Jürgen Scharhag

Athlete's Heart Right and Left Ventricular Mass and Function in Male Endurance Athletes and Untrained Individuals Determined by Magnetic Resonance Imaging

OBJECTIVES Athletes heart represents a structural and functional adaptation to regular endurance exercise. BACKGROUND While left ventricular (LV) hypertrophy of the athletes heart has been examined in many studies, the extent of right ventricular (RV) hypertrophy is still uncertain because of its complex shape and trabecular structure. To examine RV hypertrophy, we used magnetic resonance imaging (MRI) and hypothesized that athletes heart is characterized by similar LV and RV hypertrophy. METHODS The LV and RV mass, volume, and function in 21 male endurance athletes (A) (27 +/- 4 years; 70 +/- 8 kg; 178 +/- 7 cm; maximal oxygen uptake [VO(2)max]: 68 +/- 5 ml/min per kg) and 21 pair-matched untrained control subjects (C) (26 +/- 3 years; 71 +/- 9 kg; 178 +/- 6 cm; VO(2)max: 42 +/- 6 ml/min per kg) were analyzed by MRI (Magnetom Vision 1.5T, Siemens, Erlangen, Germany). RESULTS Left ventricular masses: (A: 200 +/- 20 g; C: 148 +/- 17 g) and RV masses (A: 77 +/- 10 g; C: 56 +/- 8 g) differed significantly between the groups (p < 0.001). The LV and RV end-diastolic volumes (EDV) (LV-EDV 167 +/- 28 ml [A]; 125 +/- 16 ml [C]; RV-EDV 160 +/- 26 ml [A]; 128 +/- 10 ml [C]), and stroke volumes (SV) (LV-SV: 99 +/- 18 ml [A], 74 +/- 11 ml [C]; RV-SV: 102 +/- 18 ml [A], 79 +/- 8 ml [C]) were significantly different between the athletes and control subjects (p < 0.001), whereas ejection fractions (EF) (LV-EF: 59 +/- 3% [A]; 59 +/- 6% [C]; RV-EF: 63 +/- 3% [A], 62 +/- 3% [C]) and LV-to-RV ratios were similar for both groups (LV-to-RV mass: 2.6 +/- 0.2 [A], 2.6 +/- 0.3 [C]; LV-to-RV EDV: 1.05 +/- 0.14 [A], 0.99 +/- 0.14 [C]; LV-to-RV SV: 0.98 +/- 0.17 [A], 0.95 +/- 0.17 [C]; LV-to-RV EF: 0.93 +/- 0.07 [A], 0.96 +/- 0.10 [C]). CONCLUSIONS Regular and extensive endurance training results in similar changes in LV and RV mass, volume, and function in endurance athletes. This leads to the conclusion that the athletes heart is a balanced enlarged heart.

Exercise-Induced Cardiac Troponin Elevation Evidence, Mechanisms, and Implications

Regular physical exercise is recommended for the primary prevention of cardiovascular disease. Although the high prevalence of physical inactivity remains a formidable public health issue, participation in exercise programs and recreational sporting events, such as marathons and triathlons, is on the rise. Although regular exercise training reduces cardiovascular disease risk, recent studies have documented elevations in cardiac troponin (cTn) consistent with cardiac damage after bouts of exercise in apparently healthy individuals. At present, the prevalence, mechanism(s), and clinical significance of exercise-induced cTn release remains incompletely understood. This paper will review the biochemistry, prevalence, potential mechanisms, and management of patients with exercise-induced cTn elevations.

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.

State-of-the-Art PaperExercise-Induced Cardiac Troponin Elevation: Evidence, Mechanisms, and Implications

Regular physical exercise is recommended for the primary prevention of cardiovascular disease. Although the high prevalence of physical inactivity remains a formidable public health issue, participation in exercise programs and recreational sporting events, such as marathons and triathlons, is on the rise. Although regular exercise training reduces cardiovascular disease risk, recent studies have documented elevations in cardiac troponin (cTn) consistent with cardiac damage after bouts of exercise in apparently healthy individuals. At present, the prevalence, mechanism(s), and clinical significance of exercise-induced cTn release remains incompletely understood. This paper will review the biochemistry, prevalence, potential mechanisms, and management of patients with exercise-induced cTn elevations.

Running exercise of different duration and intensity: effect on endothelial progenitor cells in healthy subjects

Background Increased numbers of circulating endothelial progenitor cells (EPC) are associated with improved vascular function. Exercise is a central component of the primary prevention of vascular diseases. The effect of physical activity on circulating EPC in healthy individuals is not known. Design A prospective crossover study. Methods and results In order to study a potential link between the extent of physical exercise and progenitor cells in humans, EPC were quantified by flow cytometry and cell culture in 25 healthy volunteers undergoing three protocols of running exercise. Intensive running, defined as 30 min at 100% of the velocity of the individual anaerobic threshold (IAT; ∼82% maximal oxygen consumption; VO2max), as well as moderate running with 30 min at 80% of the velocity of the IAT (∼68% VO2max), increased circulating EPC numbers to 235±93% and 263±106% of control levels, respectively. However, moderate short-term running for 10 min did not upregulate EPC counts. The maximum increase in circulating EPC numbers was observed 10–30 min after intensive running. Exercise increased EPC migratory and colony-forming capacity. Conclusions Intensive and moderate exercising for 30 min, but not for 10 min, increased circulating levels of EPC, which may represent an important beneficial outcome of physical exercise. The data support the notion that increased numbers of EPC correlate with cardiovascular health and suggest EPC quantification as a novel surrogate parameter of the vascular effects of exercising.

Exercise-associated increases in cardiac biomarkers.

At present, the risk of myocardial damage by endurance exercise is under debate because of reports on exercise-associated increases in cardiac biomarkers troponin and B-type natriuretic peptide (BNP); these markers are typically elevated in patients with acute myocardial infarction and chronic heart failure, respectively. Exercise-associated elevations of cardiac biomarkers can be present in elite and in recreational athletes, especially after prolonged and strenuous endurance exercise bouts (e.g., marathon and ultratriathlon). However, in contrast to cardiac patients, it is still unclear if the exercise-associated appearance or increase in cardiac biomarkers in obviously healthy athletes represents clinically significant cardiac insult or is indeed part of the physiological response to endurance exercise. In addition, elevations in cardiac biomarkers in athletes after exercise may generate difficulties for clinicians in terms of differential diagnosis and may result in inappropriate consequences. Therefore, the aim of this article is to provide an overview of exercise-associated alterations of the cardiac biomarkers troponin T and I, ischemia-modified albumin, BNP, and its cleaved inactive fragment N-terminal pro BNP for the athlete, coach, scientist, and clinician.

Post-Race Kinetics of Cardiac Troponin T and I and N-Terminal Pro-Brain Natriuretic Peptide in Marathon Runners

Annually there are cases of sudden cardiac death during and after marathon races (1)(2)(3), which has caused athletes and physicians to frequently ask whether marathon running damages the heart. Modern laboratory analyses, such as tests for cardiac troponin T and I (cTnT and cTnI) and N-terminal pro-brain natriuretic peptide (NT-proBNP), provide additional information about cardiac cell damage and wall stress with high sensitivity and specificity (4)(5)(6)(7). Previous studies have investigated cTnT and cTnI in runners, cyclists, and triathletes (8)(9)(10)(11)(12)(13)(14)(15)(16), but the results are controversial, mainly because the assays were first- (cTnI) or second-generation (cTnT) troponin assays and the cutoff points were inconsistent. In the present study we investigated cTnT and cTnI during a marathon race with third- (cTnT) and second-generation (cTnI) assays, as well as NT-proBNP. We hypothesized that marathon running may change cardiac troponin concentrations and that increased troponin concentrations are possibly associated with an increased mechanical load on the myocardium, exemplified by NT-proBNP. We investigated 46 randomly selected participants (40 males and 6 females) of the Mainz Marathon 2002 (Germany) with a mean (SD) age of 40 (7) years, a mean height of 178 (7) cm, a mean weight of 73 (9) kg, and a mean body mass index (BMI) of 23.1 (1.9). The mean running time was 239 (34) min. To allow coverage of the whole spectrum of participating runners, there were no particular exclusion criteria. All participants filled in a questionnaire to register health status, cardiovascular risk factors, and training volume. The analysis of these questionnaires revealed that runners had performed regular endurance training over the past 7 (6) years. Cardiovascular risk factors and diseases were distributed as follows: acute …

The Intensity and Effects of Strength Training in the Elderly

BACKGROUND The elderly need strength training more and more as they grow older to stay mobile for their everyday activities. The goal of training is to reduce the loss of muscle mass and the resulting loss of motor function. The dose-response relationship of training intensity to training effect has not yet been fully elucidated. METHODS PubMed was selectively searched for articles that appeared in the past 5 years about the effects and dose-response relationship of strength training in the elderly. RESULTS Strength training in the elderly (>60 years) increases muscle strength by increasing muscle mass, and by improving the recruitment of motor units, and increasing their firing rate. Muscle mass can be increased through training at an intensity corresponding to 60% to 85% of the individual maximum voluntary strength. Improving the rate of force development requires training at a higher intensity (above 85%), in the elderly just as in younger persons. It is now recommended that healthy old people should train 3 or 4 times weekly for the best results; persons with poor performance at the outset can achieve improvement even with less frequent training. Side effects are rare. CONCLUSION Progressive strength training in the elderly is efficient, even with higher intensities, to reduce sarcopenia, and to retain motor function.

Reproducibility and clinical significance of exercise-induced increases in cardiac troponins and N-terminal pro brain natriuretic peptide in endurance athletes

Background Cardiac troponins I and T and brain natriuretic peptide are the accepted standards to serologically identify myocardial necrosis and elevated wall stress. In addition, they allow risk stratification in cardiovascular patients. The clinical significance of increases in cardiac markers after strenuous endurance exercise in obviously healthy athletes is unclear. Design We therefore examined the reproducibility and clinical significance of exercise-induced increases in cardiac troponins I and T and N-terminal pro brain natriuretic peptide after two standardized endurance exercise trials in healthy endurance athletes with prior competition-induced elevations of cardiac troponins (I, 0.08–1.93 μg/l; T, 0.01–0.56 μg/l). Methods Twenty male athletes (36 ± 7 years; V O2max : 60 ± 5 ml/min per kg) completed a 1-h and a 3-h exercise study (exercise intensities 100 and 75%, respectively, of the individual anaerobic threshold) on two different days in randomized order to determine cardiac markers before, 30 min and 3h after exercise. In addition to pre- and post-exercise echocardiography including tissue Doppler imaging, delayed enhancement magnetic-resonance-imaging was performed after a 3-h exercise study to detect myocardial necrosis. Results A marginal increase in cardiac troponin I was documented after both exercise trials (from 0.02 to 0.03 μg/l; P>0.001). Cardiac troponin T remained without significant changes. N-terminal pro brain natriuretic peptide increased by 9 and 30 ng/l after 1-h and 3-h exercise studies, respectively (P>0.001). In contrast to cardiac troponins, increases in N-terminal pro brain natriuretic peptide after competition correlated with those after 1-h exercise study (ρ = 0.88) and 3-h exercise-study (ρ = 0.82). No pathologies were demonstrated by echocardiography or delayed-enhancement magnetic resonance imaging. Conclusions Due to the missing reproducibilty and evidence of myocardial damage, exercise-induced increases in cardiac troponins may represent a physiologic reaction under special conditions and seem to be without pathological significance in healthy athletes. Eur J Cardiovasc Prev Rehabil 13:388–397

Homocysteine Increases during Endurance Exercise

Abstract Hyperhomocysteinemia is a risk factor for cardiovascular and other diseases. Recently many endogenous and exogenous modulators of homocysteine (Hcy) have become known, e.g., B-vitamins. However, little is known about the effect of exercise on Hcy. The purpose of this study was to investigate the effect of three different types of acute endurance exercise on serum Hcy. We measured Hcy in 100 recreational athletes (87 males, 13 females) who participated in a marathon race (n = 46), a 100 km run (100 km; n = 12) or a 120 km mountain bike race (n = 42). Blood samples were taken before, 15 min and 3 h after the race. In athletes with pre-race Hcy >12 μmol/l we also determined folate and vitamin B12. Marathon running induced a Hcy increase of 64%, while mountain biking and 100 km running had no significant effect on Hcy. Pre-race Hcy (25th–75th percentile) overall; marathon race; 100 km; mountain bike race was 9.7 (7.1–11.5) μmol/l; 9.8 (7.4–11.1) μmol/l; 10.2 (6.6–13.2) μmol/l; 9.1 (6.9–13.5) μmol/l, respectively. At 15 min and 3 h post-race, Hcy was 11.9 (8.4–16.4) μmol/l; 16.1 (12.7–20.4) μmol/l; 9.5 (7.8–15.9) μmol/l; 8.8 (7.1–11.2) μmol/l, respectively, and 11.5 (8.9–15.7) μmol/l; 14.9 (11.5–20.0) μmol/l; 10.0 (8.1–11.8) μmol/l; 9.4 (7.4–12.1) μmol/l, respectively. The change in Hcy correlated negatively with the running time. Twenty-three athletes had pre-race Hcy levels >12 μmol/l, which were associated with relatively low folate (14.3 (11.6–18.9) nmol/l) and vitamin B12 levels (231 (183–261) pmol/l). Endurance exercise may induce a considerable Hcy increase, which varies between different disciplines and is most probably determined by the duration