Obesity is a global health concern, significantly increasing the risk of cardiovascular diseases, metabolic disorders, and autonomic dysfunction [1]. The autonomic nervous system (ANS), comprising the sympathetic and parasympathetic branches, plays a crucial role in maintaining homeostasis. Dysregulation of the ANS has been implicated in the pathophysiology of obesity and its associated comorbidities [2,3].

Recent studies have demonstrated that obesity is associated with altered autonomic function. For instance, a study by Lkhagvasuren et al. (2025) reported impaired autonomic function in obese individuals, leading to altered intestinal motility and gut dysbiosis [4]. Similarly, Phoemsapthawee et al. (2025) found that autonomic dysfunction in obesity contributes to reduced cardiovascular adaptability and increased fatigue during prolonged physical activity [5].

Autonomic function can be assessed using various non-invasive tests. The heart rate response to deep breathing, Valsalva maneuver, and orthostatic blood pressure measurements are commonly employed to evaluate parasympathetic and sympathetic activity. Studies have shown that these tests can reveal significant differences in autonomic function between obese and non-obese individuals. For example, Papadopoulos et al. (2024) conducted a meta-analysis demonstrating autonomic dysfunction in obese children and adolescents, primarily attributed to reduced vagal tone and increased sympathetic activity

[6].

Understanding the alterations in autonomic function associated with obesity is essential for early identification of individuals at risk for cardiovascular and metabolic complications. This study aims to assess autonomic function in obese individuals using standard autonomic function tests and compare the results with age- and sex-matched non-obese controls.

Study Design and Setting: This was a cross-sectional observational study conducted in an Indian medical college and hospital. The study aimed to assess the autonomic function in obese individuals and compare it with age- and sex-matched non-obese controls.

Study Population: The study included adult individuals aged 18–60 years. Participants were divided into two groups:

• Group A (Obese): Individuals with a body mass index (BMI) ≥30 kg/m²
• Group B (Control): Age- and sex-matched individuals with BMI 18.5–24.9 kg/m²

Exclusion criteria: Individuals with known cardiovascular diseases, diabetes mellitus, hypertension, neurological disorders, chronic renal or hepatic disease, current use of medications affecting autonomic function, or history of smoking/alcohol abuse were excluded.

Sample Size: Assuming a medium effect size, with α = 0.05 and power (1–β) = 0.8, the minimum sample size calculated was 60 participants per group. To account for potential dropouts, 70 participants per group were enrolled, totaling 140 participants.

Anthropometric Measurements: Height and weight were measured using a stadiometer and calibrated weighing scale, respectively. BMI was calculated using the formula: BMI=Weight (kg)/Height (m)². Waist circumference and waist-to-hip ratio were also recorded to assess central obesity.

Autonomic Function Tests: Autonomic function was evaluated using a standardized battery of non-invasive cardiovascular reflex tests:

1. Heart Rate Response to Deep Breathing (HRDB): Participants performed deep breathing at 6 breaths/min. The mean difference between maximum and minimum heart rate was calculated.
2. Valsalva Maneuver: Participants exhaled against a pressure of 40 mmHg for 15 seconds. The Valsalva ratio (maximum HR/minimum HR) was recorded.
3. Orthostatic Test: Heart rate and blood pressure were measured in supine and standing positions. The 30:15 ratio and postural blood pressure changes were analyzed.
4. Cold Pressor Test: Participants immersed their hand in ice-cold water for 1 minute, and blood pressure response was recorded.

All tests were conducted in a quiet, temperature-controlled room, with participants fasting for at least 2 hours before testing and avoiding caffeine or strenuous activity for 12 hours.

Data Collection and Analysis: Data were entered into Microsoft Excel and analyzed using SPSS version 25. Continuous variables were expressed as mean ± standard deviation, and categorical variables as frequencies and percentages. Independent t-tests were used to compare continuous variables between groups, while chi-square tests were applied for categorical variables. A p-value <0.05 was considered statistically significant.

A total of 140 participants were enrolled, with 70 individuals in the obese group and 70 in the control group. The groups were comparable in age and sex distribution (p > 0.05). As expected, BMI, waist circumference, and waist-to-hip ratio were significantly higher in the obese group compared to controls (p < 0.001) (Table 1).

The heart rate difference between maximum and minimum during deep breathing was significantly lower in obese participants (21.8 ± 4.6 bpm) compared to controls (28.4 ± 5.1 bpm, p < 0.001). Maximum heart rate was slightly lower in the obese group (94.3 ± 7.8 bpm vs. 98.7 ± 8.2 bpm, p = 0.002), while minimum heart rate was marginally higher (72.5 ± 6.5 bpm vs. 70.3 ± 6.8 bpm, p = 0.04) (Table 2).

The Valsalva ratio was significantly reduced in obese participants (1.33 ± 0.12) compared to controls (1.47 ± 0.14, p < 0.001), indicating impaired parasympathetic function in obesity (Table 3).

During postural change, the 30:15 ratio was lower in obese individuals (1.04 ± 0.06) compared to controls (1.12 ± 0.07, p < 0.001). The obese group also showed greater increases in systolic (8.5 ± 3.2 mmHg vs. 5.7 ± 2.9 mmHg, p < 0.001) and diastolic blood pressure (5.2 ± 2.4 mmHg vs. 3.8 ± 2.1 mmHg, p = 0.001) upon standing (Table 4).

The blood pressure response to cold stress was significantly exaggerated in the obese group. Systolic and diastolic blood pressure increases were higher in obese participants (18.4 ± 5.6 mmHg and 12.3 ± 4.2 mmHg, respectively) compared to controls (12.7 ± 4.9 mmHg and 8.6 ± 3.7 mmHg, p < 0.001 for both) (Table 5).

Table 1: Baseline Characteristics of Participants

Table 2: Heart Rate Response to Deep Breathing

Table 3: Valsalva Maneuver

Table 4: Orthostatic Test

Table 5: Cold Pressor Test (BP Response)

Our study corroborates emerging evidence that obesity is associated with significant autonomic dysfunction, characterized by reduced parasympathetic activity and heightened sympathetic responses. These alterations in autonomic regulation may contribute to the increased cardiovascular morbidity observed in obese individuals.

Consistent with previous studies, our findings indicate a significant reduction in parasympathetic activity among obese participants. This was evidenced by lower heart rate variability during deep breathing and a diminished Valsalva ratio. Such reductions in parasympathetic tone have been linked to an increased risk of cardiovascular events [7]. The diminished vagal activity observed in obesity may be attributed to inflammatory processes and metabolic disturbances associated with excess adiposity [8].

Our study also observed exaggerated sympathetic responses in obese individuals, as demonstrated by increased blood pressure during orthostatic and cold pressor tests. This sympathetic hyperactivity has been implicated in the pathogenesis of hypertension and other cardiovascular diseases [9]. The underlying mechanisms may involve central nervous system inflammation and altered neuroendocrine signaling pathways [10].

The identification of autonomic dysfunction in obese individuals underscores the importance of early assessment and intervention. Monitoring autonomic function could serve as a valuable tool in predicting cardiovascular risk and tailoring preventive strategies. Lifestyle modifications, including weight management and physical activity, may ameliorate autonomic imbalances and reduce associated health risks [11-13].

While our study provides valuable insights, it is cross-sectional in nature, limiting causal inferences. Future longitudinal studies are warranted to elucidate the temporal relationship between obesity and autonomic dysfunction. Additionally, exploring the effects of interventions aimed at improving autonomic function in obese individuals could further inform clinical practice.

The present study demonstrates that obesity is associated with significant autonomic dysfunction, characterized by reduced parasympathetic activity and enhanced sympathetic responses. Obese individuals exhibited lower heart rate variability during deep breathing and Valsalva maneuver, as well as exaggerated blood pressure responses to orthostatic and cold stress tests. These findings suggest that obesity not only affects metabolic and cardiovascular health but also alters autonomic regulation, potentially increasing the risk of cardiovascular morbidity. Early assessment of autonomic function in obese individuals may aid in identifying high-risk subjects and implementing timely interventions to reduce long-term complications.

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