A Cross-Sectional Comparison of Cardiac Autonomic Responses at Rest, During, and After Exercise in Young Men across Different Waist-to-Height Ratio Categories

Abstract

A waist-to-height ratio (WHtR) above 0.5 is considered a threshold for elevated cardiometabolic risk. However, whether this cutoff is associated with altered cardiac autonomic control at rest, during exercise, and throughout post-exercise recovery remains unclear. This study compared cardiac autonomic indexes between young men categorized according to WHtR. Thirteen young men (24.8 ± 4.4 years) with WHtR ≥ 0.5 (G1) and 18 age-matched men (23.1 ± 4.1 years) with WHtR < 0.5 (G2) performed a maximal graded exercise test on a treadmill. Heart rate and heart rate variability measurements were taken at rest, during exercise, and throughout recovery using a portable cardiac monitor. At rest, G1 exhibited higher resting heart rate (81 ± 13 vs. 71 ± 8 bpm; P = 0.014) and lower parasympathetic activity (P < 0.05) compared with G2. During exercise, the percentage of chronotropic response did not differ between groups (G1: 92 ± 7% vs. G2: 95 ± 7%; P = 0.233). On post-exercise recovery, G1 had decreased heart rate recovery after 300 s (G1: 60 ± 8 bpm vs. G2: 69 ± 8 bpm; P = 0.007) and decreased cardiac parasympathetic reactivation (P < 0.05) compared with G2. Overall, young men with high and low WHtR exhibit similar chronotropic responses to maximal exercise, but individuals with high WHtR have impaired baseline cardiac autonomic control and slower post-exercise cardiac autonomic recovery.

Keywords:
Chronotropic response; Heart rate recovery; Heart rate variability; Visceral adiposity.

HIGHLIGHTS

• Young men with high waist-to-height ratio have lower resting cardiac vagal tone

• Heart rate response during exercise is normal in men with high waist-to-height ratio.

• Young men with high waist-to-height ratio have slower cardiac autonomic recovery.

INTRODUCTION

Excessive fat accumulation in the body has been widely recognized over the last decades as a major risk factor for numerous health complications, particularly clinical obesity [¹]. Although these concerns are well known, a substantial body of evidence has demonstrated that a large amount of fat specifically located in the central region of the body (i.e., visceral fat) exerts a greater negative influence on cardiovascular health than fat distributed throughout the body [²,³]. In this context, anthropometric indexes such as the waist-to-height ratio (WHtR) have been proposed to stratify cardiovascular risk across different populations [³,⁴]. The WHtR can be easily calculated by dividing an individual’s waist circumference by their height and is therefore a practical tool for use in daily clinical practice [⁵]. A WHtR higher than 0.5 has been considered indicative of high risk for cardiovascular complications [⁵].

The assessment of cardiac autonomic control is one of the simplest approaches for evaluating an individual’s overall cardiovascular health status [⁶]. Cardiac autonomic responses can be evaluated by monitoring heart rate (HR) and HR variability at rest, as well as during and after a given exercise bout [⁷-⁹]. For example, the assessment of HR variability indexes at rest provides valuable information about the functioning of the sympathetic and parasympathetic branches of the autonomic nervous system [⁸,¹⁰]. In addition, the evaluation of cardiac autonomic reactivity during maximal exercise by calculating the percentage of chronotropic response is important for specifically determining the autonomic nervous system’s capacity to appropriately increase HR under physiological stress [⁷]. During the recovery period following an exercise bout, the assessment of some HR variability indexes is also important to evaluate the capacity of the autonomic nervous system to return from a condition of physiological perturbation back to rest [⁹]. Notably, these cardiac autonomic indexes obtained under different physiological states are all considered as representative markers of overall cardiovascular health [⁷].

Some studies have investigated the impact of high visceral fat accumulation on cardiac autonomic control [¹¹-¹³]. For instance, greater visceral adiposity has been associated with impaired cardiac autonomic modulation, particularly reduced parasympathetic activity, across different populations [¹¹,¹³]. In addition, higher visceral fat stores have been linked to a slower decline in HR during the first minute of post-exercise recovery [¹²]. Conversely, a study comparing groups stratified by different WHtR categories did not find differences in HR recovery or post-exercise HR variability indexes between young men with low WHtR (< 0.50) and those with high WHtR (> 0.50) [¹⁴]. However, the chronotropic response to exercise was not assessed in the aforementioned study; thus, whether abdominal fat deposition could negatively influence cardiac autonomic reactivity to exercise is still unknown. To date, no study has combined assessments of cardiac autonomic indexes at baseline, during, and after an exercise bout within a single investigation. A comparative analysis of the cardiac autonomic profile, chronotropic responses to maximal exercise, and post-exercise cardiac autonomic recovery in individuals with high and low WHtR would provide a broader understanding of the potential negative consequences of visceral fat accumulation on cardiovascular health. In addition, most evidence regarding central adiposity and autonomic function comes from older populations or individuals with morbid obesity, who often present chronotropic incompetence [¹⁵-¹⁷]. It is unclear if young men with high WHtR exhibit this same global dysfunction or if the impairment is limited to specific autonomic branches. Therefore, analyzing the response to maximal exercise and recovery is necessary to verify the extent of autonomic dysregulation in this specific age group. Furthermore, it remains unknown whether a dissociation between preserved chronotropic response and impaired post-exercise autonomic recovery may be present, which could indicate an early stage of autonomic dysfunction.

The aim of this study was to compare the baseline cardiac autonomic profile, chronotropic response to maximal exercise, and post-exercise cardiac autonomic recovery between young men with high and low WHtR. We hypothesized that young men with high WHtR would exhibit a poorer resting cardiac autonomic profile, as well as impaired chronotropic response and post-exercise cardiac autonomic recovery, compared with young men with low WHtR.

MATERIAL AND METHODS

Participants

Thirteen men with high WHtR (i.e., WHtR ≥ 0.5, G1) and 18 age-matched men with low (i.e., WHtR < 0.5, G2) were recruited to participate in this study. Some participants self-reported diagnoses of chronic diseases and the use of corresponding pharmacological treatments (Table 1). The exclusion criteria were: (a) the presence of uncontrolled or clinically unstable cardiovascular or metabolic disease; (b) articular or bone injury; and (c) the use of any medication that could influence cardiovascular response. Participants with stable and clinically controlled conditions, under regular pharmacological treatment, were not excluded, provided they had no contraindications to participation. All participants were aware of the procedures and risks of the experiment and signed an informed consent. The study was approved by the Ethics Committee of State University of Ponta Grossa (number protocol approved 1.912.887) and performed in accordance with ethical standards.

Table 1
Baseline participant’s characteristics.

Variables	G1 (n = 13)	G2 (n = 18)	P value	Cohen's d
Age, yr	24.8 ± 4.4	23.1 ± 4.1	0.285	0.397
Height, cm	175.8 ± 6.2	177.8 ± 5.1	0.336	0.356
Weight, kg	107.3 ± 7.4	71.1 ± 7.9	0.001	4.713
Waist circumference, cm	107.6 ± 6.9	78.6 ± 6.5	0.001	4.349
Waist-to-height ratio	0.61 ± 0.05	0.44 ± 0.03	0.001	4.336
Body mass index, kg/m2	34.9 ± 3,7	22.4 ± 1,9	0.001	4.255
Total body fat mass, kg	43.9 ± 9.8	11.7 ± 4.3	0.001	4.679
Total body lean mass, kg	63.7 ± 7.6	59.2 ± 5.1	0.101	0.650
Systolic blood pressure, mmHg	118.5 ± 12.2	107.3 ± 12.7	0.020	0.898
Diastolic blood pressure, mmHg	76.5 ± 12.1	66.3 ± 6.1	0.005	1.118
Time spent in regular physical activities (min/week)	180 ± 258	210 ± 211	0.719	0.132
Current smoker, n (%)	1 (8)	0 (0)	NA	NA
Chronic diseases, n (%)
Hypothyroidism	2 (15)	0 (0)	NA	NA
Type 2 Diabetes Mellitus	1 (8)	0 (0)	NA	NA
Dyslipidemia	1 (8)	0 (0)	NA	NA
Pharmacological treatment, n (%)
Antidepressants	0 (0)	1 (6)	NA	NA
Thyroid-stimulating hormone	2 (15)	0 (0)	NA	NA
Statins	1 (8)	0 (0)	NA	NA
Biguanides	1 (8)	0 (0)	NA	NA

Procedures

Initially, participants underwent a structured anamnesis to obtain information on physical activity levels, the presence of chronic diseases, and current medication use. They were asked about their regular engagement in exercise programs (e.g., resistance training, aerobic exercise) and the weekly time spent in these activities. Then, anthropometric and body composition measurements were collected. Height was measured using a stadiometer (Cardiomed, Curitiba, Paraná, Brazil) with an accuracy of 0.1 cm, and body mass was measured using a digital scale (model UM-080; Tanita, model UM-080; Amsterdam, the Netherlands) with a precision of 0.1 kg. Waist circumference was measured once, following standardized procedures, with the participant in a standing position and using a flexible tape at the midpoint between the upper border of the iliac crest and the last rib. Fat mass and lean mass were assessed using tetrapolar bioelectrical impedance analysis (Maltron, model BF906; Essex, UK), following the manufacturer’s pretest instructions. Systolic and diastolic blood pressure were measured twice (with a 3-minute interval between measurements) using an automated blood pressure cuff (Omron, model HEM-7113 INT, Omron Healthcare, Hoofddorp, the Netherlands). The average of the two measurements was considered as the resting blood pressure [¹⁸]. R-R intervals (RRi) were continuously recorded for 10 minutes using a portable cardiac monitor (Polar V800; Polar, Kempele, Finland), while participants remained seated and breathed spontaneously. Thereafter, participants performed a maximal graded exercise test, followed by a 10-minute recovery. Participants were instructed not to ingest alcohol or caffeinated beverages and not to perform vigorous physical activity during the 48 hours before visiting the laboratory for data collection.

Maximal graded exercise test and recovery period

Participants underwent a maximal graded exercise test on a treadmill (Inbramed Millennium, model ATL, Porto Alegre, Brazil). The test began at a speed of 3.2 km·h⁻¹ and 0% grade, with the speed increasing by 1.6 km·h⁻¹ every minute until the third minute. From the fourth minute until volitional exhaustion, the treadmill speed was kept constant, and the grade was increased by 2% each minute. Immediately after completing the maximal graded exercise test, participants performed an active recovery consisting of walking on the treadmill at a constant speed of 2.4 km.h⁻¹ and a 2% slope for the first five minutes. During the remaining five minutes of the recovery period, participants stepped off the treadmill and remained seated [¹⁹].

Heart rate responses during and after exercise

Chronotropic reserve during exercise was calculated using the following equation [⁷]: Chronotropic reserve (%) = [HR reserve / (220 - age - Resting HR)] x 100. Resting HR was calculated as the average HR values during the last 5 minutes of the resting RRi recording, and the highest HR value recorded during the test was defined as peak HR. The maximum predicted HR was calculated using the equation 208 - 0.7 x age [²⁰]. Heart rate reserve was calculated as the difference between maximum HR attained in the maximal graded exercise test and Resting HR. A failure to reach at least 80% of the chronotropic reserve during the maximal incremental test was characterized as chronotropic incompetence [⁷]. Moreover, HR recovery indexes were calculated as the magnitude of HR decay from maximal HR to 60, 120, 300, and 600 seconds after exercise cessation (HRR_60s, HRR_120s, HRR_300s, and HRR_600s, respectively).

Heart rate variability assessment at rest and recovery

The R-R intervals (RRi) were continuously recorded using a portable cardiac monitor (Polar V800, Kempele, Finland) for 10 minutes at rest (i.e., immediately before the maximal graded exercise test), throughout the exercise, and for 10 minutes during the recovery period. The RRi recordings from the last 5 minutes of resting and recovery conditions were considered for analysis of HR variability indexes. Firstly, the ectopic beats were visually detected in raw data and manually excluded. Thereafter, the RRi data were detrended with the smoothness priors method (k = 500) [²¹]. The HR variability indexes calculated using linear methods were: 1) standard deviation of consecutive RRi (SDNN), and 2) root mean square of the successive differences between adjacent RRi (RMSSD). RMSSD is widely recognized as an index of parasympathetic (vagal) modulation, whereas SDNN reflects overall heart rate variability, representing the combined influence of both sympathetic and parasympathetic activity [²²]. Additionally, a time-varying parasympathetic-related index - RMSSD, calculated over successive non-overlapping 60-s segments (RMSSD_60s) - was calculated throughout the 10-min recovery period [⁹]. The HR variability indexes were all calculated using Kubios HRV Standard software (ver. 3.5.0; University of Eastern Finland, Kuopio, Finland).

Statistical Analyses

The Gaussian distribution and homogeneity of variances were checked using the Shapiro-Wilk and Levene tests, respectively. The anthropometric variables, resting blood pressure, physical activity level, time to exhaustion in the maximal graded exercise test, resting HR, and HR responses during exercise and recovery were all compared between G1 and G2 groups using unpaired Student t test. Effect sizes for the t-tests were calculated and reported as Cohen’s d, where values < 0.20 indicate trivial effect, between 0.20 and 0.49 indicate a small effect, between 0.50 and 0.79 indicate a moderate effect, and ≥ 0.80 indicates a large effect [²³].

The mean RRi, RMSSD, and SDNN were compared using two-way ANOVA (group: G1 and G2; vs. time: rest and recovery). In addition, the RMSSD_60s segments were also compared using two-way ANOVA (group: G1 and G2 vs. time: 60, 120, 180, 240, 300, 360, 420, 480, 540 and 600s). The sphericity of the variances was confirmed via Mauchly’s test. When ANOVA detected a group vs. time interaction, further pairwise comparisons were performed using Fisher least significant difference (LSD) post hoc test. Effect size for F-statistics was expressed as partial eta-squared (ŋ_p²), where ŋ_p² was considered as small (ŋ_p² < 0.06), moderate (ŋ_p² between 0.06 and 0.149), or large (ŋ_p² ≥ 0.15) [²³]. Spearman’s rank correlation coefficients were calculated to examine the associations between WHtR and resting HR, and HR variability indexes at rest and during recovery. The significance was accepted when P < 0.05. The analyses were performed using Jamovi free software (version 2.3, https://www.jamovi.org).

RESULTS

The time to exhaustion in the maximal graded exercise test was significantly lower (P = 0.011) in the G1 (620 ± 151 s) when compared to the G2 (755 ± 122 s) group.

Resting HR and HR responses during exercise and recovery are shown in Table 2. As expected, resting HR was significantly higher in G1 when compared to G2 (P = 0.014). In addition, HR reserve and HRR_300s were significantly lower in G1 than in G2 (all P < 0.05). However, chronotropic reserve, peak HR, peak HR relative to maximum predicted HR, HRR_60s, HRR_120s, and HRR_600s were all similar between G1 and G2 (all P > 0.05). In addition, chronotropic incompetence was not identified in any participant either in G1 and G2 groups.

Table 2
Heart rate at rest, during and after a maximal graded exercise test.

Variables	G1 (n = 13)		G2 (n = 18)	P value	Cohen's d
Resting HR, beats/min		81 ± 13	71 ± 8	0.014	0.952
HR during exercise
Peak HR, beats/min		186 ± 8	190 ± 8	0.175	0.506
Peak HR, % of maximum predicted HR		97 ± 4	99 ± 4	0.315	0.372
HR reserve, beats/min		105 ± 15	119 ± 8	0.002	1.215
Chronotropic reserve, %		92 ± 7	95 ± 7	0.233	0.444
HR during recovery
HRR60s, beats/min		32 ± 7	35 ± 7	0.262	0.417
HRR120s, beats/min		48 ± 8	53 ± 8	0.154	0.533
HRR300s, beats/min		60 ± 8	69 ± 8	0.007	1.053
HRR600s, beats/min		80 ± 9	86 ± 9	0.090	0.639

There was a main effect of group for mean RRi (F_(1,58) = 7.84, P = 0.007, η_p² = 0.119), with lower mean RRi in the G1 than in the G2 group, regardless of time. In addition, there was a main effect of time for mean RRi (F_(1,58) = 153.81, P = 0.001, η_p² = 0.726), with lower mean RRi values during the recovery period than during resting condition. However, there was not a group vs. time interaction (F_(1,58) = 3.02, P = 0.088, η_p² = 0.049) for mean RRi (Figure 1a).

Figure 1
Differences between G1 and G2 at rest and during post-exercise recovery for (a) mean R-R intervals, (b) RMSSD, and (c) SDNN.

The ANOVA indicated a significant main effect of group for RMSSD (F_(1,58) = 7.21, P = 0.009, η_p² = 0.111), with lower RMSSD in G1 than in the G2. Moreover, there was a main effect of time for RMSSD (F_(1,58) = 113.24, P = 0.001, η_p² = 0.661), with RMSSD being lower during the recovery period than during the resting condition, regardless the group. However, the ANOVA test did not indicate a group vs. time interaction (F_(1,58) = 2.88, P = 0.095, η_p² = 0.047) for RMSSD (Figure 1b).

For SDNN, there was a main effect of group (F_(1,58) = 6.19, P = 0.016, η_p² = 0.096), with lower mean SDNN in the G1 than in the G2 group. In addition, there was a main effect of time for SDNN (F_(1,58) = 124.78, P = 0.001, η_p² = 0.683), with lower SDNN values during the recovery period than during the resting condition. However, there was not group vs. time interaction (F_(1,58) = 1.51, P = 0.223, η_p² = 0.025) for SDNN (Figure 1c).

† Significantly lower than Rest, regardless of group (P < 0.05).

The RMSSD_60s segments during post-exercise recovery are shown in Figure 2. There was a main effect of group (F_(1,58) = 6.53, P = 0.016, η_p² = 0.184) and time (F_(1,58) = 17.17, P = 0.001, η_p² = 0.372) for RMSSD_60s segments. In addition, there was a group vs. time interaction for RMSSD_60s segments. The pairwise comparisons revealed that RMSSD_60s segments were significantly lower at 420 (P = 0.024), 540 (P = 0.011), and 600 s (P = 0.008) in G1 when compared to the G2 group.

Figure 2
Root-mean-square of successive differences in the R-R intervals measured in successive non-overlapped 60 s segments (RMSSD_60s) on post-exercise recovery after maximal graded exercise test for both G1 and G2 groups.

The WHtR was significantly correlated with resting heart rate (ρ = 0.400, P = 0.026), mean RRi at rest(ρ = 0.400, P = 0.022), and RMSSD during recovery (ρ = -0.368, P = 0.048). However, WHtR did not correlate with RMSSD and SDNN at rest, and mean RRi and SDNN during post-exercise recovery (all P > 0.05).

DISCUSSION

A cross-sectional comparative analysis of the resting cardiac autonomic control, chronotropic response to maximal exercise, and post-exercise cardiac autonomic recovery between young men with high and low WHtR was conducted in this study. The main findings revealed that young men with high WHtR, compared with their low-WHtR counterparts, exhibited: (1) higher resting HR and lower baseline mean RRi, RMSSD, and SDNN, indicating impaired baseline parasympathetic activity; (2) a normal chronotropic response to maximal exercise; and (3) lower mean RRi, RMSSD, RMSSD_60s segments, SDNN, and HRR_300s during post-exercise recovery, reflecting delayed parasympathetic reactivation following maximal exercise.

An important first finding of the present study is that young men with high WHtR exhibited impaired baseline cardiac parasympathetic activity compared with those with low WHtR, as evidenced by higher resting HR and lower baseline mean RRi, RMSSD, and SDNN. This finding is consistent with cross-sectional studies showing that greater visceral adiposity negatively impacts resting cardiac vagal tone [¹¹-¹³]. However, a study that specifically compared young men with WHtR between 0.50 and 0.56 with those presenting WHtR between 0.40 and 0.449 and between 0.45 and 0.50 did not report differences in resting HR, RMSSD, or SDNN among groups [¹⁴]. The discrepancy between these findings may be explained by differences in the criteria used to classify individuals within the high-WHtR group. In the present study, no upper limit was imposed for the high-WHtR group (i.e., WHtR > 0.50), whereas in the aforementioned study, the high-WHtR group was restricted to values between 0.50 and 0.56 [¹⁴]. These methodological differences resulted in distinct group characteristics, with participants in this study exhibiting higher mean WHtR values (0.61 ± 0.05 vs. 0.53 ± 0.02), which may have led to a greater impairment of cardiac autonomic modulation.

In the present study, the chronotropic response to exercise was similar between individuals with high and low WHtR, suggesting that a large amount of visceral fat does not impair cardiac autonomic responsiveness to the physiological stress imposed by a maximal graded exercise test. While no previous study has specifically compared the chronotropic response between participants stratified by WHtR, this finding is not in line with earlier studies reporting a lower chronotropic response to exercise and a higher prevalence of chronotropic incompetence in obese compared with lean individuals [¹⁶,¹⁷]. Although the mechanisms underlying this preserved cardiac autonomic reactivity during maximal exercise in men with high WHtR are not fully understood, it can be hypothesized that impaired chronotropic responsiveness arises primarily from cardiovascular and metabolic disturbances secondary to visceral fat accumulation, rather than from excess visceral fat per se. For instance, a study reporting chronotropic impairment in obesity included individuals with a higher prevalence of concomitant cardiovascular and metabolic abnormalities, such as hypertension and diabetes mellitus [¹⁶], which are known to blunt β-adrenergic sensitivity in the sinus node and therefore the heart rate responsiveness during exercise [⁷]. For example, in the aforementioned study, the prevalence rates for hypertension and diabetes mellitus in the obese group were >80% and 17%, respectively [¹⁶]. Therefore, the excess of visceral fat per se might not be sufficient to compromise cardiac autonomic reactivity during maximal exercise, despite its negative effects on parasympathetic activity at rest and during post-exercise recovery.

The most novel finding of the present study is the dissociation between a preserved chronotropic response to maximal exercise and an impaired post-exercise parasympathetic reactivation in young men with high WHtR. This pattern suggests that autonomic dysfunction associated with central adiposity may begin with parasympathetic impairment, while sympathetic responsiveness remains preserved. This finding provides evidence of a potential early stage of autonomic dysregulation, in which alterations are not yet sufficient to impair cardiac responsiveness to exercise but are already detectable during the recovery phase. From a physiological perspective, this dissociation reinforces the importance of assessing post-exercise autonomic recovery, as resting measures or exercise responses alone may underestimate early autonomic impairment.

A final relevant finding of the present study was that young men with high WHtR exhibited delayed parasympathetic reactivation following maximal exercise, as evidenced by lower mean RRi, RMSSD, RMSSD_60s segments, SDNN, and HRR_300s throughout post-exercise recovery. This finding is not in line with a previous study that compared young men with WHtR between 0.50 and 0.56 with young men with WHtR between 0.40 and 0.449 and young men with between 0.45 and 0.50. The aforementioned differences in the criteria used to classify individuals within the high-WHtR group might also explain these discrepant results. Although the mechanisms underlying this delayed parasympathetic reactivation from maximal exercise observed in individuals with high WHtR cannot be determined from the present data and are beyond the scope of this research, this impairment may be related to chronic low-grade systemic inflammation associated with excessive visceral fat accumulation [²⁴]. Visceral adipose tissue is a major source of pro-inflammatory adipokines and cytokines, particularly interleukin-6 (IL-6), which contribute to a persistent inflammatory environment [²⁵,²⁶]. This systemic inflammatory state has been shown to negatively affect parasympathetic nervous system activity [²⁵], potentially delaying cardiac autonomic recovery from a maximal exercise bout [²⁴].

An important strength of the present study deserves to be highlighted. We simultaneously assessed multiple indexes of cardiac autonomic regulation across different physiological conditions (i.e., at rest, during exercise, and during post-exercise recovery). This methodological approach allows for a more comprehensive understanding of autonomic function under baseline conditions, as well as during the rapid adjustments required to respond appropriately to the physiological stress imposed by exercise and to facilitate the return toward homeostasis during recovery [²⁷].

On the other hand, some limitations of the present study should also be acknowledged. A first important limitation is the lack of women within the sample. As women exhibit different circadian patterns of cardiac autonomic function and distinct post-exercise autonomic recovery behavior [²⁸-³⁰], as well as sex-specific patterns of fat distribution [³¹], caution is warranted when generalizing the present findings to women. Therefore, studies comparing cardiac autonomic control among women with different WHtR categories are needed. Second, the absence of spectral analysis of frequency-domain indexes of HR variability limits a more comprehensive understanding about how WHtR influences the sympathetic component. As a reliable frequency-domain assessment requires controlled breathing during data collection [³²], future studies employing such methodological procedures would help address this gap. The small sample size, especially in the high-WHtR group, restricts the generalizability of the findings and precludes a larger extrapolation of the results. Furthermore, the inclusion of participants with clinical conditions and pharmacological treatments, although characteristic of the clinical profile associated with elevated WHtR, introduces potential confounding factors regarding autonomic regulation. Therefore, the observed distinctions should be interpreted with caution. Finally, the cross-sectional design precludes establishing causal relationships between WHtR and the observed autonomic alterations. The study also did not assess longitudinal clinical outcomes or functional performance metrics. Future investigations should employ longitudinal designs to determine if the delayed vagal recovery predicts long-term cardiovascular risk in this population. Additionally, implementing hemodynamic monitoring and inflammatory biomarkers would help elucidate the physiological mechanisms coupling visceral adiposity to the observed autonomic dysfunction.

The translational implications of these results indicate to WHtR's special therapeutic value in cardiovascular risk assessment. The observed dissociation between preserved chronotropic response during maximal exercise and delayed parasympathetic reactivation on post-exercise recovery suggests that traditional ergometric assessments that focus solely on the exertion phase may miss latent autonomic dysfunction in young men with high WHtR. As a result, a WHtR > 0.5 is a useful anthropometric marker for identifying people who need special monitoring during the fast-recovery period, particularly the first 300 seconds after exercise. Regarding exercise prescription, the delayed vagal return demands the deployment of longer active recovery procedures. This technique attempts to reduce susceptibility caused by extended sympathetic dominance and restore sympathovagal balance [⁹,²⁷].

CONCLUSION

Young men with high and low WHtR exhibit similar chronotropic responses to maximal exercise. However, individuals with high WHtR have impaired baseline cardiac autonomic control, characterized primarily by reduced parasympathetic activity, and slower post-exercise cardiac autonomic recovery, mainly due to delayed parasympathetic reactivation. These findings suggest that a greater amount of visceral fat negatively affects both resting and post-exercise cardiac autonomic regulation. Therefore, strategies aimed at mitigating these impairments and reducing associated cardiovascular health risks are desirable.

• Funding:
  This research received no external funding.
• Institutional Review Board Statement:
  The study was conducted in accordance with the Declaration of Helsinki, and approved by the Ethics Committee of State University of Ponta Grossa (number protocol approved 1.912.887).
• Informed Consent Statement:
  Informed consent was obtained from all subjects involved in the study.

Use of Generative Artificial Intelligence

The authors declare that large language models and other generative artificial intelligence (AI) or AI-assisted technologies cannot be credited as authors and have not been listed as authors of this paper.

The authors declare that they did not use artificial intelligence.

Acknowledgments:

Authors are thankful to the participants for their voluntary participation in this study.

Data Availability Statement:

Research data are available upon reasonable request for corresponding author

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• Editor-in-Chief:
  Paulo Vitor Farago

• Associate Editor:
  Bruno Pedroso

Publication Dates

• Publication in this collection
  17 Aug 2026
• Date of issue
  2026

History

• Received
  03 Feb 2026
• Accepted
  13 May 2026