Obesity is fast becoming a severe global epidemic, with its prevalence increasing significantly and steadily among young adults, especially college and university students.^1,2 Regardless of metabolic state, being overweight or obese increases the risk of unfavorable outcomes, including cardiovascular disease (CVD) risk.³ In light of the increasing prevalence of obesity, overweight, and CVD in young people, it has become imperative to determine the impact of excess adiposity on cardiac measurements as early as possible to predict the risk of comorbidities.⁴ There also is a need to identify noninvasive, low-cost, and easily administered modifiable factors that can help clinicians in early identification of individuals at risk of CVDs and to propose strategies to prevent obesity and associated cardiovascular (CV) health problems.

Given that heart rate (HR) is a precisely regulated and modifiable CV variable that plays a critical role in health and disease, its monitoring at rest, during exercise, and post-exercise can be considered as an important noninvasive clinical method and prognostic tool of investigation, which may lead to early identification of patients at risk of CVD. There is evidence that altered HR at rest and during exercise and post-exercise periods are prognostic of CV events. For example, elevated HR at rest, blunted HR response to exercise, and attenuated heart rate recovery (HRR) immediately post-exercise are associated with increased risk of CVD and mortality in populations with and without documented chronic disease.^5-7 Alterations in HR, at rest, during exercise, or post-exercise, are influenced by changes in autonomic nervous system function and cardiorespiratory fitness (CRF) of an individual.^8,9

Because obesity is an important risk factor for CVDs and can lead to cardiac autonomic dysfunction, understanding the mechanisms underlying the altered hemodynamic responses during and after exercise in obese or overweight persons is crucial. Studies have found that CRF, one of the most important determinants of overall health status and a powerful predictor of CVD mortality and morbidity, is attenuated with increasing body mass.^10,11 “CRF” refers to the ability of the circulatory and respiratory systems to efficiently supply oxygen to the working muscles during sustained physical activity. Given that CRF, obesity, and HR at rest, during exercise, and post-exercise are important risk factors for CVD, it would be of interest to examine the relationship between CRF, body mass, and HR responses at different conditions. Doing so will allow a better understanding of the potential mechanisms that mediate the links between CRF, obesity, and CVD. The ventilatory equivalent for oxygen (VEqO₂), a measure of ventilatory effectiveness, is another important determinant of health status, which has also been recognized as a significant predictor of CVD and mortality risk.^12,13 However, to the best of our knowledge, no prior investigation has compared the VEqO₂ with HR responses between overweight/obese young adults and their non-overweight/obese controls. It is also not clear if the VEqO₂ is a strong determinant of HR responses at rest and during and after exercise among overweight/obese young adults. Furthermore, few studies have shown the prevalence of impaired HR at rest, during exercise, and during recovery among overweight/obese young adults.

This study was undertaken to assess the HR responses at rest, during submaximal ergometer exercise, and during the recovery period after exercise among overweight/obese and to compare them with those of healthy-weight young adults. We also tried to determine the prevalence of impaired HR at rest, during exercise, and after exercise among overweight/obese young adults and to compare these with those of healthy-weight controls. In addition, we tested whether resting HR, exercise HR responses, and post-exercise HRR were associated with CRF and ventilatory efficiency.

Subjects

Eighty healthy young adults (30 men and 50 women) aged 23.21±2.43 years (range, 19 to 33) participated in the study. They were selected from students of Nnamdi Azikiwe University, Anambra State, Nigeria. The present study population was divided into two groups based on body mass index (BMI) ≥25 kg/m² (n=40) and controls with BMI ≥18 kg/m² but <25 kg/m² (n=40). BMI is a global measurement and was chosen as a parameter of choice for determining level of adiposity. However, there is lack of information about an optimal BMI threshold in Black African adults. A BMI cutoff of 25 kg/m² has been recommended for studies involving regions with high risk of CVDs but without a clear BMI cutoff point for overweight or obesity.¹⁴ Subjects were excluded if they were involved in any physical training program; if they were smokers, alcoholics, diabetic, hypertensive, or taking medications that could affect cardiorespiratory functions; or if they were unable to complete a moderate exercise test. Additionally, subjects with a history of unstable CV, respiratory, and peripheral vascular diseases; orthopedic or musculoskeletal lesions; or malignancy were excluded from the study. Selection of subjects was based on the outcome of a structured health and lifestyle-screening questionnaire, morphometric measurements, physical examination, and the ability of subjects to complete a submaximal moderate exercise test. Medical history, smoking history, alcohol drinking history, and history of physical training of participants were obtained from the questionnaire. Participants were instructed not to partake in any vigorous physical activity 24 hours prior to the exercise test. They were advised not to eat a heavy meal or consume alcoholic beverages or coffee before the test. Before participation, subjects were familiarized with the experimental procedures, and their informed consent (written and oral) was obtained. The investigation conformed to the principles outlined in the Declaration of Helsinki (World Medical Association, 2013). The study was approved by the Experiments and Ethics Committee of the College of Health Sciences of Nnamdi Azikiwe University.

Anthropometric measurements

Subjects heights and body weight were measured using a stadiometer and a standard scale, respectively, with the subjects in light clothing, without shoes and with the shoulders in a relaxed position and the arms hanging freely. BMI was calculated as weight (kg) divided by the square of height (m²). Hip circumference (HC) was measured at the level of the greater trochanters, and waist circumference (WC) was measured halfway between the top of the iliac crest and the lower rib border. The waist-to-hip ratio (WHR) was determined using WC and HC data.

Exercise test protocol

A symptom-limited submaximal (moderate) exercise test was performed using a mechanically braked, magnetic ergometer bicycle (American Fitness) in a well-ventilated room of about 26°C to 27°C. The subjects were asked to rest for 30 minutes in a quiet environment before participating in the test. Submaximal exercise tests are a better option than maximal exercise tests because they meet the needs of people with various functional limitations and disabilities, such as cardiopulmonary, musculoskeletal, and neuromuscular impairments and complaints.¹⁵ All experimental sessions were carried out between 8:00 AM and 12 noon. Before participation in the exercise test, the participants were asked if they adhered to instructions not to eat a heavy meal, not to consume beverages containing alcohol or coffee, and not to participate in any vigorous physical activity 24 hours before the test. Those who failed to heed pre-test instructions were not permitted to perform the test. Participants also received instructions and demonstrations on how to perform the exercise test. The testing protocol comprised an initial 1-minute warm-up exercise on the cycle ergometer at a work rate of 60 revolutions per minute with no resistance. This was followed by increased workload to elicit 60% to 70% of the individual maximum HR at a constant work rate of 60 revolutions per minute and a resistance of 1 kp (approximately 60 W) until a steady-state HR was achieved. Subjects were encouraged to sustain the exercise intensity until they achieved steady-state HR. We devised a metronome for the exercise protocol using a 60-second timer and tapping each second to help the participants and the investigator maintain a constant cycling rate of 60 rpm during the exercise test. The workload or power output (kpm/min) was computed with the formula kpm/min=[pedal rate (rpm)]×[ergometer resistance (kp)]×(6 m/rev). The kpm/min was converted to Watts (1 W=6.12 kpm/min).¹⁶ In the present study, workload (kpm/min)=60 rpm×1 kp×60=360 kpm/min=58.8 W or approximately 60 W. Steady-state HR was achieved when consecutive HRs at 1-minute intervals were within 6 bpm of each other between the 3rd minute and the last second of exercise.¹⁷ A 5-minute recovery period followed termination of the exercise, with participants maintaining an upright sitting position on the ergometer bicycle and performing active loadless pedaling on the standard ergometer.

Blood pressure, heart rate, and ventilatory measurements

The resting blood pressure (BP), HR, breathing rate (BR), and tidal volume (VT) were measured twice after 10 and 15 minutes of rest with the subject sitting in a quiet room. The resting BP and HR were measured using a mercury-column sphygmomanometer and Omron electronic monitor (HEM-712C; Omron Health Case Inc.), respectively. The BR and VT were measured using a spirometer (JY-BF II Digital spirometer; Jiangsu JInyi Instrument Technology). The average BP, HR, BR, and VT measurements were used for baseline data analysis. HR was measured continuously (at 1-minute intervals) during exercise. Immediately before exercise termination, BP, HR, BR, and VT were measured, and the values were referred to as “peak exercise value” for data analysis. Post-exercise, HR was measured first at 1 minute of recovery and subsequently at every 2-minute interval until the 5th minute.

Determination of HR outcomes

(1) In this study, high resting HR was value >76 bpm for men and >80 bpm for women and was based on the median (50th percentile) resting HR for each gender at rest.

(2) The parameters of HR response determined during the exercise test were (a) peak exercise HR; (b) percentage maximum HR expressed as [(peak HR/HRmax)×100],¹⁸ where HRmax (age-predicted maximum HR) was determined as HRmax=208–(0.7×age);¹⁹ and (c) percentage HR reserve expressed as [(peak HR–resting HR)/(age-predicted HRmax–resting HR)]×100.²⁰ For the purpose of this study, poor HR response during the submaximal exercise test was defined as the inability to achieve a percentage HR reserve ≥40%. This threshold value was based on the U.S. Department of Health recommended lower range for percentage HR reserve during moderate exercise (40% to 59%).²¹

(3) The variables of HRR after exercise were percentage HR decline at the 1st and 3rd minutes of post-exercise as well as absolute HRR. The percentage HR decline relative to peak HR was calculated as [(peak HR–1st min post-exercise HR)/(peak HR)]×100 and [(peak HR–3rd min post-exercise HR)/(peak HR)]×100, respectively.²² Absolute HRR was defined as the difference between peak exercise HR and HR during the 1st or 3rd minute of active loadless recovery. Impaired HRR was defined as a reduction of 1st minute HRR <12 bpm.²³

Determination of cardiometabolic and ventilatory parameters

(1) The peak oxygen uptake, oxygen consumption (VO₂; mL/kg/min), was determined using the equation 85.447+[9.104×sex (0=women; 1=men)]–[0.2676×age (year)]–[0.4150×body mass (kg)]+[0.1317×power output (W)]–[0.1615×peak (steady-state) HR].¹⁶ The relative VO₂ values were converted to absolute values (L/min) using the formula (relative VO₂×body weight)/1,000.

(2) The minute ventilation (VE; L/min), was calculated as the product of BR (breaths/min) and VT (L).

(3) The VEqO₂ was calculated as VEqO₂=VE (L/min)/VO₂ (L/min).²⁴

Data analysis

The descriptive data were expressed as mean and standard deviation or median (range) for continuous variables and as percentage for categorical variables. A test for normality was performed using the Shapiro Wilk’s normality test. Comparative analysis involving two continuous variables was conducted using independent sample t-test (for normally distributed data) or Mann-Whitney U-test (for abnormally distributed data). Comparative analysis involving prevalence of poor HR responses at rest and during exercise and recovery were performed using chi-square test. The Spearman’s rho correlation test was used to assess the relationships between two groups of variables. Statistical significance was set at P<0.05. All statistics were conducted using SPSS for Windows version 20.0 (IBM Co.).

The demographic and baseline characteristics of the study population indicating the mean or median age, height, weight, BMI, WC, HC, WHR, resting HR, systolic BP, diastolic BP, rate pressure product, BR, VT, and VE are shown in Table 1.

Independent sample t-test or Mann-Whitney U-test indicated significantly lower (P<0.05, P<0.01, P<0.001) mean or median HR reserve, %HR reserve, absolute 1st minute HR recovery, and percentage 1st minute post-exercise HR decline relative to peak exercise but higher 1st minute post-exercise HR and 3rd minute post-exercise HR in overweight-obese men, women, and overall subjects compared with the healthy-weight group (Table 2). The overweight-obese individuals also indicated significantly lower (P<0.01 or P<0.001) age-predicted HRmax, absolute 3rd minute HR recovery, and percentage 3rd minute post-exercise HR decline relative to peak exercise compared with the healthy-weight group in women and the overall study population but not in men alone. The peak exercise VE, VO₂, and VEqO₂ were significantly (P<0.001) lower in overweight/obese men, women, and the overall study population compared with healthy-weight controls.

Correlations between peak VO₂, peak VEqVO₂, and BMI are as shown in Figure 1. A Spearman correlation test indicated significant negative correlations between peak VO₂ and BMI in men (r=0.853, P<0.001), women (r=0.931, P<0.001), and overall population (r=0.857, P<0.001). Peak VEqVO₂ also indicated significant negative relationships with BMI in men (r=0.656, P<0.001), women (r=0.541, P<0.001), and overall population (r=0.644, P<0.001).

The correlation test also showed that peak VO₂ indicated significant negative correlations (P<0.05, P<0.01, P<0.001) with resting HR, peak HR, %HRmax achieved, 1st minute post-exercise HR, and 3rd minute post-exercise HR in men, women and combined population but positive correlations (P<0.05, P<0.01, P<0.001) with HR reserve, %HR reserve, and 1st minute %HR decline in all regimens (Table 3). Absolute HR recovery in the 1st minute and 3rd minute %HR decline indicated positive correlations (P<0.05, P<0.01) with peak VO₂ in women and combined population but not in men (P=0.089, P=0.157). No significant correlations were observed between peak VO₂ and absolute HR recovery in the 3rd minute in men (P=0.555), women (P=0.205), or combined population (P=0.336).

Data indicated significant negative correlations (P<0.01, P<0.001) between peak VEqO₂ and resting HR, in men, women, and combined population (Table 4). There were significant positive correlations (P<0.05, P<0.001) between peak VEqO₂ and HR reserve, %HR reserve, absolute HR recovery in the 1st minute, 1st minute %HR decline, absolute 3rd minute HR recovery, and 3rd minute %HR decline. Third-minute post-exercise HR indicated significant negative correlations with peak VEqO₂ in women (P=0.026) and combined population (P<0.001) but not in men. Peak HR and %HRmax indicated significant positive correlations (P<0.05) with VEqO₂ in women, but not in men or combined population. No significant correlations were observed between peak VEqO₂ and 1st minute post-exercise HR in men, women, or combined population.

The prevalence of high resting HR, impaired HR during exercise, and post-exercise period among the participants are shown in Table 5. Data indicate a higher prevalence of high resting HR among obese/overweight group in men (100% vs. 0%), women (96% vs. 4%, P<0.001), and overall population (97.5% vs. 2.5%, P<0.001) compared with the healthy-weight group. The overweight/obese persons indicated significantly higher prevalence of poor %HR reserve in men (100% vs. 73.3%, P=0.040), in women (100% vs. 64%, P=0.005), and overall (100% vs. 67.5%, P=0.014). The prevalence of impaired HR recovery in the 1st minute (men, 60% vs. 20%; women, 88% vs. 44%; overall, 77.5% vs. 35%; P<0.001) was significantly higher in the overweight/obese subjects than the healthy-weight subjects.

There are limited comparative data available on resting HR in young healthy-weight and overweight/obese adults. Our results indicate significantly lower resting HR among overweight/obese young adults than the healthy-weight group. This is in agreement with previous findings indicating the existence of a positive correlation between BMI and resting HR in obese individuals.²⁵ The overweight/obese also displayed a higher incidence of high resting HR in men (100% vs. 0%) and women (96% vs. 4%) compared with the healthy-weight persons. The alteration of resting HR in the overweight/obese may be related to autonomic abnormalities and poor CRF present in these individuals. Reduction in parasympathetic activity and predominance of sympathetic activity has been reported in obese compared to healthy-weight individuals.²⁶ Studies showing strong negative correlations between CRF and resting HR²⁷ and BMI²⁸ are in agreement with the present study, which indicated significant negative correlations between peak VO₂ and resting HR and BMI in men and women and in all individuals. Interestingly, autonomic nervous system imbalance or dysfunction and poor CRF have been implicated in the pathogenesis of CVDs, including congestive heart failure, cardiac arrhythmia, and hypertension.^29,30

The chronotropic response to submaximal exercise has not been well defined in either healthy-weight or overweight/obese young adults. Similarly, despite the well-established association between chronotropic inconvenience (CI) and prognosis of all-cause mortality in adults with obesity,^31,32 the prevalence of CI at submaximal exercise levels in overweight/obese young adults has not been investigated. Our findings showed that, in both men and women, the overweight-obese individuals showed significantly lower HR reserve and %HR reserve but no significant differences in peak HR and %HRmax achieved compared with the healthy-weight control group. In accordance with our findings, previous studies have demonstrated lower HR reserve^6,33 and similar peak HR and % predicted HRmax³⁴ in overweight/obese individuals compared with healthy-weight groups. In contrast, other studies have shown lower peak HRs^6,33 and similar HR reserve³⁴ in overweight/obese subjects than in healthy-weight individuals. Failure to achieve a predicted HR during exercise has been associated with CV events such as sick sinus syndrome, atrioventricular block, coronary artery disease, and heart failure.³⁵ HR reserve is reported to be a measure of chronotropic incompetence and an important exercise test parameter to predict CVD mortality in younger men.³⁶ The increased risk associated with impaired HR response may reflect low CRF, which has been strongly associated with clustering of cardiometabolic risk factors in youths.³⁷ Our study showed that peak VO₂ increased with increase in %HR reserve, suggesting that CRF contributed to the greater percentage HR reserve achieved by the healthy-weight adults compared with the overweight/obese individuals. Another study has suggested that impaired HR response may signify abnormalities in autonomic balance, indicating an inability of the CV system to appropriately respond to the sympathetic discharge and parasympathetic withdrawal that occurs during exercise.³⁸ The present findings suggest that the healthy-weight group, which indicated significantly higher HR reserve and %HR reserve, has a higher submaximal chronotropic competence and better autonomic response to exercise than the overweight/obese group. Interestingly, our results indicated significantly higher prevalence of poor %HR reserve in both overweight/obese men (100% vs. 73%) and women (100% vs. 64%) than in the healthy-weight group. We limited our assessment of poor exercise HR response to the lower range for percentage HR reserve during a moderate exercise test (40% to 59%) as recommended by the U.S. Department of Health physical activity guidelines. This is because the exercise test values obtained in this study were submaximal. It is unclear whether the threshold of 80% previously used for impaired HR response to maximal exercise in other studies is applicable to different age groups and those limited physically by pain and fatigue or who have abnormal gait.

The prognostic significance of HRR after exercise as a risk factor for all-cause and cardiac mortality in different cohorts of patients and in healthy subjects has been demonstrated.^7,39 However, there are limited studies on the effect of adiposity level on HRR after a submaximal exercise test among apparently healthy young adults. In this study, the overweight/obese individuals presented significantly higher 1st-minute post-exercise HR and 3rd-minute post-exercise HR values, which translated into significantly lower absolute 1st-minute HRR and percentage 1st-minute post-exercise HR decline (in both genders) as well as lower absolute 3rd-minute HRR and percentage 3rd-minute post-exercise HR decline (in women only) compared with the healthy-weight group. These findings indicate that, following a submaximal exercise test, HRR appeared slower in overweight/obese individuals than in the healthy-weight group. In agreement with our study, other cross-sectional and prospective studies have demonstrated an inverse relationship between obesity and HRR after exercise in the absence of CV risk factors.^40,41 Unlike our study, their subjects underwent maximal exercise tests. Interestingly, our study also indicated greater prevalence of impaired HRR in the 1st minute of recovery in overweight/obese individuals, suggesting a greater risk of CVDs compared with the healthy-weight group. A delayed HRR is considered a measure of autonomic imbalance,⁴² and the present finding may be a reflection of a reduction in vagal tone or an exaggerated sympathetic activation among the overweight/obese individuals. Furthermore, the slow HRR in overweight/obese person may be due to poor CRF because it has been reported that HRR is an indicator of CRF.⁴³ Our findings strengthen overweight or obesity as a risk factor for CVDs. They further confirm that submaximal exercise testing is particularly valuable during diagnostic investigations leading to early identification of patients at greater CV risk.

To the best of our knowledge, no previous study has associated the VEqO₂ with HR responses among overweight/obese young adults and their non-overweight/obese controls. The relationships observed between VEqO₂ and resting HR, %HR reserve, 1st- and 3rd-minute percentage HR decline, and 1st- and 3rd-minute HR recovery in both genders are novel findings of the present study. VEqO₂ is the ratio of VE in liters to VO₂ in liters/minute.⁴⁴ It is a feasible, objective tool used in cardiopulmonary exercise testing that provides a safe and noninvasive way to measure the ventilatory efficiency in individuals.⁴⁴ A higher value represents a greater efficiency of breathing: volumes moved at lower oxygen costs when the patient is at rest or exercising.^44,45 The present findings suggest that subjects with higher resting HR, lower %HR reserve, and blunted HR recovery are more likely to demonstrate lower respiratory efficiency than those with lower resting HR, higher %HR reserve, and faster HR recovery. Interestingly, our study indicated that overweight/obese young men and women who presented higher resting HR, lower %HR reserve, and blunted HR recovery showed significantly lower VEqO₂ (respiratory efficiency) than did the healthy-weight controls.

In conclusion, the high resting HR, submaximal chronotropic incompetence, and blunted HR recovery observed among the overweight/obese individuals in this study may be attributed to poor CRF and low respiratory efficiency. These findings may be helpful in identifying apparently overweight or obese young adults at risk of CVD and laying the groundwork for future therapeutic implications of controlling obesity and its related CVDs.

We wish to thank the staff of the Physiology Department, Nnamdi Azikiwe University, for their support and assistance. We also acknowledge the immense contributions of the students of Basic Medical Sciences, who participated in the study.

The authors declare no conflict of interest.

Study concept and design: UD; acquisition of data: RCG; analysis and interpretation of data: UD, RCG, PO, and DI; drafting of the manuscript: UD and RCG; critical revision of the manuscript: UD, RCG, PO, and DI; statistical analysis: UD and RCG; obtained funding: RCG; administrative, technical, or material support: UD, PO, and DI; and study supervision: UD.