Erythropoietin production can be enhanced by normobaric oxygen breathing in healthy humans.
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Biomedical subjects
Publications and source records attributed to J Poortmans.
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1. To address the question of whether endotoxaemia could be involved in the inflammatory response induced by long-term strenuous exercise, 18 male marathon runners [mean age 41 +/- 2 (SEM) years] were studied. Their performance in the marathon ranged from 2 h 46 min to 4 h 42 min. 2. Four venous blood samples were drawn: at rest, just before the race (baseline); within 15 min following the completion of the marathon; after 1 h of recovery; and the morning after the race. 3. The following humoral markers of the inflammatory response to exercise were measured: polymorphonuclear myeloperoxidase (MPO), anaphylatoxin C5a (C5a), tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Plasma endotoxin was measured by a sensitive and rapid chromogenic Limulus assay. All inflammatory markers were significantly increased (P < 0.001) after the race, reaching in most cases peak values in the first blood sample drawn following the completion of the marathon [MPO, 298 +/- 19 ng/ml (SEM); C5a, 1.45 +/- 0.32 ng/ml; TNF-alpha, 20 +/- 3 pg/ml; IL-6, 88 +/- 13 pg/ml] when compared with baseline [MPO, 146 +/- 16 ng/ml (SEM); C5a, 0.27 +/- 0.2 ng/ml; TNF-alpha, 12 +/- 1.5 pg/ml: IL-6, 1.0 +/- 0.5 pg/ml]. Traces of plasma endotoxin (ranging from 5 to 13 pg/ml, with one exceptionally high value of 72 pg/ml measured in one runner) were detected in seven subjects within the first hour of recovery. An ELISA method was used to determine the endogenous IgG antibodies toward a range of Gram-negative bacterial lipopolysaccharides (LPSs) of different sizes and structures. A transient decrease in certain anti-LPS activities, mainly against rough LPS, occurred in most cases in the first blood sample drawn after the race. There was no correlation between the magnitude of the inflammatory response to exercise, as assessed by the increase in blood levels of humoral markers of inflammation, and the changes in circulating endotoxin levels of anti-LPS IgG activity following the race. 4. From these results, we conclude that the mild, transient endotoxaemia detected in some of our subjects does not play a major role in the observed inflammatory response to a marathon competition.
The triad of insulin, diet and exercise has been the basis for treatment of diabetes for several decades. However, the choice of sporting activities for young diabetics requires an understanding of: a) the energy metabolism and the adaptation to physical activity in the healthy; b) the metabolic adaptation during physical activity in the diabetic child; and c) the practical recommendations concerning diet and insulin that have to be learned by the children themselves. The healthy child utilises immediately available substrates, such as ATP and creatine phosphate in much the same fashion as the adult. However, the capacity for anaerobic degradation of glycogen and glucose seems limited in the muscles of children relative to that of adults. Consequently, the adaptation to resistance exercise should be undertaken with prudence in children and adolescents. The release of insulin tends to decrease during effort. Diverse hypotheses have been proposed to explain this phenomenon. However a low concentration of insulin is required: insulin is said to play a "permissive" role. In diabetic children, an adequate insulin therapy is required to allow the full benefit of muscular activity on glucose assimilation and to reach the same level of physical performance as the non-diabetic. In the case of insufficient metabolic control, exercise can provoke severe hypoglycaemic episodes, even after muscle activity has ceased, or increase glucose levels and lead to ketoacidosis. Regular physical training induces a reduction in postexercise proteinuria measured in diabetic adolescents but its role in metabolic control remains controversial.(ABSTRACT TRUNCATED AT 250 WORDS)
Changes in platelet aggregability during maximal bicycle ergometry were studied in healthy untrained subjects. Ex vivo platelet aggregation in response to ADP and collagen was measured in whole blood by impedance aggregometry or by direct electronic counting in an Ultra-Flo 100 platelet counter. This last method revealed that the platelet aggregation induced by low concentration of ADP (0.5 - 1.0 microM) was significantly enhanced during exercise. The plasma level of beta-thromboglobulin and the urinary excretion of 2,3--dinor-6-keto prostaglandin F1 alpha were also increased. These data indicate that an intense physical exercise enhances the aggregability of human platelets and induces a compensatory increase in prostacyclin biosynthesis.
The triad of insulin, diet and exercise has been the basis for treatment of diabetes for several decades. However, the choice of sporting activities for young diabetics requires an understanding of: (a) the energy metabolism and the adaptation to physical activity in the healthy; (b) the metabolic adaptation during physical activity in the diabetic child; and (c) the practical recommendations concerning diet and insulin that have to be learned by the children themselves. The healthy child utilises immediately available substrates, such as ATP and creatine phosphate in much the same fashion as the adult. However, the capacity for anaerobic degradation of glycogen and glucose seems limited in the muscles of children relative to that of adults. Consequently, the adaptation to resistance exercise should be undertaken with prudence in children and adolescents. In diabetic children, an adequate insulin therapy is required to allow the full benefit of muscular activity on glucose assimilation and to reach the same level of physical performance as the non-diabetic. In the case of insufficient metabolic control, exercise can provoke severe hypoglycaemic episodes, even after muscle activity has ceased, or increase glucose levels and lead to ketoacidosis. Regular physical training induces a reduction in postexercise proteinuria measured in diabetic adolescents but its role in metabolic control remains controversial. If a diabetic child or adolescent follows individual recommendations concerning diet and insulin, he or she can perform physical activity much the same as a young non-diabetic. These recommendations include: (a) self-measurement of blood glucose concentration before and after exercise; (b) ingestion of carbohydrates before, during, and after exercise; (c) reduction of the insulin dose during and immediately after exercise; and (d) not choosing an injection site involved with muscular work. The only prohibited sports are those which constitute a danger to the diabetic child by provoking an eventual hypoglycaemia. The best sports are those that require progressive physical effort and that are spread out over several hours.
Validation of the maximal multistage 20 m shuttle run test with 1 min steps has been compared with a stepwise load increase on a bicycle ergometer among 201 male and female subjects ranging from 14 to 30 years. A slight underestimation of VO2 max (5.2%) amounting to 2.71 ml . min-1 . kg-1 was observed for the multistage shuttle test as compared to the bicycle test (r = 0.72). The analysis of the biological values collected after exercise does not show major differences between the two tests (plasma lactate, urinary total protein and albumin, creatinine). The renal handling of plasma proteins appears to be equally disturbed under the influence of exhaustive exercise. Maximal aerobic power regularly increases with age in both sexes, being more pronounced however for boys (1.16 to 3.37 l . min-1) than for girls (1.17 to 2.43 l . min-1) from 6 to 20 years old. Boys nearly sustain 50 ml . min-1 . kg-1 throughout childhood. On the contrary, from 8 years on girls progressively reduce their VO2 max down to 37.1 ml . min-1 . kg-1 at the age of 19. The decrease is more pronounced during the 11-16 years period. The present results constitute tentative norms on 1,025 brussels male and female subjects ranging from 6 to 23 years.
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The influence of chronic therapy with nifedipine on the pharmacokinetics of propranolol 80 mg twice daily, metoprolol 100 mg twice daily and atenolol 100 mg once daily was investigated in eight healthy volunteers. Nifedipine 10 mg three times daily did not affect the pharmacokinetics of metoprolol and atenolol whereas nifedipine shortened the time to peak plasma concentration for propranolol by about 1 h. Propranolol, metoprolol and atenolol provoked comparable decreases in heart rate measured at rest and during exercise. The beta-adrenoceptor blocking properties of propranolol, metoprolol and atenolol were not affected by concomitant therapy with nifedipine. The present study did not show significant pharmacokinetic and pharmacodynamic interactions between nifedipine and lipophilic beta-adrenoceptor blockers.
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In six insulin deprived adolescent diabetics, the influence of muscular effort equal to 50% of the VO2 max on the coefficient of glucose assimilation was evaluated. During an IVTT the coefficient of glucose assimilation at rest was (0.59). 10(-2) +/- 0.14 and it did not increase during physical activity. A minimal concentration of insulin is apparently indispensable to increase glucose utilisation during muscular effort. At higher concentrations other factors probably intervene to enhance glucose assimilation.
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Urinary total protein, albumin and beta2-microglobulin excretion during exercise on a bicycle ergometer was determined in a group of 7 adolescent male diabetics and in a comparable control group. There was no difference, neither in the diabetic group nor in the control group, in the excretion of these proteins under the provocative effect of physical exercise. These results suggest exercise may not always give a positive response and is not a discriminative function in reliable studies of renal function.
In order to obtain information concerning the CPK turnover during exercise, we have elaborated a technique to measure its activity continuously in vivo. A colorimetric method has been adapted to total blood. CPK was measured continuously in 5 physically fit athletes exercised on an ergometric bicycle for 30 min. There was practically no increase in enzymatic activity. The starting level was very high, corresponding perhaps to a "permanent state of enzyme release"; the exercise was not hard enough because of the fitness of the athletes or the maximal increase did not occur immediately after the exercise.
In an effort to determine the synthetic capacity of human kidneys for serum proteins, pieces of both kidneys removed at operation prior to transplantation were placed in organ culture. Incubation with 14C labelled amino acids and subsequent radioimmunoelectrophoresis with antisera to all five classes of immunoglobulins showed synthesis of IgG by all 5 pairs of kidneys of IgA and IgE by 4, and of IgM by 2. None synthesized IgD. Radioimmunoelectrophoresis with specific antisera to 15 non-immunoglobulin proteins revealed synthesis of lactoferrin and uromucoid while several other serum proteins, such as alpha1 antitrypsin and alpha2 macroglobulin, known for their binding properties, showed apparent synthesis. No evidence for secretory component synthesis was seen despite positive immunofluorescent localization in the tubular cells. Further, Zn alpha2 and beta2GP I also showed positive immunofluorescence but negative synthesis. It seems possible that these latter proteins may not be synthesized by the tubular cells but rather may be actively excreted or reabsorbed by them.
Four rabbit antibodies have been prepared, which are specifically directed against alpha-lactalbumins from different sources; namely human, cow, goat and sheep milk. Each of these antibodies was tested for its ability to react with, separately, each of the four proteins. The immunological reactions were assessed by means of different techniques: double immunodiffusion in agar gel as well as affinity chromatography of antibodies, using antigens covalently bound to an insoluble matrix. In each case, the strongest reaction was observed between homologous antibody and (matrix-bound) antigen; heterologous antigens were, however, also capable of cross-reaction. Whereas no cross-reaction between human alpha-lactalbumin and antibodies against the bovine protein could be evidenced by immunodiffusion, the occurrence of soluble complexes has been disclosed by means of a gel filtration technique.
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