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Cardiac Autonomic Modulation and High–Intensity Exercise

Andrey A. Porto, Vinícius Koti Kamada, Leticia Santana Oliveira, Joana Z. Chambrone, David M. Garner, Vitor E. Valenti

Andrey A. Porto, Leticia Santana Oliveira, Joana Z. Chambrone, Vitor E. Valenti, Autonomic Nervous System Study Center, UNESP, Presidente Prudente, SP, Brazil
Vinícius Koti Kamada, Department of Physical Therapy and Occupational Therapy, UNESP, Marilia, SP, Brazil
David M. Garner, Cardiorespiratory Research Group, Department of Biological and Medical Sciences, Faculty of Health and Life Sciences, Oxford Brookes University, Gipsy Lane, Oxford OX3 0BP, United Kingdom

Correspondence to: Vitor Engrácia Valenti, Departamento de Fonoaudiologia, Faculdade de Filosofia e Ciências, UNESP, Marília, SP, Brasil.
Email: vitor.valenti@marilia.unesp.br
Telephone: +55-14-3402-1324
Received: October 26, 2015
Revised: February 5, 2016
Accepted: February 8, 2016
Published online: June 10, 2016

ABSTRACT

AIM: Recently, many new ways of physical training focusing on health promotion and higher performance have been articulated. So, high intensity training has been spotlighted as the best way to improve physical aptitude and to optimize cardiorespiratory and metabolic functions. We intended to describe high intensity training protocols and their effects on cardiac autonomic regulation.

METHODS: The studies were selected in the databases PubMed, Medline, Scielo and Lilacs. The keywords cited were: Exercise, Autonomic Nervous System, Cardiovascular System, which were defined based on the MeSH.

RESULTS: The selected articles presented vagal withdrawal and increase in the sympathetic modulation during the exercise protocols. It highlighted cardiovascular overload and thus, increases in arterial pressure and heart rate, improving cardiovascular endurance over time.

CONCLUSION: The practice of exercise affects the cardiac autonomic modulation according to the level of intensity and volume advocated.

Key words: Autonomic Nervous System; Cardiovascular system; Exercise

© 2016 The Authors. Published by ACT Publishing Group Ltd.

Porto AA, Kamada VK, Oliveira LS, Chambrone JZ, Garner DM, Valenti VE. Cardiac Autonomic Modulation and High–Intensity Exercise. Journal of Cardiology and Therapy 2016; 3(3): 515-518 Available from: URL: http: //www.ghrnet.org/index.php/jct/article/view/1721

INTRODUCTION

Recently, new techniques of physical training focusing on health promotion and higher performance have been conveyed. So, the high intensity training been emphasized as an appropriate method to improve physical fitness and optimize cardiorespiratory and metabolic functions of the body. High intensity intermittent training comprises of work at high heart rate for a short period of time. In healthy adults, their oxygen consumption increases significantly[1]. Methods of resistive exercises are usually recommended to maintain good physiological health, while improving life quality and preventing chronic degenerative diseases[2].

Heart rate variability (HRV) is considered an alternative method of analysis that provides strong indications of predisposition to develop cardiovascular diseases in individuals. These include cardiac ischemia, arrhythmias and risk factors that may lead to death. Reduction in HRV inevitably occurs with the passing of time, low HRV is considered an etiological state and it is persistently linked to mortality in elderly[3]. It is extensively described in the research literature that resistive exercises benefit the musculoskeletal and endocrine systems. Still, the clinical implications in the autonomic cardiac modulation of this brand of exercise are not fully elucidated. The high intensity training protects the autonomic cardiac control against aging, as elderly athletes show similar HRV indices as young adults[4].

Identifying the precise disparities induced by high intensity exercise in HRV is of fundamental importance. Hence, many studies that analyzed the cardiac autonomic modulation through HRV in high intensity exercises were composed to better comprehend the autonomic nervous system modulation when presented with high overload. So, we aimed to describe the effect of the high intensity exercise protocols on cardiac autonomic modulation.

METHODS

The articles applied in this study were selected from the databases of PubMed, Medline, Scielo and Lilacs. For this search we applied the following keywords: Exercise, autonomic nervous system and cardiovascular system, which were defined as fundamental keywords in the health sciences (DeCS) and equally in the English language (MeSH).

These readings were gathered based on their titles, analyzed and selected according to the inclusion criteria. The title had to express high intensity exercise as its focus of study, and had to analyze the cardiac autonomic system through HRV. Afterwards, we filtered the results to identify repetitions, as the searches were made in multiple databases.

All the selected titles had their abstracts considered to retain only those that focused on the autonomic heart modulation during resistive exercise. The selected abstracts were re-analyzed to identify relevant studies that were not found in the primary search (between 2003 and 2014).

For the evaluation of the studies’ quality, we applied the PEDro scale on the manuscript presented in Table 1. The British Journal of Sports Medicine has published editorials regarding PEDro scale, supporting its use[5-7]. They presented a summary of a systematic review indexed on PEDro.

According to the PEDro’s information on the website http://www.pedro.org.au/: “PEDro is the Physiotherapy Evidence Database, which is an unrestricted database of over 32,000 randomized trials, systematic reviews and clinical practice guidelines in physiotherapy. For each trial, review or guideline, PEDro delivers the citation details, the abstract and a link to the full text, where conceivable. All trials on PEDro are independently quality assessed. These quality ratings are necessary to quickly guide users to trials that are more likely to be valid and to contain sufficient information to guide clinical practice. PEDro is produced by the Centre for Evidence-Based Physiotherapy at The George Institute for Global Health.”

The points addressed by the PEDro scale include the following criteria accordingly which are assessed in http://www.pedro.org.au/wp-content/uploads/PEDro_scale.pdf: “eligibility criteria, randomization of subjects allocation, if allocation was concealed, characteristics concerning prognostic indicators, blinding of all subjects, blinding of all therapists who administered the therapy, blinding of all assessors who measured at least one key outcome, if measures of at least one key outcome were obtained from more than 85% of the subjects initially allocated to groups, if all subjects for whom outcome measures were available received the treatment or control condition as allocated or, where this was not the case, data for at least one key outcome was analysed by “intention to treat”, if the results of between-group statistical comparisons are reported for at least one key outcome, if the study provides both point measures and measures of variability for at least one key outcome”. PEDro’s scores ranges between 0 and 11 and we standardized only studies up to 6.

The data was described in a qualitative manner, and tabulated according to the authors, year of publication, characteristics of the population, study objective, observed variables and conclusions.

RESULTS

Search and strategy of selection

149 articles were established in the first search, we then eliminated 141 articles after a second analysis, and another 4 were eliminated for not attaining the required criteria.

Characteristics of the studies selected

Table 1, organized by authors and year of publication displays the characteristics of the population, objectives, analyzed variables, PEDro scale score and their conclusions.

DISCUSSION

The study of Currie et al[8] (2014) observed enhancement in the oxygen consumption after three months of endurance training at moderate intensity with HIIT. Nevertheless, there was no more increase in peak oxygen consumption at the 6th month in patients with coronary arterial disease. They recognized that the low volume of HIIT associated to resistive exercises with an elapsed time of 20 minutes had less total workload per session than when combined with endurance training for 30 to 50 minutes. Nonetheless, there was an improvement in both group’s cardiorespiratory performance[8].

Astorino et al[9] (2000) and Marzolini et al[10] (2012) observed that resistive training associated with medium endurance training and HIIT improved cardiorespiratory capacity. Conversely, the study of Currie et al[8] (2014) did not achieve significance after three months of resistive training. This may have occurred because in the study of Currie et al[8] (2014) after the first three months, the patients reached their body’s maximum peak oxygen consumption (VO2), and they would not be able to further improve it. Taking into account the changes in the quality of life, the endurance training with resistive training was capable of raising the overall health and physiological welfare. The blood pressure and heart rate were not significantly transformed during the 6 months in either exercising groups. The lipid profile in the blood stream did not vary either, except for the high density lipoprotein, which was elevated in the groups after 6 months of training[8].

Plasma lipid levels were not changed with training in both groups, except for the high-density lipoprotein. This is because of the monitoring of patients five months before the physical training. The procedure of endurance in medium intensity consisted of continuous cycling between 51-65% of the maximum exertion in each individual. The protocol of HIIT involved 10 intermittent minutes of 1 to 85% of maximum potency (PPO) (interval of 75-93%), separated by cessations of one minute to 10% of PPO. The advancements of the exercise consisted in the elevation of the intensity each month to obtain the new ideal PPO. For the final three months, the HIIT group trained at 121% (between 100-152% of PPO, while the endurance group at 78% (60-91%) of PPO.

The resistive protocol after 3 months consisted of exercises in 2 sets, with 10 to 12 repetitions in the upper and lower limbs. The weight was established by the scale of Borg, in a score from 11 to 15[10-12]. Physical training improved the cardiorespiratory capacity in those cardiac patients. It is important to consider the weight load, intensity and duration of the training.

Guiraud et al[13] (2013) revealed that HIIT is beneficial and benign due to the increase in the parasympathetic modulation associated with a lower HR and premature ventricular contraction. Compared to the continued exercise of moderate intensity and the initial triage, there were improvements in HRV. This effect continued for 24 hours after a single exercise session, denoting the importance of this type of intervention to reduce the risk of cardiovascular incidents in patients with heart failure. The reduction of HR post exercise in HIIT is due to vagal modulation, as seen in the increase of HF. These responses may be related to the levels of angiotensin 2 and nitric oxide. The physical training delivers the action of angiotensin 2, which inhibits the vagal modulation[14].

Trained individuals have lower levels of renin plasmatic action, as a consequence of angiotensin 2 and, high values of parasympathetic modulation compared to sedentary individuals[15]. Nitric oxide has an important role in the vagal control, maximizing its action in the cardio-myocytes, while also inhibiting sympathetic activity[16,17]. The elevation in very low frequency (VLF) refers to thermoregulation and the fluctuation of the activity of the renin-angiotensin system and the function of peripheral chemoreceptors. The reduction of levels of angiotensin 2 raises VFL and improved vagal modulation[18].

There was inconsistency between the endurance exercise of medium intensity and HIIT. Although the first presented a decrease of HF, HIIT had the contradictory effect, suggesting that the benefits on HRV are related to the intensity model of HIIT. The exercises were performed on a bicycle, each session consisted of a “warming up” for 2 minutes with 50% of PPO, followed by two sets of interval at 100% of PPO. Each interval was composed of repetitive strikes of 30 seconds at 100% PPO, bounded by 30 seconds of passive rest in the seated position[19]. Four minutes of rest between the two sets was permissible, as well as one minute of rest with 25% of PPO 30 seconds after the last session of exercises[20]. It is essential to identify the most favorable length and intensity to promote the optimal HRV value, especially in heart disease patients[13].

Martinmäki et al[21] (2008) established an abrupt rise in HF in the first minute of rest post-exercise of low intensity with a reduction of HR. They advocated that this is because of a rapid vagal reactivation immediately after exercise[21]. Previously, studies illustrated that during the first minute of rest, the vagal system is the main reason of reduced HR, and this assertion is supported by other investigations of vagal activity established by methods of HRV analysis[22,23]. Martinmäki et al[21] (2008) observed a simultaneous rise in LF and HF immediately at the commencement of rest[21]. LF and HF were higher during the first minute after LI (Low intensity exercise), but after HIIT, LF retained this elevation up to the third minute, and HF up to the second minute. They elucidated that this is since the vagal reactivation, and changes in the baroreflex sensibility which is lessened during exercises of high intensity and partially restored when initiating rest. Although HRV steadied, HR still lowered until after the second minute of rest post LI, and for several minutes’ post HI. This may be explicated by the slow sympathetic reactivation. In summary, they established a greater influence on the intensity of the exercise in the LF and HF. They increased rapidly in the first minute post LI, and elevated for several minutes’ post HI, however, LF and HF were greater in the LI than in HI during the rest period. Consequently, it is suggested that there is a rapid vagal reactivation and HR restoration in low intensity exercise and, this recovery is impaired when there is excessive metabolic stress.

Lima et al confirmed that resistive exercise for the trunk and upper limbs raised the autonomic sympathetic modulation and lowered the parasympathetic cardiac modulation. The cardiac modulation was greater the more vigorous the exercise. After 1 hour at 70% of maximum workload, there was an increase in the sympathetic modulation and decrease in the parasympathetic component of HRV. These results advocate that regardless of the exercises (larger muscular groups, lower limbs, upper limbs or trunk); exercise sessions influence the cardiac autonomic modulation and was maintained for an extended period after the session[24].

In addition, the authors reported that there was orthostatic stress in the control group caused by extensive periods in the seated position, reducing venous return and raising the activity in the peripheral sympathetic nervous. Furthermore, the session of resistive exercise leads to a larger decrease of venous return since there was no post-exercise hypotension. In the study of Rezk et al[25] (2006), there were similar modifications in the cardiac autonomic modulation. Conversely, this controversy was possibly caused by the difference in the number of repetitions between the intensities in Rezk et al[25] study (2006), which was not observed by Lima et al[24,25]. Considering that individuals of the group of 70% of maximum exertion were close to fatigue which was not the case in the group of 50%. We may suggest that exhaustive resistive exercises result in a higher and longer sympathetic cardiac activation. This effect is possibly related to the higher vascular workload in vigorous exercises of high intensity, which promotes increase in the mechanoreceptors and activation of the metaboreflex due to the reduction of the blood flow.

Likewise, as a consequence it results in the deactivation of the cardiopulmonary receptors and increases HR. The resistive exercise for the trunk and upper limbs above 70% of maximum exertion represents an increase in cardiovascular risks, which is not observed at 50%, henceforth, the recommendation of exercises at 50% is the best choice to avoid risks in heart diseases patients. Still, this hypothesis still needs to be confirmed by future studies[24].

CONCLUSION

In this review, we offered important studies that aimed to clarify the effects of high intensity exercise on HRV. The practice of exercises affects the cardiac autonomic modulation according to the level of intensity and volume prescribed.

CONFLICT OF INTERESTS

There are no conflicts of interest with regard to the present study.

REFERENCES

1 Wisloff U, Støylen A, Loennechen JP, Bruvold M, Rognmo Ø, Haram PM, Tjønna AE, Helgerud J, Slørdahl SA, Lee SJ, Videm V, Bye A, Smith GL, Najjar SM, Ellingsen Ø, Skjaerpe T. Superior cardiovascular effect to aerobic interval training versus moderate continuous training in heart failure patients: a randomized study. Circulation 2007; 115(24): 3086–3094

2 Kraemer WJ, Adams K, Cafarelli E, Dudley GA, Dooly C, Feigenbaum MS, Fleck SJ, Franklin B, Fry AC, Hoffman JR, Newton RU, Potteiger J, Stone MH, Ratamess NA, Triplett-McBride T; American College of Sports Medicine. American College of Sports Medicine Position Stand. Progression models in resistance training for healthy adults. Med Sci Sports Exerc. 2002; 34(2): 364-380

3 Tsuji H, Venditti FJ Jr, Manders ES, Evans JC, Larson MG, Feldman CL, Levy D. Reduced heart rate variability and mortality risk in an elderly cohort. The Framingham Heart Study. Circulation 1994; 90(2): 878-883

4 Okazaki K, Iwasaki K, Prasad A, Palmer MD, Martini ER, Fu Q, Arbab-Zadeh A, Zhang R, Levine BD. Dose-response relationship of endurance training for autonomic circulatory control in healthy seniors. J Appl Physiol 2005; 99(3): 1041-1049

5 Kamper SJ, Moseley AM, Herbert RD, Maher CG, Elkins MR, Sherrington C. 15 years of tracking physiotherapy evidence on PEDro, where are we now? Br J Sports Med 2015; 49(14): 907-909

6 Elkins MR, Moseley AM, Sherrington C, Herbert RD, Maher CG. Growth in the Physiotherapy Evidence Database (PEDro) and use of the PEDro scale. Br J Sports Med 2013; 47(4): 188-189

7 Sherrington C, Moseley AM, Herbert RD, Elkins MR, Maher CG. Ten years of evidence to guide physiotherapy interventions: Physiotherapy Evidence Database (PEDro). Br J Sports Med 2010; 44(12): 836-837

8 Currie KD, Bailey KJ, Jung ME, McKelvie RS, MacDonald MJ. Effects of resistance training combined with moderate-intensity endurance or low-volume high-intensity interval exercise on cardiovascular risk factors in patients with coronary artery disease. J Sci Med Sport 2014; pii: S1440-2440(14)00198-4

9 Astorino TA, et al. Incidence of the oxygen plateau at VO2max during exercise testing to volitional fatigue. J Exerc Physiol Online 2000; 3(4): 1-12

10 Marzolini S, Oh PI, Brook D. Effect of combined aerobic and resistance training versus aerobic training alone in individuals with coronary artery disease: a meta-analysis. Eur J Prev Cardiol 2012; 19(1): 81-94

11 Balady GJ, Williams MA, Ades PA, Bittner V, Comoss P, Foody JA, Franklin B, Sanderson B, Southard D; American Heart Association Exercise, Cardiac Rehabilitation, and Prevention Committee; Council on Clinical Cardiology; Councils on Cardiovascular Nursing, Epidemiology and Prevention, and Nutrition, Physical Activity, and Metabolism; American Association of Cardiovascular and Pulmonary Rehabilitation. Core components of cardiac rehabilitation/secondary prevention programs: 2007 update: a scientific statement from the American Heart Association Exercise, Cardiac Rehabilitation, and Prevention Committee, the Council on Clinical Cardiology; the Councils on Cardiovascular Nursing, Epidemiology and Prevention, and Nutrition, Physical Activity, and Metabolism; and the American Association of Cardiovascular and Pulmonary Rehabilitation. J Cardiopulm Rehabil Prev 2007; 27(3): 121-129

12 Little JP, Gillen JB, Percival ME, Safdar A, Tarnopolsky MA, Punthakee Z, Jung ME, Gibala MJ. Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes. J Appl Physiol 2011; 111(6): 1554-1560

13 Guiraud T, Labrunee M, Gaucher-Cazalis K, Despas F, Meyer P, Bosquet L, Gales C, Vaccaro A, Bousquet M, Galinier M, Sénard JM, Pathak A. High-intensity interval exercise improves vagal tone and decreases arrhythmias in chronic heart failure. Med Sci Sports Exerc 2013; 45(10): 1861-1867

14 Buch AN, Coote JH, Townend JN. Mortality, cardiac vagal control and physical training–what’s the link? Exp Physiol 2002; 87(4): 423-435

15 Fagard R, Grauwels R, Groeseneken D, Lijnen P, Staessen J, Vanhees L, Amery A. Plasma levels ofrenin, angiotensin II, and 6-ketoprostaglandin F1 alpha in endurance athletes. J Appl Physiol 1985; 59(3): 947-952

16 Chowdhary S, Townend JN. Role of nitric oxide in the regulation of cardiovascular autonomic control. ClinSci (Lond) 1999; 97(1): 5-17

17 Massion PB, et al. Cardio myocyte-restricted overexpression of endothelial nitric oxide synthase (NOS3) attenuates beta-adrenergic stimulation and reinforces vagal inhibition of cardiac contraction. Circulation 2004;110(17): 2666–72

18 Taylor JA, Carr DL, Myers CW, Eckberg DL. Mechanisms underlying very-low-frequency RR-interval oscillations in humans. Circulation 1998; 98(6): 547-55

19 Meyer P, Normandin E, Gayda M, Billon G, Guiraud T, Bosquet L, Fortier A, Juneau M, White M, Nigam A. High-intensity interval exercise in chronic heart failure: protocol optimization. J Card Fail 2012; 18(2): 126-133

20 Normandin E, Nigam A, Meyer P, Juneau M, Guiraud T, Bosquet L, Mansour A, Gayda M. Acute responses to intermittent and continuous exercise in heart failure patients. Can J Cardiol 2013; 29(4): 466-471

21 Martinmäki K, Rusko H. Time-frequency analysis of heart rate variability during immediate recovery from low and high intensity exercise. Eur J Appl Physiol 2008; 102(3): 353-360

22 Goldberger JJ, Le FK, Lahiri M, Kannankeril PJ, Ng J, Kadish AH. Assessment of parasympathetic reactivation after exercise. Am J Physiol Heart Circ Physiol 2006; 290(6): H2446-52

23 Hatfield BD, Spalding TW, Santa Maria DL, Porges SW, Potts JT, Byrne EA, Brody EB, Mahon AD. Respiratory sinus arrhythmia during exercise in aerobically trained and untrained men. Med Sci Sports Exerc1998; 30(2): 206-214

24 Lima AH, Forjaz CL, Silva GQ, Menêses AL, Silva AJ, Ritti-Dias RM. Acute effect of resistance exercise intensity in cardiac autonomic modulation after exercise. Arq Bras Cardiol 2011; 96(6): 498-503

25 Rezk CC, Marrache RC, Tinucci T, Mion D Jr, Forjaz CL. Post-resistance exercise hypotension, hemodynamics, and heart rate variability: influence of exercise intensity. Eur J ApplPhysiol 2006; 98(1): 105-112

Peer reviewers: Obaida R. Rana, University Hospital Düsseldorf, Department of Cardiology, Moorenstr. 5, 40255 Düsseldorf, Germany; Patricia Massara Martinelli, PhD, Department of Morphology, O3-245, Institute of Biological Sciences, Federal University of Minas Gerais, Av Antônio Carlos, 6627, Belo Horizonte, 31270-910, Brazil.

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