[Dental implantation and general practice].
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Biomedical subjects
Publications and source records attributed to W M Schmitt.
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In a single-blind random cross-over study the influence of a Norfenefrin infusion (2-4 mg/kg per minute) on circulation, carbohydrate and fat metabolism, catecholamines, growth hormone, cortisol, and insulin was investigated. The investigations were carried out on 12 healthy male physical education students at rest and during physical exercise. Under Norfenefrin, heart rate was reduced at rest (-30%) and under low and medium work load (150 watts: -9%); under maximal work load heart rate remained unchanged. Systolic blood pressure at rest increased by 29%; the results under physical exercise differ only slightly, and during increased work load they did not differ significantly. Diastolic blood pressure, in contrast, increased at rest (+23%) and under submaximal (150 watts: +12%) and maximal work load (+12.5%). The product of systolic blood pressure and heart rate was significantly decreased at rest under Norfenefrin, whereas it tended to decrease only slightly during work load. Adrenaline remained unchanged, while noradrenaline had a tendency to decrease only slightly during submaximal work load and was significantly lower during maximal work load. Glucose, lactate, glycerol, free fatty acids, and triglycerides, as well as growth hormone, cortisol, and insulin, remained unchanged. The physical working capacity remained unaffected. These observations confirm the predominant alpha-receptor-stimulating effect of Norfenefrin. The decrease in noradrenaline during exercise indicates the ability of Norfenefrin to interfere with the autoregulation of transmitter release and to replace endogenous noradrenaline.
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The effects of beta-1-adrenergic blockade (100 mg metoprolol) on metabolism in exercise was examined in 14 healthy males who worked for 50 min on a treadmill at 65% of their maximal exercise capacity. The tests were carried out in a double blind fashion. Glucose and lactate were determined in arterialized capillary blood, free fatty acids, glycerol, growth hormone, cortisol, glucagon, insulin, testosterone, and estradiol in serum, and adrenaline and noradrenaline in plasma. Lactate and glucose were not significantly affected by beta-1-adrenergic blockade, free fatty acids and glycerol were reduced by 50% and 30% respectively as compared with the unmedicated condition. Adrenaline and noradrenaline levels were increased by 104% and 54% respectively, growth hormone by 60%, cortisol by 72%, and glucagon by 36% when compared with the control experiments. Insulin and estradiol were unaffected, testosterone was depressed by 21% under medication. The results demonstrate that during prolonged exercise beta-1-adrenergic blockade depresses lipolysis. Energetic deficiency is prevented by counter-regulatory increases of various hormones. Consequently, from the metabolic point of view there is no indication of impairment of prolonged exercise capacity under beta-1-adrenergic blockade.
Seventeen male physical education students performed three types of treadmill exercise: (1) progressive exercise to exhaustion, (2) prolonged exercise of 50 min duration at the anaerobic threshold of 4 mmol . l-1 blood lactate (AE), (3) a single bout of short-term high-intensity exercise at 156% of maximal exercise capacity in the progressive test, leading to exhaustion within 1.5 min (ANE). Immediately before and after ANE and before, during, and after AE adrenaline, noradrenaline, growth hormone, cortisol, insulin, testosterone, and oestradiol were determined in venous blood, and glucose and lactate were determined in arterialized blood from the earlobe. Adrenaline and noradrenaline increased 15 fold during ANE and 3--4 fold and 6--9 fold respectively during AE. The adrenaline/noradrenaline ratio was 1 : 3 during ANE and 1 : 10 during AE. Cortisol increased by 35% in ANE (12% of which appeared in the postexercise period) and 54% in AE. Insulin increased during ANE but decreased during AE. Testosterone and oestradiol increased by 14% and 16% during ANE and by 22% and 28% during AE. The results point to a markedly higher emotional stress and higher sympatho-adrenal activity in anaerobic exercise. Growth hormone and cortisol appear to be the more affected by intense prolonged exercise. Taking plasma volume changes and changes of metabolic clearance rates into consideration, neither of the exercise tests appeared to affect secretion of testosterone and oestradiol.
To examine the metabolic and hormonal responses to non-exhaustive steady-state exercise at the individual anaerobic threshold (IAT), 12 male physical education students performed treadmill exercise of 50 min duration. The treadmill speed equaled that at the IAT as assessed in a standardized progressive exercise test (75 +/- 2% of maximal oxygen uptake). Heart rate averaged 177.0 +/- 12.2 min-1 at 15 min and 184.5 +/- 11.5 min-1 at 50 min. After the initial adjustment, arterial lactate stabilized at individually different levels between 2.70 and 6.00 mmol/l without any substantial trend in the individual curves. Arterial glucose was unchanged throughout the test. Glycerol increased continuously to 157% above the preexercise value (P less than 0.001). The FFA blood level was not depressed but rather showed an increasing tendency between 25 and 50 min (P less than 0.05). Between 0 and 25 min, insulin decreased (P less than 0.01), growth hormone increased to 8 times its pre-exercise value (P less than 0.001), and cortisol did not show any significant changes. Between 25 and 50 min, no significant additional changes were detected for these hormones. At 15 min epinephrine and norepinephrine had increased 2.8- and 7-fold above the respective pre-exercise values (P less than 0.001); both catecholamines continued to increase until 50 min (P less than 0.001 and P less than 0.01). It is concluded that prolonged exercise at the IAT is associated with a steady-state condition in carbohydrate supply and turnover, as is suggested by the stable blood levels of glucose and lactate. The stably elevated blood level of lactate did not result in depression of the FFA blood level, suggesting unimpaired supply of FFA from extramuscular sources. Exercise at the IAT places a high load on aerobic metabolism without encountering progressive lactate accumulation and the associated metabolic effects.
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In 14 healthy physical education students the effect of acute beta 1-adrenergic blockade (100 mg metoprolol) on maximal and prolonged exercise capacity, carbohydrate and lipid metabolism, catecholamines, insulin, growth hormone, and cortisol was studied in a double-blind trial. Metoprolol had no effect on maximal oxygen uptake. The 3.5% reduction of maximal exercise capacity had to be attributed to the reduced maximal lactate concentration. Maximal heart rate was reduced by approximately 22%. At submaximal work loads (treadmill) exercise with gradually increasing velocity), lipolysis appeared to be inhibited, arterial glucose and lactate concentrations were unaffected. With metoprolol, epinephrine levels at rest and submaximal work loads were elevated; no effect was apparent at maximal loads. Norepinephrine, insulin, growth hormone, and cortisol were unaffected in exercise with increasing work loads. In prolonged exercise at a constant load of approximately 70% of maximal exercise capacity, mean heart rate was reduced by 26%. Arterial lactate and glucose levels were essentially unchanged, free fatty acids and glycerol decreased by 50 and 30% respectively. With metoprolol, epinephrine increased by 100%, norepinephrine by 50% growth hormone by 60%, and cortisol by 90%, insulin remained unchanged. The results indicate that a reduction of exercise capacity by beta 1-adrenergic blockade in patients undergoing an endurance type training for therapeutic or rehabilitative purposes is unlikely to occur. The inhibition of lipolysis under metoprolol appears to be counteracted by the increased carbohydrate utilisation and by the increased secretion of the regulating hormones.
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