Transferrin soluble receptor: a possible probe for detection of erythropoietin abuse by athletes.
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Biomedical subjects
Publications and source records attributed to G R Brisson.
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The purpose of the present study was to describe the relationship between the metabolic rate (W.kg-1 b.m.) and the oxidation rate (mg.kg-1.min-1) of exogenous glucose and fructose during prolonged exercise in 18 healthy active male volunteers (VO2max = 43-71 ml.kg-1.min-1). Each subject performed three 120-min exercises at 60% VO2max (8.5-15.0 W.kg-1.min-1) on cycle ergometer while ingesting water only or 1.33 g.k-1 (97 +/- 9 g; mean +/- SE) of 13C-glucose or 13C-fructose in water (7%). The oxidation rate of exogenous glucose and fructose increased linearly with increasing metabolic rate (r = 0.71 and 0.70, respectively, p < 0.05), the amount of exogenous glucose oxidized being significantly higher than the amount of fructose oxidized (56.1 +/- 14.2 vs 35.7 +/- 9.2 g, respectively). The respective contributions of exogenous glucose and fructose oxidation to the energy yield remain remarkably similar over the range of metabolic rate studied (14.0 +/- 2.1 and 8.9 +/- 1.6%). These observations suggest that the rate of absorption of glucose and fructose and the rate of conversion of fructose into glucose by the liver are not limiting factors for their oxidation, which could simply follow the oxidation rate of circulating glucose. From a practical point of view, these results confirm that fructose is a less efficient energy supplement than exogenous glucose for any metabolic rate sustained.
We computed the respective amounts of exogenous glucose (G) and fructose (F), which are oxidized during exercise when ingested simultaneously, with the use of 13C labeling. Six subjects exercised for 2 h at 60.7 +/- 2.9% of maximal O2 uptake on a cycle ergometer while ingesting 50 or 100 g of G or F or a mixture of 50 g each of G and F in 500 ml of water. The amount of exogenous G oxidized increased from 37.8 +/- 2.2 to 58.3 +/- 8.1 g when the total amount ingested increased from 50 to 100 g. The amount of F oxidized was significantly lower (32.2 +/- 1.2 and 45.8 +/- 2.6 g for the 50 and 100 g ingested, respectively). When 50 g each of G and F were simultaneously ingested in the same drink, the amounts oxidized (39.5 +/- 4.8 and 34.1 +/- 1.5 g, respectively) were similar to those observed when 50 g of G or F were ingested separately. The cumulative amount of exogenous hexoses oxidized (73.6 +/- 6.6 g) was 21% larger than when 100 g of G were ingested. This finding could be due to the fact that the routes for absorption and metabolism of exogenous G and F are at least partly different, resulting in less competition for oxidation when a mixture of these two hexoses is ingested than when an isocaloric amount of G is ingested. From a practical point of view, these data may provide experimental support for using mixtures of carbohydrates in the energy supplements for endurance athletes.
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This study presents a method for computing the respective amounts of two simultaneously ingested exogenous substrates (A and B) that are oxidized during a period of prolonged exercise by use of 13C labeling. This method is based on the observation that the total volume of 13CO2 produced (V13CO2tot) is the sum of 1) V13CO2 arising from the oxidation of endogenous substrates (V13CO2endo), 2) V13CO2 arising from the oxidation of substrate A (V13CO2A), and 3) V13CO2 arising from the oxidation of substrate B (V13CO2B). The equation, V13CO2tot = V13CO2endo+V13CO2A+V13CO2B, with three unknowns, can be solved from the results of three experiments conducted under the same conditions but with at least two values for the isotopic composition of A and B. This method has been used on five healthy male subjects to compute the amounts of glucose and fructose oxidized when a mixture of 15 g of glucose and 15 g of fructose is ingested (in 300 ml of water) over 60 min of cycle ergometer exercise at 65% of maximal O2 uptake. Results from three experiments indicated that 9.8 +/- 3.1 and 5.7 +/- 2.1 g of glucose and fructose, respectively, were oxidized. The total amount of exogenous carbohydrates oxidized (15.5 +/- 4.3 g) is in agreement with the oxidation rates of exogenous glucose computed in similar conditions when 30 g of glucose were ingested (13 g; Péronnet et al. Med. Sci. Sports Exercise 25: 297-302, 1993). The difference between the oxidation rates of exogenous glucose and fructose is also in line with data from the literature.
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The purpose of this study was to reassess the metabolic availability of oral glucose during prolonged exercise in man, using 13C-labeling and a computation procedure (J Appl Physiol 69:1047-1052, 1990) that correctly takes into account changes in isotopic composition of CO2 arising from oxidation of endogenous substrates (Rendo). These changes are due to glucose ingestion associated with exercise. Each of the seven subjects completed three 2-hour periods of exercise at 67% maximum oxygen consumption (VO2max) on an ergocycle, with ingestion of water (1,000 mL) or 60 g (in 1,000 mL water) of 13C-labeled glucose at two levels of enrichment (13C/12C = 1.11482% and 1.13303%). As expected, Rendo significantly increased from rest to exercise with water ingestion (1.09888% +/- .00196% to 1.09970% +/- .00175%) and with glucose ingestion (1.10002% +/- .00159%) due to changes in the respective contributions of endogenous carbohydrates and fat to energy requirements as assessed by the respiratory exchange ratio (RER). When changes in Rendo were taken into account, the estimated amount of exogenous glucose oxidized was 38.8 +/- 10.3 g. Much higher values were found when Rendo at rest or during exercise with water ingestion were used in the computation (42.3 +/- 10.3 to 65.1 +/- 20.5 g) according to the commonly used method. Examination of data in the literature indicates that the reported oxidation rate of exogenous glucose (g/min) is significantly related to oxygen consumption (VO2) (L/min; r = .592) and that exogenous glucose contributes approximately 14% to 17% to the energy requirement.(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of this investigation was to examine the effect of phenylethanolamine N-methyltransferase (PNMT) inhibition on the regulation of peripheral metabolic and hormonal responses during treadmill exercise in the rat. Changes in plasma catecholamine (epinephrine, norepinephrine, and dopamine), glucagon and glucose, and the glycogen content of the liver and two skeletal muscles were studied in four groups of rats. Two groups of rats were studied at rest: one group had been treated with LY134046, an inhibitor of PNMT, and the second group was treated with physiological saline. A third group treated with LY134046 was studied after treadmill exercise (28 m.min-1 and 8% slope). In this group of rats, exhaustion came after 37.5 +/- 7.9 minutes of exercise. In order to make appropriate comparisons, a fourth group of rats treated with physiological saline was exercised for 37.5 min. Running endurance during the treadmill exercise was thus reduced in LY134046-treated rats. Plasma epinephrine and glucagon concentrations and other metabolic (plasma glucose and gastrocnemius lateralis and superficial vastus lateralis muscles and liver glycogen contents) responses were similar between LY134046- and saline-treated rats at rest and after exercise. These results suggest that PNMT inhibition in epinephrine brain neurons might be the principal factor involved in the LY134046-induced reduction of exercise endurance.
The effective control of hypophysial prolactin (PRL) secretion with a pharmacological agent is a prerequisite for the investigation of the role of hyperprolactinemia observed during exercise. Using bromocriptine, a potent inhibitor of PRL secretion, this study established the proper experimental conditions whereby any significant increase in plasma PRL level can be prevented and basal circulating levels maintained during physical exercise. On three occasions at weekly intervals, 15 male adults, separated into two groups, exercised on an ergocycle (40 min at 65% VO2max) either 1 or 3 h after ingesting either placebo or 1.25 or 2.50 mg of bromocriptine mesylate (Parlodel; Sandoz Canada Inc., Dorval, Qué.). Under all conditions, the plasma PRL elevation observed during exercise after placebo was prevented by the administration of bromocriptine. Resting plasma PRL levels were maintained when exercise was performed 1 h after bromocriptine ingestion, but were significantly reduced when exercise was performed 3 h after administration of either bromocriptine dosages. Considering the primary and secondary effects observed, 1.25 mg of bromocriptine administered 1 h before exercise provides suitable experimental conditions to investigate the role of the increase in plasma PRL during physical exercise.
2-Deoxy-D-glucose (2-DG) is a nonmetabolizable analogue of glucose that, by competitive inhibition of glucose utilization, produces a central neuroglucopenia and a peripheral hyperglycemia. This glucopenic agent was used to gain more insight into the combined effects of central glucopenia and exercise on plasma catecholamine response. This was carried out by comparing one group of exercising (26 m/min, 0% grade) rats injected with 2-DG (2-DG-EX; 250 mg/kg iv) with two control groups: one group of exercising rats injected with a saline solution (SAL-EX) and one group of resting rats injected with 2-DG (2-DG-RE). Significant (P less than 0.05) increases in blood glucose levels were observed 10 min after administration of 2-DG (7.2-13.8 and 7.3-12.4 mmol/l in 2-DG-EX and 2-DG-RE groups, respectively). These elevated blood glucose levels were maintained throughout the experiment in the 2-DG-RE condition but decreased in 2-DG-EX rats to levels observed in the SAL-EX group after 45 min of running (13.8-8.0 mmol/l). The combination of 2-DG-induced neuroglucopenia and exercise resulted in an additive response of norepinephrine (0.59 vs. 0.34 and 0.34 ng/ml; t = 12 min) and an amplified epinephrine response (1.4 vs. 0.37 and 0.31 ng/ml; t = 12 min) compared with the responses to each stimulus alone (2-DG-EX vs. 2-DG-RE and SAL-EX, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of this study was to compare the oxidation rate of exogenous 13C-labeled medium-chain triacylglycerols (MCT) with that of an isocaloric amount of exogenous [13C]glucose and to evaluate their respective effects on endocrine and metabolic responses to moderate prolonged exercise. To take into account changes in isotopic composition of 13CO2 arising from oxidation of endogenous substrates because of exercise and/or substrate ingestion that overestimates the oxidation rate of exogenous substrates, two levels of 13C enrichment were used for each substrate. Six young healthy males (20-26 yr of age) completed five 2-h periods of exercise at 65 +/- 3% maximal O2 uptake (VO2max) on a cycle ergometer at 7-day intervals: one control exercise with water ingestion, two trials with ingestion of 25 g of [13C]MCT (trioctanoate) 1 h before exercise, and two trials with 57 g of [13C]glucose (dissolved in 1,000 ml of water) ingested during exercise. Exogenous MCT and glucose began to be oxidized within the first 30 min of exercise, and the oxidation rate increased progressively until the end of exercise for both substrates. Over the 2-h period of exercise, 13.6 +/- 3.5 g of ingested MCT and 36.4 +/- 8.2 g of exogenous glucose were oxidized, which represent 54 and 64%, respectively, of the total amount ingested. The contribution of MCT (119 +/- 31 kcal) and glucose (140 +/- 36 kcal) was not significantly different and represented 7 and 8.5%, respectively, of the total energy expenditure.(ABSTRACT TRUNCATED AT 250 WORDS)
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In the past few years significant progress has been made in the extension of storage time for red blood cells (RBCs). Albeit this, membrane still undergoes damage during conservation under blood bank conditions, reducing red cell viability following transfusion. Consequently in this study, we evaluated the presence of senescence indices (appearing on RBCs during in vivo aging) on blood bank stored RBCs, more precisely the 4.1a/4.1b ratio and the binding of autologous immunoglobulins. Although not significant, a slight increase (0.995 +/- 0.070 to 1.008 +/- 0.058) was observed in the 4.1a/4.1b ratio during the first three weeks of storage. A rapid and significant (p less than 0.001) increase in the number of cell-bound IgGs (91 +/- 22 to 913 +/- 92), following incubation with purified autologous IgGs, was observed in the first days of storage. Thus, following transfusion, binding of autologous IgGs to stored RBCs could influence post-transfusion viability.
Apart from in cystic fibrosis, where sweat analysis provides valuable diagnostic information, sweat yields remain an overlooked biological fluid. Technical problems (dilution, condensation, contamination, evaporation, etc.) linked to currently available collection procedures are of concern and thwart their use. To overcome some of these technical difficulties, an original sweat-collection technique is described. A collection capsule is created inside a flexible, adhesive and disposable anchoring membrane pasted onto the skin. A fluid-tight window is positioned in the upper part of the pocket and gives access to its content. Through the collection window, complete emptying of the sweat collector can be achieved repeatedly by suction using a vacutainer tube inserted in a tube holder equipped with a long dull needle. With prior addition of a suitable marker, fractional samplings can also be performed using a precision micropipette. This collecting method allows for kinetic studies on sweat rate and sweat content. The limited bias-inducing manipulations linked to the described technique, coupled with the ease of performing kinetic studies on sweat volume and content, make this original tool a reliable and accurate sweat-collection technique.
Exercise-induced increases in blood somatotropin (hGH) have always been considered in terms of quantity of the circulating molecules. Knowing that the hypophysis can release several GH species, we investigated the differential release in blood of total hGH (hGHT) and the main hGH variant (hGH20K) molecules in six trained male swimmers exposed to three different conditions known to favor GH release in blood: 45 min--70% maximum oxygen uptake (VO2max) bicycling and swimming, and 20 min of sauna bathing. Based on the binding specificity of hGH antibodies, hGH20K was isolated then assayed using the Nichols immunoradiometric assay system. All three experimental conditions produced significant (P less than 0.001) elevations in blood hGHT and hGH20K. In all three cases, mean blood hGH20K contribution to blood hGHT was relatively constant (11.9, SE 0.7%). Rises in rectal temperature were not statistically related to the changes in blood hGHT. This demonstration of a relatively constant elevation in hGH20K during bicycling, swimming, and sauna bathing can hardly explain the large differences in blood hGHT responses reported in literature under similar conditions.
The purpose of the present investigation was to examine the effects of hyperglycemia induced by supramaximal exercise on blood glucose homeostasis during submaximal exercise following immediately after. Six men were subjected to three experimental situations; in two of these situations, 3 min of high-intensity exercise (corresponding to 112, SD 1% VO2max) was immediately followed by either a 60-min period of submaximal exercise (68, SD 2% VO2max) or a 60-min resting period. In the third situation, subjects performed a 63-min period of submaximal exercise only. There were no significant differences between the heart rates, oxygen uptakes, and respiratory exchange ratios during the two submaximal exercise bouts (greater than 15 min) whether or not preceded by supramaximal exercise. The supramaximal exercise was associated within 10 min of the start increases (P less than 0.05) in blood glucose, insulin, and lactate concentrations. This hyperglycemia was more pronounced when subjects continued to exercise submaximally than when they rested (at 7.5 min; P less than 0.05). There was a more rapid return to normal exercise blood glucose and insulin values during submaximal exercise compared with rest. The data show that the hyperinsulinemia following supramaximal exercise is corrected in between 10-30 min during submaximal exercise following immediately, suggesting that this exercise combination does not lead to premature hypoglycemia.
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