|Year : 2020 | Volume
| Issue : 5 | Page : 2379-2383
Heart rate recovery in normal and obese males with and without parental history of cardiovascular disease
Rahul1, Narsingh Verma2, Mayank Agarwal3, Pravesh Vishwakarma4, Arvind Kanchan1, Pravesh Kumar2
1 Department of Physiology, Hind Institute of Medical Sciences, Barabanki, Uttar Pradesh, India
2 Department of Physiology, King George's Medical University, Lucknow, Uttar Pradesh, India
3 Department of Physiology, Lady Hardinge's Medical College, New Delhi, India
4 Department of Cardiology, King George's Medical University, Lucknow, Uttar Pradesh, India
|Date of Submission||21-Jan-2020|
|Date of Decision||13-Mar-2020|
|Date of Acceptance||23-Mar-2020|
|Date of Web Publication||31-May-2020|
Dr. Mayank Agarwal
474/25, New Brahm Nagar, Daliganj Crossing, Lucknow - 226 020, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
Background: Parental history of cardiovascular disease (CVD) and obesity is associated with delayed parasympathetic nervous system reactivation after exercise. Heart rate recovery (HRRe) after a minute of exercise is inversely related to cardiovascular events. Aim: To determine the effect of body mass index (BMI) and parental CVD history on HRRe in apparently healthy young Indian males. Method: The present cross-sectional experimental study involved 100 males, aged18–25 years. Subjects were divided into two equal groups based on the parental CVD history—(i) Parental CVD history present, and (ii) Parental CVD history absent. Each of these groups were further divided into two equal sub groups based on BMI—(a) BMI <23kg/m2, and (b) BMI ≥25 kg/m2. Participants exercised on the treadmill at variable speeds and grades to achieve their target HR (THR). THR was calculated by adding 60–90% HR-reserve (HRR) in their basal HR (BHR). HRR was calculated by subtracting maximal HR (MHR) from BHR. MHR was estimated by the formula: 208–0.7 × age. The HRRe was calculated by subtracting the immediate postexercise HR with the HR after a minute of rest postexercise. ANOVA with post-hoc Tukey was applied and a P value ≤0.05 was considered as statistically significant. Results: HRRe value was significantly lesser in subjects having a positive parental history of CVD than the subjects with no parental history of CVD, irrespective of BMI. Also, HRRe was inversely related to BMI. Conclusion: Not only obesity but also a family history of CVD impacts the recovery of HR after vigorous-intensity exercise.
Keywords: Body mass index, cardiovascular, family history, heart rate recovery
|How to cite this article:|
Rahul, Verma N, Agarwal M, Vishwakarma P, Kanchan A, Kumar P. Heart rate recovery in normal and obese males with and without parental history of cardiovascular disease. J Family Med Prim Care 2020;9:2379-83
|How to cite this URL:|
Rahul, Verma N, Agarwal M, Vishwakarma P, Kanchan A, Kumar P. Heart rate recovery in normal and obese males with and without parental history of cardiovascular disease. J Family Med Prim Care [serial online] 2020 [cited 2020 Sep 19];9:2379-83. Available from: http://www.jfmpc.com/text.asp?2020/9/5/2379/285071
| Introduction|| |
Heart rate recovery (HRRe) is the decrease in heart rate (HR) after 1 min (or up to 3 min) of submaximal to maximal intensity exercise cessation. HRRe is a simple, reliable, easily accessible method to monitor and assess cardiovascular health and is an important predictor of all cause mortality and death associated with cardiovascular diseases (CVD). Attenuation in HRRe is associated with adverse cardiovascular events.
The recovery in HR after exercise is affected more by parasympathetic reactivation than the sympathetic withdrawal., Autonomic nervous system dysfunction would result in attenuated HRRe and predisposition to CVD. Family history of CVD affects parasympathetic reactivation. Obese individuals have vagus nerve dysfunction. Thus, we hypothesized that parental CVD history and increased BMI would attenuate the HRRe.
To the best of the author's knowledge, none of the studies from India has reported the effect of obesity and family history of CVD on HRRe. Hence, the present study aims to observe the effect of body mass index (BMI) and family history of CVD on HRRe. Furthermore, the study results would conclude that whether obesity or family history of CVD has more impact on HRRe.
| Materials and Methods|| |
Ethical clearance reference number was 71 ECM IIB Thesis/P9, December 2015. The present population-based cross-sectional study was conducted in the Department of Physiology, King George's Medical University (KGMU), Lucknow, Uttar Pradesh, India after approval from the Institutional Ethical Committee.
The diagnosed CVD patients visiting the Cardiology Department, KGMU were counseled to send their children to the Physiology Department, KGMU for HRRe test. A structured interview and systemic examination were done before the recruitment of the subject in the study. Informed written consent was taken from each participant. ‘No’ as an answer to all the questions in Physical Activity Readiness Questionnaire, resting HR ≤100 beats per minute (bpm) or blood pressure ≤140/90 mmHg and a normal electrocardiogram (BPL Cardiart 108T-DIGI, India) were the inclusion criteria. Involvement in regular moderate-intensity physical activity in the past 6 months; history of any abnormalities like diabetes mellitus, valvular or congenital heart disease, hypertension, endocrine disorder, neuromuscular disorders (could have jeopardized the subject's health or study results); inability to follow exercise protocol were the exclusion criteria.
A total of 50 young (18–25 years), apparently healthy, male volunteers with a positive family history of CVD in their first-degree relative (mother, father or both) were involved in the study. Control group comprised of another 50 apparently healthy males that were recruited from KGMU with no history of CVD in the family. Subjects in both groups were matched by age and BMI. These groups were further divided into two equal sub-groups—(a) BMI: 18.5–22.9 kg/m2 and, (b) BMI ≥25 kg/m2 as per Asian-Pacific obesity classification by the World Health Organization.
The subjects in minimal clothing stood still on the platform of a digital weighing machine to record the weight up to the nearest 0.1 kg. The subject stood barefoot on the platform of a rigid stadiometer with straight knees, buttocks, and shoulders touching the stadiometer, and head in Frankfort plane to record the height up to the nearest 0.1 cm. BMI was calculated by the formula: weight (kg)/height (m2).
Determination of the target heart rate
First, the maximum heart rate (MHR) was calculated by the formula proposed by Tanaka et al.: 208–0.7 × age in years.,, Then, the Heart Rate Reserve (HRR) was calculated by subtracting basal heart rate (BHR) from MHR. Thereafter target HR (THR) was estimated by the equation: (0.60–0.90)×HRR + BHR. This THR keeps the exercise intensity in the vigorous range., For example, consider a 24-year-old adult who has a BHR about 75 bpm, then MHR is208–0.7 × age, i.e. 208–17 = 191.HRR is MHR–BHR, i.e. 191–75 = 116. THR range is 0.60 × HRR + BHR i.e. 0.60 × 116 + 75 = 145 bpm to 0.90 × HRR + BHR i.e. 0.90 × 116 + 75 = 179 bpm.
Exercise testing and heart rate recovery
The test was done in the morning hours (9-10 AM) atleast after 2 h of breakfast. One familiarization session and two trials were done, each separated by a week. Average value of the two trials was taken. All subjects were encouraged to walk on a motorized treadmill (Pro Bodyline Fitness 970) at variable speeds and grades (inclination or slope) to achieve their calculated THR. Subject walked/ran on the treadmill until achieved THR remained almost constant (±5 bpm) for 2 min to achieve a steady-state. HR was assessed and monitored continuously before, during and after exercise test by ‘Omron pulse oximeter ‘MD300C20’ whereas the subject was standing on the treadmill with hands placed on handrails. HRRe was calculated as the difference in the HR immediately after exercise to HR after a minute of rest postexercise.
Initial data entry was done in Microsoft Excel 2016. IBM SPSS Statistics for Windows, Version 25.0 was used to carry out further statistical analyses. Data are presented as either mean ± standard deviation. Data have been rounded off to one decimal place. Shapiro–Wilk was used to test the normality of data. ANOVA with post-hoc Tukey was applied and a P value ≤ 0.05 was considered as statistically significant. The point-biserial correlation coefficient was calculated to correlate HRRe with a positive history of CVD in normal BMI subjects. The Pearson correlation coefficient was calculated to correlate HRRe with BMI in subjects without a parental history of CVD. Linear regression analysis was done to know the R-square value. The confidence interval was 95%. Correlation coefficient was considered mild, moderate and strong for values 0.3–<0.5, 0.5–<0.7, 0.7–<0.9, respectively.
| Results|| |
[Table 1] represents the BHR, THR, and anthropometric indices of the subjects that were divided into four equal groups based on the presence or absence of parental CVD history and BMI. Subjects were comparable for age and height (P > 0.05) in all the groups. Weight and BMI of groups (both with and without CVD parental history) having BMI ≥25 were comparable (P < 0.05). BHR was non-significantly higher in groups with BMI ≥25 as compared with the groups with BMI <23 kg/m2. THR achieved after exercise was similar (P ≥ 0.97) in all the groups.
[Table 2] represents HRRe in the subjects divided into four groups. HRRe was significantly (P < 0.05) lowest in the group having a positive family history of CVD and BMI ≥ 25, followed by the groups with — negative CVD history in the family and BMI ≥ 25, positive CVD history in the family and BMI < 23, and negative family history of CVD and BMI < 23, respectively.
|Table 2: Heart rate recovery after a minute of vigorousintensity exercise|
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The point-biserial correlation coefficient was 0.413 (R2 = 0.171, P = 0.003) for the presence of parental CVD history and delayed HHRe in normal BMI subjects (n = 50). Pearson correlation coefficient was -0.598 (R2 = 0.358, P < 0.001) for BMI and HHRe in subjects (n = 50) without a family history of CVD.
| Discussion|| |
The current study involved young and apparently healthy, normal weight and obese males with and without a family history of CVD. HRRe after 1 min of vigorous-intensity treadmill exercise test was least in the obese group with a positive family history of CVD. Thus, the family history of CVD has an additional impact on attenuating HRRe in comparison to obesity as an individual factor. Moreover, a significantly mild correlation of parental CVD history with delayed HRRe was obtained in our study result. BMI has shown a moderate negative correlation with HRRe, i.e. as BMI increases HRRe attenuates.
There are considerable inter individual differences in the extent and rate of HRRe after exercise whose mechanisms are not known exactly. However, polymorphisms in the genes encoding the autonomic nervous system (sympathetic and parasympathetic) could be a possible cause., Any genetic variation and inheritance of these genes in the offsprings of CVD patients could be a cause of delayed HRRe as obtained in our study results. Ingelsson et al. involved 2982 Framingham offspring participants to perform a submaximal exercise according to standard Bruce protocol and HRRe was accessed after 3 min of exercise cessation. Ingelsson et al. reported a heritability of 34% for slow HRRe. Nederend et al. involved 491 healthy adolescent twins and their siblings to perform a maximal intensity (till exhaustion) exercise testing and reported a heritability of 60% for HRRe after a minute of exercise cessation. Parental CVD history is an established risk factor for CVD development in offspring. However, Jha et al. reported that HRRe does not depends on the parental history of hypertension and concluded that the family history of hypertension is not accompanied by autonomic nervous system dysfunction. Our study results show that the 17% attenuation in HRRe can be explained by the positive family history of CVD. It is in accordance with the previous study results.,,
A moderate and negative correlation of BMI with HRRe found in our study is in accordance with the result reported by Barbosa et al., Brinkworth et al., and Azam F et al. It was observed that a 36% change in HRRe can be explained by the presence of obesity. Barbosa et al. involved 2443 subjects of both genders, aged 20–59 years to analyze the effect of BMI on HRRe. They found that obese subjects (BMI > 30 kg/m2) had a higher basal HR compared with subjects with normal BMI which might be due to autonomic nervous system dysfunction. In our study results, basal HR was non-significantly higher in the obese group. Barbosa et al. concluded that higher BMI causes a delay in HRRe. Brinkworth et al. reported that weight loss improves the HRRe postexercise which further strengthens our study results. Azam F et al. involved 64 healthy males, aged 25–55 years and reported that the BMI is significantly and strongly correlated with slow HRRe.
The prevalence of CVD is rising in India., Family history has not been given much importance in traditional risk prediction tools. However, parental CVD history is particularly important in younger individuals that do not yet present with traditional risk factors. Thus, CVD patients visiting the hospitals must be counseled to have their children assessed for HRRe. Also, an epidemic of obesity has been established in the Indian youth.,, HRRe monitors cardiovascular health easily and can segregate high-risk individuals. Exercise restores sympathovagal balance and by prescribing an appropriate exercise protocol like eccentric exercises to these high-risk individuals would decrease the future risk of CVD morbidity and mortality and enhance the present health-related quality of life.
| Limitation of Study|| |
The study involved only young males hence results might not apply to the general population. However, as the Indian youth (15–34 years) constitutes around 35% population of the country and recent data show that India is the third most obese country in the world with the second-highest number of obese children (<20 years of age), our study results become important. Only males were included in the study to maintain the homogeneity of data.
A convenient sample size was taken in our study rather than calculating it. However, on calculating the sample size retrospectively it was found that 16 subjects were required per group for 5% alpha error and 80% power of the study. This calculation was done by using G*Power calculator v22.214.171.124. The effect size f was calculated as 1.062 from partial η2 = 0.53 (sum of squares for between groups in ANOVA for HRRe was 2541.88 and total sum of squares was 4791.56; η2 = sum of squares for between groups ÷ total sum of squares).
Standardized exercise protocol should be used to estimate MHR rather than calculating it by various available equations. However, owing to limitation of resources we have to calculate the MHR by equation by Tanaka et al. Future studies at the molecular level with larger samples, which can directly explore the heritability of delayed HRRe in individuals with a positive family history of CVD are necessary for external validation of our study results.
| Conclusion|| |
Not only obesity but also a family history of CVD impacts the recovery of HR after exercise. Obese offspring of CVD patients are at a higher risk of CVD development than obese individuals with negative parental CVD history or normal BMI offspring of CVD patients. Delayed HRRe has been associated with poor cardiovascular health. Hence, obese subjects and offspring of CVD patients should be counseled to take HRRe test. HRRe could prove to be an effective tool in reducing CVD disease burden in the country.
The authors are thankful to all the volunteers for participating in the study. Authors are grateful to the Head, Department of Physiology, King George's Medical University, Lucknow, India, for her support in the study. We are also thankful to the colleagues and faculty members of the Department of Physiology, King George's Medical University, Lucknow, India, for their support in the study.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
This research received no grant from any funding agency in the public, commercial or not-for-profit sectors.
Conflicts of interest
There are no conflicts of interest.
| References|| |
Qiu S, Cai X, Sun Z, Li L, Zuegel M, Steinacker JM, et al
. Heart rate recovery and risk of cardiovascular events and all-cause mortality: A meta-analysis of prospective cohort studies. J Am Heart Assoc 2017;6. pii: e005505.
White DW, Raven PB. Autonomic neural control of heart rate during dynamic exercise: Revisited. J Physiol 2014;592:2491-500.
Nelson C, Franks S, Brose A, Raven P, Williamson J, Shi X, et al
. The influence of hostility and family history of cardiovascular disease on autonomic activation in response to controllable versus noncontrollable stress, anger imagery induction, and relaxation imagery. J Behav Med 2005;28:213-21.
Rossi RC, Vanderlei LC, Gonçalves AC, Vanderlei FM, Bernardo AF, Yamada KM, et al
. Impact of obesity on autonomic modulation, heart rate and blood pressure in obese young people. Auton Neurosci 2015;193:138-41.
Agarwal M, Singh S, Sharma P, Saini R. Acute effect of moderate-intensity concentric and eccentric exercise on cardiac effort, perceived exertion and interleukin-6 level in physically inactive males. J Sports Med Phys Fitness 2019;59:259-66.
WHO Expert Consultation. Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies. Lancet 2004;363:157-63.
Tanaka H, Monahan KD, Seals DR. Age-predicted maximal heart rate revisited.J Am Coll Cardiol 2001;37:153-6.
Robergs RA, Landwehr R. The surprising history of the “HRmax=220-age” equation. JExerc Physiol Online 2002;5:1-10.
Franckowiak SC, Dobrosielski DA, Reilley SM, Walston JD, Andersen RE. Maximal heart rate prediction in adults that are overweight or obese.J Strength Cond Res 2011;25:1407-12.
Pescatello LS, Arena R, Riebe D, Thompson PD. ACSM's Guidelines for Exercise Testing and Prescription. 9th
ed. China: Lippincott Williams and Wilkins; 2014. p. 163-73.
Ferretti G, Fagoni N, Taboni A, Bruseghini P, Vinetti G. The physiology of submaximal exercise: The steady state concept. Respir Physiol Neurobiol 2017;246:76-85.
van de Vegte YJ, Tegegne BS, Verweij N, Snieder H, van der Harst P. Genetics and the heart rate response to exercise. Cell Mol Life Sci 2019;76:2391-409.
Kohli U, Diedrich A, Kannankeril PJ, Muszkat M, Sofowora GG, Hahn MK, et al
. Genetic variation in alpha2-adrenoreceptors and heart rate recovery after exercise. Physiol Genomics 2015;47:400-6.
Ingelsson E, Larson MG, Vasan RS, O'Donnell CJ, Yin X, Hirschhorn JN, et al
. Heritability, linkage, and genetic associations of exercise treadmill test responses. Circulation 2007;115:2917-24.
Kannel WB, Feinleib M, McNamara PM, Garrison RJ, Castelli WP. An investigation of coronary heart disease in families. The Framingham offspring study. Am J Epidemiol 1979;110:281-90.
Nederend I, Schutte NM, Bartels M, Ten Harkel AD, de Geus EJ. Heritability of heart rate recovery and vagal rebound after exercise. Eur J Appl Physiol 2016;116:2167-76.
Weijmans M, van der Graaf Y, Reitsma JB, Visseren FL. Paternal or maternal history of cardiovascular disease and the risk of cardiovascular disease in offspring. A systematic review and meta-analysis. Int J Cardiol 2015;179:409-16.
Jha A, Karki P, Agrahari R, Kumari N. Effect of exercise on heart rate recovery index in normotensive offspring with family history of hypertension. Int J Res Med Sci 2018;6:1101-5.
Barbosa Lins TC, Valente LM, Sobral Filho DC, Barbosa e Silva O. Relation between heart rate recovery after exercise testing and body mass index. Rev Port Cardiol 2015;34:27-33.
Brinkworth GD, Noakes M, Buckley JD, Clifton PM. Weight loss improves heart rate recovery in overweight and obese men with features of the metabolic syndrome. Am Heart J 2006;152:693.e1-6.
Azam F, Shaheen A, Irshad K, Liaquat A, Naveed H, Shah SU. Association of postexercise heart rate recovery with body composition in healthy male adults: Findings from Pakistan. Ann Noninvasive Electrocardiol 2019;e12711.doi: 10.1111/anec.12711.
Prabhakaran D, Singh K, Roth GA, Banerjee A, Pagidipati NJ, Huffman MD. Cardiovascular diseases in India compared with the United States.J Am Coll Cardiol 2018;72:79-95.
Prabhakaran D, Jeemon P, Sharma M, Roth GA, Johnson C, Harikrishnan S, et al
. The changing patterns of cardiovascular diseases and their risk factors in the states of India: The Global Burden of Disease Study 1990–2016. Lancet Glob Health 2018;6:e1339-51.
Bittencourt MS. Family history of cardiovascular disease: How detailed should it be?Mayo Clin Proc 2018;93:1167-8.
The GBD 2015 obesity collaborators. Health effects of overweight and obesity in 195 countries over 25 years. N
Engl J Med 2017;377:13-27.
Ng M, Fleming T, Robinson M, Thomson B, Graetz N, Margono C, et al
. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: A systematic analysis for the Global Burden of Disease Study 2013. Lancet 2014;384:766-81.
Besnier F, Labrunee M, Pathak A, Pavy-Le Traon A, Gales C, Senard JM, et al
. Exercise training-induced modification in autonomic nervous system: An update for cardiac patients. Ann Phys Rehabil Med 2017;60:27-35.
Wheatley CM, Snyder EM, Johnson BD, Olson TP. Sex differences in cardiovascular function during submaximal exercise in humans. Springerplus 2014;3:445.
Faul F, Erdfelder E, Lang AG, Buchner A. G*Power 3: A flexible statistical power analysis program for the social, behavioral, and biomedical sciences. Behav Res Methods 2007;39:175-91.
[Table 1], [Table 2]