Biomedical subjects

M Huonker

Publications and source records attributed to M Huonker.

6 recordsLinked to original sources

PubMed1991

[Metabolic and cardiovascular adaptation and the performance of professional tennis players].

14 professional tennis players of world rank were examined (7 men, mean age 23 +/- 3 years; 7 women, mean age 18 +/- 2 years). Heart volume (HV) was 11.9 +/- 0.9 ml/kg in women, 12.7 +/- 1.3 ml/kg in men, 20-30% higher than in untrained persons. Correspondingly, end-diastolic (EDV) and end-systolic volume, left-ventricular muscle mass (LVM) and stroke volume (SV) were elevated, while contractility parameters as well as the ratios of SV and of LVM to EDV and HV were within normal limits. The changes are to be taken as adaptations in the sense of athlete's heart. Maximal treadmill speed was 18 km/h in women and 19.3 km/h in men, with maximal lactate levels of 9.3 mmol/l (women) and 11.4 mmol/l (men). Anaerobic threshold was reached at a treadmill speed of 13.3 km/h (women) and 14.8 km/h (men). These data indicate a good performance range and were clearly better than in earlier groups of tennis players. This adaptation requires additional interval and endurance training. In 11 tennis players the serum concentration of magnesium and in 5 that of iron was below the recommended lower limit (magnesium: 0.8 mmol/l; iron: 14 mumols/l). Serum concentrations of creatine kinase and of lactate dehydrogenase were always two to three times higher than normal, if tennis training had taken place the day before, but all other biochemical values were within normal limits.

Adaptation, Physiological↗

PubMed1990

[Prevention and therapy of obesity with diet and sports, an ambulatory therapy program for overweight children].

Dietary restriction together with ongoing power-orientated training provide best results in the therapy and prevention of obesity. Diet can reduce the resting metabolic rate by up to 20% within 14 days. Physical activity stimulates the resting metabolic rate and counteracts this energy saving effect, but is especially important for maintaining a steady state after weight reduction. Exercise reduces the risk factors accompanying obesity by favorable adaptation of the sympathoadrenergic system to physical activity. This can be seen in the effects on heart rate, stroke volume, blood pressure, as well as glycogenolytic and lipolytic activities. Body fat especially in the abdominal area, which is particularly connected with atherogenic risk, is diminished. Weight reduction is accompanied by a decrease of the cardioprotective cholesterol fraction. Diets high in unsaturated fatty acids combined with a staying power training have a synergistic effect: they reduce a decrease of HDL. It is difficult to demonstrate risk factors connected with overweight children. However, from the preventive medicine point of view it is advisable to start with therapeutic measures during childhood. In an out-patient pilot project we surveyed 18 obese children aged 9 to 13 years. The therapy plan consisted of dietary restriction (1200 kcal/d), an exercise program performed 3 times a week, and psychological assistance. All children of 12 to 13 years arrived at an overweight level less than 20%, the younger ones displayed a lower weight reduction effect. All 18 improved their aerobic capacity. In the 1st months of treatment, HDL-cholesterol decreased slightly, but increased above pre-treatment level, later on. We did not see any vitamin deficiencies during the therapeutic regimen.

Cardiovascular System↗

PubMed1990

[Effect of beta blockade on hemodynamics in physical exertion].

Beta-receptor blocking agents are known for more than 20 years. They are of definite use in the therapy of arterial hypertension and coronary heart disease. Beta-blockers lower the sympathoadrenergic discharge to the heart and circulation, particularly if the former is increased. Beta-blockers induce a negative chronotropic and inotropic effect and inhibit beta 2-mediated vasodilation. Thus beta-sympathicolysis during physical activity results in damping of heart rate increase and of elevation of cardiac contractility. Systolic blood pressure does not increase much, and usually there is no decline in diastolic blood pressure, due to elevated peripheral resistance. With adequate dosage, there may even be a slight increase in diastolic pressure, an effect eventually vaning in chronic therapy. Pulmonary capillary wedge pressure is elevated to above normal via inhibition of contractility and relaxation of the heart. Stroke volume, cardiac output and the double-product decrease, the arteriovenous oxygen difference under exercise increases clearly and the maximum aerobic performance capacity decrease in healthy individuals. In coronary patients, this may protect against cardiac overload and increase symptom-free physical work capacity, due to a relative decrease in the myocardial O2 requirement and improved coronary perfusion resulting from prolonged diastole. With verified indication (hypertensive-hyperkinetic impairments of cardiovascular function, coronary heart disease), the goal is an overlapping, endurance-oriented training to reduce the overall sympathetic activation, in order to minimize medication in the long run.

Adrenergic beta-Antagonists↗

PubMed1989

[Doping--also a problem in general practice?].

In 1986, the Medical Commission of the IOC defined doping as the use of pharmacological substances belonging to disallowed groups of active substances (stimulants, narcotics, anabolic steroids, beta-blockers, diuretics). With certain restrictions, this applies also to alcohol, local anesthetics and corticosteroids. The use of disallowed methods (blood doping, manipulation of a urine sample) is also forbidden. These days the greatest importance is attached to anabolic steroids (including testosterone), since these substances--discontinued in good time--cannot be detected on the day of competition but still have a promoting effect on performance. Competitive sports prepared the way here for the use of anabolic steroids in general athletics and in particular usually non-olympic sports (such as bodybuilding). Against this background, effects, adverse effects and the risks of anabolic steroid use are discussed. The aim must be to prevent the use of doping, especially in uncontrollable general sports, by promoting proper awareness.

Anabolic Agents↗

PubMed1989

[Form, size and function of the sports heart--differentiation from pathological findings].

Dependent on the nature, intensity and scope of muscular exercise, regular athletic training can result in changes in the size and form of the heart, which can be recorded by radiologic and echocardiographic techniques. Brief anaerobic exercise and purely static forms of training (sprint, strength sports) do not produce substantial increases in the size of the heart, but a rotund heart shape with rounding of the cardiac tip and in some cases a discrete increase in the wall thickness of the ventricular myocardium is frequently observed. Dependent on the scope of the training and the intensity, aerobic, endurance-oriented training (endurance sports) can induce considerable enlargement of all cardiac chambers with a change in the cardiac configuration, which is most nearly comparable to combination mitral vitium. Comparison of physiological hypertrophy of the athletic heart with pathological forms of cardiac hypertrophy (such as cardiomyopathies) is in many cases not unequivocally possible with plain X-ray films, but it is usually successful with echocardiographic examination methods.

Adult↗

PubMedDate not supplied

Hepatocellular carcinoma in alcoholic liver disease: no evidence for a pathogenetic role of hepatitis B virus infection.

Hepatocellular carcinoma tissues from HBsAg-negative patients with chronic alcoholic liver disease were investigated for the presence of hepatitis B virus DNA. Southern blot analyses of DNA extracted from the hepatocellular carcinomas were negative for hepatitis B virus DNA in all 17 patients examined, at a level of sensitivity of less than 0.01 genome equivalent per cell. Similarly, in liver tissues from another 30 patients with alcoholic cirrhosis without hepatocellular carcinoma, no hepatitis B virus DNA was detectable. We conclude that in our patients there is no molecular evidence for a contribution of hepatitis B virus infection to the development of hepatocellular carcinoma in alcoholic liver disease.

Adult↗