The global prevalence of obesity has risen sharply over recent decades, and young adults now represent a substantial and growing proportion of this burden. Excess adiposity in early life is associated with the development and earlier onset of traditional cardiovascular risk factors such as hypertension, dyslipidemia and insulin resistance, which track into adulthood and increase later cardiovascular disease (CVD) risk [1].

Beyond metabolic effects, obesity exerts direct hemodynamic and structural impacts on the cardiovascular system. Adiposity increases blood volume and cardiac output, promotes sympathetic activation, and contributes to arterial stiffness and subclinical atherosclerosis; these pathophysiologic changes help explain why raised body mass is linked to higher blood pressure and left-ventricular remodeling even in otherwise young, apparently healthy individuals [2].

Obesity also alters respiratory mechanics. Increased thoraco-abdominal adipose mass reduces chest wall and lung compliance and lowers resting functional residual capacity and expiratory reserve volume. These mechanical effects commonly produce reductions in absolute spirometric volumes (notably FVC and FEV₁) while often preserving the FEV₁/FVC ratio, yielding a restrictive-pattern physiology in many obese subjects [3,4].

Cardiorespiratory fitness — typically expressed as maximal oxygen uptake (VO₂max) relative to body mass — is frequently diminished in people with obesity. Although absolute oxygen consumption (L·min⁻¹) may be similar or higher in larger individuals, VO₂max normalized to body weight (ml·kg⁻¹·min⁻¹) is generally lower in overweight and obese groups, reflecting impaired aerobic capacity per unit body mass and reduced exercise tolerance [5,6].

Despite these recognized relationships, relatively few studies have simultaneously assessed resting cardiovascular indices, detailed spirometry, and a practical field assessment of aerobic capacity (such as step-test–derived VO₂max estimates) in healthy young adult populations. A better characterization of how obesity affects these integrated cardiorespiratory parameters in early adulthood is important because impairments at a young age may herald accelerated cardiopulmonary morbidity and represent a window for preventive intervention [2,5].

Accordingly, the present study investigated the effects of obesity on resting cardiovascular measures (heart rate, blood pressure, mean arterial pressure), spirometric indices (FVC, FEV₁, FEV₁/FVC, PEFR), and estimated VO₂max (Queens College Step Test) in a cohort of healthy young adults

Study design and setting: This cross-sectional, observational study was carried out in the Department of Physiology at a tertiary care teaching hospital. Informed consent was taken from all participants.

Study population and sample size: A total of 120 young adults aged between 18–25 years were recruited. The sample was stratified into two groups:

• Obese group (n = 60): Participants with body mass index (BMI) ≥30 kg/m²
• Normal-weight group (n = 60): Participants with BMI between 18.5–24.9 kg/m²

The sample size was determined based on feasibility and previous literature reporting detectable differences in pulmonary and cardiovascular parameters between obese and non-obese individuals.

Inclusion criteria

• Apparently healthy individuals aged 18–25 years
• Non-smokers and non-alcoholics
• Willing to provide informed consent

Exclusion criteria

• History of chronic respiratory or cardiovascular disease
• Endocrine disorders (e.g., diabetes mellitus, thyroid dysfunction)
• Recent acute illness or hospitalization
• Use of medications affecting cardiovascular or respiratory function

Anthropometric measurements

Body weight was measured using a calibrated digital weighing scale, and height was recorded with a stadiometer. BMI was calculated as weight in kilograms divided by the square of height in meters. Waist and hip circumferences were measured using a non-stretchable tape to calculate the waist–hip ratio.

Cardiorespiratory parameters

1. Cardiovascular assessment: Resting heart rate and blood pressure were measured using an automated sphygmomanometer after five minutes of seated rest. Three readings were taken at two-minute intervals, and the average was recorded.
2. Respiratory assessment: Lung function tests were performed using a computerized spirometer, recording parameters such as forced vital capacity (FVC), forced expiratory volume in one second (FEV₁), and peak expiratory flow rate (PEFR).
3. Cardiorespiratory fitness: Maximal oxygen consumption (VO₂ max) was estimated using the Queens College step test, where participants performed stepping exercise at a fixed cadence, and recovery heart rate was recorded to calculate VO₂ max using standard equations.

Statistical analysis

All data were entered into Microsoft Excel and analyzed using SPSS version 25.0. Continuous variables were expressed as mean ± standard deviation. Intergroup comparisons between obese and normal-weight participants were performed using the independent sample t-test. A p-value <0.05 was considered statistically significant.

A total of 120 participants were enrolled, with 60 individuals in each group. The mean age of participants was comparable between the normal-weight and obese groups (21.2 ± 2.1 vs. 21.6 ± 2.4 years, p = 0.38). The sex distribution was also similar across groups. As expected, body weight, BMI, and waist–hip ratio were significantly higher among obese participants (p < 0.001 for all) (Table 1).

Cardiovascular parameters revealed that obese individuals had significantly elevated resting heart rate, systolic blood pressure, diastolic blood pressure, and mean arterial pressure compared to their normal-weight counterparts (all p < 0.001) (Table 2).

In terms of respiratory function, spirometric evaluation showed significantly reduced FVC, FEV₁, and PEFR values in obese participants (p < 0.001 for each). However, the FEV₁/FVC ratio did not differ significantly between the groups (p = 0.18), indicating that both groups retained a normal ventilatory pattern (Table 3).

Assessment of cardiorespiratory fitness using the Queens College Step Test demonstrated that obese participants had a higher recovery heart rate (108.4 ± 9.3 vs. 92.6 ± 7.8 bpm, p < 0.001) and a significantly lower estimated VO₂ max compared to normal-weight individuals (34.2 ± 4.9 vs. 42.1 ± 5.3 ml/kg/min, p < 0.001) (Table 4).

Table 1. Baseline characteristics of study participants

Table 2. Cardiovascular parameters

Table 3. Respiratory function tests

Table 4. Cardiorespiratory fitness (Queens College Step Test)

Our observation of higher resting systolic and diastolic blood pressure and elevated resting heart rate among obese participants aligns with multiple clinical and epidemiologic reports that link increased adiposity to early rises in blood pressure and sympathetic drive. Mechanistically, obesity increases circulating blood volume and cardiac output, augments sympathetic nervous system activity, and promotes vascular stiffening and endothelial dysfunction; these changes together raise resting cardiac workload and arterial pressure, even before clinically overt hypertension develops. Such pathophysiologic pathways have been described in contemporary reviews and mechanistic studies of obesity and cardiovascular disease [7].

The spirometric pattern we report—reduced FVC and FEV₁ with no significant reduction in FEV₁/FVC ratio—mirrors the commonly observed restrictive-type impairment associated with central adiposity. Excess truncal and abdominal fat limits diaphragmatic descent and reduces chest wall and lung compliance, lowering lung volumes (notably functional residual capacity and expiratory reserve volume) and consequently reducing measured FVC and FEV₁ in litres while often preserving the ratio. Several recent cross-sectional and population studies have demonstrated similar associations between indices of obesity (waist circumference, fat mass) and lower absolute spirometric values, supporting the mechanical explanation and highlighting that reductions in absolute volumes—rather than airflow obstruction—predominate in many otherwise healthy obese adults [8,9].

Longitudinal analyses also suggest that increasing adiposity predicts slower decline in lung function over time and that body composition (fat mass vs fat-free mass) differentially influences spirometric indices. For example, higher fat-free mass tends to be associated with larger absolute FEV₁ and FVC, whereas central adiposity (waist circumference, percent body fat) correlates inversely with these volumes—underscoring the importance of assessing body composition and fat distribution when interpreting pulmonary function in obesity. These data help explain why two individuals with the same BMI may have different pulmonary function profiles depending on their muscle mass and fat distribution [10].

The poorer cardiorespiratory fitness (lower estimated VO₂max and higher recovery heart rate) observed among obese participants is concordant with prior studies that found negative relationships between BMI and weight-normalized aerobic capacity in young adults. While absolute oxygen uptake in litres per minute may not always be lower in people with larger body mass, expressing VO₂max relative to body weight (ml·kg⁻¹·min⁻¹) reveals impaired capacity per kilogram—an important clinical metric because it relates to functional ability and cardiovascular risk. Several cross-sectional studies in young adult cohorts report similar reductions in relative VO₂max with increasing BMI, and intervention studies demonstrate improvements in VO₂max with weight loss and increased physical activity [11,12].

It is important to note limitations of field tests for VO₂max estimation such as the Queens College Step Test (QCT). Although QCT is practical for large samples and has reasonable correlation with laboratory measures in many populations, validation studies indicate that prediction equations can misestimate absolute VO₂max in certain ethnic groups and in people with high BMI; locally derived prediction equations may improve accuracy. Therefore, while our QCT-derived estimates reliably capture between-group differences in aerobic fitness, absolute VO₂max values should be interpreted with caution and ideally complemented by direct cardiopulmonary exercise testing when feasible [12].

Clinically, our results emphasize that the physiologic consequences of obesity are evident well before middle age. Elevated resting cardiovascular load and reduced pulmonary volumes and aerobic capacity in young adults may accelerate the trajectory toward symptomatic cardiopulmonary disease if excess weight persists. Early identification of these subclinical alterations provides an opportunity for targeted lifestyle and public-health interventions (weight management, structured exercise, and cardiometabolic risk screening) that could reverse or mitigate long-term risk. Recent clinical reviews and guidelines similarly advocate for early, integrated management of obesity and its cardiometabolic sequelae in adolescents and young adults [13,14].

Strengths of the present study include the concurrent assessment of resting cardiovascular indices, standardized spirometry, and a practical field test of aerobic capacity in a single young-adult cohort—allowing integrated characterization of cardiorespiratory status. However, several limitations merit mention. The cross-sectional design precludes causal inference or assessment of temporal changes. Body composition was estimated using anthropometry rather than direct methods (e.g., DXA), so residual confounding by muscle mass cannot be excluded. The VO₂max was estimated by QCT rather than measured directly; as noted above, prediction equations may be less accurate in certain subgroups. Finally, our sample size—while adequate to detect moderate between-group differences—may not have been powered to detect small effect sizes or sex-specific interactions.

The present study demonstrates that obesity in young adults is associated with significant alterations in cardiovascular and respiratory functions, as well as reduced cardiorespiratory fitness. Obese individuals exhibited higher resting heart rate and blood pressure, along with impaired spirometric indices and lower VO₂ max, compared to their normal-weight peers. These findings highlight the adverse physiological impact of obesity even in early adulthood and underscore the importance of preventive strategies, lifestyle modification, and early interventions to mitigate future cardiopulmonary morbidity.

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