Spontaneously low LDL cholesterol and reaction to exercise-induced stress.
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Biomedical subjects
Publications and source records attributed to M Halle.
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Muscular training induces structural and functional adaptations within the cardiovascular system which vary according to type, intensity and duration of muscular exertion. Dynamic muscular training for more than 5 h a week involving more than 1/6th of the skeletal muscle mass causes an increase in parasympathetic tone and an eccentric myocardial hypertrophy. The dimensions of all cardiac chambers enlarge up to 20% and the cardiac muscle mass may increase by 70%-80%. Static muscular training does not induce any change in the parasympathetic heart regulation, nor does it lead to any disproportional increase in cardiac muscle mass relative to skeletal muscle mass. However, a tendency towards a concentric myocardial hypertrophy can be observed. The effects of regular muscular training on the arteries are the subject of current scientific investigation. To explain the acute and chronic adaptations of the arterial vasculature to exercise, a "shear stress" hypothesis has been proposed. During dynamic muscular exercise the regional arterial blood flow is enhanced. This leads to an acute increase in intraluminal shear forces, which stimulates the vascular endothelium with a reactive flow-dependent regional vasodilation mediated by endothelial-derived relaxing factors (EDRF, EDNO). Chronic enhancement of shear forces induces endothelial cell-mediated alterations in gene expression (endothelin, growth factors, regulators of fibrinolysis) and chronic structural adaptations of the vascular wall (cytoskeletal redistribution, cell shape change). Recent duplex sonographic studies in humans have revealed a significant lumen increase of muscular type arteries induced by dynamic, predominantly aerobic muscular training, but not by static muscular training. These structural adaptations are confined to those arteries supplying exercising muscle groups, whereas functional adaptations with an improvement of regional compliance are found in all arteries.
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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.
Hyperfibrinogenemia and a dyslipoproteinemia characterized by reduced HDL2 cholesterol and elevated levels of small, dense LDL particles are risk factors for coronary artery disease. However, the relationship between fibrinogen and lipoproteins, in particular LDL subfractions, is uncertain. We therefore measured serum fibrinogen levels and serum concentrations of cholesterol and apolipoproteins of VLDL, IDL, six LDL, and two HDL subfractions by using the technique of density-gradient ultracentrifugation in 132 nonsmoking men without evidence of coronary artery disease or infection. Dividing the individuals into quartiles according to their fibrinogen values showed that men within the highest fibrinogen quartile (fibrinogen 2.90 to 4.34 g/L) had significantly higher concentrations of small, dense LDL (d > 1.044 g/mL) apolipoprotein B and cholesterol and lower concentrations of HDL2 cholesterol than men within the lower fibrinogen quartiles (fibrinogen < 2.55 g/L). Multivariate regression analysis revealed that the association between fibrinogen and small, dense LDL particles was independent of serum triglycerides, cholesterol, body mass index, and age. In contrast, the relationship between fibrinogen and HDL2 cholesterol was primarily influenced by triglycerides and cholesterol and not independently influenced by fibrinogen. There were no significant differences between the quartiles in terms of insulin, glucose, insulin resistance, free fatty acids, lipoprotein(a), and blood pressure. This study showed that fibrinogen is associated with the expression of a more atherogenic LDL subfraction phenotype independent of body mass index, age, other serum lipids, and insulin resistance in a healthy male nonsmoking population. The reason for this association is uncertain. These findings reinforce the evidence that fibrinogen should be determined when assessing coronary risk.
Obesity, insulin resistance (IR) with hyperinsulinemia, and a dyslipoproteinemia characterized by reduced high-density lipoprotein 2 (HDL2) cholesterol and elevated levels of small, dense low-density lipoprotein (LDL) particles are risk factors for coronary artery disease (CAD). The impact of obesity independent of hyperinsulinemia on the concentration and composition of small, dense LDL subfractions is uncertain. The aim of this study was to investigate the relationship between obesity indices, namely body mass index (BMI), skinfold measurements (SF), and waist to hip ratio (WHR), and LDL-subfraction particle concentration and composition in 200 healthy men without evidence of IR. A precise analysis of the concentration of lipids and apolipoproteins and the composition of very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and two HDL- and six LDL-subfraction particles was obtained using the technique of density-gradient ultracentrifugation. Dividing the individuals according to BMI showed that those with a BMI greater than 27 kg/m2 had significantly lower HDL2 cholesterol and apolipoprotein (apo) A-I and higher VLDL and IDL cholesterol and apo B concentrations than those with a BMI less than 25 kg/m2. Regarding LDL particles, we found that men with a BMI above 25 kg/m2 had significantly more small, dense LDL particles (d 1.044 to 1.063 g/mL) and correspondingly fewer medium, dense LDL particles (d 1.031 to 1.037 g/mL) than leaner men; those with a BMI above 27 kg/m2 had the highest concentration of circulating small, dense LDL particles. These findings were not influenced by fasting insulin concentrations, IR, or WHR.(ABSTRACT TRUNCATED AT 250 WORDS)
Working muscle plays a central role in the control of lipid metabolism. Increased physical activity induces a number of positive changes in the metabolism of lipoproteins: serum triglycerides are lowered by the increased lipolytic activity and the production of native high density lipoprotein (HDL) particles is increased. The increased lecithin: cholesterol acyltransferase activity leads to an increased production of HDL2, which in addition is catabolised more slowly due to a decreased activity of hepatic lipase. The 3 effects explain the increased HDL levels of endurance trained individuals. These effects have been demonstrated in cross-sectional as well as longitudinal studies by different groups, and can be induced by training, independent of changes in bodyweight. The influence of endurance activity on the quality and quantity of low density lipoprotein (LDL) particles is a further reason for the antiatherogenic potential of increased physical activity. It has been shown by several groups that small dense LDL particles represent a particular risk factor for atherosclerosis. Recent studies presented strong evidence that LDL level and composition can be influenced favorably by physical activity. In addition to the direct influence of physical activity on lipids and lipoproteins, physical exercise may improve the disturbances of haemorheological factors, particularly those associated with hypertriglyceridaemia. In conclusion, there is increased evidence that physical activity is able to favourably influence all 3 components of the atherogenic lipoprotein phenotype: the HDL concentration increases, the concentration of small dense LDL decreases, and serum triglycerides are reduced.
Coronary risk factors such as obesity, dyslipoproteinaemia and low physical fitness are often prevalent in childhood. In contrast, regular physical activity and healthy nutrition have been shown to be effective in primary and secondary prevention of coronary artery disease. An increment in physical activity with concomitant weight loss has a profound influence on peripheral lipoprotein metabolism and has shown to improve the atherogenic lipoprotein profile. As risk factors often track from childhood into adulthood it seems inevitable to prevent or diminish risk factors as early as possible. Therefore, intervention programmes for prevention of coronary artery disease have to be conducted in childhood. Experience from an own intervention programme of obese children has shown that the combination of intensive dietary and physical education improves physical fitness, body composition as well as lipid metabolism. Whether short-term benefits will continue into adulthood and reduce coronary artery disease in midlife will have to be shown. Nonetheless, it seems out of question that children showing risk factors such as obesity or hypercholesterolaemia will benefit from early intervention programmes when changing dietary and exercise behaviours.
Previous studies showed that probucol significantly lowered both LDL cholesterol and HDL cholesterol. In addition, there is evidence that as an essential antioxidant probucol causes variations in cellular interactions and cardiovascular functions in patients. Therefore, 14 hypercholesterolemic men were investigated before and during probucol treatment in order to document both serological and cardiovascular changes with special regard to (1) serum apolipoproteins (A-I, A-II, B, C-II, C-III, E) (2) composition and distribution of HDL and LDL subfractions, (3) cardiovascular performance using a maximum exercise stress test, and (4) induced platelet aggregation. In contrast to reduced total, LDL-, and HDL-cholesterol values, highly significant changes in serum apolipoproteins were found in apoA-I only; apoA-II was unchanged both in serum and in HDL subfractions. Despite unchanged serum apoB levels, the results showed that probucol has a significant influence on the composition (TG/FC ratio) of LDL particles of d less than 1.019 g/ml. In addition to lipoprotein-related changes, significant decreases in heart rate data and cardiac work and in lactic acid accumulation during exercise were induced by probucol administration; furthermore, adrenaline-induced platelet aggregation was also decreased. The results found significantly demonstrate that probucol acts by way of more mechanisms than cholesterol lowering alone. This aspect may be of special interest in the clinical use of probucol, because a coronary-risk-reducing therapy should not affect the lipoprotein profile only.
A method for isoelectric focusing of apolipoprotein E in an immobilized pH gradient with added carrier ampholytes has been developed. This method is an improvement over conventional isoelectric focusing of apolipoprotein E with respect to resolution, reproducibility, and simplicity. Since monosialo isoforms are resolved from the normally cofocusing asialo isoforms, unique patterns are obtained for all 6 common apolipoprotein E phenotypes. The method can also be applied to the screening of apolipoprotein A and C isoforms. Delipidated very low density lipoproteins (VLDL) have been used as the source of apolipoprotein E and C. Apolipoprotein A isoforms were focused directly from detergent-treated serum. Immunodetection of apolipoprotein E using capillary transfer was found to be compatible with the described method.
A PCO2 electrode working on the principle of electrical conductivity is described. The calibration curve can be linearized according to the formula G = Go + b square root PCO2. This linearity has been tested in the PCO2 range of 0.93-9.33 kPa (7--70 Torr). For the experiments electrodes are used which have conductivity values of about 50 nS and drifts of maximally 5%/h at a PCO2 of 5.33 kPa (40 Torr). The response time (T90) is about 20 s. The temperature sensitivity is 2.4 nS/1 K between 298 K-310 K. The standard error of the measurements is sigma = 0.33 nS. With these electrodes tissue PCO2 can be measured on the surface of various organs.
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PURPOSE: Taking pictures of the spine with Morphometric X-ray Absorptiometry (DXA) leads to a radiation dose of just 1% of conventional X-ray. Purpose of this study was to evaluate if DXA is a suitable method for sufficient measuring of the scoliosis angle. METHOD: We examined 20 patients with scolioses I. Control-pictures were made with conventional X-rays and compared to those made by DXA, measuring of scoliosis angle was performed by the method of Lippmann/Cobb. RESULTS: The difference between both methods was -10.5% DXA to conventional X-ray-each angle examined on DXA was smaller. CONCLUSION: It is possible to measure scolioses I on DXA.
We investigated the radiological findings of four patients with malignant pulmonary hemangiopericytomas, comparing plain chest radiography, CT, and MR. The radiographic presentation ranged from a small single lesion to a tumor almost completely occupying a hemithorax. Pathognomonic radiological features of malignant pulmonary hemangiopericytomas could not be established, but characteristic features include a large lobulated well-circumscribed mass with an encapsulated appearance, contrast enhancement of the margin, and no signs of surrounding compression atelectasis. The tumors were associated with late onset or a paucity of chest symptoms. Additional information regarding heterogeneity and effects on adjacent structures was provided by MR and was helpful in suggesting the diagnosis of malignant pulmonary hemangiopericytoma.