Abstract
[Purpose] To determine the optimal timing of aerobic exercise for nocturnal blood pressure (BP), this study compared the acute effects of morning and evening moderate-intensity aerobic exercise (65% heart rate reserve, 30 min) on nocturnal BP, and sleep quality. [Participants and Methods] This randomized crossover study included 15 healthy young male participants who randomly completed three experimental trials: (1) morning trial (09:30–10:00), (2) evening trial (17:30–18:00), and (3) a sedentary control trial. The exercise consisted of cycling for 30 min at 65% heart rate reserve. Nocturnal systolic BP (SBP), and sleep efficiency were assessed using the oscillometric method, and actigraphy, respectively. [Results] The morning trial produced a lower nocturnal SBP than both the evening (Cohen’s d=0.82) and control trials (Cohen’s d=1.23), whereas the evening trial also produced a lower nocturnal SBP than the control trial (Cohen’s d=0.32). Sleep efficiency was higher in the morning trial than in both the evening (Cohen’s d=5.42) and control trials (Cohen’s d=5.12). [Conclusion] Morning aerobic exercise more effectively promoted nocturnal BP dipping among healthy young men than did evening exercise.
Key words: Acute aerobic exercise, Timing, Nocturnal blood pressure
INTRODUCTION
Insomnia, which is quite common among the general population, has been associated with serious health problems, negatively impacting quality of life and having significant economic consequences1). A systematic review estimated the global prevalence of adult insomnia to be 852,325,091 (global prevalence: 16.2%), among whom 414,967,941 experienced severe insomnia (7.9%), reaffirming the need for comprehensive initiatives promoting global public and clinical sleep health2). According to the Ministry of Health, Labour and Welfare, 20.6% of Japanese people fail to get enough rest through sleep in recent years, which represents a significant increase from previously reported rates3). These trends emphasize the need for preventing and treating insomnia to reduce the risk of lifestyle-related diseases in the future and maintain long-term health4).
Cardiovascular disease (CVD) remains the leading cause of death worldwide, accounting for one-third of all deaths globally5). A critical mechanism underlying this association is the elevation of nocturnal blood pressure (BP). A prospective observational study found that the risk of composite cardiovascular outcomes was 2.15 times higher among individuals with nocturnal hypertension than among those with normal nocturnal BP6). During non-rapid eye movement (REM) sleep, parasympathetic nervous system activity increases, consequently decreasing cardiac sympathetic nervous system activity7). A decrease in sympathetic nervous system activity can cause a dipping phenomenon in which mean arterial pressure decreases by approximately 10% compared to when the person is awake8). This nocturnal reduction in BP is essential for vascular endothelial recovery and prevention of atherosclerosis progression9). During REM sleep, however, sympathetic activity increases, causing increased BP fluctuations10). Consequently, impaired sleep quality can promote sustained nocturnal BP elevation10). Indeed, studies have linked reduced sleep efficiency to a 10-mmHg increase in nocturnal BP, which has been associated with a 20% increase in CVD risk11). Therefore, reducing nighttime BP is essential for preventing CVD.
The Ministry of Health, Labour and Welfare recommends regular exercise to improve sleep quality but also emphasizes the importance of timing12). Yamanaka et al. suggested that among healthy young men, morning exercise enhances parasympathetic nervous system activity, whereas evening exercise activates sympathetic nervous system activity13). To the best of our knowledge, only one previous study has investigated the association between timing of aerobic exercise and nocturnal BP. Fairbrother et al.14) reported that when prehypertensive individuals performed aerobic exercise (30 min of treadmill exercise) in the morning and afternoon, the morning aerobic exercise promoted a greater decrease in nighttime BP than did the afternoon exercise. Although previous studies have demonstrated the acute BP-lowering effects of aerobic exercise during sleep6), research comparing the effects of different exercise timings has been lacking. Moreover, given that existing studies have been conducted on disease groups who already have vascular lesions or autonomic nervous system dysfunction, it remains unclear whether healthy young people with preserved vascular flexibility can achieve similar BP-lowering effects. Thus, the effects of exercise timing on nocturnal BP among healthy individuals remain underexplored.
Therefore, the present study aimed to determine the optimal timing for each moderate-intensity aerobic exercise session to improve nocturnal BP among healthy young men. We hypothesized that morning exercise would be more effective in reducing nocturnal BP than would evening exercise among healthy young men.
PARTICIPANTS AND METHODS
This study enrolled 15 healthy, sedentary young men (Table 1). All participants were normotensive, nonsmokers, and free from chronic diseases or any medication use. Our study protocol was approved by the Ethics Committee of Teikyo University of Science (Approval No. 24A050) and conducted in accordance with the Declaration of Helsinki and institutional guidelines for human experimentation. Prior to study initiation, a power analysis (G*Power) indicated that a minimum of nine participants was required to detect a significant effect (effect size d=0.5, power=0.80, α=0.05). All particiapnts provided written informed consent. A randomized crossover design was employed, comprising three experimental conditions: (1) morning exercise (09:30–10:00; AM), (2) evening exercise (17:30–18:00; PM), and (3) control (CON). Participants were not informed of the specific study hypothesis regarding the effects of exercise timing. To minimize the influence of individual circadian rhythms, participants were instructed to maintain a standardized sleep–wake schedule (23:00–06:00) and a consistent sleep duration for seven consecutive days prior to the first trial. Compliance was monitored using daily sleep logs and wrist actigraphy. Each trial was separated by at least a 7-day washout period to minimize carry-over effects. Participants were instructed to maintain a consistent level of physical activity across all test days, and daily step counts were recorded using a wrist actigraphy (Actigraph wGT3X-BT; ActiGraph, Pensacola, FL, USA). Participants were instructed to maintain their habitual diet throughout the study and to consume the same meals on each experimental day. During the 24 h preceding each trial, alcohol, caffeine, and vigorous physical activity were strictly prohibited. Chronotype was not assessed in the present study. Participants performed 30 min of pedaling on a cycle ergometer (Medelgo EM-400; OG Giken Co., Ltd., Okayama, Japan) at an intensity of 60 to 65% of their heart rate reserve (HRR). Heart rate (HR) was monitored continuously (Polar Unite; Polar Electro, Kempele, Finland), and the rating of perceived exertion (RPE) was assessed every 3 min using the Borg 6–20 scale. Nocturnal hemodynamics, including systolic BP (SBP) and diastolic BP (DBP), were measured using an automated oscillometric device (HEM-9601T) at baseline (pre-exercise), 02:00, and 04:0015). Mean arterial pressure (MAP) was calculated as DBP + (PP/3), whereas pulse pressure (PP) was calculated as SBP − DBP. For nocturnal BP analysis, the average values for measurements obtained at 02:00 and 04:00 were used. The intra-laboratory coefficient of variation for BP was 2 ± 1%. Sleep architecture, including total sleep time (ST; the duration of actual sleep obtained during the sleep period), sleep onset latency (SOL), sleep efficiency (SE), wake after sleep onset (WASO), and number of awakenings (NWAK) were evaluated using wrist actigraphy (Actigraph wGT3X-BT; ActiGraph, Pensacola, FL, USA)16). Data were expressed as mean ± standard deviation. Normality of data distribution was confirmed using the Shapiro–Wilk test. A repeated-measures two-way analysis of variance (trial ×time) was employed to compare hemodynamic variables. Upon detecting a significant main effect or interaction, the Bonferroni post-hoc test was used for multiple comparisons. Relative effect sizes for performance data were calculated using Cohen’s d and are defined as small (d=0.2), medium (d=0.5), or large (d=0.8). Statistical analyses were performed using SPSS (version 30; IBM, Armonk, NY, USA), with a p-value of <0.05 indicating statistical significance.
Table 1. Participant characteristics (n=15).
| Variable | |
| Age (years) | 23.9 ± 1.1 |
| Height (cm) | 171.9 ± 1.6 |
| Weight (kg) | 62.5 ± 2.2 |
| BMI (kg/m2) | 21.1 ± 0.5 |
Values are presented as mean ± standard deviation. BMI: body mass index.
RESULTS
No significant differences in HR or RPE during exercise were observed between the two exercise trials (Table 2). Compared with baseline, SBP, MAP, DBP, and HR were lower during sleep across all trials (p<0.05), whereas PP remained unchanged (Table 3). No differences in baseline BP or HR were observed among the trials (Table 3). The morning trial produced lower nocturnal SBP than did both the evening (p<0.05, Cohen’s d=0.82) and the control trials (p<0.01, Cohen’s d=1.23), whereas the evening trial also produced lower nocturnal SBP than did the control trial (p<0.05, Cohen’s d=0.32; Table 3). Nocturnal MAP (p<0.01, Cohen’s d=1.16) and HR (p<0.01, Cohen’s d=1.60) were lower in the morning trial than in the Control trial (Table 3). No inter-trial differences in nocturnal DBP or PP were observed (Table 3). ST was longer in the morning trial than the evening (p<0.01, Cohen’s d=3.35) and Control trials (p<0.01, Cohen’s d=3.37), and evening trial was longer than control trial (p<0.01, Cohen’s d=1.34; Table 4). Both the morning and evening trials produced lower SOL than the control trial (p<0.01, Cohen’s d=2.40 for morning vs. control; Cohen’s d=1.35 for evening vs. control), whereas the morning trial produced lower SOL than the evening trial (p<0.01, Cohen’s d=2.52; Table 4). SE was higher in the morning trial than in the evening trial (p<0.01, Cohen’s d=5.42) and the control trial (p<0.01, Cohen’s d=5.12; Table 4). WASO was lower in the morning trial than in the evening (p<0.01, Cohen’s d=6.83) and the control trial (p<0.01, Cohen’s d=3.35), whereas the evening trial showed higher WASO than the control trial (p<0.01, Cohen’s d=1.35; Table 4). NWAK was lower in the morning trial than in the evening trial (p<0.01, Cohen’s d=4.90) and the control trial (p<0.01, Cohen’s d=2.67), whereas the evening trial showed higher NWAK than the control trial (p<0.01, Cohen’s d=1.35; Table 4). Daily step counts did not differ among the trials (Table 5).
Table 2. Changes in mean HR and final RPE during exercise.
| Variable | Morning trial | Evening trial | Control trial |
| Mean HR (beats/min) | 148.5 ± 4.8 | 147.9 ± 5.2 | NA |
| Final RPE | 13.6 ± 0.5 | 13.5 ± 0.6 | NA |
Values are presented as mean ± standard deviation. HR: heart rate; RPE: rating of perceived exertion; NA: not applicable.
Table 3. Changes in blood pressure and heart rate.
| Variable | Morning trial |
Evening trial |
Control trial |
|||
| Pre | During sleep | Pre | During sleep | Pre | During sleep | |
| SBP (mmHg) | 106.5 ± 4.0 | 87.6 ± 3.1*#‡ | 107.0 ± 6.5 | 93.3 ± 6.4*† | 106.1 ± 6.4 | 95.8 ± 5.2* |
| MAP (mmHg) | 80.8 ± 3.6 | 61.3 ± 2.6*‡ | 80.8 ± 6.0 | 65.4 ± 5.7* | 80.4 ± 5.4 | 67.0 ± 5.4* |
| DBP (mmHg) | 67.9 ± 4.3 | 48.1 ± 3.8* | 67.8 ± 6.2 | 51.5 ± 6.0* | 67.5 ± 5.6 | 52.6 ± 6.0* |
| PP (mmHg) | 38.7 ± 4.5 | 39.5 ± 5.2 | 39.3 ± 3.6 | 41.8 ± 4.7 | 38.5 ± 4.6 | 43.2 ± 4.2 |
| HR (bpm) | 63.9 ± 5.8 | 49.4 ± 3.5*‡ | 62.0 ± 6.0 | 52.7 ± 4.6* | 64.9 ± 8.3 | 55.5 ± 4.0* |
Values are presented as mean ± standard deviation. *p<0.05 vs. pre. #p<0.05 vs. the evening trial. ‡p<0.01 and †p<0.05 vs. the control trial. SBP: systolic blood pressure; MAP: mean arterial pressure; DBP: diastolic blood pressure; PP: pulse pressure; HR: heart rate.
Table 4. Sleep state between trials.
| Variable | Morning trial | Evening trial | Control trial |
| ST (min) | 491.1 ± 8.8##‡ | 423.5 ± 3.6‡ | 412.5 ± 4.1 |
| SOL (min) | 0.0 ± 0.0##‡ | 9.2 ± 0.9‡ | 17.6 ± 1.9 |
| SE (%) | 99.0 ± 0.3##‡ | 92.6 ± 0.1 | 92.3 ± 0.1 |
| WASO (min) | 4.1 ± 1.4##‡ | 24.7 ± 0.8‡ | 16.8 ± 1.7 |
| NWAK (count) | 1.3 ± 0.4##‡ | 15.1 ± 0.3‡ | 10.8 ± 0.9 |
Values are presented as mean ± standard deviation. ‡p<0.01 vs. the control trial, ##p<0.01, vs. the evening trial. ST: total sleep time; SOL: sleep onset latency; SE: sleep efficiency; WASO: wake time after sleep onset; NWAK: number of awakenings.
Table 5. Number of steps between trials.
| Variable | Morning trial | Evening trial | Control trial |
| Number of steps (steps/day) | 8,453.7 ± 1,343.3 | 8,394.0 ± 1,340.2 | 8,450.8 ± 1,343.4 |
Values are presented as mean ± standard deviation.
DISCUSSION
The present study investigated aerobic exercise timing effects on nocturnal blood pressure in healthy young men. Morning exercise produced significantly greater nocturnal SBP reductions (Cohen’s d=0.82, percentage reduction=6.5%) and superior sleep efficiency (Cohen’s d=5.42, percentage improvement=6.9%) compared to evening exercise and control conditions. Evening exercise shortened sleep onset latency but did not improve sleep maintenance. These observations suggest that the exercise-to-bedtime timing interval may influence nocturnal BP and sleep quality.
Physiologically, both BP and HR decrease during non-REM sleep due to parasympathetic activity, a phenomenon called nocturnal dipping with cardioprotective effects17). Baseline measurements showed no significant differences, confirming adequate control. Acute aerobic exercise induces post-exercise hypotension (PEH), persisting up to 24 h 18, 19). Although both morning and evening trials reduced nocturnal SBP versus control, morning exercise produced greater reductions despite a longer exercise-to-bedtime interval—inconsistent with simple PEH decay. de Brito et al.20) reported similar timing-dependent effects in prehypertensive individuals. These observations suggest that timing interval, rather than PEH time course, might influence nocturnal BP responses, though alternative explanations remain possible.
Evening aerobic exercise effects on sleep are mixed: some studies show no impairment21, 22). while meta-analyses indicate associations between evening exercise and impaired sleep maintenance23). Consistent with meta-analytic evidence, only morning exercise improved sleep efficiency in this study. The exercise-to-bedtime timing interval could plausibly contribute to these observations. Exercise elevates sympathetic activity during and after exertion13, 24). Evening exercise, performed closer to sleep, might allow sympathetic activation to persist into early sleep. During non-REM sleep, parasympathetic activity normally predominates25); persistent sympathetic activation could interfere with this transition, potentially attenuating nocturnal SBP reduction and sleep maintenance25). Morning exercise’s longer pre-sleep interval could permit sympathetic recovery and normal parasympathetic dominance transition during sleep onset, possibly facilitating nocturnal BP reduction and sleep quality. This timing-interval-dependent mechanism is speculative. Autonomous nervous system activity, catecholamines, melatonin, and cortisol were not directly measured; therefore, whether timing interval or other factors predominate remains unknown. Future studies must directly measure heart rate variability (LF, HF, LF/HF ratio, total power), catecholamine concentrations (epinephrine, norepinephrine), melatonin, and cortisol at multiple timepoints—immediately after exercise, at bedtime, and during sleep—to test whether timing-dependent sympathetic recovery fully explains the observed effects or whether additional mechanisms contribute.
Nocturnal SBP reductions carry clinical relevance. Nocturnal BP independently predicts cardiovascular events26), and persistent nocturnal hypertension accelerates atherosclerosis progression27). Each 10-mmHg nocturnal SBP increase associates with approximately 15–20% increased CVD risk9). Concurrent improvements in SE and nocturnal SBP reduction following morning exercise might provide synergistic cardiovascular benefits, though this remains speculative without direct hemodynamic measurement.
The study has several limitations. First, findings were limited to healthy young men; generalizability to women, older adults, and clinical populations is unknown. Second, actigraphy cannot identify sleep stages necessary for comprehensive hemodynamic analysis8). Third, autonomic and endocrine variables were not measured; this prevents confirmation of proposed mechanisms. Fourth, chronotype was not assessed. Although timing interval may provide a more direct mechanistic explanation than circadian factors, neither was directly tested. Future studies should measure heart rate variability (LF, HF, LF/HF ratio, total power), catecholamines (epinephrine, norepinephrine), melatonin, and cortisol to directly test whether timing-dependent sympathetic recovery or other mechanisms explain the observed timing-dependent effects.
In conclusion, morning aerobic exercise appears to be the most effective strategy for reducing nocturnal BP and enhancing SE among healthy young men. Although evening exercise may facilitate sleep onset, it may also impair sleep maintenance and attenuate the nocturnal BP-lowering response. Therefore, appropriate management of exercise timing is critically important for the simultaneous reduction of cardiovascular burden and maintenance of high-quality sleep.
Funding
This work was supported by JSPS KAKENHI Grant Number JP 23K10645.
Conflict of interest
The authors declare no conflicts of interest.
Funding Statement
This work was supported by JSPS KAKENHI Grant Number JP 23K10645.
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