Anabolic steroid-induced echocardiographic characteristics of professional football players?
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Biomedical subjects
Publications and source records attributed to Wilfried Kindermann.
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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 micromol/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) micromol/l; 9.8 (7.4-11.1) micromol/l; 10.2 (6.6-13.2) micromol/l; 9.1 (6.9-13.5) micromol/l, respectively. At 15 min and 3 h post-race, Hcy was 11.9 (8.4-16.4) micromol/l; 16.1 (12.7-20.4) micromol/l; 9.5 (7.8-15.9) micromol/l; 8.8 (7.1-11.2) micromol/l, respectively, and 11.5 (8.9-15.7) micromol/l; 14.9 (11.5-20.0) micromol/l; 10.0 (8.1-11.8) micromol/l; 9.4 (7.4-12.1) micromol/l, respectively. The change in Hcy correlated negatively with the running time. Twenty-three athletes had pre-race Hcy levels > 12 micromol/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 and intensity of exercise. Furthermore, about 25% of recreational endurance athletes exhibited hyperhomocysteinemia in association with low vitamin B12 and folate levels.
BACKGROUND: Since homocysteine (Hcy) is a risk factor for cardiovascular and other diseases, it is important to know how exercise can modify it. Previous studies have suggested that endurance training influences Hcy. However, little is known about the effect of training intensity on Hcy. MATERIALS AND METHODS: We investigated Hcy, vitamin B12, vitamin B6, folate and methylmalonic acid (MMA) before and after 3 weeks of volume-oriented training (VOL) (30 km/week) and high-intensity interval training (HIT) (20 km/week) in 20 young swimmers (16 +/- 2 years). Afterward, the athletes completed 5 days of recovery training. RESULTS: The training induced a Hcy increase in HIT and VOL (6.47 +/- 0.95 micromol/l vs. 7.44 +/- 1.17 micromol/l and 7.33 +/- 1.92 micromol/l vs. 8.28 +/- 1.42 micromol/l, respectively) that persisted during the recovery period (8.02 +/- 1.69 micromol/l and 8.00 +/- 1.81 micromol/l, respectively). Vitamin B12 was unchanged after the training (539 +/- 166 ng/l vs. 556 +/- 192 ng/l and 480 +/- 144 ng/l vs. 491 +/- 124 ng/l, respectively) but decreased during the recovery period (459 +/- 134 ng/l and 451 +/- 116 ng/l, respectively). Folate showed an increase during the training (9.07 +/- 2.01 microg/l vs. 11.71 +/- 4.08 microg/l and 10.34 +/- 2.32 microg/l vs. 11.13 +/- 4.64 microg/l, respectively), which was reversible by the end of the recovery training (8.57 +/- 1.98 microg/l and 9.60 +/- 2.38 microg/l, respectively). Vitamin B6 and MMA did not change. For none of the measured parameters were there significant differences between HIT and VOL. CONCLUSION: Three weeks of strenuous swimming caused a prolonged Hcy increase, which was accompanied by changes in vitamin B12 and folate. The magnitude of these effects was not influenced by the training intensity.
BACKGROUND: In patients with chronic heart failure, exercise limitation cannot be exclusively attributed to cardiac dysfunction. During progression of the disease, peripheral factors have a growing impact on functional capacity. Chronic underperfusion of skeletal muscles, inactivity and a harmful effect of neuroendocrine stimulation lead to a myopathy syndrome characterized by atrophy, a shift in muscle fiber type and a loss of capillaries and mitochondria, which cause reduced muscle strength and aerobic capacity. Unlike left ventricular systolic function, which is a poor predictor of exercise tolerance in patients with chronic heart failure, parameters characterizing the myopathy syndrome correlate well with functional capacity. In the last 20 years, numerous studies have demonstrated that chronic heart failure patients in NYHA classes II and III benefit from physical training without deterioration of their cardiac function. EFFECTS OF EXERCISE TRAINING: Physical activity primarily improves muscle function and increases maximal as well as submaximal exercise capacity. Advantageous effects have also been observed with regard to neuroendocrine stimulation. The effect on central hemodynamics is much smaller and indirectly mediated by a trend towards decreased peripheral resistance. Left ventricular diameters, ejection fraction and filling pressures do not show significant changes. The gain in exercise capacity is usually accompanied by an improvement in symptom status and quality of life. Recent studies indicate that prognosis may also be improved by exercise training. CONVERSION INTO CLINICAL PRACTICE: Although continuous exercise training (mainly by use of cycle ergometry) has been investigated most thoroughly, there is an increasing number of studies reporting beneficial effects of interval and resistance training. Before starting a standardized training program, functional limitation and training intensity should be determined by an appropriate stress test. During the first training sessions, patients should always be supervised by a physician. In order to increase efficiency and feasibility of the exercise therapy, home-based training should be engaged as soon as a stable condition during repeated training sessions has been proven.
OBJECTIVES: Athlete's heart represents a structural and functional adaptation to regular endurance exercise. BACKGROUND: While left ventricular (LV) hypertrophy of the athlete's 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 athlete's 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 athlete's heart is a balanced enlarged heart.
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The multitude of publications regarding overtraining syndrome (OTS or 'staleness') or the short-term 'over-reaching' and the severity of consequences for the athlete are in sharp contrast with the limited availability of valid diagnostic tools. Ergometric tests may reveal a decrement in sport-specific performance if they are maximal tests until exhaustion. Overtrained athletes usually present an impaired anaerobic lactacid performance and a reduced time-to-exhaustion in standardised high-intensity endurance exercise accompanied by a small decrease in the maximum heart rate. Lactate levels are also slightly lowered during submaximal performance and this results in a slightly increased anaerobic threshold. A reduced respiratory exchange ratio during exercise still deserves further investigation. A deterioration of the mood state and typical subjective complaints ('heavy legs', sleep disorders) represent sensitive markers, however, they may be manipulated. Although measurements at rest of selected blood markers such as urea, uric acid, ammonia, enzymes (creatine kinase activity) or hormones including the ratio between (free) serum testosterone and cortisol, may serve to reveal circumstances which, for the long term, impair the exercise performance, they are not useful in the diagnosis of established OTS. The nocturnal urinary catecholamine excretion and the decrease in the maximum exercise-induced rise in pituitary hormones, especially adrenocorticotropic hormone and growth hormone, and, to a lesser degree, in cortisol and free plasma catecholamines, often provide interesting diagnostic information, but hormone measurements are less suitable in practical application. From a critical review of the existing overtraining research it must be concluded that there has been little improvement in recent years in the tools available for the diagnosis of OTS.