Deepayan Sarkar¹, Anindya Roy², Paramita Nag³, Gargi Barat⁴, Enakshi Ghosh^5*

 

{¹Junior Resident (3rd year), Department of Ophthalmology} {²Associate Professor and HOD, Department of Physiology}

Raiganj Government Medical College, Raiganj, Uttar Dinajpur, West Bengal, INDIA.

³Demonstrator, ⁴Junior Resident II^nd Year, ⁵Associate Professor, Department of Anatomy, R.G. Kar Medical College, Kolkata, INDIA.

Email: drenakshighosh@gmail.com

 

 

Heart rate variability (HRV) is the physiological phenomenon of variation in time interval between heart beats. Variation in the beat-to-beat interval is a physiological phenomenon⁴.HRV has an ubiquitous relationship with all biological functions of the body. The HRV data can be collected by non-invasive procedures and is subject friendly. Presently, it is studied widely in India and abroad, its clinical implications are also emerging gradually. The SA node receives several different inputs and the R-R interval and its variation are the results of these inputs. The main inputs are from the sympathetic and the parasympathetic nervous system⁵.Most widely used methods of HRV analysis are Time Domain method, Frequency Domain method, Non-linear method, Geometric method. In this study we will study HRV by Frequency Domain Method. This method is chosen as, by this method in stable standardized conditions no other factor other than the current autonomic tone contributes in HRV.⁶So, by calculating HRV by FFT method we can measure accurately the effect of persisting autonomic tone on the heart. The Frequency domain is calculated by Fast Fourier Transformation (FFT). The frequency domain in short term recording has 3 components- Very low Frequency (VLF), Low Frequency (LF), High Frequency (HF). Of these, the physiological aspect of VLF is less defined. Sympathetic tone is believed to influence the LF component whereas both sympathetic and parasympathetic activity has an effect on the HF component. The heart rate is increased by sympathetic activity and decreased by parasympathetic (vagal) activity. The balance between the effects of the sympathetic and parasympathetic systems is called sympathovagal balance and it reflects in the beat-to-beat changes of the cardiac cycle. The ratio of the power (LF/HF) is used as a measure of sympathovagal balance^{. 7} Obesity is a clinical condition in which excess body fat has accumulated to that extent that it has negative impact on health. Excessive body weight is associated with diseases like cardiovascular diseases, diabetes mellitus type 2, obstructive sleep apnoea, cancers etc. In the cardiovascular system it causes diseases like ischemic heart disease, congestive heart failure, high blood pressure.⁸ Obesity is measured by particular anthropometric parameters, though body mass index (BMI) is the standard measure of obesity, it is seen that waist hip ratio (WHR) is well correlated with the clinical implications of obesity and abnormal fat deposition in the body.⁹ Recent studies also prove that the WHR is a better indicator of cardiac status than the BMI.¹⁰ In this study both the parameters BMI and WHR are taken for anthropometric correlation. This study shows the effect of obesity on ANS which is evident by HRV analysis. Sex of a person by itself is an independent variable that is seen to affect the HRV of an individual.¹¹ It is seen in females that a considerable change in HRV is noted during the different phases of the menstrual cycle, this change is due to the effect of different sex hormones attaining their peaks in different phases.¹² These hormones lay their effect on the heart rate and HRV of an individual. Present study aims to discover if any significant difference in HRV persists among males and females in resting condition and after submaximal exercise. The subjects were given a sub maximal graded exercise in which the intensity of exercise gradually increases. The exercise was given according to the modified Blake-Bruce Protocol.¹³ A treadmill exercise was given to the subject until. was reached. This was measured by a pulse oxymeter. When the pulse rate reaches 128 beats/min (for males) and 138 beats/min(for females) it indicates 50% of VO₂max. The exercise was then terminated. The subject was then immediately laid in supine condition to record the HRV. The last two decades has witnessed the recognition of a significant relationship between the ANS and cardiovascular mortality, including sudden cardiac death. Experimental evidence for an association between diseases of cardiovascular system (cardiac autoneuropathy) either increases the sympathetic or reduces the vagal activity this has spurred the efforts for the development of quantitative markers for autonomic activity.¹⁵ Reduced HRV and heart rate has been shown to be a predictor of mortality after acutemyocardial infarction(AMI).^16,17,18A range of other conditions are also associated with HRV, including congestive heart failure, diabetic neuropathy, depression, post-cardiac transplant, susceptibility to SIDS and poor survival in premature babies. The purpose of this study is to find out if a single bout of sub-maximal exercise (50% VO₂ max.)can cause change in HRV and how it varies with gender and anthropometric parameters. This study will show how gender and obesity influences the HRV which is a measure of autonomic nervous system. This study also lays clinical standards of the HRV in correlation with obesity and sex hormones which would effectively help a physician to diagnose and treat an obese patient or a patient undergoing hormone replacement therapy(HRT).

 

AIMS AND OBJECTIVES

• To find out the changes in HRV among males and females in the age group of 17-25 years at rest.
• To find out the changes of HRV after a single bout of sub maximal treadmill exercise (50% of VO₂ max.) in the same subjects.
• To find out the correlations between the HRV parameters at rest and after the exercise with BMI and WHR in the study group.

 

METHODOLOGY

• Type of study-             Observational.
• Study Design-            Cross sectional.
• Study Population- Young healthy adults of 17-25 years age group, both males and females.
• Study Site- Human Research Laboratory, Department of Physiology, R.G Kar Medical College and Hospital, Kolkata, West Bengal.
• Sample Size- 60 young healthy adult subjects; 30 males and 30females.
• Selection Criteria- Young Healthy Adults of 17-25 years age group males and females not suffering from any sort of disease or disability or not associated with regular strenuous activities (including exercises) which effectively changes

the basal heart rate.

G. Exclusion Criteria:

• Hypertensive subjects.
• Smoker, Addicts.
• Subjects suffering from any cardiovascular diseases.
• Subjects recovering from any major ailment.
• Subjects with any sort of disease or disability.
• Menstruating female subjects.
• Athletes or Trained Subjects.

 H. Instruments Used

• Measuring tape.
• Physiograph Polyrite-D instrument and accessories.
• Computerized Treadmill.
• Fingertip pulse oxymeter.
• Mercury Sphygmomanometer and Stethoscope.
• Stadiometer and Weighing scale.
• Glucometer and kit.       
• Computerised Electrocardiograph.
• Electrode jelly.

I. Data collection procedure:

1. Questionnaire: Includes History, General Examination and Systemic Examinations.

2. Investigations:

• Blood Pressure (BP) and Pulse monitoring.
• Blood Glucose (Random).                                                             
• Computerized Electrocardiogram (12 leads):-ECG of the subjects were done and checked before the study to detect any cardiovascular disease and expert opinion was sought whenever required.

J. Statistical Tools: Statistical analysis was done by SPSS version -17 using Unpaired student T-Test, Paired Student T- test and Pearson Correlation Test. P value <0.05 was taken as significant value.

K. Ethical Consideration: Ethical clearance has been taken from the ‘Ethics Committee’ of R.G Kar Medical College and Hospital, Kolkata.

L.Written Consent: Written consent was taken from all subjects taking part in this study after proper explanation of the study, procedures and its impacts.

M. Measurement of HRV:

a) Pre-study criteria:

A modified questionnaire (Mayo Autonomic Laboratory, Mayo Clinic, Rochester, Minnesota)²⁶ containing subject particulars, personal habits, family history and a detailed history of any illness or treatment were recorded. General physical examinations were done. Pre-test instructions were given to avoid consumption of any drugs or food that may alter the autonomic function, 48 hours prior to the test. The subjects were advised to have sound sleep the night before. On the day of the test subjects were not permitted to have tea, coffee, food or drugs from three hours prior to the tests.

b) Procedure:

• The room temperature of the lab was maintained at 18-25 ᵒC. The subjectscame for the study, following all the above criteria. Consent of the subject was taken for the study.
• Data for Waist-Hip ratio [WHR=Waist Circumference (in cms.)/Hip Circumference (in cms.)] and for Body Mass Index[BMI] was then collected.
• The subject was rested on a bed comfortably for 30 minutes.
• ECG and pulse rate were recorded with Digital Physiograph (Polyrite D) for 5 minutes in supine position.
• Then the subject was made to walk on the treadmill as per the pre-determined protocol.The heart rate was monitored by the pulse oxymeter. When the pulse rate reaches 128 beats/min (for males) and 138 beats/min(for females) the exercise was terminated. 14
• The subject was immediately laid on the bed in supine position and the ECG was recordedwith digital Physiograph for 5 min.

c) Measurement of WHR and BMI:

i.    Waist Circumference- It is the point midway between lower rib and iliac crest i.e., 1cm below theumbilicus.

ii.   Hip Circumference- It is measured as the widest girth of the hip.

iii.  BMI measurement: It was measured by Quitlet index i e. Weight in kg / (Height in Metre)2

WHR:

i. Normal= 0.80-0.87(males) , 0.67-0.75(females).

ii. Overweight = 0.88-0.99(males), 0.76-0.84(females).

iii. Obese = ≥1(males), ≥0.85(females).

BMI- (kg/m²):

i.<18.50 (underweight)

ii.18.50-24.99 (normal)

iii.25-29.99 (overweight)

iv.≥30.00 (obese).²⁷

d) Analysis of the recordings: In frequency domain [in short term recordings (2-5 minutes)], spectral components are:

• Very low frequency (VLF) : 0.04 Hz.
• Low Frequency (LF) : 0.04 to 0.15 Hz.
• High Frequency (HF) : 0.15 to 0.4 Hz.

The physiological component of VLF is much less defined. The measurement of VLF, LF, and HF power components was be taken in absolute values of power (milliseconds squared). LF and HF values were also measured in normalized units, which represent the relative value of each power component in proportion to the total power minus the VLF component. The representation of LF and HF in normalized units emphasizes the controlled and balanced behaviour of the two subdivisions of the ANS.²⁸The data of LF/HF ratio was collected and tabulated using suitable statistical techniques and was then analysed to find the correlations, if any.

 

OBSERVATIONS AND RESULTS

Table 1: Gender wise distribution of subjects

 

Figure 1: The pie diagram shows the distribution of study subjects according to gender.

 

Table 1 and Fig.1 shows that: 50% of the subjects taken for the study were males and 50% were females.

 

Table 2: Age wise distribution of subjects

 

Figure 2: The bar diagram shows the distribution of subjects according to gender and age.

Table 2 and Fig. 2 shows that:Among the 30 male.Among the 30 female subjects taken 18 were of the age group 17-20 (≤20) years and 12 were of the age subjects taken 13 were of the age group 17-20 (≤20) years and 17 were of the age group of 21-25 (21) years group of 21-25 (21) years.

Table 3: Base line charecteristics of the subjects

*p<0.05 = Significant.

Table 3 shows that male and female were age matched. There was no significant differences in BMI,WHR and pulse rate except height and weight that was found to be significantly (p<0.05) more in males than females.

Table 4: Comparision of BMI with Gender of the subjects

 

Figure 3: The bar diagram shows the distribution of BMI with gender of the subjects.

 

Table 4 and Fig. 3 shows that among the study subjects maximum number of subjects were normal (46.67% males and 50% females)where as only 13.33% males and 3.33% female were underweight, 26.67% males and 16.67% females were overweight and 13.33% males and 30% females were obese.

 

Table 5: Comparison ofWaist-Hip Ratio (WHR) with Gender

 

Figure 4: The bar diagram shows the distribution of study subjects acoording to WHR and Gender.

Table 5 and Fig.4 shows that among the female only 6.67%were normal but 46.67% were obese and 46.67% were overweight. Whereas among the male maximum number of subjects were overweight (50%) , 6.67% males were obese. Only 43.3% males were in normal category.

Table 6: Comparision of LF/HF Ratio with gender after sub-maximal exercise

*p<0.05 = Significant.

Table 6 shows that there is a significant difference of resting LF/HF values among males and females.After a single bout of sub-maximal exercise there is no significant change in LF/HF values in males,but there is significant change in LF/HF values in females after the exercise. There is no significant change in LF/HF ratio among males and females after the exercise.

TABLE 7: Correlation of BMI and LF/HF ratio (HRV parameters) for Pre and Post Exercise in Males

 

Figure 5: The scatter diagram shows the correlation between pre-exercise LF/HF ratio with BMI among males; Figure 6: The scatter diagram shows the correlation between post-exercise LF/HF ratio with BMI among

males

Table 7 and scatter-diagrams (Fig.5 and Fig. 6 ) shows that Pre- Exercise LF/HF ratio in Males has weak positive correlation (r=0.251)with BMI and Post Exercise LF/HF ratio in Males has weak negative correlation (r=-0.023) with BMI and that correlations were not significant (p >0.05).

Table 8: Correlation of WHR and LF/HF ratio (HRV parameters) for Pre and Post Exercise in Males

 

Figure 7: The scatter diagram shows the correlation between pre-exercise LF/HF ratio with WHR among males.Figure 8:The scatter diagram shows the correlation between post-exercise LF/HF ratio with WHR among males.

 

Table 8 scatter diagrams (Fig.7 and Fig. 8) shows that Pre- Exercise LF/HF ratio in Males has positive correlation with WHR and Post- Exercise LF/HF ratio in Males has weak positive correlation with WHR but that was not significant.

TABLE 9:Correlation of BMI and LF/HF ratio (HRV parameters) for Pre and Post Exercise in Females

*p<0.05 = Significant.

 

Figure 9: The scatter diagram shows the correlation between pre-exercise LF/HF ratio with BMI among females; Figure 10: The scatter diagram shows the correlation between post-exercise LF/HF ratio with BMI among females.

 

Table 9, Fig.9, Fig.10 shows that Pre-Exercise LF/HF ratio in Females has negative correlation with BMI and that is significant whereas Post-Exercise LF/HF ratio in Females has negative correlation with BMI but that is not significant.

 

TABLE 10: Correlation of WHR and LF/HF ratio (HRV parameters) for Pre and Post Exercise in Females

*p<0.05 = Significant.

 

Figure 11: The scatter diagram shows the correlation between pre-exercise LF/HF ratio with WHR among females; Figure 12: The scatter diagram shows the correlation between post-exercise LF/HF ratio with WHR among females.

 

Table 10, Fig.11 and Fig.12 shows that Pre Exercise LF/HF ratio in Females has significant association with WHR but Post Exercise LF/HF ratio in Females has Significant negative correlation with WHR.

 

DISCUSSION

The HRV is due to autonomic modulation over the cardiac activity and it is well known that the decrease in HRV indicates sympathetic activity and increase in HRV is due to parasympathetic influence. So, decrease in LF/HF indicates decrease in sympathetic activity and increase in LF/HF indicates increase in parasympathetic activity. Deep breathing activates parasympathetic nervous system whereas during exercise the sympathetic activity is kindled. In the present study, the basal HRV (resting period) of males are significantly more than females indicating sympathetic activity is more in male than female. According to Kuo et al.’s study middle-aged females have a more dominant parasympathetic regulation.²⁹The reason for this is paradoxical autonomic control in adolescent age, lies in the onset of secretion of sex hormones. The female sex hormones play a vital role in increasing the vagal activity. This increases the parasympathetic activity in young adolescent girls. This is also shown in the study conducted by A. S. Leicht, et al., in which it was shown that there is an increased vagal tone in girls during ovulation and he concluded that it was due to increased endogenous oestrogen level.³⁰As there is an increased level of sex hormones especially oestrogen during the adoloscence, this causes an increased parasympathetic activity by increasing the vagal tone which maintains a low resting LF/HF ratio in females. Physical exercise is associated with parasympathetic withdrawal and increased sympathetic activity resulting in heart rate increase. The rate of post-exercise cardio deceleration is used as an index of cardiac vagal reactivation. Analysis of HRV can provide useful information about autonomic control of the cardiovascular system. In our study the subjects were asked to perform sub-maximal exercise (50% of VO₂ max.) to assess their sympathetic activity. When HRV was taken immediately after exercise,while the male HRV values was more than their respective resting HRV though not significant , the female HRV was significantly more than their respective resting HRV; indicating the anticipatory response of exercise, which is mediated through sympathetic activity is more in female. During exercise the heart rate increases, so should the activity of the sympathetic nervous system but in the study we find only a marginal rise in LF/HF ratio. This can be explained on the lines of homeostasis in which the body tries to maintain an equilibrium condition. The sympathetic activity (LF) increases but simultaneously the parasympathetic activity (HF) also increases to maintain equilibrium. This saves the heart from an overdose of sympathetic stimulation, suggesting a more stable autonomic environment for the heart.³¹The results can also be described as, the study being conducted on sub-maximal exercise the sympathetic nervous system did not reach to its peak values hence though there was increase in LF/HF ratio, there was no significant change in LF/HF ratio, this is on lines of the study conducted by Ana Márciados Santos António et al.³² Several authors have observed that obesity and weight loss affect HRV.^{33,34,35,36,37} Diet induced weight loss improved baroreceptor sensitivity and metaboreflex in obese subjects. ^38,39 However, others^40,41,42 have detected no association between HRV and BMI. A study conducted by Breno Quintella Farah, et al. ²² on HRV and its relationship with central and general obesity showed that the body mass index showed no significant correlation with any heart rate variability parameter. Our study agrees with those studies which show no association between HRV and BMI in case of males. In the present study (Table no.7, Fig.5and6)it is seen that there is no significant correlation of both Pre and Post exercise LF/HF ratio with BMI in males. But in our study it shows that with increasing BMI in females the LF/HF ratio decreases in both resting and post-exercise conditions and that association is significant only in pre-exercise condition. It has been documented with various methods in experimental⁴³ and clinical studies ^31,44,45,46that parasympathetic activity is decreased in obesity. Katarzyna Piestrzeniewicz et al.⁴⁷demonstrated a negative correlation between waist circumference and the parameters reflecting parasympathetic activity. Disparate results come from the study by Kim et al.²³ who revealed a negative correlation between HRV and waist to hip ratio. In our study (Table no.8, Fig.7 and 8) there is no significant correlation of pre and post exercise LF/HF ratio with Hip ratio in males, but in case of females (Table no.10, Fig.11 and 12) it was found that in post exercise conditions LF/HF ratio has a significant negative correlation with WHR. Physical exertion acutely increases cardiac output and results in a redistribution of blood flow to meet the metabolic demands of active skeletal muscle. After exercise, there is a prompt decrease in cardiac output as physiological activity returns towards resting conditions. Specialized afferent receptors, such as metaboreceptors and baroreceptors, are highly involved with the changes in cardiovascular-autonomic modulation during and after exercise. However, increased intramuscular fat reduces skeletal muscle uptake of glucose and attenuates acidosis during exercise⁴⁸, and therefore, could lower the activation of the metaboreceptors⁴⁹. Furthermore, reduced baroreflex sensitivity following brisk walking has been reported in obese compared to lean women⁵⁰. Consequently, it appears that the afferent feedback mechanisms that normally result in an appropriate autonomic adjustment of the cardiovascular system during and following exercise is impaired with obesity⁴⁹, which help to explain the results of the current study.

 

CONCLUSION

Obesity is frequently associated with sympathovagal imbalance characterized by depressed parasympathetic tone and increased sympathetic activity. The present work opines that the females have higher parasympathetic activity than males. Observing the association between WHR and BMI with HRV in healthy female persons suggests that ANS dysfunction can be detected early and at relatively young age, therefore providing an opportunity for early intervention. Present study also shows that there is an increase in LF/HF values among males and females after a single bout of sub-maximal exercise though the change is not significant. So, exercise therapy programs of variable intensities may increase HRV in obese individual. Future investigations on larger groups of patients, with HRV in response to stimuli, complex evaluation of ANS including baroreceptor reactivity as well as prospective study with follow-up observation are warranted to thoroughly elucidate the impact and mechanism of adverse effects of obesity on cardiac function. Further research is needed to identify exercise regimen that produces optimal improvement in HRV. It also needs to be evaluated whether exercise interventions are effective in long-term therapies for stimulating favourable ANS alterations.

 

Acknowledgement: Indian Council of Medical Research.STS2014(REFERENCE ID: 2014-00536)

              

REFERENCES

1. “Autonomic nervous system" -Dorland's Medical Dictionary,30th Ed. Elsevier.
2. Arthur C.Guyton and John.H.E. Hall. Text book of Medical Physiology (12th. edition), published by Elsevier, division of Reed Elsevier India Private Ltd, New Delhi, India: Page No.729-730.
3. Rang, Dale, Ritter and Moore (2003). Pharmacology 5th ed. Churchill Livingstone. p. 127. ISBN 0-443-07145-4.
4. Corr PB, Yamada KA.“Mechanisms controlling cardiac autonomic function and relation to arrhythmogenesis.” . The Heart and Cardiovascular System, NY. 1986:1343-1403.
5. http://en.wikipedia.org/wiki/Heart_rate_variability.- Variation.
6. www.biocomtech.com/hrv-science/heart rate variability methods. Biochem technologies.
7. “Heart Rate Variability Standards of Measurement, Physiological Interpretation and Clinical use”. Circulation.1996:1043-1065. Doi:10.1161/0.1 CIR 93. 5.1043.
8. Haslam DW, James WP (2005). "Obesity". Lancet366 (9492): 1197– 209. doi:10.1016/S0140-6736(05)67483-1. PMID 16198769.
9. Rudolf E Noble,et al. “Waist to Hip Ratio versus BMI as predictor of cardiac risk in obese adult women”-West J. Med.Apr; 2001; 174(4):240-241
10. Mørkedal, Bjørn; et al. (2011). "Informativeness of indices of blood pressure, obesity and serum lipids in relation to ischaemic heart disease mortality: the HUNT-II study". European Journal of Epidemiology26 (6): 457–461. doi:10.1007/s10654-011-9572-7. ISSN 0393-2990. PMC 3115050. PMID 21461943.
11. “Sex realated differences in auto modulation of Heart Rate in Middle aged subjects” – Circulation:1996;122-125. American Heart Association.
12. GD Allen “Heart rate variability and endogenous sex hormones during the menstrual cycle in young women.”Experimental PhysiologyMay 1, 2003;88, 441-446.
13. HANSON,“Clinical Exercise Training”. Sport Medicine. pg. 13-40
14. Nooman and Dean “Submaximal Exercise Testing: Application and Interpretation” Clinical Physical Therapy , Vol.- 80, No.8, August 2000. Pg-787.
15. “Heart Rate Variability Standards of Measurement, Physiological Interpretation, and Clinical Use”- Marek Malik et al. Circulation. 1996; 93: 1043-1065 doi: 10.1161/01.CIR.93.5.1043.
16. Bigger JT Jr, Fleiss JL, Steinman RC, Rolnitzky LM, Kleiger RE, Rottman JN. (1992). "Frequency domain measures of heart period variability and mortality after myocardial infarction". Circulation.85 (1): 164–171. doi:10.1161/01.CIR.85.1.164. PMID 1728446. 
17. Kleiger RE, Miller JP, Bigger JT Jr, Moss AJ. (1987). "Decreased heart rate variability and its association with increased mortality after acute myocardial infarction". Am J Cardiol.59 (4);pg: 256–262. doi:10.1016/0002-9149(87)90795-8. PMID 3812275. 
18. Abildstrom SZ, Jensen BT, Agner E et al. (2003). "Heart rate versus heart rate variability in risk prediction after myocardial infarction". Journal of Cardiovascular Electrophysiology14 (2): 168–73. doi:10.1046/j.1540-8167.2003.02367.x. PMID 12693499
19. IO’ Brein , PO’ Hare , et al.“Heart Rate Variability in healthy subjects ; effect of age and the derivation of normal ranges for test of Autonomic Function” –Br.Heart J1986;55;348-354; doi:10.1136/hrt55.4.348.
20. Farinatti PT1, Brandão C. “Acute effects of stretching exercise on the heart rate variability in subjects with low flexibility levels.”-J Strength Cond Res; 2011 Jun; (6):1579-85. doi:10.1519/JSC.0b013e3181e06ce1.
21. Dr. Sanhita Rajan Walawalkar “ A study on variation in HRV with change in posture in Young Adult Indian Males”-. JMSCR Vol.2 Issue. 3, Page- 503-514, March 2014.
22. Breno Quintella Farah; Wagner Luiz do Prado, et al.“ Heart rate variability and its relationship with central and general obesity in obese normotensive adolescents”. Einstein (Sao Paulo) Vol.11 no.3. Sao Paulo July/Sept 2013.
23. Jeong A Kim, et al.“Heart Rate variability and Obesity Indices”-. http.//www.jabfp.org. Pg.- 97-103.
24. “Obesity and autonomic function in adolescence.” -Riva P, Martini G, Rabbia F, Milan A Clin Exp Hypertension. 2001 Jan-Feb;23(1-2):57-67. PMID: 11270589.
25. R.Sinnereich, et al. “Five minute recordings of heart rate variability for population studies; repeatability and age-sex charecteristics.” Heart 1998;80; Pg-156-162.
26. Low PA: Laboratory evaluation of autonomic function, Clinical Autonomic Disorders: Evaluation and Management, 1997.Low PA: Lippincott – Raven Publishers, Philadelphia,( 2nd Edn.) , Page No. 179 – 206.
27. Preventive and Social Medicine. K.Park. 22nd Edition.Page-369-370.
28. www.physionet.org/physiotools/ecgsyn/paper/node 3.html. Paper-8/10/2013-“Heart Rate Variability”.
29. Terry B. J.Kuoet al. “ Effect of aging on gender differences in neural control of heart rate.”American Journal of Physiology - Heart and Circulatory PhysiologyPublished 1 December 1999Vol. 277no. 6, H2233-H2239
30. S. Leicht, D. A. Hirning and G. D. Allen “Sex hormone influences on heart rate control”- Exp Physiol 88.3. Pg.no.- 444.
31. Pober DM1, Braun B, Freedson PS. “Effects of a single bout of exercise on resting heart rate variability.”- Med Sci Sports Exerc. 2004 Jul;36(7):1140-8.
32. Ana Márcia dos Santos António, et al. “Cardiac autonomic responses induced by a single bout of exercise with flexible pole” - International Archives of Medicine 2014, 7:40.
33. Muscelli E, Emdin M, Natali AA et al. “Autonomic et hemodynamic responses to insulin in lean and obese humans”. J Clin Endocrinol Metab, 1998; 83: 2084–2090.
34. Rabbia F, Silke B, Conterno A et al. “Assessment of cardiac autonomic modulation during adolescent obesity.”Obes Res, 2003; 11: 541–548.
35. Karason K, Molgaard H, Wikstrand J, Sjostrom L.”Heart rate variability in obesity and the effect ofweight loss”. Am J Cardiol, 1999; 83: 1242–1247.
36. Nault I, Nadreau E, Paquet C et al. “Impact of bariatricsurgery-induced weight loss on heart rate variability”.Metabolism, 2007; 56: 1425–1430.
37. Ito H, Ohshima A, Tsuzuki M et al. “Effects of increasedphysical activity and mild calorie restrictionon heart rate variability in obese women”. Jpn Heart J,2001; 42: 459–469.
38. Grassi G et al. “Body weight reduction, sympathetic nerve traffic, and arterial baroreflex in obese normotensive humans.”Circulation 97:2037–2042.
39. Trombetta IC et al.(2003) “Weight loss improves neurovascular and muscle metaboreflex control in obesity”. Am J Physiol Heart Circ Physiol;pg: 285:H974–H982. doi:10.1152/ajpheart.01090.2002.
40. Kim JA, Park YG, Cho KH et al. “Heart rate variabilityand obesity indices: emphasis on the response tonoise and standing.”J Am Board Fam Pract, 2005; 18:97–103.
41. Antelmi I, DePaula RS, Shinzato AR, Peres CA,Mansur AJ, Grupi CJ. “Influence of age, gender, body mass index and functional capacity on heart ratevariability in a cohort of subjects without heart disease.”Am J Cardiol, 2004; 93: 381–385.
42. Madsen T, Christensen JH, Toft E, Schmidt EB. “C-reactive protein is associated with heart rate variability”Ann Noninvasive Electrocardiol, 2007; 12:216–222.
43. Van Villet BN, Hall JE, Mizelle HL, Montani JP,Smith Jr MJ. “Reduced parasympathetic control of heart rate in obese dogs.”Am J Physiol, 1995; 269: 629–637.
44. Peterson HR, Rothschild M, Weinberg CR, Fell RD,McLeish KR, Pfeifer MA. “Body fat and the activity of the autonomic nervous system.”N Engl J Med, 1988; 318: 1077–1083.
45. Zahorska-Markiewicz B, Kuagowska E, Kucio C,Klin M. “Heart rate variability in obesity”. Int J Obes Relat Metab Disord.1993; 17: 21–23.
46. Piccirillo G, Vetta F, Viola E et al. “Heart rate and blood pressure variability in obese normotensive subjects.”Int J Obes Relat Metab Disord, 1998; 22: 741–750.
47. Katarzyna Piestrzeniewicz et al. “Obesity and heart rate variability in men with myocardial infarction”.Cardiology Journal 2008, Vol. 15, No. 1, pp. 43–49
48. Sherman WM, Katz AL, Cutler CL, Withers RT, Ivy JI (1988) “Glucose transport: locus of muscle insulin resistance in obese Zucker rats.”Am J Physiol. pg:255:E374–E382.
49. Dipla K, Nassis GP, Vrabas IS (2012)” Blood pressure control at rest and during exercise in obese children and adults.” J Obes 147385. doi:10.1155/2012/147385.
50. Figueroa A, Baynard T, Fernhall B, Carhart R, Kanaley JA (2007a) “Impaired postexercise cardiovascular autonomic modulation in middle-aged women with type 2 diabetes.” Eur J Cardiovascular 14:237–243.