Next Article in Journal
Fast Inverse Distance Weighting-Based Spatiotemporal Interpolation: A Web-Based Application of Interpolating Daily Fine Particulate Matter PM2.5 in the Contiguous U.S. Using Parallel Programming and k-d Tree
Previous Article in Journal
Family-Related Opinions and Stressful Situations Associated with Psychological Distress in Women Undergoing Infertility Treatment
 
 
Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
IJERPH
Volume 11
Issue 9
10.3390/ijerph110909082
ijerph-logo
Submit to this Journal Review for this Journal Propose a Special Issue
► Article Menu

Article Menu

share Share announcement Help format_quote Cite question_answer Discuss in SciProfiles
first_page
settings
Order Article Reprints
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Article

Endurance Sport and “Cardiac Injury”: A Prospective Study of Recreational Ironman Athletes

by
Roman Leischik
* and
Norman Spelsberg
School of Medicine, Faculty of Health, Witten/Herdecke University, Elberfelder Str. 1, 58095 Hagen, Germany
*
Author to whom correspondence should be addressed.
Int. J. Environ. Res. Public Health 2014, 11(9), 9082-9100; https://doi.org/10.3390/ijerph110909082
Submission received: 20 July 2014 / Revised: 18 August 2014 / Accepted: 24 August 2014 / Published: 3 September 2014
Browse Figure
Versions Notes

Abstract

:
Background: Participation in triathlon competitions has increased in recent years. Many studies have described left or right ventricular injury in endurance athletes. The goal of this study was to examine the right and left ventricular cardiac structures and function and dynamic cardio-pulmonary performance in a large cohort of middle- and long-distance triathletes. Methods: 87 triathletes (54 male and 33 female) were examined using spiroergometry and echocardiography. The inclusion criterion was participation in at least one middle- or long distance triathlon. Results: Male triathletes showed a maximum oxygen absorption of 58.1 ± 8.6 mL/min/kg (female triathletes 52.8 ± 5.7 mL/min/kg), maximum ergometer performance of 347.8 ± 49.9 W (female triathletes 264.5 ± 26.1 W). Left ventricular ejection fraction (EF) was normal (male triathletes EF: 61.9% ± 3%, female triathletes EF: 63.0% ± 2.7%) and systolic right ventricular area change fraction (RV AFC%) showed normal values (males RV AFC%: 33.5% ± 2.2%, females 32.2% ± 2.8%). Doppler indices of diastolic function were normal in both groups. With respect to the echocardiographic readings the left ventricular mass for males and females were 217.7 ± 41.6 g and 145.9 ± 31.3 g, respectively. The relative wall thickness for males was 0.50 ± 0.07, whereas it was 0.47 ± 0.09 for females. The probability of left ventricular mass >220 g increased with higher blood pressure during exercise (OR: 1.027, CI 1.002–1.052, p = 0.034) or with higher training volume (OR: 1.23, CI 1.04–1.47, p = 0.019). Conclusions: Right or left ventricular dysfunction could not be found, although the maximal participation in triathlon competitions was 29 years. A left ventricular mass >220 g is more likely to occur with higher arterial pressure during exercise and with a higher training volume.

1. Introduction

The possibility of myocardial damage due to physical activity has been known since ancient times. According to legend, a soldier named Pheidippides (more likely Philippides) dropped dead after running to Athens from the battle at Marathon with the news of victory [1]. A soldier or courier, he is purported to have already run 240 km from Athens to Sparta and back before running a marathon distance to Athens, and the truth about his story is unknown [2]. What is clear, however, is that this death is the first recorded sport-related death.
Some papers have reported on common deaths in triathlon competitions [3] and exercise-induced cardiac fatigue in triathlon competitions [4,5] and other endurance disciplines [6,7]. The problem of cardiac injury with endurance sports is a complex issue [7,8,9]. Figure 1 shows some factors that might influence cardiac injury in endurance athletes.
Ijerph 11 09082 g001 1024
Figure 1. Factors that might influence heart function during endurance sport.
Figure 1. Factors that might influence heart function during endurance sport.
Ijerph 11 09082 g001
Triathlon is an endurance sport, especially when performed in middle- and long-distance formats (e.g., middle/long distance Ironman: a 1.9/3.8 km swim, a 90/180 km bicycle ride and a 21.1/42.2 km run), mainly under aerobic conditions. It is particularly important for triathletes to perform at sub-maximal levels over a long period to avoid reaching a state of exhaustion [10,11]. Amateur athletes typically take 5 to 6.5 h for middle-distance events and 10 to 16 h for long-distance events. Such long periods of stress require that both the amateur and the top athletes be adequately trained and have sufficient aerobic capacity [10]. A number of studies with small cohorts have reported spiroergometric data [12,13,14,15]. Problems regarding the condition of athletes’ hearts have been identified [16]. These problems are mainly known from observations of professional cyclists [17] and elite runners [18]. Regarding the literature about “exercise-induced” cardiac fatigue and “athlete’s heart”, the following questions have to be asked:
-
Are there signs of cardiac “fatigue” when triathletes have trained hard over a period of years? Are there risks for right ventricular or left ventricular dysfunction for amateur athletes?
-
What type of athletes’ hearts or what type of hypertrophy, concentric or eccentric, is found most often in triathletes?
-
Are there signs of reduced physiological performance?

2. Experimental Section

2.1. Participants

Eighty-seven triathletes were examined, including 54 males and 33 females. All triathletes were examined by echocardiography (except three males) and spiroergometry. Triathletes underwent their annual medical check-up or examination for training preparation in 2011/2012, which would have been performed as part of the normal clinical routine. All examinations were performed by Dr. Roman Leischik or Dr. Norman Spelsberg. The participants were invited to participate in the study during their routine check-up or routine training preparation, and announcements in social media and triathlon clubs were also made. Dr. Roman Leischik is the medical supervisor of the Triathlon Club PV-Witten since 2007. This study was prospective in design.

2.2. Methods: Echocardiography and Spiroergometry

A Vivid 7 echocardiograph, produced by General Electric (Fairfield, CT, USA) was used for the examinations. The Ergobike 8I, produced by Daum (Fürth, Germany), and the Metalizer 3B, produced by Cortex (Leipzig, Germany), were used for the spiroergometric examination.
To compare the data from elite triathletes with those of non-elite triathletes, both males and females were divided into two groups according to their aerobic capacity (relative VO2/min/kg at the aerobic threshold). The 20 males and 15 females with the highest values were designated as elite.
All triathletes were examined in a single day using first echocardiography and then spiroergometry. All examinations were performed in 2011 and 2012 at the Sports Medicine Center, Hagen, Germany. The spiroergometry was performed in the following manner: the stress test was conducted in stages after successful gas and volume calibration at 50 W for 3 min, 100 W for an additional 3 min, after which it increased by another 30 W for 3 minutes. The test ended when the subject was exhausted.
The echocardiographic analysis was conducted according to general recommendations [19,20]. The formula recommended by the American Society of Echocardiography (ASE) was used to calculate the muscle mass. EDV and ESV were determined as monoplane by the modified Simpson method.
The spiroergometric analyses were conducted according to the literature. VAT was determined as the first non-linear increase in the ventilatory equivalent for oxygen without a simultaneous increase of the ventilatory equivalent for CO2. RCP was determined as a simultaneous non-linear increase of both ventilatory equivalents according to recommendations [21,22]. VO2max was registered as the highest average value of oxygen absorption over 30 seconds. Elite triathletes were identified by their aerobic capacity. The 20 males and 15 females with the best values of relative oxygen uptake (in mL/min/kg) were classified as elite.

2.2.1. Ethics Statement

All athletes gave verbal and written consent to voluntary performance testing and for use of their data in this study. All data were anonymized. Triathletes underwent their annual medical check-up or examination for training preparation in 2011/2012, which would have been performed in any case as it is clinical routine. The study was approved as a doctoral dissertation by the Dissertation Audit Committee of the University Witten/Herdecke. All examinations (echocardiography and spiroergometry) were a part of the routine clinical and diagnostic care for the triathletes. All examinations were performed by two experienced investigators (see chapter methods). This study did not introduce any pharmaceutical interventions or changes in the clinical course of the triathletes.

2.2.2. Statistical Analyses

The entire statistical analysis was designed as follows. Stata/IC 11.2 for Windows was used for data preparation and statistical analysis. The Mann-Whitney U-Test was used to compare the groups. The Kaplan-Meier product limit method and the Cox proportional hazards model were used to estimate the odds ratios for analysis of the relationship between arterial pressure and the probability of a left ventricular muscle mass (LVM) >220 g. All statistical tests were two-sided, with a significance level of 0.05.

3. Results and Discussion

3.1. Participants Characteristics

Anthropometric data and the general cardiac parameters of the participants are listed in Table 1.
Male triathletes have significant greater weight, BMI, and BSA than female triathletes, but lower body fat (12% vs. 22.8%). Heart cavities and stroke volume are significant larger, without differences in systolic function (EF) or diastolic function (Doppler parameters).
Table
Table 1. Anthropometric and structural echocardiographic characteristics of the study population.
Table 1. Anthropometric and structural echocardiographic characteristics of the study population.
ParametersMaleFemaleMann-Whitney U-Test p-value
nMvSdnMvSd
Age (years)5438.111.83334.38.10.137
Weight (kg)5476.88.93361.57.80.001
Size (cm)54182.46.733168.86.40.001
BMI (kg/m²)5423.01.833321.62.280.001
BSA (m²)541.970.14331.700.130.001
%body fat5412.53.63322.84.70.001
Ao512.900.37332.470.240.001
LA512.540.28332.350.250.002
LAV (mL)5129.17.83327.49.30.254
IVS thickness diastolic (cm)511.230.13331.020.170.001
IVS thickness systolic (cm)511.670.18331.440.220.001
PWT diastolic (cm)511.220.14331.020.160.001
PWTs (cm)511.700.17331.480.200.001
Relative wall thickness510.500.07330.470.090.066
LVEDD (cm)514.80.38334.40.320.001
LVESD (cm)513.30.29332.90.270.001
LVM (g)51217.741.633145.931.30.001
LVM (g/m²)51110.521.83385.818.70.001
LVEDV (mL)51138.522.333105.017.80.001
LVESV (mL)5152.79.93338.97.10.001
SV (mL)5185.714.03366.111.30.001
EF (%)5161.93.03363.02.70.292
LVOT VMax (m/s)510.800.13320.860.130.047
MV EMax (m/s)510.530.10330.560.120.091
MV AMax (m/s)510.360.06330.380.090.569
MV E/A Ratio511.480.31331.540.340.407
RV parasternal513.180.13332.400.180.001
RV AFC%5133.52.23332.22.80.005
n = number; Mv = mean value; Sd = standard deviation; BMI = body mass index; BSA = body surface area; Ao = aortic diameter; LA = left atrial diameter in cm; LAV = left atrial end-systolic volume; IVS = interventricular septum; PWT = diastolic posterior wall thickness; PWTs = systolic posterior wall thickness; RWT = relative wall thickness (formula: 2 × PWT/LVEDD); LVEDD = left ventricular end-diastolic diameter; LVESD = left ventricular end-systolic diameter; LVM = left ventricular mass; LVM (g/m2 ) = LVM/BSA; LVEDV = left ventricular end-diastolic volume; LVESV = left ventricular end-systolic volume; d = diastolic; s = systolic; SV = stroke volume; EF = left ventricular ejection fraction in %; LVOT VMax = left ventricular outflow tract velocity; MV EMax = early (E) mitral velocity; MV AMax = mitral A (atrial) velocity; RV parasternal = RV diameter from parasternal view in cm; RV AFC = right ventricular area fractional change in %.

3.1.1. Echocardiography

Myocardial hypertrophy was common and was classified according to Lang et al. [19] (Table 2 and Table 3).
Table
Table 2. Myocardial hypertrophy in male triathletes.
Table 2. Myocardial hypertrophy in male triathletes.
Left VentricleNormalLightModerateStrong
LVEDD51 (100%)000
IVSD3 (5.9%)39 (76.5%)9 (17.6%)0
PWT4 (7.8%)37 (72.5%)10 (19.7%)0
LVM (g/m²)31 (60.8%)11 (21.6%)7 (13.7%)2 (3.9%)
LVEDV *44 (86.3%)4 (7.8%)2 (3.9%)1 (2.0%)
* Reference values according to Lang et al. [19]; LVEDD: left ventricular end-diastolic diameter; IVSD: interventricular septum diastolic thickness; PWT: diastolic posterior wall thickness; LVM (g/m²): Left ventricular mass/BSA; LVEDV: left ventricular end-diastolic volume.
Table
Table 3. Myocardial hypertrophy in female triathletes.
Table 3. Myocardial hypertrophy in female triathletes.
Left VentricleNormalLightModerateStrong
LVEDD33 (100%)000
IVSD12 (36.4%)18 (54.5%)3 (9.1%)0
PWT12 (36.4%)18 (54.5%)3 (9.1%)0
LVM (g/m²)26 (78.8%)4 (12.1%)1 (3.0%)2 (6.1%)
LVEDV *18 (54.5%)5 (15.2%)8 (24.2%)2 (6.1%)
* Reference values according to Lang et al. [19]; LVEDD: left ventricular end-diastolic diameter; IVSD: interventricular septum-end-diastolic thickness; PWT: diastolic posterior wall thickness; LVM (g/m²): Left ventricular mass/BSA; LVEDV: left ventricular end-diastolic volume.
In the study population, concentric changes of the left ventricle characterized the echocardiographic morphological picture. Concentric remodeling for males was found in 26 cases and concentric hypertrophy was observed in 21 cases. One male triathlete had eccentric hypertrophy, and three had normal myocardial anatomy. Seventeen females displayed concentric remodeling, and 6 females had concentric hypertrophy. Cardiac adaptation forms are visualized in Table 4.
Table
Table 4. Cardiac adaptation in the study collective *.
Table 4. Cardiac adaptation in the study collective *.
RWT >0.42 cmConcentric RemodelingConcentric Hypertrophy
Males: 26Males: 21
Females: 17Females: 6
RWT <0.42 cmNormalEccentric Hypertrophy
Males: 3Males: 1
Females: 9Females: 1
* Reference values and definition according to Lang et al. [19]; RWT: relative wall thickness (formula: 2 × PWT/LVEDD).
The classification into types of hypertrophy followed the criteria of Lang et al. [19]. Right ventricular remodeling or other pathological findings in the right ventricle were not found. Left ventricular function was excellent in all triathletes, even if they trained hard and had finished middle- or long-distance triathlons.

3.1.2. Spiroergometry/Physiological Performance

Oxygen absorption, ergometer performance and heart rate with VAT, RCP and at peak capacity are shown in Table 5 (males) and Table 6 (females).
Table
Table 5. Males: heart rate, oxygen uptake and power output according to performance.
Table 5. Males: heart rate, oxygen uptake and power output according to performance.
MeasurementsElite MalesNon-Elite Malesp-Value *
nMvSdnMvSd
AT (aerobic threshold)
HR20160.49.134144.913.00.000
aVO2203.850.46343.140.520.000
rVO22053.15.23439.85.50.000
%VO2max2082.46.63473.911.70.004
Watt20314.547.034259.744.10.000
RCP (respiratory compensatory point, anaerobic threshold)
HR20170.87.434157.712.20.000
aVO2204.370.61343.590.480.000
rVO22060.16.63445.45.10.000
%VO2max2092.36.93484.410.40.003
Watt20346.348.634289.738.20.000
Peak capacity
HR20180.47.134144.913.00.000
aVO2max204.70.7344.30.60.060
rVO2max2064.76.73454.27.10.000
Wattmax20367.047.634336.548.30.026
n = number; Mv = mean value; Sd = standard deviation; aVO2 = absolute VO2max in L/min; rVO2 = relative VO2 in mL/kg−1·min−1; * = of the Mann-Whitney U-Test; HR = heart rate; Watt = power output.
Table
Table 6. Females: heart rate, oxygen uptake and power output according to performance.
Table 6. Females: heart rate, oxygen uptake and power output according to performance.
MeasurementsElite FemalesNon-Elite Femalesp-Value *
nMvSdnMvSd
VAT (ventilatory aerobic threshold)
HR15160.614.518138.619.90.002
aVO2152.760.35181.990.460.001
rVO21545.55.41832.73.80.001
%VO21581.27.01864.412.90.001
Watt15230.024.518162.241.40.001
RCP (respiratory compensation point, anaerobic threshold)
HR15169.812.618152.321.00.016
aVO2153.060.28182.330.560.001
rVO21546.814.91837.46.30.001
%VO2max1591.76.71875.314.70.001
Watt15252.523.818195.044.00.001
Peak capacity
HR15179.710.018179.87.60.971
aVO2max153.40.3183.10.30.006
rVO2max1556.15.71850.14.10.004
Wattmax15274.032.518256.716.40.097
n = number; Mv = mean value; Sd = standard deviation; aVO2 = absolute oxygen uptake in L/min; rVO2 = relative oxygen uptake in mL/kg−1·min-1; * = Mann-Whitney U-Test; HR = heart rate; Watt = power output; max = maximum.

3.1.3. Left Ventricular Hypertrophy

According to the values reported by Devereux et al. [23] and Bove et al. [24], we divided male triathletes into two groups, group 1 with LVM >220 g and group 2 with LVM <220 g, to assess the possible reasons for left ventricular hypertrophy. The significant differences between the two groups are visible in Table 7.
Table
Table 7. Differences between males with LV-mass >220 g and <220 g.
Table 7. Differences between males with LV-mass >220 g and <220 g.
LV Mass (ASE) gMale < 220 gMales > 220 gp-Value
nMvSdnMvSdMann-Whitney U-Test
VO2AT273.20.5243.70.50.001
Training distance bike27190.365.824250.2600.004
SV (Teich) mL276311.72472.913.30.006
SV index (Teich) mL/m²2732.25.923366.30.018
Left atrium (cm)272.460.27242.640.270.020
WattsAT27265.646.624301.353.40.023
Training time bike2772.2248.62.40.034
Training time (overall)2715.72.72417.83.30.035
Wattmax27336.741.924363.856.60.042
Training time swimming273.21.2243.81.40.049
RRsWattmax27188.120.424199.619.90.055
RRsAT2717824.624192.920.50.056
VO2max274.30.5244.60.80.059
VO2AT: oxygen uptake at the aerobic threshold (VAT) in L/min; Training-distance bike: kilometers/week; SV (Teichholz) mL: left ventricular stroke volume; Training time bike: hours/week Training time overall: hours/week Wattmax: maximal power; Training time swimming: hours/week; RRsWattmax: systolic arterial pressure during maximal exercise; RRsAT: systolic arterial pressure at the aerobic threshold; VO2max: maximal oxygen uptake in L/min.
Additional results about the possible reasons for LV hypertrophy were calculated by odds ratios (Table 8).
Table
Table 8. Probability of LVM >220 g: odds ratios.
Table 8. Probability of LVM >220 g: odds ratios.
ParametersLVMOR95%-CIp-Value
<220 g (n = 27)>220 g (n = 24)
MvSDMvSD
BPsRest125.410.8130.815.71.0310.9891.0740.148
BPs Aero.thresh.178.024.6192.920.51.0271.0031.0510.025
BPs Anae.thresh.185.221.5198.822.31.0271.0021.0520.034
BPsWmax188.120.4199.619.91.0271.0001.0540.050
Tr.time swim3.21.23.81.41.460.952.250.081
Tr.time bike7.02.28.62.41.331.061.660.015
Tr.time run4.91.54.91.21.050.701.560.823
Training time15.72.717.83.31.231.041.470.019
Triathlon since y14.59.015.710.31.010.961.070.654
BPs = systolic blood pressure (mmHg); Tr.time = training time in hours/week; Aero.thresh. = aerobic threshold; Anae.thresh. = anaerobic threshold; y = years.
With respect to the relationship between arterial hypertension and myocardial hypertrophy, 32 male triathletes had a wall thickness >1.2 cm, whereas 19 had a thickness <1.2 cm. In these male athletes, the mean arterial blood pressure values of 196.9 mmHg and 187.9 mmHg (p = 0.075) were measured at the maximal watts level (Wmax). The odds ratios showed a significant relationship between the arterial pressure values during exercise (at the aerobic and anaerobic threshold). There was an additional relationship between the overall training time and a LVM >220 g (Table 8).

3.1.4. Training Habits/History

The mean training times were similar in male and female triathletes (Table 9). The mean time for swimming was 3.5 h/week, for biking 6–8 h a week, for running 5 h a week. Total training time was 14–15 h/week. The maximal training time for triathlon was 29 years for a 64 years old male triathlete. The oldest female triathlete was 45 years old and had trained for triathlons for 5 years. Four athletes had a history of Chlamydia pneumoniae infections.
Table
Table 9. Training habits/week.
Table 9. Training habits/week.
TrainingsMalesFemalesTimes/distances
nMvSdnMvSd
Swimming543.51.28333.61.19hours
547.83.9337.53.5km
Biking547.82.39336.62.05hours
54218.668.933168.570.9km
Running544.91.36335.11.36hours
5452.413.33351.514km
Tr.time/week5416.73.13315.53.3hours
Triathlon years549.06.4336.44.5years
Sport years5414.99.43313.76.8years
Mv = mean value; Sd = standard deviation.

3.2. Discussion

Sports-related cardiac injury is a very broadly discussed issue [7,8,9]. The most substantial cardiac injury is sport-related sudden death. Most cases of sudden death in athletes over 35 years of age are caused by coronary disease [25], and their prognoses depend on the coronary arteriosclerosis burden [26] rather than on a possible increase in biomarkers during competition. The sudden deaths of young athletes <35 years (Table 10) typically have different causes (hypertrophic cardiomyopathy, coronary disease, coronary anomalies, myocarditis and arrhythmogenic right ventricle) [27,28,29,30].
In this study, pathological structural cardiac changes could not be observed. The dynamic physiological performance of the triathletes showed high baseline values without functional signs of cardio-pulmonary impairment.
Table
Table 10. Causes of sudden cardiac death in young athletes 12–35 years old (percentages).
Table 10. Causes of sudden cardiac death in young athletes 12–35 years old (percentages).
Causes of cardiac sudden deathMaron [27]Corrado [29]Solberg [30]Marijon [28]
Aortic rupture2.21.84.32
Aortic stenosis/cong. HD1.8 4.36
ARVC422 4
Channelopathies (QT, WPW)31.88.712
Coronary artery anomalies24113.3
Coronary disease318486
Dilatative CM21.8 4
Hypertrophic CM361.84.310
MVP47.3 2
Myocarditis5.49224
Possible HCM11.3 4
Riva muscle bridge2.23.6 2
Unclear 1.8 36
n = 1049n = 55n = 22n = 50
cong. HD = congenital heart disease; ARVC = arrhythmogenic right ventricular cardiomyopathy; QT = QT-syndrome (including Romano-Ward syndrome and Jervell-Lange-Nielsen syndrome); WPW = Wolff-Parkinson-White syndrome; CM = cardiomyopathy; HCM = hypertrophic cardiomyopathy; MVP = mitral valve prolapsed.

3.2.1. Cardiac Adaptation to Exercise and Left Ventricular Hypertrophy

The specific endurance training of triathletes leads to physiological changes in their performance parameters [31] and results in changes in cardiac function or cardiac structures [32]. This adaptation is linked to the nature and magnitude of the physical exercise [16,33]. The physiological adaptation is a “harmonic increase in [the] size” of a healthy heart caused by physical activity [34]. The term “athlete’s heart” [16] has been used since 1899 [35]. The sudden death of athletes is more often a problem for male athletes [28]. Different causes of sudden death [27], (silent coronary disease [30], hypertrophic cardiomyopathy [27] and arrhythmogenic right ventricular cardiomyopathy [29]) have been reported. Cardiovascular adaptations to exercise have been systematically defined and differ according to the type of conditioning endurance training [33,36,37]. Cycling and rowing have the biggest effects on the cavity size and wall thickness [27,38].
Concentric hypertrophy in triathletes has already been described [39]. Douglas et al. [40] suggested that athletes developed hypertrophy from the systolic blood pressure increase during exercise, which could be explained by the frequency of the training. The diastolic function was normal under these conditions.
In the present study, odds ratio analysis showed a relationship between myocardial thickening and exercise arterial pressure. Intense, long-term training with exercise-induced blood pressure elevation can lead to hypertrophy that mimics the conditions of pathological arterial pressure changes. The male triathletes with a wall thickness >1.2 cm had higher arterial pressure (196.9 mmHg vs. 187.9 mmHg; p = 0.075) at the peak capacity (maximum wattage), but this difference was not significant. This difference was found only in males; the average arterial pressure values for females were not different and did not increase. Indicators of an increase in wall thickness additional other than dilatation have been confirmed in a study of female athletes [41] that compared long-distance and short-distance runners. Endurance training for females causes an increase in the wall thickness rather than the dilatation of the left ventricle. However, the RWT reported in that study is significantly lower than what we observed (0.384 ± 0.052). The basic assumption for triathletes that this sport can lead to eccentric rather than to concentric hypertrophy was not confirmed in this study. There were signs of remodeling with primarily concentric hypertrophy in the female subjects in the present study. Concentric remodeling for males was found in 26 cases, and concentric hypertrophy could be observed in 21 cases. Concentric remodeling and concentric hypertrophy are more common in male athletes [16]. Different authors have concluded that strength training predominantly leads to concentric hypertrophy and endurance training leads to eccentric hypertrophy [42]. In this study, concentric remodeling was the most frequently observed. George et al. [16] reported that the expected pattern of eccentric enlargement was replaced by a pattern of concentric or symmetric enlargement in groups of highly trained athletes. Generally, the adaptation of the cardiac mass does not appear to depend on the type of conditioning [16]. In our opinion, the results of wall thickness measurements depend on the cohort size, age and gender.
In 1989, Douglas et al. [43] published a comparison of 36 triathletes comprising 17 normal control and 15 high-pressure subjects. The authors reported that the triathletes underwent cardiac adaptations similar to pressure overload of the left ventricle and described an RWT of 0.41. In these triathletes, the left ventricular muscle mass was positively correlated with the systolic blood pressure during exercise.
The difference between triathletes and cycle racers is that the training not only takes place under strength/endurance conditions, as during a cycle race, but it also occurs under running conditions. Modified strength training also results in different changes in the cardiac structures of triathletes compared to professional cycle racers [44]. In a study of 14 professional cycle racers, the authors found that the left ventricular muscle mass as well as the diastolic cardiac parameters resulted in eccentric hypertrophy more than concentric hypertrophy, which contrasts with our study. The functional changes of the cardiac structures for triathletes resemble the changes in runners [45].

3.2.2. Right or Left Ventricular “Fatigue”

Some papers have reported that excessive endurance training may cause negative remodeling of cardiac structures [9,46,47]. Predominantly, ultra-marathons and Ironman-distance triathlons can cause transient overload of the right ventricle [46,47,48]. Fibrosis of the left ventricle in older runners is a possible cause of death [49,50]. Diverse patterns of myocardial fibrosis were reported by Wilson et al. [50]. Heidbüchel [51] postulates that load-induced, right ventricular arrhythmogenic cardiomyopathy could lead from repetitive microtrauma to chronic and structural changes of the right ventricle and “pro-arrhythmogenesis”. In his view, ventricular tachycardia originating from the right ventricle is responsible for the acute deaths. His hypothesis is based on a retrospective analysis of electrophysiological examinations in 2003 [52].
The discussion concerning cardiac injury and endurance sports is ongoing [7,8,9,53]. Pelliccia et al. [54] examined the left ventricular function of 114 Olympic athletes in a long-term follow-up study. The global left systolic function was unchanged, and wall motion abnormalities were absent. D’Andrea et al. [55] examined the right ventricle function in 650 top-level athletes and found enlarged right ventricular and right atrial dimensions; they described this as a “physiologic phenomenon.” Additionally, long-term-training marathon runners did not suffer any long term injury of the right ventricle (including examination by advanced strain technology) [56].
The systolic function of the left ventricle was not negatively influenced in our study cohort. The right ventricular fractional area change was normal in all triathletes. The oldest triathlete in our study had competed in triathlons for 29 years. The diastolic function in our cohort was not materially impaired. The E/A ratio, however, was slightly lower, as reported by Douglas et al. [40]. The impact of exercise-induced arterial hypertension (EIAH) is known in healthy subjects [57]. There is strong evidence that athletes have a higher incidence of atrial fibrillation [58,59] and bradyarrhythmias with increasing age [58,60]. We do not know the definitive reasons for this (increased atrial pressure?), but EIAH and LVM can cause atrial fibrillation in endurance athletes. The general prevalence or incidence of EIAH in athletes is unknown. The problem of EIAH seems to occur more in male competitive athletes who undergo a vigorous training schedule [57]. Low-intensity training and aerobic exercise have been shown to help decrease blood pressure [61,62]. The hypertensive or non-hypertensive response to exercise seems to be related to hereditary factors [63], to aging or to the individual arterial stiffness [64]. It is crucial to define the people who are at risk and to start therapy if possible [65]. In our daily practice, we treat subjects with low-dose ACE inhibitors or AT1-blockers before training or competition. The dosage should be tested using an exercise test. The present study shows the relationship between EIAH and cardiac hypertrophy (Table 5).

3.2.3. Dynamic Physiological Performance

A prerequisite of successful participation in middle- and long-distance triathlons is sufficient aerobic capacity [31]. It also appears that this is essential for avoiding possible damage due to long-term endurance training [4]. In the present study, 54 male athletes had a VO2max of 58.1 mL/kg−1·min−1 and a VAT of 44.7 mL/kg−1·min−1. These data are in agreement with published data from smaller studies. The VO2 for the VAT was between 34 and 49 mL/kg−1·min−1 body weight in previously published studies, which depends on the subject group. The maximum oxygen absorption in the previously published studies had a range of 43 to 74 mL/kg−1·min−1 body weight among the different groups that were examined. In contrast, studies of groups with, for example, five world-class athletes [66] report higher results. However, it can be postulated that a VO2max >55 mL/kg−1·min−1 body weight is a good marker for successful participation in an Ironman competition at both middle and long distances. The oxygen absorption at the aerobic threshold should be >45 mL/min/kg body weight for males and >35 mL/kg−1·min−1 body weight for females. In the present study, the examinations always took place using egometric peak capacity by bicycle; treadmill data can differ depending on the athletes’ background [13]. Bunc et al. [67] propose the use of VO2max values for young Olympic triathletes, with males having an average of >65 mL/min/kg and females >60 mL/min/kg. This pertains to elite triathletes. In smaller studies using bicycle ergometry, the maximum oxygen absorption values for female athletes (e.g., [68]) averaged 57.5 mL/kg−1·min−1 body weight, and the average oxygen absorption value for ten Olympic-level female athletes [69] was at VAT of 37.7 mL/min/kg body weight. The overall male and female group examined here had a physiological profile that matches well-trained and ambitious triathletes, though it does not compare to the equivalent values for world-class athletes.
When comparing the performance values of elite and non-elite male athletes (Table 2) in the present study, a significant difference was observed, as expected (relVO2max for males 64 ± 6.7 vs. 54.9 ± 6.7 mL/kg−1·min−1 and VO2 for VAT 53.1 ± vs. 39.8 ± 5.5 mL/kg−1·min−1). A similar difference in the range of VO2max was observed for female athletes (Table 3). In summary, the results from this study show a difference in VO2max, which is not as high as observed in triathletes examined in other studies. The values determined for German elite and amateur athletes are within the range of internationally determined parameters.

3.2.4. Study Limitations and Future Directions

The cross-sectional design of this study did not allow us to exclude the possibility of negative effects of endurance sport in the triathletes, although our data suggest that our examined triathletes had no significant signs of cardiac injury except for the signs of the hypertrophy. The pathological relevance of the athletes’ hypertrophy is under discussion. Confirmatory longitudinal studies are necessary. It is not possible to exclude, that using of strain or tissue Doppler technique might provide diagnosis of abnormal cardiac function. Biplane analysis of the ventricular volumes might provide small changes in the stroke volume analysis, but in participants without regional wall motion abnormalities or cardiac infarction they are negligible.

4. Conclusions

The data of the present study on German triathletes participating in the middle- and long-distance events allow for the practical use of this information as a routine part of sports medicine in classifying the efficiency of performance diagnostic centers. In males, the training goals aim for an aerobic capacity of VAT = 45 mL/kg−1·min−1, (males) or 35 mL/kg−1·min−1 (females). In terms of the echocardiographic measurement, we can expect concentric remodeling/concentric hypertrophy. Valve dysfunctions are possible but rare. Accordingly, the blood pressure values should be thoroughly examined during routine or pre-event check-up. We conclude that the relationship between myocardial thickening and arterial blood pressure during exercise remains an open issue. With respect to echocardiography, we did not observe cardiac dysfunction in our athletes.
The idea of exercise-induced cardiac disease was suggested by Heidbüchel [51] and LaGerche [46] but the data are controversial [8,53]. In our cohort, with the mean time of participation in triathlon competitions of 9.0 years in males and 6.4 years in females (Table 9, we did not find the negative long-term effects on cardiac structures that had been proposed for exercised-induced cardiac fatigue. The longest time for participating in triathlon competitions was 29 years (one 64-year-old triathlete, with Ironman-distance times of ca. 11 h).
There is no doubt that athletes have a higher incidence of atrial fibrillation [58] and bradyarrhythmias [60]. Elite athletes (particularly men) have improved longevity because of the rare occurrence of cardiovascular disease [70]. Early death in individuals due by myocardial fibrosis is possible [49]. The general incidence of exercise-induced cardiac injury is not known, and the dose of exercise bouts and individual sensitivity has yet to be defined and should be evaluated in further prospective studies [71]. In all athletes with suspicious inflammation/myocarditis or in cases of power/performance lost, blood tests must be performed, especially for Chlamydia pneumoniae [72] or other bacterial/viral infections. The impact of exercise-induced arterial hypertension in endurance athletes remains an open issue [57]. Abnormal exercise-induced cardiac hypertrophy might be a risk factor for arrhythmia [57]. Further prospective studies on possible cardiac “negative remodeling” due to participation in sports (exercise-induced cardiac fatigue) with larger cohorts and under clearly defined conditions should be conducted. In addition, the optimal training volume of physical activity concerning the general survival rate should be investigated prospectively. Considering the dominant probability of coronary heart disease in ambitious athletes >35 years, risk stratification with exercise-tests/imaging techniques [73,74] is advisable in addition to basic examination (medical history/physical examination/12-channel-ECG). Marijon et al. [28] reported a five-fold higher cardiac mortality in young, ambitious competitive athletes (relative risk 9.8, 95%, CI 3.7 to 16) than in non-competitive athletes (2.2, 95%, CI 1.4 to 3.0). This fact supports the need for a more detailed examination of athletes <35 years and to identify people who are at risk.
Given the value of competitive sporting activities to hobby-athletes, the media, and other industries, physical activity in the general population is of fundamental importance [75]. Further prospective examinations and studies about the long-term adverse effects of endurance sports should be performed.

Acknowledgments

The authors thank Birgit Dworrak for help in preparation of references and text and Karin Worst for preparing the tables.

Author Contributions

Roman Leischik has the original idea for the study and drafted the manuscript, which was revised, read and approved by both authors. Norman Spelsberg conceived and participated in project design and coordination. He performed the examinations and was responsible for data cleaning and carried out the analyses together with Roman Leischik. Both authors were responsible for recruitment and follow-up of study participants.

Conflicts of Interest

The authors declare no conflict of interest.

References

  1. Potts, S. Marathon, Battle of (490 BCE). Encycl. War 2012. [Google Scholar] [CrossRef]
  2. Frost, F. The dubious origin of marathon. Am. J. Anc. Hist. 1979, 4, 159–163. [Google Scholar]
  3. Harris, K.M.; Henry, J.T.; Rohman, E.; Haas, T.S.; Maron, B.J. Sudden death during the triathlon. Jama 2010, 303, 1255–1257. [Google Scholar] [CrossRef]
  4. Douglas, P.S.; O’Toole, M.L.; Hiller, W.D.; Hackney, K.; Reichek, N. Cardiac fatigue after prolonged exercise. Circulation 1987, 76, 1206–1213. [Google Scholar] [CrossRef]
  5. Rifai, N.; Douglas, P.S.; O’Toole, M.; Rimm, E.; Ginsburg, G.S. Cardiac troponin T and I, echocardiographic [correction of electrocardiographic] wall motion analyses, and ejection fractions in athletes participating in the Hawaii Ironman Triathlon. Am. J. Cardiol. 1999, 83, 1085–1089. [Google Scholar]
  6. Neilan, T.G.; Januzzi, J.L.; Lee-Lewandrowski, E.; Ton-Nu, T.-T.; Yoerger, D.M.; Jassal, D.S.; Lewandrowski, K.B.; Siegel, A.J.; Marshall, J.E.; Douglas, P.S. Myocardial injury and ventricular dysfunction related to training levels among nonelite participants in the Boston marathon. Circulation 2006, 114, 2325–2333. [Google Scholar] [CrossRef]
  7. Oxborough, D.; Birch, K.; Shave, R.; George, K. Exercise-induced cardiac fatigue”—A review of the echocardiographic literature. Echocardiography 2010, 27, 1130–1140. [Google Scholar] [CrossRef]
  8. Leischik, R. Endurance sport and cardiac injury. Pol. J. Cardiol. Kardiol. Polska 2014, 72, 311–321. [Google Scholar] [CrossRef]
  9. O’Keefe, J.H.; Harshal, R.P.; Lavie, C.J.; Magalski, A.; Vogel, R.A.; McCiiough, P.A. Potential adverse cardiovascular effects from excessive endurance exercise. Mayo Clin. Proc. 2012, 87, 587–595. [Google Scholar] [CrossRef]
  10. O'Toole, M.L.; Douglas, P.S. Applied physiology of triathlon. Sports Med. 1995, 19, 251–267. [Google Scholar] [CrossRef]
  11. O'Toole, M.L.; Hiller, D.B.; Crosby, L.O.; Douglas, P.S. The ultraendurance triathlete: A physiological profile. Med. Sci. Sports Exerc. 1987, 19, 45–50. [Google Scholar]
  12. Hue, O. Prediction of drafted-triathlon race time from submaximal laboratory testing in elite triathletes. Can. J. Appl. Physiol. 2003, 28, 547–560. [Google Scholar] [CrossRef]
  13. Hue, O.; Le Gallais, D.; Chollet, D.; Prefaut, C. Ventilatory threshold and maximal oxygen uptake in present triathletes. Can. J. Appl. Physiol. 2000, 25, 102–113. [Google Scholar] [CrossRef]
  14. Laursen, P.B.; Rhodes, E.C.; Langill, R.H.; McKenzie, D.C.; Taunton, J.E. Relationship of exercise test variables to cycling performance in an Ironman triathlon. Eur. J. Appl. Physiol. 2002, 87, 433–440. [Google Scholar] [CrossRef]
  15. Laursen, P.B.; Shing, C.M.; Tennant, S.C.; Prentice, C.M.; Jenkins, D.G. A comparison of the cycling performance of cyclists and triathletes. J. Sports Sci. 2003, 21, 411–418. [Google Scholar] [CrossRef]
  16. George, K.P.; Wolfe, L.A.; Burggraf, G.W. The ‘athletic heart syndrome’. A critical review. Sports Med. 1991, 11, 300–330. [Google Scholar] [CrossRef]
  17. Abergel, E.; Chatellier, G.; Hagege, A.A.; Oblak, A.; Linhart, A.; Ducardonnet, A.; Menard, J. Serial left ventricular adaptations in world-class professional cyclists: Implications for disease screening and follow-up. J. Am. Coll. Cardiol. 2004, 44, 144–149. [Google Scholar] [CrossRef]
  18. Fagard, R.; Van den Broeke, C.; Amery, A. Left ventricular dynamics during exercise in elite marathon runners. J. Am. Coll. Cardiol. 1989, 14, 112–118. [Google Scholar] [CrossRef]
  19. Lang, R.M.; Bierig, M.; Devereux, R.B.; Flachskampf, F.A.; Foster, E.; Pellikka, P.A.; Picard, M.H.; Roman, M.J.; Seward, J.; Shanewise, J. Recommendations for chamber quantification. Eur. J. Echocardiogr. 2006, 7, 79–108. [Google Scholar] [CrossRef]
  20. Nagueh, S.F.; Appleton, C.P.; Gillebert, T.C.; Marino, P.N.; Oh, J.K.; Smiseth, O.A.; Waggoner, A.D.; Flachskampf, F.A.; Pellikka, P.A.; Evangelisa, A. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. Eur. J. Echocardiogr. 2009, 10, 165–193. [Google Scholar] [CrossRef]
  21. Beaver, W.L.; Wasserman, K.; Whipp, B.J. A new method for detecting anaerobic threshold by gas exchange. J. Appl. Physiol. 1986, 60, 2020–2027. [Google Scholar]
  22. Wasserman, K.; Whipp, B.J.; Koyl, S.N.; Beaver, W.L. Anaerobic threshold and respiratory gas exchange during exercise. J. Appl. Physiol. 1973, 35, 236–243. [Google Scholar]
  23. Devereux, R.B.; Alonso, D.R.; Lutas, E.M.; Gottlieb, G.J.; Campo, E.; Sachs, I.; Reichek, N. Echocardiographic assessment of left ventricular hypertrophy: Comparison to necropsy findings. Am. J. Cardiol. 1986, 57, 450–458. [Google Scholar] [CrossRef]
  24. Bove, K.E.; Rowlands, D.T.; Scott, R.C. Observations on the assessment of cardiac hypertrophy utilizing a chamber partition technique. Circulation 1966, 33, 558–568. [Google Scholar] [CrossRef]
  25. Wike, J.; Kernan, M. Sudden cardiac death in the active adult: Causes, screening, and preventive strategies. Curr. Sports Med. Rep. 2005, 4, 76–82. [Google Scholar] [CrossRef]
  26. Mohlenkamp, S.; Leineweber, K.; Lehmann, N.; Braun, S.; Roggenbuck, U.; Perrey, M.; Broecker-Preuss, M.; Budde, T.; Halle, M.; Mann, K.; et al. Coronary atherosclerosis burden, but not transient troponin elevation, predicts long-term outcome in recreational marathon runners. Basic Res. Cardiol. 2014, 109, 391. [Google Scholar] [CrossRef]
  27. Maron, B.J.; Thompson, P.D.; Ackerman, M.J.; Balady, G.; Berger, S.; Cohen, D.; Dimeff, R.; Douglas, P.S.; Glover, D.W.; Hutter, A.M. Recommendations and considerations related to preparticipation screening for cardiovascular abnormalities in competitive athletes: 2007 Update a scientific statement from the American Heart Association Council on nutrition, physical activity, and metabolism: Endorsed by the American College of Cardiology Foundation. Circulation 2007, 115, 1643–1655. [Google Scholar] [CrossRef]
  28. Marijon, E.; Tafflet, M.; Celermajer, D.S.; Dumas, F.; Perier, M.C.; Mustafic, H.; Toussaint, J.F.; Desnos, M.; Rieu, M.; Benameur, N.; et al. Sports-related sudden death in the general population. Circulation 2011, 124, 672–681. [Google Scholar]
  29. Corrado, D.; Basso, C.; Rizzoli, G.; Schiavon, M.; Thiene, G. Does sports activity enhance the risk of sudden death in adolescents and young adults? J. Am. Coll. Cardiol. 2003, 42, 1959–1963. [Google Scholar] [CrossRef]
  30. Solberg, E.E.; Gjertsen, F.; Haugstad, E.; Kolsrud, L. Sudden death in sports among young adults in Norway. Eur. J. Cardiovasc. Prev. Rehabil. 2010, 17, 337–341. [Google Scholar]
  31. Suriano, R.; Bishop, D. Physiological attributes of triathletes. J. Sci. Med. Sport 2010, 13, 340–347. [Google Scholar] [CrossRef]
  32. Atchley, A.E., Jr.; Douglas, P.S. Left ventricular hypertrophy in athletes: Morphologic features and clinical correlates. Cardiol. Clin. 2007, 25, 371–382. [Google Scholar] [CrossRef]
  33. Utomi, V.; Oxborough, D.; Ashley, E.; Lord, R.; Fletcher, S.; Stembridge, M.; Shave, R.; Hoffman, M.D.; Whyte, G.; Somauroo, J.; et al. Predominance of normal left ventricular geometry in the male ‘athlete’s heart’. Heart 2014, 100, 1264–1271. [Google Scholar]
  34. Dickhuth, H.; Hipp, A.; Niess, A.; Röcker, K.; Mayer, F.; Horstmann, T. Differenzialdiagnostik der physiologischen Herzhypertrophie (Sportherz). Deutsche Zeitschrift für Sportmedizin 2001, 52, 205–210. [Google Scholar]
  35. Henschen, S. Skilanglauf und Skiwettlauf. Eine medizinische Sportstudie. Mitt. Med. Klin. Upsala 1899, 2, 74. [Google Scholar]
  36. Morganroth, J.; Maron, B.J.; Henry, W.L.; Epstein, S.E. Comparative left ventricular dimensions in trained athletes. Ann. Intern. Med. 1975, 82, 521–524. [Google Scholar] [CrossRef]
  37. Utomi, V.; Oxborough, D.; Whyte, G.P.; Somauroo, J.; Sharma, S.; Shave, R.; Atkinson, G.; George, K. Systematic review and meta-analysis of training mode, imaging modality and body size influences on the morphology and function of the male athlete’s heart. Heart 2013, 99, 1727–1733. [Google Scholar] [CrossRef]
  38. Fagard, R.H. Impact of different sports and training on cardiac structure and function. Cardiol. Clin. 1997, 15, 397–412. [Google Scholar]
  39. Douglas, P.S.; O’Toole, M.L.; Katz, S.E.; Ginsburg, G.S.; Hiller, W.D.; Laird, R.H. Left ventricular hypertrophy in athletes. Am. J. Cardiol. 1997, 80, 1384–1388. [Google Scholar] [CrossRef]
  40. Douglas, P.S.; O’Toole, M.L.; Hiller, W.D.; Reichek, N. Left ventricular structure and function by echocardiography in ultraendurance athletes. Am. J. Cardiol. 1986, 58, 805–809. [Google Scholar] [CrossRef]
  41. Venckunas, T.; Lionikas, A.; Marcinkeviciene, J.E.; Raugaliene, R.; Alekrinskis, A.; Stasiulis, A. Echocardiographic parameters in athletes of different sports. J. Sports Sci. Med. 2008, 7, 151–156. [Google Scholar]
  42. Pluim, B.M.; Zwinderman, A.H.; van der Laarse, A.; van der Wall, E.E. The athlete’s heart a meta-analysis of cardiac structure and function. Circulation 2000, 101, 336–344. [Google Scholar] [CrossRef]
  43. Douglas, P.S. Cardiac considerations in the triathlete. Med. Sci. Sports Exerc. 1989, 21, S214–S218. [Google Scholar] [CrossRef]
  44. Bekaert, I.; Pannier, J.L.; Van de Weghe, C.; van Durme, J.P.; Clement, D.L.; Pannier, R. Non-invasive evaluation of cardiac function in professional cyclists. Br. Heart J. 1981, 45, 213–218. [Google Scholar] [CrossRef]
  45. Fagard, R.; Aubert, A.; Staessen, J.; Eynde, E.V.; Vanhees, L.; Amery, A. Cardiac structure and function in cyclists and runners. Comparative echocardiographic study. Br. Heart J. 1984, 52, 124–129. [Google Scholar] [CrossRef]
  46. La Gerche, A.; Burns, A.T.; Mooney, D.J.; Inder, W.J.; Taylor, A.J.; Bogaert, J.; MacIsaac, A.I.; Heidbüchel, H.; Prior, D.L. Exercise-induced right ventricular dysfunction and structural remodelling in endurance athletes. Eur. Heart J. 2012, 33, 998–1006. [Google Scholar] [CrossRef]
  47. Karlstedt, E.; Chelvanathan, A.; Da Silva, M.; Cleverley, K.; Kumar, K.; Bhullar, N.; Lytwyn, M.; Bohonis, S.; Oomah, S.; Nepomuceno, R.; et al. The impact of repeated marathon running on cardiovascular function in the aging population. J. Cardiovasc. Magn. Reson. 2012, 14, 58. [Google Scholar] [CrossRef]
  48. Oomah, S.R.; Mousavi, N.; Bhullar, N.; Kumar, K.; Walker, J.R.; Lytwyn, M.; Colish, J.; Wassef, A.; Kirkpatrick, I.D.; Sharma, S.; Jassal, D.S. The role of three-dimensional echocardiography in the assessment of right ventricular dysfunction after a half marathon: Comparison with cardiac magnetic resonance imaging. J. Am. Soc. Echocardiogr. 2011, 24, 207–213. [Google Scholar] [CrossRef]
  49. Whyte, G.; Sheppard, M.; George, K.; Shave, R.; Wilson, M.; Prasad, S.; O’Hanlon, R.; Sharma, S. Post-mortem evidence of idiopathic left ventricular hypertrophy and idiopathic interstitial myocardial fibrosis: Is exercise the cause? Br. J. Sports Med. 2008, 42, 304–305. [Google Scholar] [CrossRef]
  50. Wilson, M.; O’Hanlon, R.; Prasad, S.; Deighan, A.; Macmillan, P.; Oxborough, D.; Godfrey, R.; Smith, G.; Maceira, A.; Sharma, S.; et al. Diverse patterns of myocardial fibrosis in lifelong, veteran endurance athletes. J. Appl. Physiol. 2011, 110, 1622–1626. [Google Scholar] [CrossRef]
  51. Heidbuchel, H.; Prior, D.L.; La Gerche, A. Ventricular arrhythmias associated with long-term endurance sports: What is the evidence? Br. J. Sports Med. 2012, 46 (Suppl. 1), i44–i50. [Google Scholar] [CrossRef]
  52. Heidbuchel, H.; Hoogsteen, J.; Fagard, R.; Vanhees, L.; Ector, H.; Willems, R.; Van Lierde, J. High prevalence of right ventricular involvement in endurance athletes with ventricular arrhythmias. Role of an electrophysiologic study in risk stratification. Eur. Heart J. 2003, 24, 1473–1480. [Google Scholar]
  53. Scharhag, J.; Lollgen, H.; Kindermann, W. Competitive sports and the heart: Benefit or risk? Dtsch Arztebl Int. 2013, 110, e11–e12. [Google Scholar]
  54. Pelliccia, A.; Kinoshita, N.; Pisicchio, C.; Quattrini, F.; DiPaolo, F.M.; Ciardo, R.; Di Giacinto, B.; Guerra, E.; De Blasiis, E.; Casasco, M.; et al. Long-term clinical consequences of intense, uninterrupted endurance training in Olympic athletes. J. Am. Coll. Cardiol. 2010, 55, 1619–1625. [Google Scholar]
  55. D’Andrea, A.; Riegler, L.; Golia, E.; Cocchia, R.; Scarafile, R.; Salerno, G.; Pezzullo, E.; Nunziata, L.; Citro, R.; Cuomo, S. Range of right heart measurements in top-level athletes: The training impact. Int. J. Cardiol. 2013, 164, 48–57. [Google Scholar] [CrossRef]
  56. Simsek, Z.; Tas, M.H.; Gunay, E.; Degirmenci, H. Speckle-tracking echocardiographic imaging of the right ventricular systolic and diastolic parameters in chronic exercise. Int. J. Cardiovasc. Imaging 2013, 29, 1265–1271. [Google Scholar] [CrossRef]
  57. Leischik, R.; Spelsberg, N.; Niggemann, H.; Dworrak, B.; Tiroch, K. Exercise-induced arterial hypertension—An independent factor for hypertrophy and a ticking clock for cardiac fatigue or atrial fibrillation in athletes? F1000Research 2014, 3. [Google Scholar] [CrossRef]
  58. Calvo, N.; Brugada, J.; Sitges, M.; Mont, L. Atrial fibrillation and atrial flutter in athletes. Br. J. Sports Med. 2012, 46 (Suppl. 1), i37–i43. [Google Scholar]
  59. Leischik, R.; Littwitz, H. Slow recovery of the right and left ventricular deformation after conversion from atrial fibrillation. Am. J. Sports Sci. 2014, 2, 13–16. [Google Scholar]
  60. Andersen, K.; Farahmand, B.; Ahlbom, A.; Held, C.; Ljunghall, S.; Michaelsson, K.; Sundstrom, J. Risk of arrhythmias in 52 755 long-distance cross-country skiers: A cohort study. Eur. Heart J. 2013, 34, 3624–3631. [Google Scholar]
  61. Rogers, M.W.; Probst, M.M.; Gruber, J.J.; Berger, R.; Boone, J.B., Jr. Differential effects of exercise training intensity on blood pressure and cardiovascular responses to stress in borderline hypertensive humans. J. Hypertens. 1996, 14, 1369–1375. [Google Scholar]
  62. Kelley, G.A.; Sharpe Kelley, K. Aerobic exercise and resting blood pressure in older adults: A meta-analytic review of randomized controlled trials. J. Gerontol. A Biol. Sci. Med. Sci. 2001, 56, M298–M303. [Google Scholar] [CrossRef]
  63. Walker, A.J.; Bassett, D.R., Jr.; Duey, W.J.; Howley, E.T.; Bond, V.; Torok, D.J.; Mancuso, P. Cardiovascular and plasma catecholamine responses to exercise in blacks and whites. Hypertension 1992, 20, 542–548. [Google Scholar] [CrossRef]
  64. Laurent, S.; Cockcroft, J.; Van Bortel, L.; Boutouyrie, P.; Giannattasio, C.; Hayoz, D.; Pannier, B.; Vlachopoulos, C.; Wilkinson, I.; Struijker-Boudier, H. Expert consensus document on arterial stiffness: Methodological issues and clinical applications. Eur. Heart J. 2006, 27, 2588–2605. [Google Scholar]
  65. Vanhees, L.; Fagard, R.; Lijnen, P.; Amery, A. Effect of antihypertensive medication on endurance exercise capacity in hypertensive sportsmen. J. Hypertens. 1991, 9, 1063–1068. [Google Scholar]
  66. Schabort, E.J.; Killian, S.C.; St Clair Gibson, A.; Hawley, J.A.; Noakes, T.D. Prediction of triathlon race time from laboratory testing in national triathletes. Med. Sci. Sports Exerc. 2000, 32, 844–849. [Google Scholar] [CrossRef]
  67. Bunc, V.; Heller, J.; Horcic, J.; Novotny, J. Physiological profile of best Czech male and female young triathletes. J. Sports Med. Phys. Fitness 1996, 36, 265–270. [Google Scholar]
  68. O’Toole, M.L.; Douglas, P.S.; Hiller, W.D. Lactate, oxygen uptake, and cycling performance in triathletes. Int. J. Sports Med. 1989, 10, 413–418. [Google Scholar]
  69. Schneider, D.A.; Pollack, J. Ventilatory threshold and maximal oxygen uptake during cycling and running in female triathletes. Int. J. Sports Med. 1991, 12, 379–383. [Google Scholar] [CrossRef]
  70. Gajewski, A.K.; Poznanska, A. Mortality of top athletes, actors and clergy in Poland: 1924–2000 follow-up study of the long term effect of physical activity. Eur. J. Epidemiol. 2008, 23, 335–340. [Google Scholar] [CrossRef]
  71. Lee, I.M.; Skerrett, P.J. Physical activity and all-cause mortality: What is the dose-response relation? Med. Sci. Sports Exerc. 2001, 33, S459–S471; discussion S493–S494. [Google Scholar]
  72. Wesslen, L.; Pahlson, C.; Lindquist, O.; Hjelm, E.; Gnarpe, J.; Larsson, E.; Baandrup, U.; Eriksson, L.; Fohlman, J.; Engstrand, L.; et al. An increase in sudden unexpected cardiac deaths among young Swedish orienteers during 1979–1992. Eur. Heart J. 1996, 17, 902–910. [Google Scholar] [CrossRef]
  73. Leischik, R.; Dworrak, B.; Littwitz, H.; Gulker, H. Prognostic significance of exercise stress echocardiography in 3329 outpatients (5-year longitudinal study). Int. J. Cardiol. 2007, 119, 297–305. [Google Scholar] [CrossRef]
  74. La Gerche, A.; Baggish, A.L.; Knuuti, J.; Prior, D.L.; Sharma, S.; Heidbuchel, H.; Thompson, P.D. Cardiac imaging and stress testing asymptomatic athletes to identify those at risk of sudden cardiac death. JACC Cardiovasc. Imaging 2013, 6, 993–1007. [Google Scholar] [CrossRef]
  75. Warburton, D.E.; Nicol, C.W.; Bredin, S.S. Health benefits of physical activity: The evidence. CMAJ 2006, 174, 801–809. [Google Scholar] [CrossRef]

Share and Cite

MDPI and ACS Style

Leischik, R.; Spelsberg, N. Endurance Sport and “Cardiac Injury”: A Prospective Study of Recreational Ironman Athletes. Int. J. Environ. Res. Public Health 2014, 11, 9082-9100. https://doi.org/10.3390/ijerph110909082

AMA Style

Leischik R, Spelsberg N. Endurance Sport and “Cardiac Injury”: A Prospective Study of Recreational Ironman Athletes. International Journal of Environmental Research and Public Health. 2014; 11(9):9082-9100. https://doi.org/10.3390/ijerph110909082

Chicago/Turabian Style

Leischik, Roman, and Norman Spelsberg. 2014. "Endurance Sport and “Cardiac Injury”: A Prospective Study of Recreational Ironman Athletes" International Journal of Environmental Research and Public Health 11, no. 9: 9082-9100. https://doi.org/10.3390/ijerph110909082

APA Style

Leischik, R., & Spelsberg, N. (2014). Endurance Sport and “Cardiac Injury”: A Prospective Study of Recreational Ironman Athletes. International Journal of Environmental Research and Public Health, 11(9), 9082-9100. https://doi.org/10.3390/ijerph110909082

Article Metrics

Back to TopTop