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      BRADYCARDIA IN ATHLETES: DOES THE TYPE OF SPORT MAKE ANY DIFFERENCE? – A SYSTEMATIC REVIEW Translated title: BRADICARDIA EN ATLETAS: ¿LA MODALIDAD DEPORTIVA IMPORTA? - UNA REVISIÓN SISTEMÁTICA Translated title: BRADICARDIA EM ATLETAS: A MODALIDADE ESPORTIVA IMPORTA? – UMA REVISÃO SISTEMÁTICA

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          Abstract

          ABSTRACT Bradycardia in athletes can range from moderate to severe, and the factors that contribute to slow heart rate are complex. Studies investigating the mechanisms associated with this condition are controversial, and may be linked to the form of exercise practiced. A systematic literature review was conducted to discuss bradycardia mechanisms in athletes who practice different forms of sport. The databases consulted were Pubmed (MEDLINE), Clinical Trials, Cochrane, Scopus, Web of Science, SciELO, Sport Discus and PEDro. The search included English language articles published up to January 2019, that evaluated athletes who practiced different forms of sport. One hundred and ninety-three articles were found, ten of which met the inclusion criteria, with 1549 male and female athletes who practiced diverse forms of sport. Resting heart rate and cardiac structure were studied in association with the form of sport practiced, through heart rate variability, electrocardiogram, echocardiogram and pharmacological blockade. The studies suggest that a slow resting heart rate cannot be explained by increased vagal modulation alone, but also includes changes in cardiac structure. According to the studies, different sports seem to produce different cardiac responses, and the bradycardia found in athletes can be explained by non-autonomic and autonomic mechanisms, depending on the type of effort or the form of sport practiced. However, the mechanism underlying the slow heart rate in each form of sport is still unclear. Level of evidence II; Prognostic studies - Investigating the effect of a patient characteristic on the outcome of disease.

          Translated abstract

          RESUMEN La bradicardia en atletas puede variar de moderada a grave, y los factores que contribuyen para la reducción de la frecuencia cardíaca son complejos. Los estudios que investigan los mecanismos asociados a la bradicardia son controvertidos y, posiblemente, vinculados al tipo de ejercicio. Se realizó una investigación bibliográfica sistemática para discutir los mecanismos de bradicardia en atletas de diferentes modalidades deportivas. Las bases de datos consultadas fueron Pubmed (MEDLINE), Clinical Trials, Cochrane, Scopus, Web of Science, SciELO, Sport Discus y PEDro. Se incluyeron artículos en inglés, que evaluaron a atletas de diferentes modalidades deportivas, publicados hasta enero de 2019. Se encontraron ciento noventa y tres artículos y diez cumplieron con los criterios de inclusión, totalizando 1549 hombres y mujeres atletas de diversas modalidades deportivas. La frecuencia cardíaca en reposo y la estructura cardíaca fueron estudiadas en asociación con la modalidad deportiva, por variabilidad de la frecuencia cardíaca, electrocardiograma, ecocardiograma y bloqueo farmacológico. Los estudios sugieren que la reducción de la frecuencia cardíaca en reposo no es explicada sólo por el aumento de la modulación vagal, sino también por alteraciones de la estructura cardíaca. De acuerdo con los estudios, los diferentes deportes parecen producir diferentes respuestas cardíacas y la bradicardia encontrada en atletas puede explicarse por mecanismos no autonómicos y autonómicos. Este hallazgo parece depender del tipo de esfuerzo o modalidad deportiva practicada. Sin embargo, el mecanismo involucrado en la reducción de la frecuencia cardíaca en cada modalidad deportiva aún no está claro. Nivel de evidencia II; Estudios pronósticos - investigación del efecto de característica de un paciente sobre el desenlace de la enfermedad.

          Translated abstract

          RESUMO A bradicardia em atletas pode variar de moderada a grave, e os fatores que contribuem para a redução da frequência cardíaca são complexos. Estudos que investigam os mecanismos associados à bradicardia são controversos e, possivelmente, ligados ao tipo de exercício. Realizou-se uma pesquisa bibliográfica sistemática para discutir os mecanismos de bradicardia em atletas de diferentes modalidades esportivas. As bases de dados consultadas foram Pubmed (MEDLINE), Clinical Trials, Cochrane, Scopus, Web of Science, SciELO, Sport Discus e PEDro. Foram incluídos artigos em inglês, que avaliaram atletas de diferentes modalidades esportivas, publicados até janeiro de 2019. Cento e noventa e três artigos foram encontrados e dez preencheram os critérios de inclusão, perfazendo 1.549 homens e mulheres atletas de diversas modalidades esportivas. A frequência cardíaca em repouso e a estrutura cardíaca foram estudadas em associação com a modalidade esportiva, por variabilidade da frequência cardíaca, eletrocardiograma, ecocardiograma e bloqueio farmacológico. Os estudos sugerem que a redução da frequência cardíaca em repouso não é explicada apenas pelo aumento da modulação vagal, mas também por alterações da estrutura cardíaca. De acordo com os estudos, diferentes esportes parecem produzir diferentes respostas cardíacas e a bradicardia encontrada em atletas pode ser explicada por mecanismos não autonômicos e autonômicos. Este achado parece depender do tipo de esforço ou modalidade esportiva praticada. No entanto, o mecanismo envolvido na redução da frequência cardíaca em cada modalidade esportiva ainda não está claro. Nível de evidência II; Estudos prognósticos – Investigação do efeito de característica de um paciente sobre o desfecho da doença.

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          Most cited references29

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          Neural regulation of heart rate variability in endurance athletes and sedentary controls.

          The aim was to examine the cardiac autonomic responses to orthostatic stress and recovery from steady state exercise in endurance trained athletes and sedentary subjects. The power spectrum of heart rate variability was measured before and after exercise in 10 male long distance runners and 14 male sedentary control subjects. Both groups were comparable in sex, age, and body mass index. Continuous ECG recordings were obtained during the following physiological manoeuvres: 45 min supine rest state; 10 min standing; 15 min steady state exercise at 50% maximum workload, and 15 min while supine during post-exercise recovery. The resting heart rate of athletes was lower than controls, at 52(SD 4.9) v 67(8.7) beats.min-1, p < 0.001. Power spectrum analysis was performed using autoregressive modelling. The resting high frequency (HF) vagal component was higher in athletes than controls, at 62 (10.7) v 44(22.4) beats.min-1.Hz-1, p < 0.05. The resting low frequency (LF) peak power was significantly reduced in athletes, at 54(9.9) v 70(19.5) in control, p < 0.05. Although no group differences were observed during upright posture or exercise, the LF:HF area ratio had already returned to pre-exercise levels within 5 min of recovery in athletes. Conversely, it required up to 15 min of recovery before a noticeable decrease in the LF:HF area ratio was seen in controls. These data support the hypothesis that endurance training modifies heart rate control in whole or in part through neurocardiac mechanisms.
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            Intrinsic sinus and atrioventricular node electrophysiologic adaptations in endurance athletes.

            In the present study, we evaluated sinus and atrioventricular (AV) node electrophysiology of endurance athletes and untrained individuals before and after autonomic pharmacologic blockade. Endurance athletes present a higher prevalence of sinus bradycardia and AV conduction abnormalities, as compared with untrained individuals. Previous data from our laboratory suggest that nonautonomic factors may be responsible for the longer AV node refractory period found in well-trained athletes. Six aerobically trained male athletes and six healthy male individuals with similar ages and normal rest electrocardiograms were studied. Maximal oxygen uptake (O(2)max) was measured by cardiopulmonary testing. The sinus cycle length (SCL), AV conduction intervals, sinus node recovery time (SNRT), Wenckebach cycle (WC) and anterograde effective refractory period (ERP) of the AV node were evaluated by invasive electrophysiologic studies at baseline, after intravenous atropine (0.04 mg/kg) and after addition of intravenous propranolol (0.2 mg/kg). Athletes had a significantly higher O(2)max as compared with untrained individuals. The SCL was longer in athletes at baseline, after atropine and after the addition of propranolol for double-autonomic blockade. The mean maximal SNRT/SCL was longer in athletes after atropine and after propranolol. The WC and anterograde ERP of the AV node were longer in athletes at baseline, after atropine and after propranolol. Under double-pharmacologic blockade, we demonstrated that sinus automaticity and AV node conduction changes of endurance athletes are related to intrinsic physiology and not to autonomic influences.
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              Effects of endurance training on resting and post-exercise cardiac autonomic control.

              Endurance training induces reductions in both resting and postexercise heart rate (HR). If adaptation in cardiac autonomic regulation is a contributing factor in these reductions, changes in cardiac autonomic nervous system (ANS) should correspond to those in HR during an endurance-training program. We investigated the changes in resting and postexercise HR variabilities (both in the time and frequency domain) over a 6-wk training program. HR variability was measured five times in an endurance-training group (N = 7) and four times in a control group (N = 5) during the course of study. Endurance training decreased HR and increased indices of parasympathetic modulation measured both at rest and during postexercise recovery periods. Noteworthy is that no changes in either HR or indices of ANS modulation measured during postexercise recovery periods were detectable after the first 7 d of the study despite continued changes in resting HR and indices in ANS modulation measured between the 7th and 42nd days of the endurance-training program. The study demonstrates that with endurance-training changes in cardiac ANS modulation partly contribute to a decrease in HR at rest and during postexercise recovery period, and that adaptation of the cardiac autonomic control occurs sooner in immediate postexercise periods than at rest.
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                Author and article information

                Journal
                rbme
                Revista Brasileira de Medicina do Esporte
                Rev Bras Med Esporte
                Sociedade Brasileira de Medicina do Exercício e do Esporte (São Paulo, SP, Brazil )
                1517-8692
                1806-9940
                October 2020
                : 26
                : 5
                : 449-453
                Affiliations
                [1] Brasília DF orgnameUniversity of Brasília orgdiv1Faculty of Physical Education orgdiv2Exercise Physiology Laboratory Brazil
                Article
                S1517-86922020000500449 S1517-8692(20)02600500449
                10.1590/1517-8692202026052019_0001
                5fa908e0-347b-4f35-8a25-ce1b0f0c2eb9

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                : 20 May 2020
                : 23 May 2019
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 32, Pages: 5
                Product

                SciELO Brazil

                Categories
                Systematic Review Article

                Fisiologia cardiovascular,Bradycardia,Sistema nervioso autónomo,Sistema nervoso autônomo,Sports,Athletes,Cardiovascular physiology,Bradicardia,Autonomic nervous system,Deportes,Atletas,Fisiología cardiovascular,Esportes

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