Right and Left Ventricular Function and Mass in Male Elite Master Athletes: A Controlled Contrast-Enhanced Cardiovascular Magnetic Resonance Study.

BACKGROUND: It is under debate whether the cumulative effects of intensive endurance exercise induce chronic cardiac damage, mainly involving the right heart. The aim of this study was to examine the cardiac structure and function in long-term elite master endurance athletes with special focus on the right ventricle by contrast-enhanced cardiovascular magnetic resonance. METHODS AND RESULTS: Thirty-three healthy white competitive elite male master endurance athletes (age range, 30-60 years) with a training history of 29±8 years, and 33 white control subjects pair-matched for age, height, and weight underwent cardiopulmonary exercise testing, echocardiography including tissue-Doppler imaging and speckle tracking, and cardiovascular magnetic resonance. Indexed left ventricular mass and right ventricular mass (left ventricular mass/body surface area, 96±13 and 62±10 g/m(2); P<0.001; right ventricular mass/body surface area, 36±7 and 24±5 g/m(2); P<0.001) and indexed left ventricular end-diastolic volume and right ventricular end-diastolic volume (left ventricular end-diastolic volume/body surface area, 104±13 and 69±18 mL/m(2); P<0.001; right ventricular end-diastolic volume/body surface area, 110±22 and 66±16 mL/m(2); P<0.001) were significantly increased in athletes in comparison with control subjects. Right ventricular ejection fraction did not differ between athletes and control subjects (52±8 and 54±6%; P=0.26). Pathological late enhancement was detected in 1 athlete. No correlations were found for left ventricular and right ventricular volumes and ejection fraction with N-terminal pro-brain natriuretic peptide, and high-sensitive troponin was negative in all subjects. CONCLUSIONS: Based on our results, chronic right ventricular damage in elite endurance master athletes with lifelong high training volumes seems to be unlikely. Thus, the hypothesis of an exercise-induced arrhythmogenic right ventricular cardiomyopathy has to be questioned.

Validity of Lactate Thresholds in Inline Speed Skating.

Lactate thresholds are commonly used as estimates of the highest workload where lactate production and elimination are in equilibrium (maximum lactate steady state [MLSS]). However, because of the high static load on propulsive muscles, lactate kinetics in inline speed skating may differ significantly from other endurance exercise modes. Therefore, the discipline-specific validity of lactate thresholds has to be verified. Sixteen competitive inline-speed skaters (age: 30 ± 10 years; training per week: 10 ± 4 hours) completed an exhaustive stepwise incremental exercise test (start 24 km·h, step duration 3 minutes, increment 2 km·h) to determine individual anaerobic threshold (IAT) and the workload corresponding to a blood lactate concentration of 4 mmol·L (LT4) and 2-5 continuous load tests of (up to) 30 minutes to determine MLSS. The IAT and LT4 correlated significantly with MLSS, and the mean differences were almost negligible (MLSS 29.5 ± 2.5 km·h; IAT 29.2 ± 2.0 km·h; LT4 29.6 ± 2.3 km·h; p > 0.1 for all differences). However, the variability of differences was considerable resulting in 95% limits of agreement in the upper range of values known from other endurance disciplines (2.6 km·h [8.8%] for IAT and 3.1 km·h [10.3%] for LT4). Consequently, IAT and LT4 may be considered as valid estimates of the MLSS in inline speed skating, but verification by means of a constant load test should be considered in cases of doubt or when optimal accuracy is needed (e.g., in elite athletes or scientific studies).

Competitive sports and the heart: benefit or risk?

BACKGROUND: Controversy surrounds the cardiac effects of competitive sports and the athlete's heart. In this review, we present and discuss the main cardiological findings in competitive athletes. METHOD: Selective review of pertinent literature retrieved by a search with the keywords "athlete's heart," "ECG," "echocardiography," "endurance exercise," "longevity," and others. RESULTS: Regular exercise leads to functional and structural adaptations that improve cardiac function. Athlete's heart, which develops rarely, is a typical finding in endurance athletes. This condition is characterized by physiological, harmonically eccentric hypertrophy of all cardiac chambers. The athlete's ECG can be used to distinguish physiological, training-related changes from pathological training-unrelated changes. The athlete's heart function is normal at rest and increases appropriately during exercise. The cardiac markers troponin and B-type natriuretic peptide are within the normal range in healthy athletes at rest, but can temporarily be mildly elevated after exhausting endurance-exercise, without evidence of myocardial damage. The epidemiological data suggest that participation in competitive sports increases life expectancy. CONCLUSION: Competitive exercise does not induce cardiac damage in individuals with healthy hearts, but does induce physiological functional and structural cardiac adaptations which have positive effects on life expectancy.

Intensity control in swim training by means of the individual anaerobic threshold.

This study aimed at evaluating the homogeneity of physiological responses during swim training bouts with intensities prescribed by reference to the individual anaerobic threshold (IAT). Eighteen competitive front crawl swimmers (female 5, male 13, 10 long-distance, and 8 short-distance swimmers [LDSs, SDSs], age: 17 ± 1.7 years, training history: 7.0 ± 2.8 years, training volume per week: 35 ± 5.7 km) performed an incremental swimming test to determine the IAT. Within a maximum of 3 weeks, 4 training programs were conducted: 20 × 100-m low-intensity endurance training (EN(low), 97% IAT), 5 × 400-m high-intensity endurance training (EN(high), 101% IAT), 5 × 200 m (IT1, 105% IAT), and 10 × 100 m (IT2, 108% IAT) intensive interval training. Blood lactate concentrations (bLa) were determined during each training session. The results are given as median (25th and 75th percentiles). During EN(low) and EN(high), the mean bLas were 1.8 mmol·L(-1) (1.3/3.0 mmol·L(-1)) and 4.4 mmol·L(-1) (3.9/6.4 mmol·L(-1)). The bLas were higher during both IT programs: IT1, 6.3 mmol·L(-1) (5.6/7.2 mmol·L(-1)); IT2, 5.8 mmol·L(-1) (5.0/6.5 mmol·L(-1)). The bLas of most individuals were close to the median values (±2.4 mmol·L(-1)). However, in each of the training programs, some subjects showed bLa values that were clearly above (3-7 mmol·L(-1) higher). In particular, SDSs reached higher bLas at the same intensity compared with LDSs. It is concluded that intensity prescriptions by means of IAT seem to elicit an expected metabolic response in approximately 85% of swim training sessions. The observed average bLa is in the range of those recommended in the scientific literature.

Polymorphisms in the IGF1 signalling pathway including the myostatin gene are associated with left ventricular mass in male athletes.

BACKGROUND: Athlete's heart as an adaptation to long-time and intensive endurance training can vary considerably between individuals. Genetic polymorphisms in the cardiological relevant insulin-like growth factor 1 (IGF1) signalling pathway seem to have an essential influence on the extent of physiological hypertrophy. OBJECTIVE: Analysis of polymorphisms in the genes of IGF1, IGF1 receptor (IGF1R) and the negative regulator of the cardiac IGF1 signalling pathway, myostatin (MSTN), and their relation to left ventricular mass (LVM) of endurance athletes. METHODS: In 110 elite endurance athletes or athletes with a high amount of endurance training (75 males and 35 females) and 27 male controls, which were examined by echocardiographic imaging methods and ergometric exercise-testing, the genotypes of a cytosine-adenine repeat polymorphism in the promoter region of the IGF1 gene and a G/A substitution at position 3174 in the IGF1R gene were determined. Additionally, a mutation screen of the MSTN gene was performed. RESULTS: The polymorphisms in the IGF1 and the IGF1R gene showed a significant relation to the LVM for male (IGF1: p=0.003; IGF1R: p=0.01), but not for female athletes. The same applies to a previously unnoticed polymorphism in the 1 intron of the MSTN gene, whose deletion allele (AAA→AA) appears to increase the myostatic effect (p=0.015). Moreover, combinations of the polymorphisms showed significant synergistic effects on the LVM of the male athletes. CONCLUSIONS: The authors' results argue for the importance of polymorphisms in the IGF1 signalling pathway in combination with MSTN on the variant degree of physiological hypertrophy of male athletes.

Ergogenic effects of inhaled beta2-agonists in non-asthmatic athletes.

The potential ergogenic effects of asthma medication in athletes have been controversially discussed for decades. The prevalence of asthma is higher in elite athletes than in the general population. The highest risk for developing asthmatic symptoms is found in endurance athletes and swimmers. In addition, asthma seems to be more common in winter-sport athletes. Asthmatic athletes commonly use inhaled beta2-agonists to prevent and treat asthmatic symptoms. However, beta2-agonists are prohibited according to the "Prohibited List of the World Anti-Doping Agency" (WADA). Until the end of 2009 an exception was only allowed for the substances formoterol, salbutamol, salmeterol, and terbutaline by inhalation, as long as a so-called therapeutic use exemption has been applied for and was granted by the relevant anti-doping authorities. From 2010 salbutamol and salmeterol are allowed by inhalation requiring a so called declaration of use.

Benefits and limitations of cardiovascular pre-competition screening in international football.

BACKGROUND: Competitive sport can serve as a trigger for sudden cardiac death (SCD). The majority of athletes who die suddenly have previously unsuspected structural heart disease. Medical evaluation before competition offers the potential to identify cardiovascular abnormalities in asymptomatic athletes. Consensus on the ideal screening programme has not been reached. So, a cardiovascular pre-competition screening of elite football players was developed and implemented prior to the 2006 FIFA World Cup Germany to detect SCD risk factors. METHODS: Medical history, physical examination, 12-lead resting- and exercise electrocardiogram (ECG) and echocardiography results of the players were recorded on a standardised form by the team physicians and submitted after the final match for retrospective evaluation by two blinded independent cardiologic reviewers. RESULTS: Response rate was 82% (605 of 736 players). Completeness and quality of the recordings and examination methods differed amongst teams. In 25 players (4.8%), the examining physicians evaluated the resting ECG as pathological. Suspicious echocardiographic findings demanding further investigations to rule out serious cardiovascular disease existed in 1% of the players. CONCLUSION: Cardiovascular pre-competition screening proved feasible in international elite football teams, but turned out to be vital to ensure high quality of data, particularly with regard to stress testing and echocardiography. The screening concept was revised mainly to improve completeness and quality of data acquisition. Resting ECG and echocardiography were retained, but it is questionable if exercise testing should be included in this context.

Exercise at given percentages of VO2max: heterogeneous metabolic responses between individuals.

PURPOSE: Given percentages of VO(2max) are widely used for training and study purposes although they might not result in homogeneous metabolic strain. Therefore, the homogeneity of metabolic responses to prolonged exercise at fixed percentages of VO(2max) should be investigated. PROCEDURES: Twenty-one healthy male subjects (29+/-5 years, 77+/-8 kg, VO(2max): 59.9+/-11.8 ml min(-1)kg(-1)) performed two incremental tests to exhaustion on a cycle ergometer to determine VO(2max). Subsequently, two 60 min tests at 60 and 75% VO(2max) were conducted in randomised order. VO(2) was kept constant by adjusting the work rate. Blood lactate (La) responses as primary outcome variable to quantify metabolic strain were assessed. FINDINGS: Mean La was 2.1+/-1.1 mmol l(-1) (min-max: 0.7-5.6 mmol l(-1)) during the 60% VO(2max) test and 4.6+/-1.9 mmol l(-1) (min-max: 2.2-8.0 mmol l(-1)) during the 75% VO(2max) test. The coefficients of variation of La amounted for 52.4 and 41.3% during the 60 and 75% VO(2max) test, respectively. La responses did not differ significantly between three subgroups of the subjects (N=7 with VO(2max)<55 ml min(-1)kg(-1), N=7 with VO(2max) 55-65 ml min(-1)kg(-1), and N=7 with VO(2 max)>65 ml min(-1)kg(-1); P>or=0.08). CONCLUSION: Altogether, prolonged exercise at given percentages of VO(2max) leads to inhomogeneous metabolic strain as indicated by the large variability of La responses. This holds true even in subgroups of similar aerobic capacity. Thus, intensity prescription for endurance training and study purposes should not be solely based upon percentages of VO(2max) when a comparable metabolic strain is intended.

Physical exercise prevents cellular senescence in circulating leukocytes and in the vessel wall.

BACKGROUND: The underlying molecular mechanisms of the vasculoprotective effects of physical exercise are incompletely understood. Telomere erosion is a central component of aging, and telomere-associated proteins regulate cellular senescence and survival. This study examines the effects of exercising on vascular telomere biology and endothelial apoptosis in mice and the effects of long-term endurance training on telomere biology in humans. METHODS AND RESULTS: C57/Bl6 mice were randomized to voluntary running or no running wheel conditions for 3 weeks. Exercise upregulated telomerase activity in the thoracic aorta and in circulating mononuclear cells compared with sedentary controls, increased vascular expression of telomere repeat-binding factor 2 and Ku70, and reduced the expression of vascular apoptosis regulators such as cell-cycle-checkpoint kinase 2, p16, and p53. Mice preconditioned by voluntary running exhibited a marked reduction in lipopolysaccharide-induced aortic endothelial apoptosis. Transgenic mouse studies showed that endothelial nitric oxide synthase and telomerase reverse transcriptase synergize to confer endothelial stress resistance after physical activity. To test the significance of these data in humans, telomere biology in circulating leukocytes of young and middle-aged track and field athletes was analyzed. Peripheral blood leukocytes isolated from endurance athletes showed increased telomerase activity, expression of telomere-stabilizing proteins, and downregulation of cell-cycle inhibitors compared with untrained individuals. Long-term endurance training was associated with reduced leukocyte telomere erosion compared with untrained controls. CONCLUSIONS: Physical activity regulates telomere-stabilizing proteins in mice and in humans and thereby protects from stress-induced vascular apoptosis.