Patterns of Ventricular Tachyarrhythmias Associated WithTraining, Deconditioning and Retraining in Elite Athletes Without
Cardiovascular Abnormalities
Alessandro Biffi, MDa,*, Barry J. Maron, MDb, Franco Culasso, MDc, Luisa Verdile, MDa,Fredrick Fernando, MDd, Barbara Di Giacinto, MDa, Fernando M. Di Paolo, MDa,
Antonio Spataro, MDa, Pietro Delise, MDe, and Antonio Pelliccia, MDa
Ventricular tachyarrhythmias commonly occur in trained athletes during ambulatoryHolter electrocardiography and are usually associated with a benign course. Such arrhyth-mias have been demonstrated to be sensitive to short periods of athletic deconditioning;however, their response to retraining is not known. Twenty-four hour Holter electrocar-diographic monitoring was performed at peak training and after 3 to 6 months of decon-ditioning and was repeated in the present study after 2, 6, and 12 months of retraining in37 athletes with frequent and complex ventricular tachyarrhythmias and without cardio-vascular abnormalities. These subjects showed partial (101 to 500 ventricular prematurecomplexes [VPCs]/24 hours) or marked (<100 VPCs) reversibility of arrhythmias afterdeconditioning. Retraining initially resulted in a significant increase in arrhythmia fre-quency compared with deconditioning (from 280 � 475 to 1,542 � 2,186 VPCs; p � 0.005),couplets (0.14 � 0.42 to 4.4 � 8.2; p � 0.005), and nonsustained ventricular tachycardia(from 0 to 0.8 � 1.8; p � 0.02). Subsequently, a progressive reduction was seen in thefrequency of all ventricular arrhythmias during the 1 year of training to well below that atthe peak training levels (VPCs 917 � 1,630, couplets 1.8 � 4.2, and nonsustained ventric-ular tachycardia 0.4 � 1.2). Such annual arrhythmia reduction was significantly greaterstatistically in those athletes with marked reversibility after deconditioning than in theathletes with partial reversibility (69 � 139 vs 1,496 � 1,917 VPCs/24 hours, respectively;p � 0.007). No cardiac events or symptoms occurred during 1 year of follow-up. Inconclusion, in elite athletes without cardiovascular disease, a resumption in intense trainingafter deconditioning was associated with variable, but prolonged, suppression of ventric-ular ectopy. The absence of adverse clinical events or symptoms associated with theresumption of training supports the continued eligibility in competitive sports for suchathletes and is also consistent with the benign nature of physiologic athlete’s heart
Ventricular tachyarrhythmias are not uncommon find-ings on ambulatory Holter electrocardiogram (ECG) intrained athletes1–3 and have usually been associated withbenign outcomes in the absence of cardiovascular abnor-malities.4,5 Such arrhythmias have been demonstrated to besensitive to short periods of athletic deconditioning6 andlargely independent of training-related physiologic left ven-tricular (LV) remodeling.7,8 However, the course of theentricular tachyarrhythmias after the resumption of phys-cal training and competition (occurring after a period ofomplete deconditioning) is unknown. This becomes a rel-
aInstitute of Sports Medicine and Science, Italian National OlympicCommittee, Rome, Italy, bHypertrophic Cardiomyopathy Center, Minne-apolis Heart Institute Foundation, Minneapolis, Minnesota; cUniversity of
ome “La Sapienza,” Rome, Italy; dSant’Andrea Hospital, Rome, Italy;nd eDivision of Cardiology, Hospital of Conegliano, Conegliano, Italy.
Manuscript received September 1, 2010; manuscript received and acceptedOctober 26, 2010.
vant issue in clinical practice, because athletes with fre-uent and complex ventricular arrhythmias in the absence oftructural heart disease often represent clinical managementilemmas, including the decisions regarding sports disqual-fication versus eligibility. The aim of the present study waso assess, in a unique subset of elite athletes, the responsend clinical significance of ventricular tachyarrhythmias onesumption of exercise and competition after a forced periodf deconditioning.
ethods
The case records of the Institute of Sports Medicine andcience were reviewed, and 355 athletes who had met theollowing criteria were selected with 24-hour ambulatoryHolter) ECG: (1) �3 ventricular premature complexesVPCs) on the at rest 12-lead ECG (n � 337); and/or (2) aistory of palpitations (n � 18). Of the 355 athletes, 284ith �2,000 VPCs/24 hours, who were allowed to continue
n competition and training, were excluded from the presentnalysis.4 The remaining 71 athletes with frequent and/or com-
lex ventricular arrhythmias (arbitrarily defined as �2,000
698 The American Journal of Cardiology (www.ajconline.org)
VPCs and/or �1 burst of nonsustained ventricular tachycar-dia [NSVT]) were considered for inclusion in the presentstudy. One of these athletes died suddenly from arrhythmo-genic right ventricular cardiomyopathy (ARVC) and wasexcluded because he had not undergone detraining. Of theremaining 70 athletes, 50 were without detectable cardio-vascular abnormalities, and the other 20 had structural car-diac diseases, including ARVC (n � 6), mitral valve
rolapse (n � 6), myocarditis (n � 4), and dilated car-iomyopathy (n � 4). These latter athletes with cardiacisease were excluded from sports activity (and from theresent study) in accordance with the current Italian guide-ines.9 Of the 50 athletes with no cardiovascular abnormal-ties, 37 (75%) had shown a partial (101 to 500 VPCs/24ours; n � 21) or marked (�100 VPCs; n � 16) revers-bility of the ventricular arrhythmias within the 3- to-month period of deconditioning. These 37 athletes re-umed training and competition (after deconditioning) for a-year period (mean 12 � 0.6 months) and represent theresent study group. The inclusion and exclusion criteria,hich have taken into account the criteria of the Strength-
ning the Reporting of Observational Studies in Epidemi-logy (STROBE) statement,10 are presented in Figure 1.
The study athletes were engaged in a variety of sportsdisciplines, most commonly soccer (n � 10 [27%]), basket-ball (n � 6 [16%]), and volleyball (n � 4 [10%]). They also
Figure 1. Flow chart showing inclusion (Left) and exclusion (Right) criteriaused in this study design.
presented a broad spectrum of athletic achievement, with 13
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699Arrhythmias and Conduction Disturbances/Training-Related Ventricular Tachyarrhythmias
(35%) participating at an elite level, including 9 who hadcompeted in the Olympic Games or World Championships.The mean age of the athletes was 24 � 10 years (range 18to 33), and 28 (75%) were men. All athletes were asymp-tomatic. At the subsequent Holter electrocardiographicmonitoring, no athlete was taking antiarrhythmic or othercardioactive medications. The operators who analyzed theHolter ECGs were unaware of the phase of deconditioningor retraining.
The 24-hour ambulatory (Holter) ECGs were initiallyrecorded during the periods of peak training, includingconditioning sessions (average 1 hour in duration), similarto that generally performed by the athlete; the remainingtime was occupied by the usual daily activities, which couldhave involved recreational physical activity. The data re-lated to 24-hour Holter ECGs during peak training in the 37athletes constituting the study group have been previouslyreported.4
The athletes underwent a complete deconditioning pe-riod of �3 consecutive months (mean 19 � 6 weeks, range12 to 24). This period was selected, because it has beenpreviously shown to be sufficient to reverse the cardiovas-cular adaptations induced by physical training, includingLV hypertrophy.11 After deconditioning, each athlete un-derwent a second cardiovascular assessment that also in-cluded a 24-hour Holter ECG performed under the sameconditions as at peak training. The data relative to thisdeconditioning period have been previously reported.6 Afterthe period of deconditioning, each athlete resumed compet-itive sports without restriction, according to the usual pro-gram and intensity of their athletic training. Each athleteunderwent additional cardiovascular assessments, including24-hour ambulatory [Holter] ECGs performed under thesame conditions as previously, at 2, 6, and 12 months ofretraining. These latter 24-hour Holter ECGs included con-ditioning sessions similar to that performed at the initial(peak training) and second (deconditioning) 24-hour Holter
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Figure 2. Scatter plot of number of VPCs/24 hours of each athlete at peacontinued lines) showing gradual and progressive reduction of ventricularretraining.
ECGs. The data obtained from the athletes at 2, 6, and 12
months of retraining were compared to those obtained atpeak conditioning and at deconditioning.
In the previous study of deconditioning,6 we assembleds a control group, 148 athletes without structural heartisease, of similar age to the study subjects (26 � 10 years),ith less frequent ventricular arrhythmias (�2,000 VPCs/4 hours, mean 1,211 � 850, and without NSVT). The 148ontrols underwent a second Holter ECG 3 to 6 months aftereak training, maintaining the same level of training, andithout previous deconditioning. The period between theseHolter recordings obtained during training (19 � 4
eeks, range 12 to 24) was the same as between thective training and deconditioned phases in the 37 ath-etes of our study group.
The echocardiographic studies were performed at peakraining, after deconditioning, and 2.6 and 12 months ofetraining using commercially available instruments (Sonos500, Philips, Cleveland, Ohio). Images of the heart werebtained in multiple cross-sectional planes using standardransducer positions. The LV cavity dimensions, anterior,entricular, septal, and posterior free wall thicknesses andeft atrial dimensions were obtained from the M-mode echo-ardiograms, in accordance with previous recommenda-ions.12 The LV mass was calculated using the formula ofevereux et al13 and normalized to the body surface area.The mean, median, and SDs for VPCs, couplets, and
NSVT were computed at different points (peak condition-ing, deconditioning, and retraining at 2, 6, and 12 months).Comparisons between the mean values were performed us-ing the paired t test or Mann-Whitney U test, as appropriate.The same analyses were performed in the 2 subgroups ofathletes with either partial (�100 VPCs/24 hours) ormarked (�100 VPCs/24 hours) reversibility of arrhythmiasafter deconditioning. The data were then log transformed (toachieve approximately normal distributions), and the differ-ences in VPCs at retraining (2, 6, and 12 months) werecompared with those at deconditioning. Finally, we applied
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ing, deconditioning, and retraining at 2, 6, and 12 months (connected by(with the exception of an initial increase after 2 months) during 1 year of
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a linear regression model (to avoid the problem of multiple
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700 The American Journal of Cardiology (www.ajconline.org)
testing) to assess the relation of VPC frequency with re-training at 2, 6, and 12 months and at deconditioning.
Results
At the initial assessment, during the peak training period,the frequency of VPCs/24 hours was 2,140 to 43,221 (mean10,405 � 9,605; Table 1 and Figure 2). Of the 37 athletes,23 (62%) had �1 couplet (mean 35.2 � 73, range 1 to 321);21 (57%) also had 1 to 179 bursts of NSVT (mean 7.7 �29.5), consisting of 3 to 28 consecutive beats, at a heart rateof 130 to 270 beats/min.
After the deconditioning period, the study group showeda significant reduction in VPCs (98%), couplets (98%), andNSVT (100%; p �0.005 with respect to peak training). Theindividual subject analysis showed that after decondition-ing, all 37 athletes had either partial (�100 to 500 VPCs/24hours; n � 21) or marked (�100 VPCs; n � 16) revers-bility of ventricular tachyarrhythmias (Figure 2). Only 4 of3 athletes showed the persistence of ventricular coupletsfter deconditioning (3 athletes had 1 couplet/24 hours andathlete had 2 couplets/24 hours). None of the 21 athletesith NSVT at peak training had NSVT after decondition-
ng. After deconditioning, the athletes resumed their train-ng programs and participated in competitive sports eventsithout restriction.After 2 months of retraining, the number of VPCs sig-
ificantly increased compared to that at deconditioning to,542 � 2,186 (p �0.005; 80% change). The number ofouplets increased to 4.4 � 8.2 (p �0.005; 95% change)nd NSVT to 0.8 � 1.8 (p �0.02; 90% change). Neverthe-ess, the VPC, couplet, and NSVT frequency remained atignificantly less than that peak training levels (p �0.01;able 1). Individual subject analysis showed a significant
ncrease in ventricular tachyarrhythmias within 2 months ofetraining in 18 athletes (49% change; to 500 to 2,000PCs/24 hours; p �0.001 compared with deconditioning),
ncluding 9 with a marked increase in this arrhythmia (to2,000 VPCs/24 hours). The remaining 19 athletes showed
onsignificant change in VPCs with respect to the decon-itioning period (to 0 to 500 VPCs/24 hours; p � 0.78;igure 2). Couplets significantly reappeared compared to
he deconditioning levels after 2 months of retraining in 18thletes (48% change; from 1 to 34 couplets/24 hours; p �.002) and NSVT in 13 athletes (35% change; from 1 to 10
Table 2Different response in ventricular ectopy during 1 year of retraining in elitdeconditioning
Variable
Athletes With Marked Reversibility(�100 VPCs/24 hours; n � 16)
pisodes of NSVT/24 hours; p � 0.0001). Increased ar- s
hythmia frequency at 2 months of retraining was greater inhe athletes with previous partial reversibility of VPC fre-uency than in those with marked reversibility (2,054.6 �,446 vs 790.2 � 1,514 VBCs/24 hours; p � 0.084; Table 2).
After 6 months of retraining, the VPCs showed a de-rease to 1,087 � 1,830 (i.e., 30% change with respect tohat at 2 months of retraining; Figure 2). A similar trend wasvident for complex arrhythmias, with couplets decreasingo 3.0 � 5.6 (32% change compared with at 2 months ofetraining) and NSVT to 0.6 � 1.6 (25% change). After 6onths of retraining, the VPC, couplet, and NSVT frequency
emained at significantly less than peak training levels (p �0.01).ndividual subject analysis showed no significant changes from 2o 6 months in the number of athletes with 500 to 2,000 VPCs/24ours (from 19 to 15 athletes; p � 0.53). No difference was alsoound in those athletes who showed a marked increase of arrhyth-ia at 2 months of retraining (to �2,000 VPCs/24 hours)
from 9 athletes at 2 months to 8 athletes at 6 months ofetraining; p � 0.94). Athletes with less-frequent ventricularrrhythmias (0 to 500 VPCs/24 hours) remained substan-ially unchanged from 2 to 6 months of retraining (18 vs 22thletes, respectively; p � 0.52; Figure 2). The number ofthletes with couplets and NSVT showed no significantariation from 2 to 6 months of retraining (from 18 to 16thletes, p � 0.91; and from 13 to 11 athletes, p � 0.83,espectively). Furthermore, individual subject analysishowed that the 16 athletes with marked reversibility ofentricular tachyarrhythmias after deconditioning had a sig-ificantly greater decrease in arrhythmias at 6 months ofetraining (to 139.4 � 216 VPCs/24 hours) compared to thatf the 21 athletes with only partial reversibility, for whomhis arrhythmia remained consistent (1,734.4 � 2,152PCs; p � 0.007; Table 2).After 1 year of retraining, VPCs continued to decrease to
17 � 1,630 (i.e., 16% change with respect to 6 months ofetraining; Figure 2). Couplets and NSVT also showed andditional decrease to 1.8 � 4.2 (40% change compared tohat at 6 months of retraining) and to 0.4 � 1.2 (35%hange), respectively. VPCs, couplets, and NSVT continuedo remain at significantly less than the peak training levelsp �0.01; Table 1). Individual subject analysis showed noignificant changes from 6 to 12 months in athletes with 500o 2,000 VPCs/24 hours (from 15 to 14 athletes; p � 0.97).
not significant reduction was found in the athletes who
es with partial or marked reversibility of arrhythmias after
PCs p Value
Athletes With Partial Reversibility(�100 VPCs/24 hours; n � 21)
howed a marked increase of arrhythmia at 2 months of
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701Arrhythmias and Conduction Disturbances/Training-Related Ventricular Tachyarrhythmias
retraining (to �2,000 VPCs/24 hours; from 8 athletes at 6months to 4 athletes at 12 months of retraining; p � 0.21).The athletes with less-frequent ventricular arrhythmias (0 to500 VPCs/24 hours) remained substantially unvaried from 6to 12 months of retraining (22 vs 23 athletes, respectively;p � 0.97; Figure 2). Also, the athletes with couplets andNSVT did not show a significant variation from 6 to 12months (from 16 to 11 athletes, p � 0.36; and from 11 to 7athletes, p � 0.40, respectively). Furthermore, individualsubject analysis showed that athletes with marked revers-ibility of arrhythmias with deconditioning continued to havea more prolonged suppression of VPCs at 1 year of retrain-ing compared to athletes with partial reversibility (69 � 139vs 1,496 � 1,917 VPCs; p � 0.007; Table 2). Linear regres-ion analysis applied to the differences in VPC frequencyetween deconditioning and the 3 phases of retraining showedstatistically significant association between retraining at 6
nd 12 months compared to that at deconditioning.Of the 37 athletes, 30 (81%) showed a pattern of VPC
orphology consistent with a right ventricular outflow tractrigin and 7 a fascicular origin (19%). Of the 30 athletesith a right ventricular origin of VPCs, 28 had an inferior
xis and 2 showed an indeterminate axis. Ventricular ar-hythmias with marked reversibility showed a right ventric-lar outflow tract origin, with an inferior axis in all 16thletes.
At peak training, the LV mass index was 114 � 23 g/m2.After deconditioning, it had decreased to 94 � 19 g/m2 (p
0.001). During retraining, the LV mass index had increasedo 96 � 18 g/m2 at 2 months (p � 0.61), 101 � 21 g/m2 at
6 months (p � 0.27), and 110 � 19 g/m2 at 12 months (p�0.05). The changes in LV mass index with training did notdiffer between the 18 athletes who experienced a reappear-ance of ventricular tachyarrhythmias with retraining and the19 athletes without a reappearance of arrhythmias (95 � 11vs 96 � 10 g/m2 at 2 months of retraining, p � 0.55). Nosignificant structural or functional abnormality of the rightventricle was identified in any athlete.
No cardiac events or symptoms occurred in the athleteswith or without a reappearance of ventricular tachyarrhyth-mias during the 1-year follow-up period, during whichtraining and competition had been resumed.
The cardiovascular evaluations with at rest and exerciseECGs and 2-dimensional echocardiography at 2, 6, and 12months of retraining in all athletes and selectively withcardiac magnetic resonance (n � 30), signal-averaged elec-trocardiography (n � 37), programmed ventricular stimula-tion (n � 13), and myocardial biopsy (n � 2) did not detectpreviously unrecognized cardiovascular abnormalities inany athlete. Only 2 of the 37 athletes incurred ventriculartachyarrhythmias during exercise testing; the remaining 35athletes had a complete disappearance of arrhythmia duringexercise. No athlete experienced cardiac symptoms duringexercise testing. In the 13 athletes who underwent an elec-trophysiologic study, either no arrhythmia or only a non-sustained ventricular response (3 to 5 consecutive ectopicbeats) was induced by programmed ventricular stimulation.None of the athletes underwent radiofrequency catheterablation.
In the 148 control athletes, who had not modified their
physical conditioning, no significant variability in ventric-
ular arrhythmias was found between the 2 ambulatoryHolter ECGs obtained during training (19 � 4 weeks apartduring the training period). The mean number of VPCs onthe first Holter ECG was 1,211 � 850 and was 1,050 � 648on the second (p � 0.28). Also, no significant differencewas found with regard to couplets and NSVT (0 vs 0).
Discussion
We had previously observed that intense athletic condi-tioning was not uncommonly associated with the occurrenceof frequent and/or complex ventricular tachyarrhythmias onambulatory Holter ECGs.4 Despite the presence of suchtachyarrhythmias, the risk of sudden death has proved to beexceedingly low during an 8-year follow-up period (annualmortality rate 0.17%). In a subsequent study,6 we demon-trated that these arrhythmias are sensitive to shorts periodsf deconditioning, independent of whether structural car-iovascular abnormalities are present.
The present study has extended these observations byssessing a unique subset of 37 elite athletes without car-iovascular abnormalities who had demonstrated partial orarked reversibility of frequent and/or complex ventricular
achyarrhythmias with deconditioning, at which point theyesumed training and competition. The decision to resumeraining in athletes with frequent ventricular tachyarrhyth-ias reversed by deconditioning was justified by the ab-
ence of structural cardiovascular abnormalities and by ourrevious experience with 284 athletes with less frequentrrhythmias (�2,000 VPCs/24 hours), who did not developnfavorable consequences during an 8-year follow-up pe-iod during which training and competition continued.4
The major finding of the present study was that, althoughretraining was initially associated with an increase in ven-tricular tachyarrhythmias (after 2 months), a gradual andprogressive regression of all forms of arrhythmia were sub-sequently observed during the remainder of the 1-year fol-low-up period (ultimately to a level significantly below thatof peak training). Such regression was most evident in thoseathletes with marked reversibility of arrhythmias after de-conditioning in contrast to that of athletes with only partialreversibility. Therefore, a single period of physical decon-ditioning appeared to convey a prolonged suppressive effecton ventricular ectopy, even after a 1-year resumption ofintense exercise training. Furthermore, the resumed physicalretraining was not associated with cardiac symptoms, clin-ical events, or evolving expression of cardiac disease14 in allthletes with frequent ventricular tachyarrhythmias sensi-ive to deconditioning. Therefore, we believe that the de-onditioning strategy could be regarded as a useful clinicalool in managing competitive athletes with frequent and/oromplex ventricular tachyarrhythmias in the absence ofeart disease, supporting the recommendation stated in theecent international guidelines on sports eligibility.9,15,16
The observed changes in ventricular arrhythmias duringthe 1-year period could have resulted theoretically from theresolution of a previously unrecognized myocardial process(e.g., myocarditis) or might represent the preclinical expres-sion of disease states such as ARVC or hypertrophic car-diomyopathy.14 However, the latter consideration seems
highly unlikely to explain the findings in all or most athletes
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702 The American Journal of Cardiology (www.ajconline.org)
in the present analysis. Also, a normal QT interval on a12-lead ECG largely excluded ion channelopathies, whichcould have been responsible for the arrhythmogenicity inathletes with structurally normal hearts.2,17–19 Currently, wedo not have data regarding the retraining in the other 13athletes who were excluded from the present study becauseof frequent and/or complex ventricular tachyarrhythmias(�2,000 VPCs/24 hours) and were not allowed to resumetraining because of a lack of ventricular arrhythmia revers-ibility with deconditioning (Figure 1). Our prudent decisionwas determined by the consideration that, although these 13athletes had a good prognosis at the 1-year follow-up ex-amination, we could not exclude the possibility that such afavorable outcome was also influenced by the withdrawalfrom regular training. The persistence (or increased fre-quency) of complex ventricular tachyarrhythmias over time(and despite suspension of training) might represent the firstexpression of a clinically silent arrhythmogenic cardiomy-opathy, as suggested by the athlete who continued compet-itive sports against medical advice and died suddenly fromARVC.4,18
The mechanisms that explain the changes in ventriculartachyarrhythmias with deconditioning and retraining areunresolved but appear to be independent of conditioning-related physiologic cardiac remodeling. Our findings havedemonstrated that changes in the LV mass with physicaltraining did not differ between the athletes with and withouta reappearance of ventricular tachyarrhythmias during re-training, and are consistent with our previous observationsin which no correlation was evident between the frequencyor complexity of ventricular ectopy and the magnitude oftraining-induced LV hypertrophy.7,8 Furthermore, the grad-ual increase in LV mass observed from 2 months to 1 yearof retraining was associated with a parallel regression, andnot an increase, in all forms of ventricular tachyarrhythmiasduring the same period. Although less intensive condition-ing regimens could theoretically be responsible for a reduc-tion in ventricular ectopy in some athletes during the re-training phase, this was an unlikely explanation, becauseretraining was permitted without restriction for all athletes(and was confirmed by a progressive increase in LV massduring the same period).
Other factors and mechanisms can potentially promoteventricular arrhythmogenicity in conditioned athletes. Au-tonomic nervous system adaptations induced by a varyingintensity of physical training have been reported to have arole in the genesis of ventricular tachyarrhythmias in sus-ceptible subjects.20–23 It is possible that in our unique co-ort of elite athletes, a shift in cardiovascular autonomicodulation from parasympathetic to sympathetic predomi-
ance because of an intensive and systematic training reg-men24 might have predisposed our athletes to electricalnstability, triggering ventricular tachyarrhythmias. The res-lution of arrhythmias with deconditioning and their reap-earance in the early stage of retraining could have beenonsistent with such a neural hypothesis. However, it cannotxplain the gradual reduction of ventricular tachyarrhyth-ias during continued training period during a 1-year fol-
ow-up period. Furthermore, the possible influence of theormonal changes (in particular of the cortisol and adrena-
ine levels) induced by prolonged and intensive training on
yocardial irritability should be taken into account.25,26
Thus, we propose a prolonged “antiarrhythmic” effect ofdeconditioning in sensitive athletes, in which ventricularectopic foci might become less prone to autonomic influ-ences over time. However, we wish to underscore that ourdata need to be confirmed by other studies in larger athleticpopulations. Also, a limitation of the present study was theabsence of a control group of athletes (with �2,000VPCs/24 hours and NSVT) who had not undergone periodsof deconditioning and retraining and their relation to ven-tricular arrhythmias. The acquisition of these data couldbetter exclude the influence of day-to-day variability of anectopic burden as a confounder in the present study and ofregression toward the mean as a potential explanation forreduction in ectopy over time. Finally, in none of our ath-letes were antiarrhythmic or other cardioactive medicationsadministered. Each athlete underwent multiple comprehensivescreenings for performance-enhancing drugs in accord withrecommendations of the World AntiDoping Agency and In-ternational Olympic Committee,27 thereby excluding the pres-ence of steroids, amphetamines, cocaine, growth hormones,and erythropoietin.
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703Arrhythmias and Conduction Disturbances/Training-Related Ventricular Tachyarrhythmias
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