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Efectos de entrenamiento de la resistencia en la variabilidad del ritmo cardíaco y la susceptibilidad a la muerte súbita cardíaca

Efectos de entrenamiento de la resistencia en la variabilidad del ritmo cardíaco y la susceptibilidad a la muerte súbita cardíaca

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Published by: Natanael Martin Osorio Hidalgo on Apr 06, 2014
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doi:10.1152/japplphysiol.01328.2005 100:896-906, 2006. First published 1 December 2005;
 J Appl Physiol
George E. Billman and Monica Kukielka
regulationprotection is not due to enhanced cardiac vagalvariability and susceptibility to sudden cardiac death: Effects of endurance exercise training on heart rate
You might find this additional info useful...
44 articles, 29 of which can be accessed free at:This article cites http://jap.physiology.org/content/100/3/896.full.html#ref-list-18 other HighWire hosted articles, the first 5 are:This article has been cited by [PDF][Full Text][Abstract], August 1, 2008; 93 (8): 931-944.
BillmanCarlos L. del Rio, Tom A. Dawson, Bradley D. Clymer, David J. Paterson and George E.
myocardial ischaemia in dogs: heart rate-mediated attenuationEffects of acute vagal nerve stimulation on the early passive electrical changes induced by
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T. A. Dawson, D. Li, T. Woodward, Z. Barber, L. Wang and D. J. Paterson
gene transferCardiac cholinergic NO-cGMP signaling following acute myocardial infarction and nNOS
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Gyorke, Cynthia A. Carnes and Paul M. L. JanssenKaylan M. Haizlip, Michelle M. Monasky, Nitisha Hiranandani, William S. Harris, Sandor George E. Billman, Yoshinori Nishijima, Andriy E. Belevych, Dmitry Terentyev, Ying Xu,
myocardial infarctions: in vivo and in vitro studies3 fatty acids on ventricular function in dogs with healed
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George E. Billman and William S. Harris
responses to myocardial ischemia or submaximal exerciseEffect of dietary omega-3 fatty acids on the heart rate and the heart rate variability
including high resolution figures, can be found at:Updated information and services http://jap.physiology.org/content/100/3/896.full.html can be found at:
 Journal of Applied Physiology
about Additional material and information http://www.the-aps.org/publications/japplThis infomation is current as of June 3, 2011. 
ISSN: 0363-6143, ESSN: 1522-1563. Visit our website at http://www.the-aps.org/.Physiological Society, 9650 Rockville Pike, Bethesda MD 20814-3991. Copyright © 2006 by the American Physiological Society.those papers emphasizing adaptive and integrative mechanisms. It is published 12 times a year (monthly) by the American publishes original papers that deal with diverse areas of research in applied physiology, especially
 Journal of Applied Physiology
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Effects of endurance exercise training on heart rate variability andsusceptibility to sudden cardiac death: protection is not due to enhancedcardiac vagal regulation
George E. Billman and Monica Kukielka
 Department of Physiology and Cell Biology, The Ohio State University, Columbus, Ohio
Submitted 19 October 2005; accepted in final form 23 November 2005
Billman, George E., and Monica Kukielka.
 Effects of enduranceexercise training on heart rate variability and susceptibility to suddencardiac death: protection is not due to enhanced cardiac vagal regu-lation.
 J Appl Physiol
 100: 896–906, 2006. First published December1, 2005; doi:10.1152/japplphysiol.01328.2005.—Low heart rate vari-ability (HRV) is associated with an increased susceptibility to ven-tricular fibrillation (VF). Exercise training can increase HRV (anindex of cardiac vagal regulation) and could, thereby, decrease therisk for VF. To test this hypothesis, a 2-min coronary occlusion wasmade during the last min of a 18-min submaximal exercise test in dogswith healed myocardial infarctions; 20 had VF (susceptible), and 13did not (resistant). The dogs then received either a 10-wk exerciseprogram (susceptible,
 9; resistant,
 8) or an equivalentsedentary period (susceptible,
 11; resistant,
 5). HRV wasevaluated at rest, during exercise, and during a 2-min occlusion at restand before and after the 10-wk period. Pretraining, the occlusionprovoked significantly (
0.01) greater increases in HR (suscepti-ble, 54.9
 8.3 vs. resistant, 25.0
 6.1 beats/min) and greaterreductions in HRV (susceptible,
0.3 vs. resistant,
0.8ln ms
) in the susceptible dogs compared with the resistant animals.Similar response differences between susceptible and resistant dogswere noted during submaximal exercise. Training significantly re-duced the HR and HRV responses to the occlusion (HR, 17.9
11.5beats/min; HRV,
0.8, ln ms
) in the susceptible dogs; similarresponse reductions were noted during exercise. In contrast, thesevariables were not altered in the sedentary susceptible dogs. Posttrain-ing, VF could no longer be induced in the susceptible dogs, whereasfour sedentary susceptible dogs died during the 10-wk control period,and the remaining seven animals still had VF when tested. Atropinedecreased HRV but only induced VF in one of eight trained suscep-tible dogs. Thus exercise training increased cardiac vagal activity,which was not solely responsible for the training-induced VF protec-tion.parasympathetic nervous system; ventricular fibrillation; myocardialischemia; myocardial infarction
 control have beenassociated with an increase risk for sudden death (44). Kleigerand coworkers (3, 28) found that the patients recovering frommyocardial infarctions with the smallest heart rate variability[HRV; a noninvasive index of cardiac parasympathetic regu-lation (6, 40, 47)] had the greatest risk of dying suddenly. Therelative risk of mortality was 5.3 times greater in patients withan R-R interval variability
50 ms compared with patientswith variability
100 ms. This initial observation has beenconfirmed in numerous clinical studies (1, 21). For example,the ATRAMI (Autonomic Tone and Reflexes After MyocardialInfarction) group found that postmyocardial infarction patientswith either low HRV or reduced baroreflex sensitivity had amuch greater risk of sudden death than those with well-preserved cardiac vagal function (31).Similar results have been obtained in animal studies. Ourlaboratory previously reported that HRV was much lower inanimals susceptible to ventricular fibrillation compared withanimals resistant to these malignant arrhythmias (7, 12, 18, 22).In particular, the susceptible animals exhibited a much greaterreduction (withdrawal) of vagal activity in response to eithersubmaximal exercise (7, 18, 22) or acute myocardial ischemia(12, 18, 22) than did the resistant dogs. In a similar manner,bilateral vagotomy (13) or the cholinergic antagonist atropineincreased arrhythmia formation (14), whereas cholinergic ago-nists or electrical stimulation of the vagus nerves increasedventricular fibrillation threshold, antagonized the effects of sympathetic stimulation, and decreased the incidence of ven-tricular fibrillation (4, 27, 29, 48). These data demonstrate thatsubnormal cardiac parasympathetic regulation increases therisk for malignant arrhythmias, whereas interventions thatenhance cardiac vagal function can protect against ventricularfibrillation. However, to be an effective antiarrhythmic ther-apy, an intervention not only must increase baseline vagalactivity but also must maintain this enhanced activity when theheart is stressed, as during myocardial ischemia. Indeed, lowdoses of cholinergic antagonists paradoxically increased thebaseline cardiac vagal activity (30) but failed to maintain thisincrease in HRV when the heart was stressed by either sub-maximal exercise or a coronary artery occlusion (18). As aconsequence, this intervention proved to be ineffective in theprevention of lethal arrhythmias induced by acute myocardialischemia (18, 25).It is well established that regular exercise can improvecardiac autonomic balance (increasing parasympathetic whiledecreasing sympathetic regulation of the heart) (5, 42). In bothhumans and animals, heart rate at submaximal workloads islower in trained individuals compared with sedentary controls(5, 42), while the presence of a resting bradycardia is fre-quently used to confirm that training has been effective (17, 34,45). Exercise training programs can increase HRV in patientsrecovering from myocardial infarction (32, 33, 35, 39) and mayreduce the incidence of sudden death and arrhythmias in bothhuman and animal models (8, 23, 32, 37, 38, 41). In a similarmanner, meta-analysis of 22 randomized trials of rehabilitationwith exercise after myocardial infarction found that exercise
Address for reprint requests and other correspondence: G. E. Billman, Dept.of Physiology and Cell Biology, The Ohio State Univ., 304 Hamilton Hall,1645 Neil Ave., Columbus, OH 43210-1218 (e-mail: billman.1@osu.edu).The costs of publication of this article were defrayed in part by the paymentof page charges. The article must therefore be hereby marked “
in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
 J Appl Physiol
 100: 896–906, 2006.First published December 1, 2005; doi:10.1152/japplphysiol.01328.2005.8750-7587/06 $8.00 Copyright
 2006 the American Physiological Society http://www.jap.org896
  on J  un e 3  , 0  j   a p. p y  s i   ol   o g y . o g ownl   o a d  e d f   om 
training elicited significant reductions in both reinfarction andthe incidence of sudden death (38). In animals, regular exerciseeither increased the electrical current necessary to induceventricular fibrillation (37, 41) or reduced the susceptibility toventricular fibrillation induced by myocardial ischemia (8, 24).However, the contributions of changes in cardiac autonomicbalance to the protection afforded by exercise training were notextensively examined in these studies and remain largely to bedetermined. Although exercise training has been shown toincrease baseline HRV in animals prone to lethal arrhythmias(24), the effects of this intervention on HRV when the heart isstressed (i.e., during exercise or coronary occlusion) remain tobe determined.Therefore, it was the purpose of this study to investigate theeffects of exercise training on HRV and susceptibility toventricular fibrillation using a conscious canine model of sudden death. Specifically, the hypothesis that exercise trainingwould increase HRV even during physiological stress (exerciseor acute ischemia) and, thereby, could prevent ventricularfibrillation induced by myocardial ischemia was tested.The present study demonstrates that exercise training im-proves cardiac autonomic function such that cardiac vagalregulation is maintained even when the heart is stressed byeither exercise or acute myocardial ischemia in animals withhealed infarctions. Furthermore, exercise training completelysuppressed ventricular fibrillation induced by myocardial is-chemia. However, because atropine pretreatment did not rein-troduce lethal arrhythmias in these dogs, the exercise-inducedprotection from ventricular fibrillation did not result solelyfrom enhanced cardiac vagal regulation.
The principles governing the care and use of animals as expressedby the Declaration of Helsinki, and as adopted by the AmericanPhysiological Society, were followed at all times during this study. Inaddition, the Ohio State University Institutional Animal Care and UseCommittee approved all the procedures used in this study.
Surgical preparation.
 Sixty heartworm-free mongrel dogs weigh-ing 15.4–24.5 kg (19.1
0.4 kg) were used in this study. The animalswere anesthetized and instrumented as previously described (7, 12, 18,22). Briefly, using strict aseptic procedures, a left thoracotomy wasmade in the fourth intercostal space. The heart was exposed andsupported by a pericardial cradle. The left circumflex coronary arterywas dissected free of the surrounding tissue. Both a 20-MHz pulsedDoppler flow transducer and a hydraulic occluder were then placedaround this vessel. Two pairs of silver-coated copper wires were alsosutured on the epicardial surface of the heart and used to obtain aventricular electrogram (from which heart rate and various indexes of HRV were measured, see below). One pair of electrodes was placedin the potentially ischemic area (lateral left ventricular wall, an areaperfused by the left circumflex artery) and the other pair in anonischemic region (right ventricular outflow tract). A two-stageocclusion of the left anterior descending artery was then performedapproximately one-third the distance from its origin to produce ananterior wall myocardial infarction. This vessel was partially occludedfor 20 min and then tied off.
 HRV protocols.
 The studies began 3–4 wk after the production of the myocardial infarction (see flow chart, Fig. 1). First, over the periodof 3–5 days, the dogs learned to run on a motor-driven treadmill. Thecardiac response to submaximal exercise was then evaluated asfollows: exercise lasted a total of 18 min with workload increasingevery 3 min. The protocol began with a 3-min warm-up period, duringwhich the dogs ran at 4.8 kilometers per hour (kph) at 0% grade. Thespeed was then increased to 6.4 kph, and the grade increased every 3min (0, 4, 8, 12, and 16%). The submaximal exercise test was repeatedthree times (1/day). Before the third submaximal exercise test, acatheter was placed percutaneously in a cephalic vein to administerthe muscarinic antagonist, atropine sulfate (50
g/kg), 3 min beforethe end of the exercise period. On a subsequent day, with the dogslying quietly unrestrained on a table, a 2-min left circumflex coronaryocclusion was made. At least 48 h after the completion of thesestudies, the animals were tested for susceptibility to ventricularfibrillation using an exercise plus ischemia test that is described in thefollowing section. Heart rate, left circumflex blood flow, and HRVwere monitored continuously throughout the exercise or occlusionstudies. These studies were repeated after the completion of the 10-wk exercise training or the 10-wk sedentary time period.
 Exercise plus ischemia test: classification of the dogs.
 The suscep-tibility to ventricular fibrillation was tested as previously described (7,12, 18, 22) (Fig. 1). Briefly, the animals ran on a motor-driventreadmill while workload progressively increased until a heart rate of 70% of maximum (
210 beats/min) had been achieved. During thelast minute of exercise, the left circumflex coronary artery wasoccluded, the treadmill stopped, and the occlusion maintained for anadditional minute (total occlusion time
 2 min). The exercise plusischemia test reliably induced ventricular flutter that rapidly deterio-rated into ventricular fibrillation. Therefore, large metal plates (11-cmdiameter) were placed across the animal’s chest so that electricaldefibrillation (Zoll M series defibrillator, Zoll Medical, Burlington,MA) could be achieved with a minimal delay but only after the animalwas unconscious (10–20 s after the onset of ventricular fibrillation).Of the 60 animals that underwent surgery, 21 animals could not betested due to either death within 72 h of the myocardial infarction(
 14, 23.3%) or occluder failure (
 7). Thus the exercise plusischemia test was performed on 39 of the original 60 animals. Theocclusion was immediately released if ventricular fibrillation oc-curred. Twenty-six dogs developed ventricular fibrillation (suscepti-ble), whereas the remaining 13 did not (resistant). Three susceptibleanimals were not successfully defibrillated and, as such, were notavailable for additional studies. This exercise plus ischemia test, using
Fig. 1. Flow chart illustrating the sequences of events in this study. Three tofour weeks after myocardial infarction, the dogs were classified as susceptibleor resistant to ventricular fibrillation (VF) with an exercise plus ischemia test.The animals were then randomly assigned to either 10-wk exercise (Ex)training program or a 10-wk sedentary period. The exercise plus ischemia testwas repeated at the end of the 10-wk period. n, No. of animals; defib,defibrillate.
 J Appl Physiol
 VOL 100
 MARCH 2006
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