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Biomedical subjects

A Orsetti

Publications and source records attributed to A Orsetti.

At least 19 recordsLinked to original sources
PubMed1999

Effects of zinc supplementation on blood rheology during exercise.

We previously reported a higher blood viscosity at corrected hematocrit (45%) (explained by a higher value of erythrocyte rigidity) in football players with low serum zinc (Zn) and thus presumably Zn deficiency; subjects with low serum zinc had also an impairment in performance. This interventional study was undertaken in order to assess the effects of zinc supplementation (compared to placebo) on blood rheology and performance either at rest or during exercise. Ten male healthy volunteers (age: 26+/-1.3 yr; weight 67.9+/-2.24 kg; height 177+/-3 cm) received at random order either zinc (20 mg/day) and placebo, according to a double blind cross-over procedure, during seven days. In each case on the eighth day they performed a 25 min submaximal exercise-test. At rest blood viscosity at corrected hematocrit 45% (gamma = 1000 s(-1)) was lower after Zn (3.56+/-0.14 vs. 4.13+/-0.16 mPa.s, p = 0.009), explained by a lower RBC rigidity index 'k' according to Quemada's equation (1.65+/-0.07 vs. 1.84+/-0.08, p = 0.03). Hematocrit and plasma viscosity were unchanged, but RBC aggregation was decreased (laser retrodiffusion-derived aggregation time 'Ta' 3.52+/-0.51 vs. 2.75+/-0.59, p = 0.02). The increase in blood viscosity during exercise is lower after Zn than placebo. Blood viscosity at corrected hematocrit 45% remains unchanged during exercise after Zn, yet it increases after placebo. RBC rigidity index 'k' remains lower during exercise after Zn. The rating of perceived exertion (Borg's scale) at the 20th minute of exercise is lower after zinc (5.6+/-0.4 vs. 6.6+/-0.4, p = 0.008). This study confirms that Zn improves erythrocyte deformability, decreases the exercise-induced acute increase in blood viscosity, and improves exercise tolerance. Since Zn deficiencies are not unfrequent in sportsmen, these findings may be potentially relevant to sports nutrition.

Adult↗
PubMed1998

Negative correlation between plasma fibrinogen and insulin sensitivity measured with the minimal model technique.

We aimed at investigating relationship between plasma fibrinogen and insulin sensitivity, which are two major determinants of metabolic Syndrome X (insulin resistance syndrome). We designed a prospective study of 27 non-diabetic, non-hypertensive subjects, presenting a wide range of body mass index BMI (10 men, 17 women; mean age+/-SEM: 35.9+/-2.2 years; BMI ranging from 21.1-45.2 kg/m2). Insulin sensitivity was assessed with the minimal model procedure, over a 180 min intravenous glucose tolerance test with iterative sampling. Fibrinogen levels were determined by the method of Clauss. The insulin sensitivity index SI (i.e., the slope of the dose-response relationship between insulin increased above baseline and glucose disposal) ranged from 0.0009 to 16 x 10(-4) min(-1)/(microU/ml), with a mean value of 4.76+/-0.73 x 10(-4). Mean values of plasma fibrinogen were 3.33+/-0.13 g/l, ranging from 2.21 to 5.07 g/l. There were highly significant negative correlations between SI and the level of plasma fibrinogen (r = -0.61, p = 0.0007) and between the basal effect of insulin BIE and plasma fibrinogen (r = -0.521, p = 0.005). Basal insulin was positively correlated to fibrinogen (r = 0.386, p = 0.046). When we analysed the data using partial correlation analysis, the negative relation between SI and fibrinogen was maintained independently from BMI (r = -0.45, p < 0.05). These data establish a strong negative association between insulin sensitivity and fibrinogen, involved in the increased cardiovascular risk of metabolic Syndrome X.

Adult↗
PubMed1998

The triphasic effects of exercise on blood rheology: which relevance to physiology and pathophysiology?

The life-extending effects of regular exercise are related to a decrease in both coronary and peripheral vascular morbidity, associated with some improvements in cardiovascular risk factors. A possible link between the beneficial metabolic and hemodynamic effects of exercise could be blood rheology, which is markedly affected by exercise. We propose here a description of the hemorheological effects of exercise as a triphasic phenomenon. Short-term effects of exercise are an increase in blood viscosity resulting from both fluid shifts and alterations of erythrocyte rheologic properties (rigidity and aggregability). Increased blood lactate, stress, and acute phase play a role in this process. Middle-term effects of regular exercise are a reversal of these acute effects with an increase in blood fluidity, explained by plasma volume expansion (autohemodilution) that lowers both plasma viscosity and hematocrit. Long-term effects further improve blood fluidity, parallel with the classical training-induced hormonal and metabolic alterations. While body composition, blood lipid pattern, and fibrinogen improve (thus decreasing plasma viscosity), erythrocyte metabolic and rheologic properties are modified, with a reduction in aggregability and rigidity. On the whole, these improvements reflect a reversal of the so-called "insulin-resistance syndrome" induced by a sedentary lifestyle. Since impaired blood rheology has been demonstrated to be at risk for vascular diseases, the hemorheologic effects of exercise can be hypothesized to be a mechanism (or at least a marker) of risk reversal. This latter point requires further investigation. The physiological meaning of the triphasic pattern of exercise-induced alterations of blood rheology is uncompletely understood, but increased blood fluidity may improve several steps of oxygen transfer to muscle, as clearly demonstrated in hypoxic conditions. Increasing evidence emerges from the literature, that blood fluidity is a physiological determinant of fitness.

Exercise↗
PubMed1997

Metabolic and hormonal responses during repeated bouts of brief and intense exercise: effects of pre-exercise glucose ingestion.

We investigated metabolic and hormonal responses during repeated bouts of brief and intense exercise (a force-velocity test; Fv test) and examined the effect of glucose ingestion on these responses and on exercise performance. The test was performed twice by seven subjects [27 (2) years] according to a double-blind randomized crossover protocol. During the experimental trial (GLU), the subjects ingested 500 ml of glucose polymer solution containing 25 g glucose 15 min before starting the exercise. During the control trial (CON), the subjects received an equal volume of sweet placebo (aspartame). Exercise performance was assessed by calculating peak anaerobic power (W(an,peak)). Venous plasma lactate concentration increased significantly during the Fv test (P < 0.001), but no difference was found between CON and GLU. Blood glucose first decreased significantly from the beginning of exercise up to the 6-kg load (P < 0.001) and then increased significantly at W(an,peak) and for up to 10 min during the recovery period (P < 0.001) in both CON and GLU. Insulin concentrations decreased significantly in both groups, but were higher at W(an,peak) in GLU compared with CON (P < 0.05). Glucagon and epinephrine did not change significantly in either group, but epinephrine was significantly lower in GLU after glucose ingestion (P < 0.05) and at W(an,peak) (P < 0.05). W(an,peak) was not significantly different between CON and GLU. In conclusion, blood glucose and insulin concentrations decreased during repeated bouts of brief and intense exercise, while blood lactate concentration increased markedly without any significant change in glucagon and epinephrine concentrations. Glucose ingestion altered metabolic and hormonal responses during the Fv test, but the performance as measured by W(an,peak) was not changed.

Adult↗
PubMed1997

[Interrelation of visceral fat and muscle mass in non insulin-dependent diabetes (type II): practical implications].

Insulin resistance, which is found in 85-95% of non-insulin-dependent diabetes mellitus (NIDDM) patients, results from three factors: genetic background (which has been widely investigated), nutritional status (mostly obesity and fat distribution) and exercise. Upper body obesity, which can be found in 85% of these subjects, can increase muscular insulin resistance through several mechanisms, the best known being a free fatty acid-induced decrease in intracellular free CoA/acylCoA that inhibits the stimulatory effect of insulin on glycolysis, glucose transport across cell membrane, and glycogen storage. However, muscle insulin resistance in NIDDM exists before adiposity and is likely to induce it. Actually, muscles of subjects at risk for NIDDM exhibit a very early defect in both glycogen storage ability and free fatty acid oxidation capacity that can impair fuel utilization and increase fat storage. Regular exercise induces muscular metabolic changes which can compensate for those diabetogenic defects and thus prove useful in the management of NIDDM. Moreover, exercise has been shown to prevent subjects at risk for NIDDM from developing overt diabetes.

Abdomen↗
PubMed1996

Increased insulin sensitivity and basal insulin effectiveness in postprandial reactive hypoglycaemia.

Glucose clamp experiments have shown that patients with reactive postprandial hypoglycaemia (PRH) frequently have an increased glucose disposal, but the relative involvement of insulin sensitivity (SI) and glucose effectiveness (Sg) in this process remains unknown. The minimal model approach was used to compare 13 patients in whom moderate reactive hypoglycaemia ( < 3.3 mmol) had been previously diagnosed and 13 matched controls. The intravenous glucose tolerance test (IVGTT, 0.5 g/kg glucose IV) with 0.02 U/kg insulin given at the 19th min and frequent sampling over 180 min shows that PRH patients exhibit a higher glucose tolerance coefficient Kg (2.99 +/- 0.26 vs 2.19 +/- 0.12; P < 0.02), higher SI [22.9 +/- 6.4 vs 7.18 +/- 0.14 min-1/(microU/ml). 10(-4); P < 0.01] and higher Sg (3.84 +/- 0.35 vs 2.92 +/- 0.79 min-1. 10(-2); P < 0.05). The increase in Sg is explained by an increase in its component basal insulin effectiveness (BIE: 1.2 +/- 0.27 min-1.10(-2) in PRH subjects vs 0.58 +/- 0.07; P < 0.05) rather than an increase in Sg at zero insulin. The increase in BIE results from the high values of SI. In 4 PRH subjects SI and Sg were within the normal range, and the increase in Kg evidenced in the 9 others was explained by an increase in SI alone in 3 cases, in Sg alone in 1 case, and both SI and Sg in 5 cases. Thus, in sedentary subjects, the previously reported rise in tissue glucose assimilation is mainly explained by an increased insulin-mediated glucose disposal rather than non-insulin-mediated glucose disposal.

Adult↗
PubMed1996

Endogenous oploid peptides stimulate post-exercise insulin response to glucose in rats.

Exercise is associated with profound changes in glucose metabolism and insulin secretion. Endogenous opioid peptides may be involved in these metabolic adaptations. To gain insights into this hypothesis, we studied the effects of the opioid antagonist naloxone on the insulin response to glucose after a 2.5 h exercise bout, either by means of an intravascular glucose tolerance test in male Wistar rats or from rat islets of Langerhans isolated just after exercise. There was a tenfold increase in plasma beta-endorphin concentrations (9.8 +/- 2.1 vs. 114.2 +/- 22.0 fmol/ml, p < 0.001) in animals killed immediately after exercise. The in vivo post-exercise peak insulin response to glucose was markedly reduced compared to resting controls (p < 0.01). Interestingly, naloxone (10 mg/kg) still further decreased the insulin response compared to saline injected exercised rats (p < 0.05), but did not alter the response from resting animals. The post-exercise insulin response to 8.3 mM glucose was significantly reduced compared to resting rat islets (p < 0.05) and was further inhibited when naloxone (10 mu M) was added to the culture medium (p < 0.05). In another experiment, we also tested the effect of 10(-8) and 10(-6) M beta-endorphin on control islets. Both concentrations of beta-endorphin significantly increased the islet insulin response to 8.3 mM glucose (p < 0.05) and this effect was completely blocked by naloxone. These results suggest that endogenous opioid peptides participate in the physiological adaptation to exercise stress in maintaining post-exercise insulin response to glucose.

Adaptation, Physiological↗
PubMed1996

[Blood viscosity is correlated with insulin resistance].

The insulin resistance syndrome (or syndrome X) is a cluster of symptoms (dyslipidemia, impaired glucose tolerance, overweight, hypertension) associated with a higher risk of atherosclerosis. It has been suggested that hemorheological abnormalities, often found in association with most of these symptoms, may be a part of this syndrome, and possibly play a role in the circulatory abnormalities. In 22 nondiabetic women (20-54 years) presenting a wide range of body mass index (from 20 to 48 kg/m2), insulin sensitivity was assessed with the minimal model procedure, over a 180 min intravenous glucose tolerance test with frequent sampling. The insulin sensitivity index SI (i.e. the slope of the dose-response relationship between insulin increased above baseline and glucose disposal) ranges between 0.1 and 20.1 x 10(-4) min-1/microU/ml) i.e all the range of insulin sensitivity. SI was negatively correlated with blood viscosity (r = -0.530 p < 0.02), body mass index (r = 0.563 p < 0.01) and baseline insulinemia (r = 0.489 p < 0.05). These correlations were independent of each other and were not explained by relationships between SI and fibrinogen or blood lipids. Thus, blood fluidity is correlated with insulin sensitivity when it is measured with an accurate technique, suggesting that blood hyperviscosity is a symptom of insulin resistance that might be involved in the cardiovascular risk of this syndrome.

Adult↗
PubMed1995

Evaluation of a standardized hyperglucidic breakfast test in postprandial reactive hypoglycaemia.

The oral glucose tolerance test is not specific for diagnosing postprandial reactive hypoglycaemia, since it too frequently induces low blood glucose values in subjects who have never complained of symptoms of this. By contrast, the mixed meal tests are deceptive for this purpose because they do not induce hypoglycaemia in subjects who have complained of of hypoglycaemic symptoms. We investigated the frequency of hypoglycaemia after a standardized hyperglucidic breakfast test in three groups of subjects:group A, 43 control subjects; group B, 38 postprandial reactive hypoglycaemic patients; group C, 1193 asymptomatic subjects undergoing assessment of glycoregulation. In the 38 subjects with suspected reactive hypoglycaemia the mean blood glucose nadir was 3.48 +/- 0.08 mmol/l, i.e. lower than in control subjects (4.83 +/- 0.13 p < 0.0001). Blood glucose levels less than 3.3 mmol/l were found in 47.3% of subjects with suspected postprandial reactive hypoglycaemia (group B), i.e more frequently than in control subjects (group A: 2.2% p = 1.6 x 10(-6)) and asymptomatic subjects (group C: 1% p = 8 x 10(-22)). This markedly higher frequency of low blood glucose values in subjects with postprandial symptoms compared with control and asymptomatic subjects suggests that this test detects a tendency to hypoglycaemia after a standardized hyperglucidic breakfast. Since this test mimics average French eating habits, the results suggest that the patients undergo such symptoms in their everyday life, and that the hyperglucidic breakfast test is a simple alternative to ambulatory glucose sampling for diagnosis of postprandial reactive hypoglycaemia.

Adult↗
PubMed1995

Effects of zamic as a means for zinc supplementation in growing children.

We investigated the effects of zinc supplementation in case of moderate growth retardation in which GH treatment could not be used. Zamic (ZA, an association containing arginine, L-methionine, and zinc; from Aguettant pharmaceuticals) was compared with arginine aspartate (AA) (5 g) in a crossover randomized trial (6 mo of each treatment at random order over 1 yr). We present preliminary results of 24 children who completed the study (3 girls, 21 boys, age 9-13 yr). Subjects had to be prepubertal, with no GH deficiency diagnosed. In 15 subjects growth velocity was lower than 5 mm/mo: In this case ZA improved growth velocity (rising from 3.105 +/- 0.229 to 5.4 +/- 0.69 mm/mo p < 0.01), whereas the effect of AA was not significant. The increase in growth velocity was higher with ZA (+2.44 +/- 0.657 mm/mo) than AA (+0.438 +/- 0.450 mm/mo) p < 0.05. These results suggest that ZA is more efficient than AA, consistent with the hypothesis that zinc needs are increased in those children in this period of life.

Adolescent↗
PubMed1995

Influence of short-term submaximal exercise on parameters of glucose assimilation analyzed with the minimal model.

After exercise, glucose uptake in tissues increases by insulin-dependent and -independent mechanisms. We evaluated whether these two effects of exercise on glucose disposal can be detected with the minimal model technique. Seven healthy volunteers were submitted at random order to two frequently sampled intravenous glucose tolerance test (FSIVGTTs), one at rest and the other 25 minutes after a 15-minute exercise test. This exercise included 5 minutes of increasing workload on a cycloergometer followed by 10 minutes at 85% of the maximal theoretic heart rate. Bergman's minimal model of insulin action was used to analyze the two FSIVGTTs and produced the following parameters: coefficient of glucose tolerance (Kg), ie, the slope of the exponential decrease in glycemia between 4 and 19 minutes after intravenous glucose; insulin sensitivity (Sl); and glucose effectiveness at basal insulin (Sg). Sg was divided into its two components: basal insulin effectiveness ([BIE] Sl x basal insulin) and glucose effectiveness at zero insulin ([GEZI] Sg-BIE). After the exercise bout, subjects had an increased Kg (3.44 +/- 0.44 v 2.06 +/- 0.28 x 10(-2).min-1, P < .02), Sl (11.43 +/- 1.27 v 6.23 +/- 0.97 x 10(-4) microU/mL.min-1, P < .01), and Sg (4.40 +/- 0.55 v 2.81 +/- 0.36 x 10(-2).min-1, P < .02). The increase in Sg was mainly explained by a 60% increase in GEZI (3.6 +/- 0.57 v 2.25 +/- 0.36 x 10(-2).min-1, P < .02), but also by an increase in BIE (0.80 +/- 0.12 v 0.47 +/- 0.08 x 10(-2).min-1, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Effects of naloxone opiate blockade on the immunomodulation induced by exercise in rats.

The purpose of this study was to examine the possible involvement of the endogenous opiate system in the changes in immune competence induced by isolated exercise. Male untrained rats were subjected to a 2.5 hours swimming exercise bout. Animals were killed 15 min after the end of the exercise. The concentration of leukocytes, lymphocytes, monocytes and granulocytes and T4 (T-helper), T8 (T-suppressor/cytotoxic), interleukin-2 receptor (IL-2R) and transferrin receptor (TrfR) positive lymphocytes were determined both in peripheral blood and spleen by flow cytometric analysis. Exercise resulted in a significant decrease in 1) blood lymphocyte and splenic granulocyte number (p < 0.05), 2) blood and splenic T4 positive lymphocytes and T4/T8 ratio (p < 0.05), and 3) blood and splenic IL-2R and TrfR positive lymphocytes (p < 0.05). The injection of the opiate blocker naloxone to exercising rats induced a decrease in the concentration and proportion of T8 positive lymphocytes, thereby restoring a normal T4/T8 ratio both in peripheral blood and spleen. Naloxone had no effect in control animals. The concentration and proportion of IL-2R and TrfR positive lymphocytes were not affected by naloxone. The mechanisms of the immunomodulation induced by isolated intense exercise are unclear. These data suggest that endogenous opiates participate in the alteration of cell-mediated immunity associated with exercise by modulating the T8 (suppressor/cytotoxic)-cell activity.

Animals↗
PubMed1995

Protective effect of gamma-hydroxybutyrate and nicotinamide on low-dose streptozotocin-induced diabetes in mice.

The purpose of this study was to investigate the effect of a treatment by gamma-hydroxybutyrate (GHB) and nicotinamide (NA) on low-dose streptozotocin (STZ)-induced diabetes in mice. Mean plasma glucose level was significantly elevated in mice given STZ by day 12 after the first STZ injection compared to controls (15.0 +/- 4.7 vs 8.0 +/- 1.6 mmol/l, p < 0.001) and 100% of the animals were severely diabetic by day 18. Plasma glucose levels remained in the normal range and no diabetic values were found in mice treated with combined treatment by GHB and NA for 25 days. However, hyperglycemia and glycosuria appeared within one week after discontinuation of the treatment. Treatment by either GHB or NA alone had only a slight and transient effect in preventing hyperglycemia. In vitro experiment on isolated pancreatic islets demonstrated that STZ-induced loss of insulin response to glucose was also counteracted by incubation with GHB and NA (Peak insulin response to 16.4 mM glucose: 0.69 +/- 0.31 vs 3.03 +/- 0.67 microU/islet/min), but not by GHB or NA alone. These results indicate that GHB and NA have complementary effects in preventing STZ-induced beta cell damage both in vivo and in vitro. This should be taken into account for future preventive strategies in human insulin-dependent diabetes mellitus.

Animals↗
PubMed1994

Plasma beta-endorphin, corticotrophin and growth hormone responses to exercise in pubertal and prepubertal children.

An increase in plasma beta-endorphin concentrations during exercise has been reported in adult men and women by several investigators. However, very little is known about this physiological hormonal response to exercise in children. In this study, we investigated plasma beta-endorphin, ACTH and GH responses to exercise in 40 prepubertal and pubertal children. Subjects were recruited as part of a population of children and adolescents presenting growth retardation and were selected on the basis of the absence of any clinical or biological signs of endocrine or metabolic disease. There were 16 girls and 24 boys with 24 prepubertal and 16 pubertal individuals. A standardised 15 min workload on cycloergometer was used to progressively increase the heart rate of the children up to 90% of the theoretical maximal value. Exercise resulted in a significant increase (p < 0.01) in plasma beta-endorphin (mean +/- SEM) (4.26 +/- 0.47 vs 5.74 +/- 0.56 fmol/ml), ACTH (3.71 +/- 0.41 vs 6.2 +/- 0.62 fmol/ml) and GH (147 +/- 29 vs 364 +/- 67 fmol/ml). The percentage of children with significant hormonal response to exercise was about 75% for each of the 3 hormones but only 3 of the 40 children studied did not show any hormonal response to exercise. Exercise-induced increases in plasma beta-endorphin and ACTH were significantly correlated (p < 0.01). By contrast, there was no significant relationship between GH and beta-endorphin or ACTH values. Furthermore, whereas exercise-induced plasma GH increase was significantly higher in pubertal than in prepubertal children (p < 0.001), corresponding beta-endorphin and ACTH levels were quite similar in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

The magnitude, the kinetics and the metabolic efficiency of first-phase insulin response to intravenous glucose are related.

We investigated the relationship between the kinetics, the magnitude and the metabolic efficiency of first-phase insulin response (FPIR) to intravenous glucose. Twenty healthy control subjects and fifty first degree relatives of Type 1 diabetic patients were studied using a standardized protocol for the intravenous glucose tolerance test (IVGTT). The first significant increase in plasma insulin concentrations above baseline appeared as early as the 2nd min (1 min before the end of glucose injection, fast response) in 80% of controls and 70% of relatives, and at the 3rd min or later (delayed response) in the remaining subjects. The greatest delay in insulin release (5th min) was observed in 4 of 6 relatives of Type 1 diabetic patients with impaired FPIR. In the controls and the relatives, the subjects with a fast insulin response had a significantly higher FPIR (controls 215.4 +/- 93.5 vs 59.7 +/- 5.6 microU/ml, p < 0.001 and relatives 143.5 +/- 61.8 vs 55.9 +/- 27.7 microU/ml, p < 0.001) and showed better glucose assimilation (controls 3.05 +/- 1.05 vs 1.64 +/- 0.16%/min, p < 0.05 and relatives 2.6 +/- 0.96 vs 1.6 +/- 0.85%/min, p < 0.01) during IVGTT than the subjects with a delayed response. Moreover, for normal FPIR values in the group of relatives of Type 1 diabetic patients, a fast response was associated with a significantly better glucose assimilation as assessed by the incremental area under the glucose curve (358.6 +/- 64.7 vs 539.2 +/- 67.7 mmol/l per 90 min, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Determination of urinary testosterone and epitestosterone during pubertal development: a cross-sectional study in 141 normal male subjects.

OBJECTIVES: Exogenous testosterone administration is classically detected by measuring the ratio of testosterone to epitestosterone in urine. Athletes are considered to be positive for drug abuse if the urinary testosterone to epitestosterone ratio is greater than 6. We aimed at investigating the urinary excretion of testosterone and epitestosterone during pubertal development. DESIGN: We performed a cross-sectional study of 141 normal male subjects between ages 8 and 26 years. PATIENTS: We studied 141 subjects: 32 at stage 1 of Tanner, 27 at stage 2, 30 at stage 3, 25 at stage 4 and 27 at stage 5. MEASUREMENTS: Subjects performed a 24-hour urine collection. Urinary testosterone and epitestosterone were measured by gas chromatography-mass spectrometry with selected ion monitoring. RESULTS: Urinary testosterone was 20.5 +/- 1.7 nmol/24 h (mean +/- SEM) at stage 1, 49 +/- 2.9 at stage 2, 98.8 +/- 3.4 at stage 3, 371.8 +/- 21.8 at stage 4 and 403.4 +/- 16.1 nmol/24h at stage 5. Urinary epitestosterone was 13.1 +/- 1.5 nmol/24h at stage 1, 29.1 +/- 3.3 at stage 2, 48.3 +/- 3.7 at stage 3, 156.3 +/- 14.8 at stage 4 and 221.1 +/- 18.6 nmol/24h at stage 5. The urinary excretions of both steroids increased significantly during puberty and were highly correlated with chronological age (P < 0.001). Comparison of the correlation slopes (P < 0.001) showed that the urinary profiles of testosterone and epitestosterone are not parallel during pubertal development. Two subjects presented a testosterone to epitestosterone ratio above 6, corresponding to a low urinary concentration of epitestosterone, without pathological explanation. CONCLUSION: Testosterone and epitestosterone do not present the same urinary profiles throughout puberty. Marked increases of the testosterone to epitestosterone ratio can be observed at this period and may interfere with doping tests.

Adolescent↗