The electrocardiographic early repolarization (ER) pattern is associated with idiopathic ventricular fibrillation and increased long-term cardiovascular mortality. Whether structural cardiac aberrations influence the phenotype is unclear. Since ER is particularly common in athletes, we evaluated its prevalence and investigated predisposing echocardiographic characteristics and cardiopulmonary exercise capacity in a cohort of elite athletes.

A total of 623 elite athletes (age 21 ± 5 years) were examined during annual preparticipation screening from 2006 until 2012 including electrocardiography, echocardiography, and exercise testing. ECGs were analyzed with focus on ER. All athletes participated in a clinical follow-up.

The prevalence of ER was 17% (108/623). ER-positive athletes were predominantly male (71%, 77/108), showed a lower heart rate (57.1 ± 9.3 bpm versus 60.0 ± 11.2 bpm; p = 0.015) and a higher lean body mass compared to ER-negative participants (88.1% ± 5.6% versus 86.5% ± 6.3%; p = 0.015). Echocardiographic measurements and cardiopulmonary exercise capacity in male and female athletes with and without ER largely showed similar results. Only the notching ER subtype (n = 15) was associated with an increased left atrial diameter (OR 7.01, 95%CI 1.65-29.83; p = 0.008), a higher left ventricular mass (OR 1.02, 95%CI 1.00-1.03; p = 0.038) and larger relative heart volume (OR 1.01, 95%CI 1.00-1.01; p = 0.01). During a follow-up of 7.4 ± 1.5 years, no severe cardiovascular event occurred in the study sample.

In elite athletes presence of ER is not associated with distinct alterations in echocardiography and cardiopulmonary exercise. Athletes presenting with ER are rather male, lean with a low heart rate.

Hypertension is a complex disease that constitutes an important public health problem and demands many studies in order to understand the molecular mechanisms involving his pathophysiology. Therefore, an increasing number of studies have been conducted and new therapies are continually being discovered. In this context, exercise training has emerged as an important non-pharmacological therapy to treat hypertensive patients, minimizing the side effects of pharmacological therapies and frequently contributing to allow pharmacotherapy to be suspended. Several mechanisms have been associated with the pathogenesis of hypertension, such as hyperactivity of the sympathetic nervous system and renin-angiotensin aldosterone system, impaired endothelial nitric oxide production, increased oxygen-reactive species, vascular thickening and stiffening, cardiac hypertrophy, impaired angiogenesis, and sometimes genetic predisposition. With the advent of microRNAs (miRNAs), new insights have been added to the perspectives for the treatment of this disease, and exercise training has been shown to be able to modulate the miRNAs associated with it. Elucidation of the relationship between exercise training and miRNAs in the pathogenesis of hypertension is fundamental in order to understand how exercise modulates the cardiovascular system at genetic level. This can be promising even for the development of new drugs. This article is a review of how exercise training acts on hypertension by means of specific miRNAs in the heart, vascular system, and skeletal muscle.

Recent reports provide indirect evidence of myocardial injury and ventricular dysfunction after prolonged exercise. However, existing data is conflicting and lacks direct verification of functional myocardial alterations by CMR [cardiac MR (magnetic resonance)]. The present study sought to examine structural myocardial damage and modification of LV (left ventricular) wall motion by CMR imaging directly after a marathon. Analysis of cTnT (cardiac troponin T) and NT-proBNP (N-terminal pro-brain natriuretic peptide) serum levels, echocardiography [pulsed-wave and TD (tissue Doppler)] and CMR were performed before and after amateur marathon races in 28 healthy males aged 41 ± 5 years. CMR included LGE (late gadolinium enhancement) and myocardial tagging to assess myocardial injury and ventricular motion patterns. Echocardiography indicated alterations of diastolic filling [decrease in E/A (early transmitral diastolic filling velocity/late transmitral diastolic filling velocity) ratio and E' (tissue Doppler early transmitral diastolic filling velocity)] postmarathon. All participants had a significant increase in NT-proBNP and/or cTnT levels. However, we found no evidence of LV LGE. MR tagging demonstrated unaltered radial shortening, circumferential and longitudinal strain. Myocardial rotation analysis, however, revealed an increase of maximal torsion by 18.3% (13.1 ± 3.8 to 15.5 ± 3.6 °; P=0.002) and maximal torsion velocity by 35% (6.8 ± 1.6 to 9.2 ± 2.5 °·s-1; P<0.001). Apical rotation velocity during diastolic filling was increased by 1.23 ± 0.33 °·s-1 after marathon (P<0.001) in a multivariate analysis adjusted for heart rate, whereas peak untwist rate showed no relevant changes. Although marathon running leads to a transient increase of cardiac biomarkers, no detectable myocardial necrosis was observed as evidenced by LGE MRI (MR imaging). Endurance exercise induces an augmented systolic wringing motion of the myocardium and increased diastolic filling velocities. The stress of marathon running seems to be better described as a burden of myocardial overstimulation rather than cardiac injury.

Chronic dynamic exercise leads to regulative and structural adaptations of the heart (athlete's heart). To what extent the enlargement and physiologic hypertrophy of the heart lead to changes in the function of the valves, particularly regurgitation, is not yet clear. The aim of this study was to examine the regurgitation levels of different states of "athlete's heart."

Our study population consisted of 5124 healthy subjects (4046 male and 1078 female, 18-60 years), regularly exercising 1 to 20 h/wk. Subjects were divided into 3 groups depending on their relative heart volumes (RHVs): (1) very enlarged heart group (VEHG; male, n = 1251; female, n = 201), with RHVs of greater than 14 (male) and 13 (female) mL/kg; (2) mildly enlarged heart group (MEHG; male, n = 702; female, n = 224), with RHVs of 12 to 14 (male) and 11 to 13 (female) mL/kg; and (3) control subjects (CS; male, n = 2093; female, n = 653), with RHVs of less than 12 (male) and 11 (female) mL/kg.

According to US Food and Drug Administration criteria for valve regurgitation, it could be shown by Doppler sonography that as physiologic enlargement and hypertrophy increased significantly, the frequency and severity of aortic valve regurgitation (mean +/- SD: VEHG, 0.04 +/- 0.09; MEHG, 0.09 +/- 0.10; CS, 0.10 +/- 0.11; P < .05) and high mitral regurgitation (VEHG, 0.10 +/- 0.17; MEHG, 0.20 +/- 0.29; CS, 0.26 +/- 0.32; P < .01) decreased. On the contrary, pulmonary regurgitation (VEHG, 0.79 +/- 0.45; MEHG, 0.47 +/- 0.33; CS, 0.35 +/- 0.38; P < .01) and tricuspid valve regurgitation (VEHG, 0.42 +/- 0.29; MEHG, 0.47 +/- 0.33; CS, 0.35 +/- 0.38; P < .01) increased highly significantly with heart size.

These findings strongly support the view of athlete's heart as a physiologic adaptation of the heart, at least on the left side, not causing increased valvular regurgitation.

Improvement to maximal oxygen uptake is mainly due to myocardial adaptations brought about by physical training. As a consequence, the athlete's heart echocardiographic modifications associated with these adaptations are already well-known. We studied the relationships between maximal oxygen uptake (ml/min) and resting echocardiographic patterns in three athlete groups.

Tumbling (n=16), canoeing (n=12), cycling (n=12) and untrained (n=19) participants performed clinical examination and an echocardiogram. Trained groups performed a maximal graded exercise test on a cycle ergometer with gas exchange analysis.

Sport-specific cardiac hypertrophy was observed. No significant echocardiographic difference was noted between untrained and tumbling participants. Canoeists showed higher end-diastolic thickness of the interventricular septum (P<0.001) and left ventricle mass (P<0.05) than untrained and higher posterior wall thickness (P<0.001) and than untrained and tumbling participants. In comparison between untrained, tumbling and cycling participants, left ventricular end-diastolic diameter (P<0.001) and left ventricular mass (P<0.001) was higher in cyclists. In trained subjects studied as a global group, the main linear correlation with maximal oxygen uptake concerned left ventricular end-diastolic diameter (r=0.92; P<0.001), left ventricular mass (r=0.60; P<0.001) and to a lesser extent aortic (r=0.39; P<0.01) and left atrium (r=0.36; P<0.05) diameters and E (r=0.38; P<0.05) and A (r=-0.33; P<0.05) Doppler peak velocities. Each trained group showed specific correlations between echocardiographic parameters and absolute maximal oxygen uptake. No further correlation was noted with left ventricular end-diastolic diameter or left ventricle mass when each group was studied individually.

In athletes, maximal oxygen uptake is partly linked to some resting echocardiographic parameters. Specific relationships between maximal oxygen uptake and some echocardiographic parameters in relation to the sport practised are also observed.

Athlete's heart represents a structural and functional adaptation to regular endurance exercise.

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.

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).

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]).

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.

The mechanisms by which endurance training produces physiological hypertrophy have been thoroughly investigated but not with young athletes. The aim of our study was to investigate arterial blood pressure exercise responses in young athletes who started heavy training by the age of 11, participating in metabolically different sports (cycling, kayaking, and soccer) and to analyse the influence that arterial blood pressure at maximum exercise and VO(2) max could have on the development of cardiac mass in these subjects.

We studied a group of well trained normotensive male subjects, comprising 37 cyclists, 15 soccer players and 12 canoeists (mean age, 16+/-1 years). Evaluation included a clinical history and physical examination, M-mode and two-dimensional echocardiography, 12-lead resting electrocardiogram and a graded exercise test with direct determination of VO(2) max. Systolic and diastolic blood pressure were measured at rest and maximum exercise. Determination of the left ventricular mass index (LVMI) was performed using Devereux's formula with correction for the body surface area.

Cyclists showed values of LVMI in g m(-2) significantly higher than those of other subjects (123 vs. 92 and 113). Canoeists showed the maximal arterial blood pressure at maximum exercise in mmHg (190 vs. 172 and 170) and cyclists showed the maximal VO(2) ml kg(-1) min(-1) uptake (57.6 vs. 48.5 and 53.3). A linear correlation was found between LVMI and VO(2) max (r=0.4727, P<0.001) and this correlation was also significant with systolic blood pressure at maximum exercise (r=0.2909, P<0.01). No differences in LVMI were found when comparing those subjects who presented systolic blood pressure at maximum exercise equal or greater than 195 mmHg with those who presented less than this value.

It can be concluded that VO(2) max is the variable that better correlates with the LVMI. Athletes who reach greater systolic blood pressures at peak exercise have a tendency to develop greater LVMI. In comparison with soccer players and canoeists, cyclists are the sportsmen who develop a greater LVMI and VO(2) max.

A potential confounding factor in the interpretation of left ventricular (LV) structural and functional data in female subjects could be menstrual phase or contraceptive use upon assessment. To date no study has addressed this issue.

Seventeen eumenorrheic (EU; mean +/- SD age = 21 +/- 3 yr) and 14 combined-oral contraceptive pill-using (COC: mean +/- SD age = 21 +/- 3 yr) females volunteered to participate. The EU had stable menstrual cycles and the COC had all been using the same pill preparation for a minimum of 6 months. Echocardiographic examinations occurred during the mid-follicular phase and mid-luteal phases in the EU and during mid-consumption and mid-end of withdrawal in the COC. LV structure and function were assessed using M-mode and pulsed-wave Doppler echocardiography. Data were compared via Student t-tests and limits of agreement (LoA) were calculated.

Structure and function did not significantly differ between phases of the menstrual cycle or between consumption and withdrawal of oral contraception (P > 0.05). However, there was considerable variance in the LoA between variables. Smaller LoA were reported for those variables directly measured from echocardiograms compared with those from derived data. For example, in a measured variable such as LV internal dimension in diastole, the LoA data represented a variation of +/- 0.4 mm (+/- 1%) between phases. Conversely, data for LV mass, a derived variable, reported LoA values of +/- 15 g (10%) between phases. The LoA were consistent between EU and COC. Variation in both measured and derived variables were within, or close to, accepted limits of measurement or biological error.

It would seem that in studies assessing LV structure and function in women the influence of menstrual phase or oral contraceptive use is of minor significance.

In this study, we investigated resting left ventricular dimensions and function in trained female rowers, canoeists and cyclists. In male populations, such athletes have demonstrated the largest left ventricular wall thicknesses and cavity dimensions. Echocardiograms were analysed from 24 athletes (rowers and canoeists, n = 12; cyclists, n = 12) and 21 age-matched controls to measure left ventricular end-diastolic dimension and volume, and septal (ST) and posterior wall (PWT) thicknesses. Left ventricular mass was calculated from M-mode data. Systolic and diastolic function were calculated from M-mode and Doppler echocardiography, respectively. Height, body mass, body surface area and fat-free mass were determined anthropometrically. The athletes were well matched with the controls for all anthropometric variables except fat-free mass (rowers and canoeists 49.7+/-3.6 kg, cyclists 48.0+/-3.8 kg, controls 45.0+/-5.4 kg; P < 0.05). The left ventricular end-diastolic dimension, mass and volume, and septal and posterior wall thicknesses, were all significantly greater in the athletes than the controls (P < 0.05). These differences persisted (except for left ventricular end-diastolic dimension) even after allometric adjustment for group differences in fat-free mass. Stroke volume was larger (rowers and canoeists 102+/-13 ml, cyclists 103+/-16 ml, controls 80+/-15 ml; P < 0.05) in both groups of athletes but all other functional data were similar between groups. As in male athletes, female rowers, canoeists and cyclists displayed significantly larger left ventricular cavity dimensions and wall thicknesses than controls.

Heart dimensions, left ventricular function, and internal dimensions of limb arteries, as well as physical fitness, were examined in sedentary male subjects with paraplegia (SP, N = 20), national elite male athletes with paraplegia (PA, N = 29), and untrained able-bodied males (AB, N = 30).

All subjects underwent two-dimensional echocardiography, duplex sonography of common femoral artery and subclavian artery at rest, and an incremental wheelchair ergometer exercise test.

Heart volume in relation to body weight was not different in PA as compared with that in AB (11.5 +/- 1.6 vs 11.6 +/- 2.2 mL.kg-1; mean +/- SD), whereas SP showed significantly lower values (9.7 +/- 1.5 mL.kg-1). Left ventricular ejection fraction was similar in all subjects (59.9-60.8%). In relation to body surface area, subclavian artery cross-sectional area was significantly higher in PA compared with that in AB and SP, respectively (PA: 0.32 +/- 0.05, AB: 0.21 +/- 0.06, SP: 0.22 +/- 0.05 cm2/m2). The corresponding values for the common femoral artery were significantly lower in all subjects with paraplegia as compared with those in AB, whereas no difference was found between PA and SP (AB: 0.31 +/- 0.05, PA: 0.14 +/- 0.05, SP: 0.15 +/- 0.04 cm2/m2). Peak oxygen uptake (VO2peak) determined in the wheelchair ergometer exercise test was within the same range in PA and AB, but significantly (P < 0.05) lower in SP (PA: 34.5 +/- 4.3, AB: 31.5 +/- 4.1, SP: 23.9 +/- 3.8 mL.kg-1.min-1).

In conclusion, cardiac dimensions and VO2peak of PA were larger than in SP but do not exceed those of AB. Intensive wheelchair training was associated with larger dimensions of the subclavian arteries in PA, whereas a hypotrophy of the common femoral artery was found in SP and PA compared with that in AB.

Relationships between echocardiographic dimensions and the Heath-Carter anthropometric somatotype were considered in healthy, non-obese children (8-11 year olds, n = 143), adolescents (12 15 year olds, n = 216) and young adults (16-24 years, n = 190). Cardiac dimensions, measured by M-mode echocardiography at end-diastole, included left ventricular internal diameter (LVIDd), posterior wall thickness (PWTd), and interventricular posterior wall thickness (STd). Left ventricular mass (LVM) and left ventricular end-diastolic volume (LVEDV) were estimated. Partial correlations between cardiac dimensions and each somatotype component were calculated, controlling for age and the other two components. Only 9 out of 45 correlations in males and 7 of 45 correlations in females were significant (p < or = 0.05). LVM, LVEDV, and LVIDd were significantly related to somatotype in males, demonstrating significant positive correlations with mesomorphy (r = 0.25, 0.29 and 0.29, respectively) and ectomorphy (r = 0.22. 0.37, and 0.37, respectively), and LVEDV and LVIDd were related to endomorphy (r = 0.24 and 0.25, respectively) in 8-11 year old boys. In 8-11 year old females, endomorphy was related to STd (r = 0.41) and LVM (r = 0.34), while mesomorphy was related to PWTd (r = -0.34) and ectomorphy was related to PWTd (r = -0.36). In 12-15 year old females, mesomorphy was related to STd (r = 0.26) and in 16-24 year old females, endomorphy was related to LVIDd (r = 0.29) and LVEDV (r = 0.32). Overall, the correlations between somatotype and cardiac dimensions were low, ranging from -0.36 to +0.41, with no clear pattern in either sex. Additionally, a backward stepwise regression analysis indicated that body size was more important in predicting echocardiographic dimensions than somatotype. Thus, physique, as estimated with the Heath-Carter anthropometric somatotype, is not related to echocardiographic dimensions in children, youths and young adults.

Physical exercise has become a well-established concept in the secondary prevention of coronary artery disease. We investigated the exercise requirements of extensive highland mountain hiking (8.7 km, 470 m to 1220 m over sea level, average incline 8.5%, mean walking velocity < 3 km x h-1) in 11 regularly exercising male patients with history of MI and stable coronary artery disease (CAD; mean age +/- SD:61.0 +/- 3.9 yr) and 9 age-matched male healthy controls (CO; mean age +/- SD:61.2 +/- 5.0 yr). All subjects underwent continuous ECG monitoring; arterial blood pressure and blood lactate concentrations were measured several times during mountain hiking. Before and after exercise, cardiac dimensions and functions were assessed by two-dimensional echocardiography and Doppler echocardiography. The mean exercise levels for heart rate and blood lactate were compared with the corresponding data of a multistage upright cycle ergometry. Clinical manifestations of coronary insufficiency, left ventricular myocardial dysfunction, or cardiac arrhythmias > Lown IIIb were not observed in any case. No significant differences in left atrial and left ventricular dimensions and no changes in systolic left ventricular function compared with the preexercise values were found after the mountain hike tour. Doppler echocardiography demonstrated significant changes in diastolic left ventricular function in CAD, but not in CO. The peak exercise intensity during mountain hiking was equivalent to a workload of 100-125 W (1.25-1.5 W x kg-1 body weight) in a multistage upright cycle ergometry. Extensive highland mountain hiking may be a low risk alternative within the outpatient rehabilitation program for secondary prevention of CAD for MI patients with a cycle ergometric exercise tolerance > 1.5 W x kg-1 body weight.

Fifteen athletes were investigated 24 h before, 1 h after, and 20 h after an exhaustive exercise stress test (mean duration 68 min). Testing for cytokines was done in serum, urine, and the supernatants of whole blood cell cultures, which were stimulated with lipopolysaccharide (LPS), concanavalin A (Con A), or phythaemagglutinin (PHA). Elevated levels of interleukin 6 (IL-6) and soluble IL-2 receptor (sIL-2R) were found 1 h after the run in both serum and urine samples. TNF-alpha in serum was also increased, whereas IL-2 in urine was decreased after the exercise. All other testings in serum and urine (including IFN-gamma) gave borderline or negative results. In cell cultures, the LPS-induced release of the inflammatory cytokines TNF-alpha, IL-1, and IL-6 was suppressed 1 h after exercise. Also, the Con-A-induced and LPS-induced release of IFN-gamma, and the PHA-induced release of IL-2 were suppressed 1 h after exercise. In contrast, Con-A-induced release of IL-2 was mildly increased after the run. We conclude that exercise of the intensity and duration described here causes an activation of the immune system, which is immediately counter-regulated. Twenty hours after the exercise, most of the observed changes were back to pre-exercise levels, indicating only a short duration for this suppressive counter-regulation.

Elevated concentrations of lipoprotein(a) [Lp(a)] have been shown to be an independent risk factor for atherosclerotic disease. Physical activity and physical fitness have been shown to improve lipoprotein metabolism and reduce the risk of coronary artery disease. Studies on the influence of physical activity and physical fitness on Lp(a) levels including a large number of endurance as well as power athletes have not been performed before. Therefore, we determined parameters of physical fitness (maximal oxygen consumption), physical activity, and lipoproteins in 105 endurance athletes, 57 power athletes, and 87 sedentary young men. As expected, we found that endurance athletes with a good physical fitness had significantly higher concentrations of high-density lipoprotein cholesterol than power athletes and sedentary controls. Regarding mean Lp(a) levels (rocket immunoelectrophoresis), however, there were no significant differences between endurance athletes, power athletes, and sedentary controls. Even when including only those with Lp(a) values > 10 mg.dl-1, no differences were observed between the groups. These findings indicate that intensive training over years and good aerobic fitness improve the ratio of low-density lipoprotein to high-density lipoprotein cholesterol but have no or only minor effects on Lp(a) concentrations.

Development of the concept of "athlete's heart" is traced through early clinical and radiographic studies to modern echocardiography and magnetic resonance imaging. It is noted that the lower limits of criteria for the diagnosis of a "pathological" enlargement of the heart have frequently been revised in an upward direction, as the prevalence of large hearts has been recognised in both endurance and power sports competitors who are in good health. Belief that hypertrophic cardiomyopathy is the commonest cause of sports related death in young adults is traced to weak diagnostic criteria and frequent republication of a very small group of cases. Although the existence of a congenital myocardial dystrophy is now well established, this condition is extremely rare, and has no particular predilection for athletes. Genetically based screening tests may become available in the future, but the exclusion of young adults from sports participation on echocardiographic criteria appears costly and ineffective. For most people, the development of a large heart is not a pathological sign--rather, it is a desirable outcome that will enhance performance on the sports field, and will allow longer independence in old age.

Using a 3 x 3 Latin Square design, a possible interaction between diprafenone HCl a class IC antiarrhythmic drug with nonspecific beta-antagonist activity and propranolol HCl was investigated in nine young, healthy, caucasian, male volunteers. The volunteers randomly received 3 single-dose treatments: (A) 200 mg DHCl, (B) 80 mg PHCl, and (C) 200 mg DHCl and 80 mg PHCl. Scheduled blood samples were taken and plasma concentrations of both diprafenone and propranolol were measured by sensitive and specific assay methods. Lead II electrocardiogram intervals at rest, heart rate during erect bicycle ergometry, and echocardiographic variables at rest and shortly after exercise were recorded. The data analysis used compartment model independent methods. There was no evidence for a pharmacokinetic interaction between the two drugs. With DHCl, two of the nine subjects showed greatly increased areas under the plasma concentration-time curves and apparent disposition half-lives in the presence and absence of PHCl, indicating that metabolism of diprafenone may be subject to pharmacogenetic polymorphism. There was evidence for a pharmacodynamic interaction between DHCl and PHCl regarding the negative chronotropic effect at rest and during exercise. There was no difference in the pharmacodynamics and tolerability of the three treatments in suspected "poor" and "extensive metabolizers" of DHCl.

We examined the influence on heart rate, blood pressure, lactate, glucose, and catecholamine levels of moderate recreational swimming at a mean time of 5.2 to 9 minutes with mean speed of 0.33 to 0.49 m/s in 25 CHD patients and 8 healthy control subjects. During swimming, changes in these exercise-related parameters were observed such as were only found in seated ergometry trials at levels above 100 to 175 W. We consider these changes tolerable for patients with mild left heart damage (n = 13; ejection fraction 54 +/- 7%; exercise capacity 2.1 +/- 0.4 W/kg). They may indicate overexertion in patients with marked damage to the left heart (n = 12; ejection fraction 44 +/- 5%; exercise capacity 1.3 +/- 0.4 W/kg). Six of the 12 patients with marked left heart damage stopped swimming before the planned time had elapsed for subjective (overexertion) or objective (arrhythmia) reasons.

Findings of 185 patients and 271 control subjects are presented for the assessment of work capacity in hypertensive individuals (primary hypertension); an attempt at classification by hypertensive stage is seen as an essential presupposition. The subdivision into three stages recommended by the Experts' Commission of the WHO places the effects of hypertension on the organism, especially on the heart, in the focal point. This appears justified from a prognostic, pathophysiological, and therapeutic point of view. Hemodynamics in the examined patients undergo increasing impairment in relation to the stage of hypertension with a decrease in maximum cardiac index and work capacity and an increase in myocardial oxygen requirement. Initially, only the diastolic cardiac function is impaired; however, in advanced stages, the systolic function of the heart is impaired as well. Evaluation of work capacity is usually possible from a cardiac point of view by means of noninvasive echocardiographic and spiroergometric methods. The mass/volume ratio of the left cardiac ventricle and the relationship between left ventricular muscle mass (or volume) and work capacity are especially important. Both experience characteristic changes depending on the stage of hypertension and thus permit precise determination of work capacity, progress controls, and delineation from physiological cardiac hypertrophy (athletic heart).

The object of this study was to investigate the possible concentric increase in the left ventricular (LV) wall thickness by intensive strength training and to differentiate between the specific effect of the strength training itself and the influence of anabolic drugs. In this study 21 top-level bodybuilders [users of anabolic steroids (A): n = 14; non-users (N): n = 7] underwent one-dimensional and two-dimensional echocardiography as well as a cycle ergometer test. In both groups blood pressure at rest and during ergometric exercise was within the normal range. In spite of the same amount of time being spent on training, A showed significantly better power results than N. Total heart volume (A = 11.3 +/- 0.9 ml.kg-1; N = 11.9 +/- 0.9 ml.kg-1) and LV muscle mass were almost identical in A and N and correlated significantly with body weight and lean body mass respectively. The body dimension-related diastolic LV diameter was significantly lower in A (0.567 +/- 0.062 mm.kg-1) than in N (0.639 +/- 0.040 mm.kg-1). An increase in the LV posterior wall (p less than 0.01) and septum thickness (ns) resulted in increased LV wall thickness:diameter (p less than 0.01) and LV muscle mass:volume (p less than 0.05) ratios in A (0.458 +/- 0.590; 1.38 +/- 0.25 g.ml-1) in comparison to N (0.356 +/- 0.077; 1.16 +/- 0.17 g.ml-1). The septal:posterior wall thickness ratio was similar for both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Six male non-endurance trained subjects (S) and six marathon runners (M) underwent graded treadmill exercise (T) and isoproterenol stimulation (I; 2 and 4 microgram X min-1). beta-adrenergic receptor density was additionally determined as the amount of 3H-Dihydroalprenolol (DHA) specifically bound on intact polymorphonuclear leucocytes. Heart rate, VO2 uptake, lactate, plasma noradrenaline, and adrenaline were estimated during T. Heart rate, stroke volume, cardiac output, as well as lactate, glucose, free fatty acids (FFA), and glycerol levels in the blood were determined during I. M showed the known training-dependent responses during T, such as lower heart rates, lactate levels, and plasma catecholamines at identical work loads, as well as higher VO2 max than S. I-induced cardiac output increase was quite similar in both groups. Stroke volume, however, increased significantly in M and stayed constant in S. Lactate decreased (S), glucose increased significantly (M), glycerol increased similarly in both groups, FFA rise was less marked in S. I-induced stroke volume response (I) may be indicative of a more economic regulation of heart work in M than S. Lactate decrease and less marked FFA increase, as observed in S, may be the result of a somewhat higher cardiac energy demand, dependent on less economic heart work. Higher DHA-binding as observed in M, as well as stroke volume response and glucose increase, may be indicators of a training-dependent rise in sensitivity to catecholamines. The unsolved question is, however, to what extent beta-receptor responses in intact blood cells are significant for receptor behavior in other organs.