Pecanha et al. 2017).

The current investigation has several strengths but also has limitations. For instance, characteristics of the experimental protocol must be considered when interpreting our findings. The main characteristics include the time of day, the intensities for light exposure, and the exercise protocol (type, intensity, and duration). Additional limitations are related to the subject group. The present findings should not be generalized to women, older adults, and subjects with clinical conditions. Future studies should replicate our findings in other participant groups. As strengths of our study, we provide a standardized meal before every experiment to exclude the impact of different diets on performance or cardiac autonomic modulation between the conditions; the workloads and intensities used were consistent between both experimental conditions; and the visits were conducted at the same day of the week, facilitating the subjects to follow a similar routine on the day before the experiment.

In healthy young adult men, BL did not impact postexercise HR and cardiac sympathovagal balance. However, DL exposure decreased cardiac sympathovagal balance, which was compensated by a greater increase from pre- to postexercise. Thus, moderate aerobic exercise has a greater impact on cardiac autonomic modulation than light exposure, and their effects are not additive. Future investigations are warranted to study the DL effects on cardiac autonomic control as well as the effects of BL exposure at other times of the day and with other exercise protocols.

Acknowledgments

We thank all the subjects who participated in this study.

Funding

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP), Grant/Award Number: 2019/24327-5, 2022/ 12605-3 and 2018/05226-0 (to JCN, CLMF, and LCB); Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), Grant/Award Number: 302309/2022-5 (to CLMF); American Heart Association (AHA), Grant/Award Number: 24CDA1267757 (to LCB); National Institutes of Health Grant/Award Number: R01HL163232 (to SST).

Footnotes

Disclosure Statement

No potential conflict of interest was reported by the author(s).

Data Availability Statement

Data will be available upon reasonable request.

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