Showing papers by "Maastricht University published in 1989"

Study on food intake and energy expenditure during extreme sustained exercise: the Tour de France.

Abstract: Food intake and energy expenditure (EE) were studied in five cyclists during the 22-day race of the Tour de France. The course is about 4000 km including 30 mountain passages (up to 2700 m altitude) and can be considered as one of the most strenuous endurance endeavors. Nutritional intake was calculated from daily food records. EE was estimated from sleeping time and the low activity period. EE during cycling was predicted based on detailed information. Mean energy intake (EI) was 24.7 MJ with a highest mean daily EI of 32.4 MJ. Mean EE was 25.4 MJ with a highest mean daily EE of 32.7 MJ. Relative contribution of protein, CHO, and fat was 15, 62, and 23 En% resp. 49% of EI was taken during the race resulting in a CHO intake of 94 g.h-1 representing 69 en%. It is questioned whether this amount of CHO is optimal in relation to CHO oxidation and performance. About 30% from CHO intake came from CHO-rich liquids. High EI resulted in high Ca and Fe intake. For vitamins, especially B1, this relation was not found. Vitamin B1 nutrient density dropped to 0.25 mg/4.2 MJ during the race caused by a large intake of refined CHO-rich food items. However, vitamin supplementation was high. Daily water intake was 6.71 with extremes up to 11.81. Therefore, the strategy of intake of large quantities of CHO-rich liquids seems to be the appropriate answer to maintain energy and fluid balance under these extreme conditions.

Echography of the Inferior Vena Cava is a Simple and Reliable Tool for Estimation of ‘Dry Weight’ in Haemodialysis Patients

Abstract: Using echography, the diameter of the inferior vena cava (IVC) and its decrease on deep inspiration (collapse index) were evaluated in haemodialysis patients. The diameter of the IVC was expressed as an index to the body surface area (VCD) in mm/m2. Non-linear regression analysis in predicting mean right atrial pressure by VCD (mm/m2) and collapse index revealed a good correlation (r = 0.92; P less than 0.001) in both measurements. These results indicate that the IVC indices can be used as a parameter for both high and low filling pressures. Over-hydration (mean right atrial pressure greater than 7 mmHg) was defined as a collapse index of less than 40% and a VCD of more than 11.5 mm/m2, and underhydration (mean right atrial pressure less than 3 mmHg) as a VCD of less than 8 mm/m2 and collapse index of above 75%. In 22 patients in whom dry weight was determined on clinical grounds, only six had a correct dry weight according to IVC indices. Reliability of IVC indices for estimation of body fluid status was proved by the fact that during haemodialysis with fluid removal, postdialysis underhydrated patients according to IVC indices showed a decrease of mean arterial pressure and stroke volume, and an increase of heart rate. No such changes were observed in postdialysis normovolaemic and hypervolaemic patients, according to the vena cava indices. Furthermore, blood volume in normo- and hypervolaemic patients decreased much less than in hypovolaemic patients, despite the same amount of ultrafiltration. Total blood volume (ml/m2) and VCD (mm/m2) correlated significantly (r = 0.61; P less than 0.001), whereas there was no significant correlation between collapse index and blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Nonischemic ventricular tachycardia. Clinical course and long-term follow-up in patients without clinically overt heart disease.

Abstract: This report describes the clinical, laboratory, and electrophysiologic features of 52 patients with ventricular tachycardia (VT) who had no clinical evidence of heart disease. The mean age of patients was 36 years, cardiovascular collapse occurred in 18 patients (35%), and exercise-related symptoms were present in 24 of 49 patients (49%). There were 20 patients with sustained monomorphic VT, 11 with incessant VT, and 21 with nonsustained VT. Abnormalities were present in 14 of 38 patients (37%) during echocardiography and in 21 of 47 patients (45%) who underwent cardiac catheterization. During baseline evaluation while patients were not receiving antiarrhythmic drugs, ambulatory monitoring and exercise testing showed an 88% and 57% incidence, respectively, of nonsustained or sustained monomorphic VT, whereas 31 of 50 patients (62%) had inducible VT (requiring an infusion of isoproterenol in 11 patients) during programmed electrical stimulation. The clinical VT (when a 12-lead electrocardiogram was available for analysis) had a left bundle branch block (LBBB) configuration in 20 of 33 patients (61%) and a right axis deviation in 17 of 33 patients (51%). The VT occurring during exercise testing and programmed electrical stimulation had the same configuration as the clinical VT in 22 of 22 patients. Three patients have received an antitachycardia pacemaker, and one patient underwent endocardial resection. Forty-eight patients (92%) were treated medically. One patient died of cancer; the remaining 47 patients were alive at a mean follow-up of 96 months after initial symptoms and 46 months after programmed electrical stimulation. We conclude that in patients without clinical evidence of heart disease, VT may be incessant, sustained, or nonsustained and that VT originates from the right ventricular outflow tract in more than 50% of patients. Although cardiac abnormalities may be found in more than 30% of patients, the exact significance of these abnormalities is unclear because of the absence of progressive changes and the excellent prognosis of this group of patients.

Explanatory Models in the Processing of Science Text: The Role of Prior Knowledge Activation Through Small-Group Discussion

Abstract: Two experiments assessed effects of activation of prior knowledge through small-group discussion. Subjects were given a description of natural phenomena and were asked to elaborate on possible explanations for them. In Experiment 1, small groups of subjects were presented with a problem describing the behavior of a blood cell in pure water and in a salt solution. No additional text was studied. The experimental subjects produced more than twice as many propositions about osmosis (i.e. the biological process explaining the blood cell's behavior) as a control group produced. Experiment 2 investigated effects of problem analysis on subsequent text processing for subjects with imprecise prior knowledge (novices) and subjects with precise knowledge (experts). Recall of the text showed considerable facilitative effects of problem analysis. Results are explained in terms of faster accessibility of prior knowledge and better integration of new information into explanatory models that may exist before, or are actively constructed during, problem analysis. Attempts to understand the physical world involve the use of cognitive structures that represent mechanisms or principles underlying the phenomena observed. These cognitions may vary from highly sophisticated to quite naive. They may emerge as the result of formal education but often are constructed "spontaneously" while a person is experiencing the phenomena concerned. Take thunder and lightning. By scientists, this natural phenomenon is interpreted in terms of large differences in electrical potential between clouds charged with static electricity and the earth. Young children however, generally favor explanations involving the clash of clouds, and in earlier centuries thunder was attributed to the rage of the gods. These naive "mental models" are, like the models of science, not merely descriptive of what is going on in the outer world. They are truly "explanatory," because they clarify why the world is as it is. In addition, these conceptions can be considered models because they usually consist of a set of concepts connected by causal links that help to interpret the phenomena concerned in terms of the underlying structure of these phenomena (Clement, 1979; Gentner & Stevens, 1983).

Thin-Basement-Membrane Nephropathy in Adults with Persistent Hematuria

Abstract: Thin-basement-membrane nephropathy, also called benign recurrent hematuria, is characterized by diffuse thinning of the glomerular basement membrane and by hematuria. To determine the incidence of thin-basement-membrane nephropathy among patients with idiopathic hematuria, we conducted a prospective study in the nephrology units of three large hospitals in the Netherlands. Eighty normotensive adults without azotemia underwent renal biopsy because of recurrent macroscopic hematuria (n = 26) or persistent microscopic hematuria (n = 54). Idiopathic IgA nephropathy was found in 27 of the 80 patients. Light microscopical examination showed that 42 patients had normal renal tissue. The remaining 11 patients had mesangioproliferative glomerulonephritis (n = 5), interstitial nephritis (n = 3), or focal global glomerulosclerosis (n = 3). Tissue from the 42 patients whose renal biopsy specimens were normal when examined with light microscopy was analyzed morphometrically with electron microscopy to determine the thickness of the glomerular basement membrane. Two subsets of patients were identified by this analysis. In 18, thin-basement-membrane nephropathy was found (mean basement-membrane thickness [+/- SE], 191 +/- 28 nm; normal, 350 +/- 43 nm); all but one of these 18 patients had microscopic hematuria, which persisted during follow-up (median duration, 50 months). (Of the 54 patients who presented with microscopic hematuria, 17 [31 percent] had thin-basement-membrane nephropathy.) The thickness of the glomerular basement membrane was normal in the other 24 patients (361 +/- 69 nm); during follow-up, hematuria disappeared in all 13 of these patients who had macroscopic hematuria, and hematuria resolved in 5 of the 11 patients who had microscopic hematuria. We conclude that in patients with persistent microscopic hematuria, the incidence of thin-basement-membrane nephropathy is similar to that of idiopathic IgA nephropathy. Morphometric analysis of the thickness of the glomerular basement membrane should be included in the workup of adults with persistent microscopic hematuria that is not of urologic origin.

Exercise-induced activation of the branched-chain 2-oxo acid dehydrogenase in human muscle

Abstract: The present study was conducted to investigate the metabolic regulation of the oxidation of branched-chain amino acids (BCAA) by exercise in human skeletal muscle. Five trained male volunteers were exercised on a cycle ergometer at 70% +/- 10% (mean +/- SD) of their maximal oxygen consumption (VO2max). Percutaneous quadriceps muscle biopsies were obtained under local anaesthesia at rest and after 30 and 120 min of exercise. In the muscle samples the active and total amount of the branched-chain 2-oxo acid dehydrogenase complex (BC-complex), the regulatory enzyme in the oxidative pathway of the BCAA, were measured. Glycogen content and activity of mitochondrial marker enzymes were also measured. Blood samples were obtained every 20 min for the measurement of metabolites. Heart rate and rated perceived exertion on the Borg scale were recorded every 10 min. At rest 4.0% +/- 2.5% of the BC complex was active, after 30 min of exercise 9.9% +/- 9.0% and after 120 min 17.5% +/- 8.5% (mean +/- SD). Exercise did not change the total activity. The largest activation was seen in two of the subjects who developed higher blood lactates early on during exercise and decreased their muscle glycogen more (indications of anaerobic metabolism). These data demonstrate that in trained individuals significant increases in the activity of the BC-complex occur only after prolonged intense exercise. In spite of the 4-fold activation, the data support the classical view that amino acids and protein do not contribute substantially as an energy source during exercise, since VO2 increased more than 20-fold.

Lipid alterations in isolated, working rat hearts during ischemia and reperfusion: its relation to myocardial damage.

Abstract: Disturbances in lipid metabolism may play an important role in the onset of irreversible myocardial damage. To investigate the effect of ischemia and reperfusion on lipid homeostasis and to delineate its possible consequences for myocardial damage, Krebs-Henseleit-perfused, working rat hearts were subjected to various periods of no-flow ischemia (10 to 90 minutes) with or without 30 minutes of reperfusion. During ischemia, the rise in nonesterified fatty acids (NEFAs) was preceded by the accumulation of substantial amounts of glycerol, indicating the presence of an active triacylglycerol-NEFA cycle. The subsequent rise in NEFAs (from 0.25 to 1.64 mumol/g dry residue wt after 90 minutes [means]) coincided with the reduction of ATP to values lower than 10 mumol/g dry wt and the rise of AMP, a potent inhibitor of acyl-coenzyme A synthetase, to values exceeding 2 mumol/g dry wt, making the latter compound a good candidate to hamper the turnover of endogenous lipids during prolonged ischemia. Reperfusion resulted in an additional rise in NEFAs (up to 4.1 mumol/g dry residue wt after 60 minutes of ischemia). Neither ischemia nor reperfusion resulted in significant decreases in the tissue content of triacylglycerols and the various phospholipids. During reperfusion recovery of stroke volume was still adequate at tissue NEFA levels thought to be incompatible with normal mitochondrial function. A positive correlation (r = 0.81) was found between NEFA content of reperfused hearts and cumulative release of lactate dehydrogenase during reperfusion. Accordingly it is concluded that 1) reperfusion results in additional changes in myocardial lipid homeostasis, 2) the accumulating NEFAs are compartmentalized, possibly at the cellular level, and 3) the accumulation of NEFAs is a sensitive marker for myocardial cell damage.

The relative importance of the factors II, VII, IX and X for the prothrombinase activity in plasma of orally anticoagulated patients.

Abstract: The individual importance of each of the four vitamin K-dependent clotting factors on the generation of prothrombinase activity in the plasma of orally anticoagulated patients has been investigated Addition of purified factors VII, IX or X to plasma from deeply anticoagulated patients (International Normalized Ratio 28-48) did not influence the amount of prothrombinase activity or the amount of thrombin formed Only the prothrombin level in the plasma determines the course of thrombin generation Addition of increasing amounts of purified factor II, VII, IX or X to plasmas deficient in respectively factor II, VII, IX or X showed that the prothrombinase activity increases linearly with the concentration of factor II added and that the concentration below which the factors VII, IX and X start to have a measurable effect on prothrombinase activity are 5%, 20%, and 30%, respectively Half maximal prothrombinase activity was found at about 1% factor VII, 5% factor IX and 8% factor X respectively From these observations we conclude that primarily the variation in factor II level determines thrombin generation and hence presumably the antithrombotic effect of oral anticoagulant therapy It therefore seems likely that, for the control of oral anticoagulant therapy, tests that reflect factor II activity would be suitable

Loss of membrane phospholipid asymmetry during activation of blood platelets and sickled red cells; mechanisms and physiological significance.

Abstract: Membrane phospholipid asymmetry is considered to be a general property of biological membranes. Detailed information is presently available on the non-random orientation of phospholipids in red cell- and platelet membranes. The outer leaflet of the lipid bilayer membrane is rich in choline-phospholipids, whereas amino-phospholipids are abundant in the inner leaflet. Studies with blood platelets have shown that these asymmetries are not maintained when the cells are activated in various ways. Undoing the normal asymmetry of membrane phospholipids in activated blood cells is presumably mediated by increased transbilayer movement of phospholipids. This process, which leads to increased exposure of negatively charged phosphatidylserine at the outer surface, plays an important physiological role in local blood clotting reactions. A similar phenomenon occurs in sickled red cells. Phospholipid vesicles breaking off from reversibly sickled cells contribute similarly to intravascular clotting in the crisis phase of sickle cell disease. The loss of membrane phospholipid asymmetry in activated platelets seems to be strictly correlated with degradation of cytoskeletal proteins by endogenous calpain. It is remarkable that membrane phospholipid asymmetry can be (partly) restored when activated platelets are treated with reducing agents. This leads to disappearance of phosphatidylserine from the outer leaflet where it was previously exposed during cell activation. These observations will be discussed in relation to two mechanisms which have been recognized to play a role in the regulation of membrane phospholipid asymmetry; i.e. the interaction of aminophospholipids to cytoskeletal proteins, and the involvement of a phospholipid-translocase catalyzing outward-inward transbilayer movement of amino-phospholipids.

Plasma-amino acid profiles in sepsis and stress.

Abstract: Sepsis has been associated with specific plasma amino acid patterns. Sixty-five patients were prospectively investigated as to whether these patterns are indeed sepsis specific, or specific for metabolic stress without concomitant sepsis, or associated with the presence of organ failure. Virtually all aminoacid levels were decreased by 10-30% (p less than 0.05), whereas cystine and phenylalanine were significantly elevated. These changes were more pronounced in severe sepsis. Organ failure was not associated with significantly altered amino acid profiles. No differences were found between sepsis and stress without signs of sepsis. In addition, imminent death was not associated with aberrant amino acid profiles. We conclude that sepsis and metabolic stress are associated with changes in plasma amino acid profiles, but that such changes are aspecific and therefore poor indicators of disease severity.

The effect of trace amounts of tissue factor on thrombin generation in platelet rich plasma, its inhibition by heparin

Abstract: Amounts of human brain thromboplastin that do not stimulate thrombin generation in platelet poor plasma, were shown to advance by about 4 min an explosive formation of thrombin that occurs after recalcification in the presence of blood platelets. This synergistic effect is inhibited by the specific thrombin inhibitor hirudin and mimicked by adding low concentrations (less than 5 nM) of thrombin to platelet rich plasma. It is our conclusion that small amounts of thrombin, generated under the influence of thromboplastin induced procoagulant activity in the blood platelets. This activity is most likely mainly due to procoagulant phospholipids. Heparin inhibits this effect and retards the explosive thrombin formation. It does not, however, diminish the peak amount of thrombin eventually formed, because heparin neutralizing material released from the activated platelets quenches the heparin effect.

Fluid intake and gastrointestinal problems in runners competing in a 25-km race and a marathon

Abstract: A group of 114 previously untrained subjects, 31 females and 83 males, was followed for 18 months while training for a marathon. Forty-four of the subjects completed a survey regarding fluid intakes and gastrointestinal (GI) disturbances during competition for both their first 25-km race (run after 1 year of training) and their first marathon. GI problems were common. Among the individuals surveyed, 25% had GI complaints in the 25-km race. In the marathon, 52% complained of GI distress. In general, fluid consumption was low (25 km means = 109 ml; marathon w = 577 ml). Body weight losses in the marathon were substantial (w = 3.2%, BW; range 1.5%-6.2%) indicating sweat losses greater than fluid replacement. These losses were greater in men than in women (men w = 3.4% BW; women w = 2.6% BW). GI complaints were not associated with larger drink intakes. In contrast, dehydration above a certain limit appears to increase the frequency of GI disorders. In the marathon, 80% of the runners who lost greater than 4% BW had GI problems. It is possible that reduced blood flow to the GI region is compromised via the exercise itself as well as by a reduced blood volume, which may disrupt normal secretion/absorption of the digestive tract. It may also be that a rising core body temperature, associated with decreased sweating at high levels of dehydration, may be related to GI dysfunction.

Anorectal function: defecographic measurement in asymptomatic subjects.

Abstract: A study of anorectal function during fluoroscopically monitored defecation was conducted in 32 asymptomatic subjects. Two observers independently measured various parameters on defecograms and reviewed video recordings during the subjects' squeezing, rest, and straining. There was a wide range of measurements for the anorectal angle, the position of the anorectal junction, perineal motility, and anal canal width. Interobserver variation of these measurements was large. In 17 subjects, both observers agreed that rectal emptying was incomplete. In 10 patients, there was agreement on the presence of rectal wall changes such as intussusception, rectocele, and mucosal prolapse. Defecographic measurements should be interpreted with caution and should not be used as the only criteria for treatment. Anatomic changes of the anorectal region during straining at defecation do not necessarily cause symptoms but may be a precursor of clinical disorders. Defecography is useful in the detection of these abnormalities.

Effect of the notochord on proliferation and differentiation in the neural tube of the chick embryo

Abstract: After implantation of a notochord fragment lateral to the neural tube in a 2-day chick embryo, at 4 days the ipsilateral neural tube half was increased in size and axons left the neural tube in a broad dorsoventral area (van Straaten et al. 1985). This enlargement appears to coincide with an increased area of AChE-positive basal plate neuroblasts, as determined with scan-cytophotometry. The effect was ipsilateral and local: clear effects were seen only when the implant was localized less than 80 microns from the neural tube and over 120 microns from the ventral notochord. In order to investigate the expected enhancement of proliferation, the mitotic density and the number of cells at the site of the implant at 3 days was determined and the mitotic index calculated. All three parameters showed an increase. It was concluded that the cell cycle was shorter in the implant area relative to the control area, at least during the third day. At 4 days the number of cells was still increased, predominantly in the basal plate. It appeared that the numerical increase was for the larger part due to neuroblasts. The synergism of two notochords thus resulted in enhancement of proliferation and differentiation in the neural tube. It is suggested that the notochord merely regulates and arranges the surrounding sclerenchymal cells, which are the effective cells in the regulation of neural tube development.

Exposure of endogenous phosphatidylserine at the outer surface of stimulated platelets is reversed by restoration of aminophospholipid translocase activity.

Abstract: Phosphatidylserine (PS) in the plasma membrane of nonactivated human platelets is almost entirely located on the cytoplasmic side. Stimulation of platelets with the Ca2+ ionophore A23187 or combined action of collagen plus thrombin results in a rapid loss of the asymmetric distribution of PS. Also, treatment with the sulfhydryl-reactive compounds diamide and pyridyldithioethylamine (PDA) causes exposure of PS at the platelet outer surface. PS exposure is sensitively measured as the catalytic potential of platelets to enhance the rate of thrombin formation by the enzyme complex factor Xa-factor Va, since this reaction is essentially dependent on the presence of a PS-containing lipid surface. In this paper we demonstrate that endogenous PS, previously exposed at the outer surface during cell activation or sulfhydryl oxidation, can be translocated back to the cytoplasmic leaflet of the membrane by addition of dithiothreitol (DTT) but not by nonpermeable reducing agents like reduced glutathione. Treatment of platelets with trypsin or chymotrypsin, prior to addition of DTT, inhibits the inward transport of exposed PS. Moreover, severe depletion of metabolic ATP, as obtained by platelet stimulation with A23187 in the presence of metabolic inhibitors, though not inhibiting PS exposure at the outer surface, blocks the translocation of endogenous PS to the internal leaflet of the plasma membrane. These results strongly indicate the involvement of a membrane protein in the inward transport of endogenous PS. Recently, an aminophospholipid-specific translocase in the platelet membrane was postulated on the basis of the inward transport of exogenously added PS (analogues) [Sune, A., Bette-Bobillo, P., Bienvenue, A., Fellmann, P., & Devaux, P.F. (1987) Biochemistry 26, 2972-2978].(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise and training effects on gastric emptying of carbohydrate beverages.

Abstract: Carbohydrate containing drinks are commonly consumed as an ergogenic aid during endurance sports activities. The efficacy of a given drink is limited by the rate of absorption, which is in turn limited by gastric emptying. A myriad of factors influence gastric emptying. The influence of several of these factors (training status, exercise intensity, and carbohydrate composition) was investigated by repeated experiments using a nasogastric tube and a modification of the technique of George. A group of well-trained bicyclists and a group of untrained subjects performed similar experiments. Three different carbohydrate containing drinks (15 g.100 ml-1 glucose (G), 15 g.100 ml-1 maltodextrin plus 3 g.100 ml-1 fructose (MD), 7 g.100 ml-1 sucrose (I] and artificially sweetened water were compared during rest and 50 and 70% Wmax bicycling. Experimental design was crossover. There was a trend for the carbohydrate drinks to empty initially more slowly under the influence of exercise. Differences in drink volume remaining in the stomach were significant (P less than 0.05), with I at 10 min (70%, mean = 48.9%; rest, mean = 30.5%) and at 20 min (70%, mean = 28.9%; rest, mean = 23.8%) and with MD at 10 min (70%, mean = 71.1%; rest, mean = 55.9%). A similar trend was also seen with 50% Wmax exercise; however, this trend was only significant with MD at 10 min (50%, mean = 72.1%; rest, mean = 55.9%). Drink composition was a much stronger inhibitor of gastric emptying. However, all drinks emptied exponentially with fast-phase initial emptying rates. No differences in gastric emptying or secretion were observed between trained and untrained subjects.

Eating, drinking, and cycling. A controlled Tour de France simulation study, Part I.

Abstract: Sustained exhausting exercise is thought to depress appetite and food intake. The aim of the present investigation was to study the effect of intensive cycling exercise, with an energy expenditure comparable to values derived from the Tour de France, on food and fluid intake, energy balance, nitrogen balance, and nutrient oxidation. Thirteen highly trained cyclists consuming a normal carbohydrate (CHO)-rich diet (60 En%) were studied during a 7-day stay in a respiration chamber. Two preparation days were followed by a standardized resting day (3), after which the subjects completed two exhausting exercise days (4-5). On day 6 the standardized resting day was repeated. Food and fluid intake were measured by weighed procedure. Energy expenditure was calculated from continuous gas analysis. Energy and nitrogen losses were calculated from all measured excretes. The results showed that energy balance (EB) and nitrogen balance (NB) were positive on the first resting day and became negative on the exercise days. EB was positive again on the recovery day whereas NB remained negative. Nitrogen losses almost balanced N intakes (1.7 g.kg-1) indicating an increased protein requirement. CHO oxidation exceeded CHO intake indicating endogenous CHO depletion. Contribution of CHO to energy exchange decreased from 51.4% +/- 3.1% on day 4 to 40.6% +/- 3.4% on day 5; this decrease was compensated by an increased fat oxidation. The food consumption pattern during days 4 and 5 was not different from days 2 and 6. In-between meal consumption accounted for 30.5%-34.3% of total energy intake. Fluid consumption was adequate to compensate for the losses.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in Basal Plasma Testosterone, Cortisol, and Dehydroepiandrosterone Sulfate in Previously Untrained Males and Females Preparing for a Marathon

Abstract: In the present study 25 males and 11 females were monitored for an 18- to 20-month training period during which the training distance was gradually increased. The training period was divided into three periods of 6, 5, and 7 months, respectively. The first, second, and third period were concluded with a 15-, 25-, and 42-km road race, respectively. The competitive distance always exceeded the maximal distance covered in any previous training session. Before and after three contests of 15, 25, and 42.195 km, the plasma concentration of testosterone, cortisol, and dehydroepiandrosterone sulfate (DHEAS) were determined. The decrease of plasma testosterone concentration in males was dependent on the distance of the contests. Moreover, the plasma testosterone concentration was increased in males during the course of the training period. In females no clear relation between plasma testosterone levels and the contests could be observed, and no changes in basal levels were found in the course of the training period. DHEAS seems to be a more useful stress marker than the plasma cortisol concentration. The plasma levels of this hormone remained elevated both in males and females for 1-2 days after the contests. The amplitude of DHEAS increments, however, was greater after the marathon.

Lymphocyte homing receptors and adhesion molecules in intravascular malignant lymphomatosis.

Abstract: Intravascular malignant lymphomatosis (IML) is a highly malignant, recently recognized form of lymphoma. It is characterized by multifocal proliferation of malignant lymphocytes within small blood vessels, primarily in the central nervous system and skin, frequently resulting in circulatory disturbances. The cause of the impaired capability of the malignant lymphocytes to extravasate has remained unclear. We analyzed the presence of immunoreactivity for certain homing receptor and adhesion molecules associated with lymphocyte extravasation in 3 patients with this disease. Compared with nonneoplastic leukocytes, large malignant lymphocytes appeared either negative or only weakly positive for the leukocyte surface glycoprotein, CD 18 that is the beta chain of the CD 11 a/CD 18 complex (lymphocytefunction associated antigen-1, LFA-1), which mediates cell-to-cell adhesion of lymphocytes. On the other hand, antibody to one of the proposed ligands for this complex, intercellular adhesion molecule-1, gave positive reactivity both on lymphocytes and on endothelial cells. Further, the malignant lymphoid cells stained positively with Hermes-3 antibody, which recognizes a common structure of CD44 class of molecules involved in lymphocyte homing. It was also shown that HECA-452 antigen, a marker of high endothelial venules (HEV) supporting lymphocyte extravasation, can be synthesized by an IML patient even at the site of inflammation but it is not prerequisite for extravasation of inflammatory lymphocytes. Our results suggest that the deficiency or absence of the adhesion molecule CD 11 a/CD 18 may contribute to the inability of the malignant lymphoid cells to extravasate in IML, and perhaps also to the high malignancy of this form of lymphoma.

Eating, drinking, and cycling. A controlled Tour de France simulation study, Part II. Effect of diet manipulation.

Abstract: Field studies during the Tour de France indicated that cyclists consume 30% of daily energy intake as liquid carbohydrate (CHO)-enriched nutrition with the goal of maintaining energy and CHO balance. The aim of the present investigation was to study the effect of such dietary manipulation during 2 days of long-lasting exhausting cycling on food and fluid intake, energy balance, nitrogen balance, and nutrient oxidation. Thirteen highly trained cyclists were divided into two subgroups receiving ad libitum either a primarily maltodextrin-based beverage (Mf) (20% w/v, 85% maltodextrin, 15% fructose) or a 50/50% composed fructose-maltodextrin (FM) beverage in addition to their normal diet. The study was performed during a 7-day stay in a respiration chamber (2 preparation days, 1 standardized resting day, 2 cycling days, 1.5 standardized recovery days), allowing for continuous gas analysis, weighed food and fluid intake procedure, and collection of excretes. The data of this study were compared with data from the same subjects receiving a normal CHO-rich diet (N) (60 En%) in a separate experiment. The results showed that the cyclists receiving Mf were able to maintain EB during sustained exercise days in contrast to when receiving N and to subjects receiving FM. With Mf treatment CHO intake increased, up to 80 En% (17.5 +/- 1.0 g.kg-1 BW) and carbohydrate balance remained positive. The subjects receiving FM had the largest CHO oxidation, calculated from R. Protein oxidation significantly increased in N and FM as a result of exercise but not in Mf. The latter subjects were in slightly negative nitrogen balance at a protein intake level of 1.4 g.kg-1 BW.(ABSTRACT TRUNCATED AT 250 WORDS)

Fatty acid composition of umbilical arteries and veins: Possible implications for the fetal EFA-status

Abstract: Fatty acid compositions were determined of phospholipids, isolated from umbilical arteries and veins, obtained from Dutch neonates after vaginal delivery, terminating normal pregnancy. The fatty acid profiles of the cord vessels were characterized by the absence of eicosapentaenoic (timnodonic) acid, a low (2–3%) content of linoleic acid and reasonable amounts of arachidonic acid (10–15%) and docosahexaenoic (cervonic) acid (3–5%). Significant amounts of Mead acid (1–4%) and its direct elongation product (0.5–2%) were also observed. In each cord, the efferent blood vessels contained significantly more Mead acid and other fatty acids of the oleic acid (n−9) family and less fatty acids of the linoleic (n−6) and linolenic (n−3) families than the afferent blood vessel. This indicates that the essential fatty acid (EFA) status of ‘downstream’ neonatal tissue may be marginal. No signs of EFA-deficiency were observed in endothelial and smooth muscle cells in culture, or in blood vessels from adults. In all cords 22∶5(n−6) was significantly higher in the artery compared to the vein, whereas for all other (n−6) fatty acids this difference was negative. Since the synthesis of 22∶5(n−6) is known to be stimulated when the required amount of cervonic acid, 22∶6(n−3), is too low, our observations also suggest that the cervonic acid status of the neonates investigated was not optimal. Further studies are in progress to relate these findings to maternal EFA status and complications of pregnancy.

The mode of action of low molecular weight heparin preparation (PK10169) and two of its major components on thrombin generation in plasma.

Abstract: We studied the mode of action of the low molecular weight heparin PK10169 and two of its constituent fractions: EMT 966 High Molecular Weight Fraction and EMT 967 Low Molecular Weight Fraction. EMT 966 like standard heparin, acts primarily on thrombin formed and not on prothrombinase (S type heparin). In contrast EMT 967 has no direct effect on thrombin. At high concentrations, it inhibits the prothrombinase complex (P type heparin). PK10169, that contains the two EMTs shows both activities: antithrombin and antiprothrombinase (mixed type heparin). The addition of increasing amounts of EMT 967 to a constant amount of EMT 966 does not influence the breakdown constant of endogenous thrombin which is determined by the concentration of EMT 966 only. This demonstrates the absence of competition for AT III between the two components of PK10169. In platelet rich plasma, EMT 966 inhibits and postpones thrombin generation more efficiently than unfractionated heparin, probably because it is less sensitive to neutralization by platelet components (platelet factor 4). Amounts of EMT 967 that hardly inhibit thrombin generation in platelet rich plasma enhance the effect of EMT 966 probably by neutralizing platelet factor 4.