Journal of Obesity & Metabolic Syndrome



J Obes Metab Syndr 2023; 32(1): 87-97

Published online March 30, 2023

Copyright © Korean Society for the Study of Obesity.

Heart Rate Responses at Rest, during Exercise and after Exercise Periods in Relation to Adiposity Levels among Young Nigerian Adults

Uchechukwu Dimkpa *, Robert C. Godswill, Peter Okonudo, David Ikwuka

Human Physiology Department, Faculty of Basic Medical Sciences, Nnamdi Azikiwe University, Nnewi Campus, Nnewi, Nigeria

Correspondence to:
Uchechukwu Dimkpa
Human Physiology Department, Faculty of Basic Medical Sciences, Nnamdi Azikiwe University, Nnewi Campus, P.M.B. 5025, Nnewi, Nigeria
Tel: +234-7037362106

Received: September 12, 2022; Reviewed : November 6, 2022; Accepted: December 16, 2022

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Background: There is a dearth of comparative studies on heart rate (HR) abnormalities at rest, chronotropic responses during submaximal exercise, and such responses during recovery from submaximal exercise between healthy-weight and overweight/obese young adults.
Methods: Eighty healthy young adults (30 men and 50 women) aged 19 to 33 years participated in the present study. A symptom-limited, submaximal, cycle ergometer exercise test of intensity targeted at 60% to 70% of the subject’s age-predicted maximum HR was performed. The HR, blood pressure, and minute ventilation were measured at rest and during exercise. Post-exercise, HR was first measured at 1 minute of recovery and then every 2 minutes until the 5th minute.
Results: Our results showed significantly higher resting HR (P<0.001), lower percentage HR reserve during exercise (P<0.001), and slower HR recovery after exercise (P<0.05, P<0.01, or P<0.001) in overweight/obese men and women than in the non-overweight/obese controls. The prevalence of high resting HR, submaximal chronotropic incompetence, and blunted HR recovery were more common in the overweight/obese individuals than in the healthy-weight controls. Peak VO2 and ventilatory equivalent for oxygen were associated with resting HR, exercise HR parameters, and post-exercise HR recovery indices in both men and women.
Conclusion: High resting HR, submaximal chronotropic incompetence, and blunted HR recovery in overweight/obese individuals in this study may be attributed to poor cardiorespiratory fitness and low respiratory efficiency.

Keywords: Overweight, Obesity, Heart rate, Young adult, Cardiorespiratory fitness, Prevalence, Exercise test

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.


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 reserve6,33 and similar peak HR and % predicted HRmax34 in overweight/obese individuals compared with healthy-weight groups. In contrast, other studies have shown lower peak HRs6,33 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.

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.

Fig. 1. Scatterplot diagrams showing the correlations between (A, B, C) peak oxygen consumption (VO2), (D, E, F) peak ventilatory equivalent for oxygen (VEqVO2), and body mass index (BMI) in men, women, and overall population.

Demographic and baseline characteristics of the study population

Variable Men (n= 30) Women (n= 50) All (n= 80)

< 25 kg/m2 (n= 15) ≥ 25 kg/m2 (n= 15) P < 25 kg/m2 (n= 25) ≥ 25 kg/m2 (n= 25) P < 25 kg/m2 (n= 40) ≥ 25 kg/m2 (n= 40) P
Age (yr) 23.0 (21–26) 24.0 (20–28) 0.174 21.0 (19–31) 23.0 (20–33) 0.001 22.0 (19–31) 24.0 (20–33) 0.001
Height (m) 1.7 ± 0.1 1.8 ± 0.1 0.253 1.6 ± 0.1 1.6 ± 0.04 0.528 1.7 ± 0.1 1.7 ± 0.1 0.342
Weight (kg) 66.2 ± 3.5 88.6 ± 10.9 < 0.001 59.1 ± 6.1 81.7 ± 14.7 < 0.001 61.8 ± 6.3 84.3 ± 13.7 < 0.001
BMI (kg/m2) 21.8 ± 1.3 28.1 ± 2.3 < 0.001 21.9 ± 2.6 29.7 ± 4.3 < 0.001 21.9 ± 2.2 29.1 ± 3.7 < 0.001
WC (cm) 30.5 ± 1.3 35.4 ± 3.0 < 0.001 30.1 ± 3.3 36.8 ± 4.5 < 0.001 30.2 ± 2.7 36.3 ± 3.9 < 0.001
HC (cm) 34.4 ± 2.3 39.8 ± 3.1 < 0.001 37.0 ± 3.1 43.6 ± 4.4 < 0.001 36.1 ± 3.0 42.2 ± 4.4 < 0.001
WHR 0.9 ± 0.04 0.9 ± 0.05 0.727 0.8 ± 0.04 0.84 ± 0.04 0.002 0.83 ± 0.06 0.86 ± 0.05 0.029
Resting HR (bpm) 68.0 (61–72) 83.0 (80–87) < 0.001 70.0 (62–81) 83.0 (80–93) < 0.001 69.5 (61–81) 83.0 (80–93) < 0.001
Resting SBP (mmHg) 110 (98–120) 120 (95–130) 0.009 100 (90–112) 116 (100–137) < 0.001 101.5 (90–120) 119.5 (95–137) < 0.001
Resting DBP (mmHg) 71.0 (62–81) 73.0 (61–80) 0.870 70.0 (60–80) 79.0 (69–100) < 0.001 70.5 (60–81) 78.0 (61–100) 0.002
Resting RPP (× 103) 7.5 (6.1–8.6) 9.9 (7.6–11.0) < 0.001 7.1 (6.1–8.9) 9.7 (8.0–12.7) < 0.001 7.3 (6.1–8.9) 9.8 (7.6–12.7) < 0.001
Resting BR (breaths/min) 14.0 (13–15) 19.0 (18–21) < 0.001 15.0 (14–18) 19.0 (18–25) < 0.001 14 (13–18) 19.0 (18–25) < 0.001
Resting VT (L) 0.5 (0.5–0.6) 0.4 (0.4–0.5) < 0.001 0.5 (0.4–0.6) 0.4 (0.4–0.5) < 0.001 0.5 (0.4–0.6) 0.4 (0.4–0.5) < 0.001
Resting VE (L/min) 7.5 (7.5–7.8) 8.3 (8.1–8.8) < 0.001 7.1 (6.8–8.3) 8.4 (8.1–9.7) < 0.001 7.6 (6.8–8.3) 8.4 (8.1–9.7) < 0.001

Values are presented as median (range) or mean± standard deviation.

BMI, body mass index; WC, waist circumference; HC, hip circumference; WHR, waist hip ratio; HR, heart rate; SBP, systolic blood pressure; DBP, diastolic blood pressure; RPP, rate pressure product; BR, breathing rate; VT, tidal volume; VE, minute ventilation.

Heart rate responses and indices of cardiometabolic and ventilatory efficiency of the study population

Variable Men (n= 30) Women (n= 50) All (n= 80)

< 25 kg/m2 (n= 15) ≥ 25 kg/m2 (n= 15) P < 25 kg/m2 (n= 25) ≥ 25 kg/m2 (n= 25) P < 25 kg/m2 (n= 40) ≥ 25 kg/m2 (n= 40) P
Age-predicted HRmax 191.9 ± 1.2 191.3 ± 1.6 0.205 193.3 (186–195) 191.9 (185–194) 0.001 192.6 (186–195) 191.2 (185–194) 0.001
Peak HR (bpm) 115.1 ± 4.2 117.9 ± 8.5 0.254 117.0 (102–132) 119.0 (104–125) 0.915 116.0 (102–132) 119.0 (104–128) 0.378
% HRmax achieved 60.0 ± 2.2 61.6 ± 4.3 0.195 61.7 (52.4–69.3) 62.5 (54.4–65.4) 0.734 60.5 (52.4–69.3) 62.7 (54.4–66.9) 0.277
HR reserve (bpm) 46.7 ± 5.0 35.2 ± 7.5 < 0.001 46.0 (37–68) 34 (24–43) < 0.001 46.0 (37–68) 35.0 (24–45) < 0.001
%HR reserve achieved 36.1 ± 2.7 23.4 ± 2.4 < 0.001 31.6 (21.2–47.1) 23.1 (21.4–31.2) < 0.001 35.7 (21.2–47.1) 23.1 (21.4–31.2) < 0.001
Post-exercise HR1-min (bpm) 100.2 ± 6.3 107.4 ± 4.9 0.002 100.8 ± 10.7 110.1 ± 4.5 < 0.001 100.6 ± 9.2 109.1 ± 4.8 < 0.001
Absolute HRR1-min 14.9 ± 5.7 10.5 ± 6.0 0.05 15.6 ± 6.3 6.5 ± 5.6 < 0.001 15.3 ± 6.0 8.0 ± 6.0 < 0.001
% HR1-min decline 12.9 ± 4.9 8.7 ± 4.6 0.023 13.3 ± 4.9 5.4 ± 4.8 < 0.001 13.1 ± 4.9 6.6 ± 4.9 < 0.001
Post-exercise HR3-min (bpm) 92.9 ± 6.2 98.0 ± 5.3 0.023 88.7 ± 8.5 99.4 ± 5.1 < 0.001 90.3 ± 7.9 98.8 ± 5.2 < 0.001
Absolute HRR3-min 22.1 ± 6.1 19.9 ± 6.5 0.347 27.6 ± 9.4 17.2 ± 5.7 < 0.001 25.6 ± 8.7 18.2 ± 6.1 < 0.001
% HR3-min decline 19.2 ± 5.1 16.7 ± 4.7 0.171 23.4 ± 6.2 14.7 ± 4.6 < 0.001 21.8 ± 6.1 15.4 ± 4.7 < 0.001
Peak VE (L/min) 43.7 (42–44.8) 15.5 (14.5–15.9) < 0.001 42.1 (14.5–45.6) 15.5 (14.5–18.2) < 0.001 43.7 (14.5–45.6) 15.5 (14.5–18.2) < 0.001
Peak VO2 (mL/kg/min) 50.2 ± 1.4 40.2 ± 5.0 < 0.001 43.9 (36.6–50.7) 36.0 (18.1–42) < 0.001 48.5 (36.6–51.9) 36.9 (18.1–49.3) < 0.001
Peak VEqO2 13.1 ± 0.5 4.3 ± 0.2 < 0.001 16.6 (5.2–18.4) 5.6 (5.0–8.9) < 0.001 15.8 (5.2–18.4) 5.3 (4.0–8.9) < 0.001

Values are presented as mean± standard deviation or median (range).

HR, heart rate; HR1-min, 1st minute heart rate decline; HRR, heart rate recovery; HR3-min, 3rd minute heart rate decline; VE, minute ventilation; VO2, oxygen consumption; VEqO2, ventilatory equivalent for oxygen.

Spearman rho correlation analysis between peak VO2 and HR parameters at rest, during exercise, and after exercise

Peak VO2 vs. R (P)

Men Women All
Resting HR –0.858 (< 0.001) –0.932 (< 0.001) –0.868 (< 0.001)
Peak HR –0.383 (0.037) –0.487 (0.001) –0.462 (< 0.001)
% HRmax achieved –0.403 (0.027) –0.515 (< 0.001) –0.485 (< 0.001)
HR reserve 0.555 (0.001) 0.476 (0.001) 0.452 (< 0.001)
%HR reserve achieved 0.596 (0.001) 0.324 (0.022) 0.366 (0.001)
Post-exercise HR1-min –0.680 (< 0.001) –0.773 (< 0.001) –0.750 (< 0.001)
Absolute HRR1-min 0.316 (0.089) 0.419 (0.002) 0.378 (0.001)
% HR1-min decline 0.416 (0.022) 0.522 (< 0.001) 0.458 (< 0.001)
Post-exercise HR3-min –0.550 (0.002) –0.691 (< 0.001) –0.571 (< 0.001)
Absolute HRR3-min 0.112 (0.555) 0.182 (0.205) 0.109 (0.336)
% HR3-min decline 0.265 (0.157) 0.328 (0.020) 0.289 (0.009)

Values are presented as Spearman’s correlation coefficient (P-value).

VO2, oxygen consumption; HR, heart rate; HR1-min, 1st minute heart rate decline; HRR, heart rate recovery; HR3-min, 3rd minute heart rate decline.

Spearman rho correlation analysis between peak VEqO2 and HR parameters at rest, during exercise, and after exercise

Peak VEqO2 vs. R (P)

Men Women All
Resting HR –0.591 (0.001) –0.515 (< 0.001) –0.608 (< 0.001)
Peak HR 0.182 (0.337) 0.355 (0.011) 0.105 (0.355)
% HRmax achieved 0.172 (0.353) 0.362 (0.010) 0.101 (0.371)
HR reserve 0.833 (< 0.001) 0.835 (< 0.001) 0.715 (< 0.001)
%HR reserve achieved 0.917 (< 0.001) 0.963 (< 0.001) 0.859 (< 0.001)
Post-exercise HR1-min –0.233 (0.214) –0.069 (0.636) –0.195 (0.083)
Absolute HRR1-min 0.420 (0.021) 0.537 (< 0.001) 0.426 (< 0.001)
% HR1-min decline 0.465 (0.010) 0.528 (< 0.001) 0.448 (< 0.001)
Post-exercise HR3-min –0.212 (0.260) –0.314 (0.026) –0.383 (< 0.001)
Absolute HRR3-min 0.387 (0.034) 0.617 (< 0.001) 0.472 (< 0.001)
% HR3-min decline 0.431 (0.017) 0.641 (< 0.001) 0.227 (0.043)

Values are presented as Spearman’s correlation coefficient (P-value).

VEqO2, ventilatory equivalent for oxygen; HR, heart rate; HR1-min, 1st minute heart rate decline; HRR, heart rate recovery; HR3-min, 3rd minute heart rate decline.

Incidence of high resting HR, poor exercise HR, and impaired post-exercise HR of the study population

Variable Men Women All

< 25 kg/m2 (n= 15) ≥ 25 kg/m2 (n= 15) P < 25 kg/m2 (n= 25) ≥ 25 kg/m2 (n= 25) P < 25 kg/m2 (n= 40) ≥ 25 kg/m2 (n= 40) P
High resting HR 0 15 (100)* - 1 (4.0) 24 (96.0) < 0.001 1 (2.5) 39 (97.5) < 0.001
Poor %HR reserve 11 (73.3) 15 (100) 0.04 16 (64.0) 25 (100) 0.005 27 (67.5) 40 (100) 0.014
Impaired 1st minute HR recovery 3 (20.0) 9 (60.0) < 0.001 11 (44.0) 22 (88.0) < 0.001 14 (35.0) 31 (77.5) < 0.001

Values are presented as number (%).

*Chi-square test could not be performed due to a zero data point (0%).

HR, heart rate.

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