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Biomedical subjects

A Nadeau

Publications and source records attributed to A Nadeau.

At least 163 records · Page 9Linked to original sources
PubMed1986

Heredity and changes in hormones and metabolic rates with short-term training.

The purpose of this experiment was to assess the effects of a 22-day training program on resting metabolic rate (RMR), thermic effect of a meal (TEM), and associated hormonal changes. Six pairs of male monozygotic twins were submitted to a 22-day ergocycle exercise program designed to induce a deficit in energy balance of 4.2 MJ per day. RMR and TEM after a 4.2-MJ meal challenge were measured before and after training. Results indicated that RMR and TEM did not change significantly, although a large variation in response between twin pairs was observed. Moreover, training reduced (P less than 0.05) basal and postprandial insulin response, plasma thyroid hormones triiodothyronine (T3), thyroxine (T4), and FT4 (P less than 0.05). Absolute changes in RMR and TEM exhibited significant within-pair resemblance in response, with intraclass correlations reaching r = 0.81 (P less than 0.05) and r = 0.72 (P less than 0.05), respectively. Changes in T4 and FT4 also exhibited moderate within-pair resemblance (0.42 less than or equal to r less than or equal to 0.71). These results suggest that short-term exercise training does not modify RMR and TEM but can significantly decrease plasma levels of insulin and thyroid hormones. Moreover, the similarity of response within twin pairs suggests that heredity plays a role in determining RMR, TEM, and thyroid hormone adaptation to exercise training generating a negative energy balance.

Adolescent↗
PubMed1986

The role of body fat in insulin sensitivity of endurance athletes.

The purpose of the study was to assess the role of adiposity in the enhanced insulin sensitivity observed in endurance athletes (EA). An oral glucose tolerance test (75 g glucose) was administered to nine EA and to 23 sedentary subjects (SS). Two different strategies were used to investigate the problem. First, body composition indicators and Vo2max were correlated with the delta insulin and delta glucose areas measured for 180 minutes following glucose ingestion. These correlation analyses were performed for the two groups combined (n = 32). No significant correlations were observed between either fat weight or percent body fat versus delta insulin, delta glucose or delta glucose/delta insulin areas. Moreover, no significant correlation was observed between the several subcutaneous fat indicators and delta insulin, delta glucose and delta glucose/delta insulin areas. The second strategy consisted of comparing EA to SS when percent body fat difference was eliminated. This was achieved by two different methods, first by covariance analysis and second by comparing subsamples of trained and non-trained subjects paired with respect to percent body fat. These two comparisons revealed that even when adiposity was equal between the groups, a significantly greater insulin sensitivity was observed in the EA group (p less than 0.01). The present results suggest that adiposity is not the determining factor for the increased insulin sensitivity of trained subjects.

Adipose Tissue↗
PubMed1985

Contribution of the exercise-induced increment in glucose storage to the increased insulin sensitivity of endurance athletes.

The present study was designed to evaluate the contribution of the exercise-induced increment in glucose storage to the increased insulin sensitivity characterizing endurance athletes. Plasma glucose and insulin were measured during an oral glucose tolerance test (OGTT) in six endurance athletes. Glucose storage and lipid oxidation during this test were also determined using indirect calorimetry. These measurements were compared to those obtained in five non-trained subjects who were tested before and during the three days following a 90-min cycle ergometer exercise performed at 69% of their VO2max. As expected, preexercise values of non-trained subjects revealed a much higher insulin response to glucose, and a lower glucose storage and lipid oxidation compared to results obtained in endurance trained individuals. Glucose tolerance was comparable in both groups. The morning following the exercise test, i.e. about 16 h after exercise, glucose storage was significantly increased in non-trained subjects to a level similar to that found in trained subjects. Surprisingly, this was accompanied by higher values of glucose during the OGTT without significant changes in insulinaemia. This impairment in glucose homeostasis was transitory since glucose tolerance had returned to control level on day 2 after exercise. At that time, the increase in glucose storage was less pronounced than in day 1. On day 3 after exercise, glucose and insulin responses to glucose were similar to preexercise values. These results indicate that the increase in glucose storage by acute exercise is not systematically associated with an improved glucose homeostasis, suggesting that other adaptive mechanisms also contribute to the improvement of insulin sensitivity in endurance athletes.

Adult↗
PubMed1985

Contribution of postexercise increment in glucose storage to variations in glucose-induced thermogenesis in endurance athletes.

The present study was undertaken to evaluate the contribution of an increment in glucose storage to the reduced glucose-induced thermogenesis (GIT) characterizing endurance-trained individuals. For that purpose, glucose storage and GIT were determined during an oral glucose tolerance test (OGTT) in eight elite endurance athletes exercising between 6 and 16 h/week. Their values were compared with those obtained in five nontrained subjects submitted to two OGTT, i.e., before and 16 h after they had performed a 90-min vigorous exercise. As expected, endurance athletes exhibited a reduced GIT and a greater glucose storage during the OGTT in comparison to the preexercise values of nontrained subjects. Once the latter subjects had performed the 90-min exercise, their glucose storage during the OGTT was similar to the level found in athletes. This adaptation was accompanied by a significant reduction in GIT, which corresponded to 47% of the difference observed between trained and nontrained subjects when both groups maintained their usual life habits. Unlike GIT, resting metabolic rate (RMR) was found to be higher in athletes than in nontrained individuals. When subdividing the athletes into two subgroups on the basis of the duration of their weekly training, it was found that RMR was mainly elevated in those performing the higher amount of exercise. These results demonstrate that the reduced GIT characterizing endurance-trained individuals is partly explained by an increase in glucose storage during an OGTT. As further discussed, this reduced GIT is likely an indirect consequence of modifications of other energy-requiring energy processes rather than a direct result of the postexercise increment in glucose storage.

Adipose Tissue↗
PubMed1985

Hyperglycemic effect of high doses of dobutamine in the rat: studies of insulin and glucagon secretion.

The influence of dobutamine on glucoregulation has been assessed in the rat during and after an intravenous infusion given at the following doses: 0, 0.1, 1.0, 10, 100, and 1000 micrograms X kg-1 X min-1. Plasma glucose, insulin, and glucagon levels were measured at 15-min intervals in unanesthetized previously cannulated rats. Basal glucose levels were preserved with the less than or equal to 10 micrograms X kg-1 X min-1 doses. At the greater than or equal to 100 micrograms X kg-1 X min-1 doses, a marked hyperglycemic effect was observed, partly attributable to some inhibitory effect of dobutamine on glucose-induced insulin secretion and to its stimulatory effect on glucagon secretion. Such data suggest that dobutamine may disturb the normal glucose homeostasis, particularly in situations of deficient insulin reserve.

Animals↗
PubMed1985

Diminished glucagon response to epinephrine in physically trained diabetic rats.

The effect of physical training on glucose, insulin, and glucagon response to epinephrine was assessed in normal and diabetic rats. Male Wistar rats were injected with streptozocin (STZ, 45 mg/kg) and those presenting 1 wk later a blood glucose value between 250 and 400 mg/dl were retained in the protocol and randomly assigned to a sedentary or trained group. Similar studies were conducted in control animals. Physical training was done on a treadmill according to a 10-wk program. Epinephrine (0.75 microgram/kg/min) was infused intravenously (i.v.) in previously cannulated rats for 1 h and arterial blood samples obtained at 15-min intervals for glucose, insulin, and glucagon measurements. Pancreatic insulin and glucagon content was also determined. Basal glucose levels were significantly lower in trained than in sedentary diabetic rats (P less than 0.01). The hyperglycemic response to epinephrine was diminished by 19% and 23% in trained control and diabetic animals, respectively, with a faster return to baseline after stopping epinephrine infusion in both trained groups. Although in nondiabetic rats this could be related to some diminution in the suppressive effect of epinephrine on insulin secretion, this was not the case in diabetic animals. Moreover, while training did not modify epinephrine-induced glucagon response in control rats, the twofold greater (P less than 0.01) glucagon response observed in sedentary diabetic rats was restored to normal in trained diabetic rats. After stopping epinephrine infusion, glucagon levels dropped below the baseline in both groups of trained rats but not in their sedentary counterparts. These effects of training on glucagon response could not be explained by changes in pancreatic glucagon content.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Plasma, adrenal, and heart catecholamines in physically trained normal and diabetic rats.

This study was designed to evaluate the possibility that the enhanced insulin sensitivity of physically trained normal and diabetic rats is due to adaptive changes in the adrenergic system. Mild diabetes mellitus was induced in male Wistar rats with streptozocin (STZ, 45 mg/kg i.v.) and a 10-wk conditioning program was conducted by having the animals run on a treadmill. Rats were cannulated 16 h after the last period of exercise and blood sampling was obtained 48 h later for basal plasma glucose, insulin, epinephrine, and norepinephrine determination. Catecholamine measurements were also made in adrenals, atria, and ventricles from sedentary control, trained control, sedentary diabetic, and trained diabetic rats. The previously reported beneficial effect of physical training on diabetes mellitus was reproduced. While diabetes mellitus did not modify the catecholamine levels, the training program provoked an increase in plasma epinephrine concentrations, with a concomitant significant rise in adrenal epinephrine content. In heart tissue, the epinephrine values also tended to be increased by training although statistical significance was not reached. These data suggest that basal secretion of epinephrine is somewhat increased in trained rats. Whether this may trigger adaptive changes that could be involved in the beneficial effect of physical training on experimental diabetes mellitus remains to be elucidated.

Adrenal Glands↗
PubMed1983

The influence of high carbohydrate diet on plasma glucose and insulin of trained subjects.

In previous studies we have shown that when endurance athletes refrain from daily exercise for three days, they rapidly loose their enhanced insulin sensitivity. This finding suggests that a precompetitive high carbohydrate diet with reduced training might alter plasma glucose and insulin regulation. To test this hypothesis, six long distance runners were recruited to participate in a five-day experiment. During the first two days, the subjects fasted while running 16 km d-1. Thereafter, they consumed 16.3 MJ (3900 kcal) and 539 g carbohydrate per day for three days while remaining inactive. Before and after each portion of this experiment, an intravenous glucose tolerance test (IVGTT) was performed in fasting state. As expected, fasting with exercise induced a considerable deterioration of glucose tolerance, as reflected by lower K value and higher total area glucose during IVGTT. The high carbohydrate refeeding restored glucose tolerance to a level comparable to that observed when subjects maintain their usual life habits. However, while a decrease in insulin sensitivity is observed in subjects inactive for three days, the insulin sparing effect of exercise training is retained if this period of inactivity is preceded by two days of fast accompanied by exercise. These results show that glucose disposal and insulin response to glucose injection are not adversely modified by the precompetitive "glycogen loading" procedure.

Blood Glucose↗
PubMed1983

Daily variations of plasma glucose and insulin in physically-trained and sedentary subjects.

The variations in plasma glucose and insulin levels were measured at 30-minute intervals throughout the day in physically trained and in sedentary subjects. The subjects exercised for 75 minutes at 65% of VO2max in the first experiment and refrained from heavy exercise in the second experiment. In all situations the physically trained subjects overall had lower plasma glucose and insulin levels than the nontrained subjects. In addition, the positive correlation between plasma glucose and plasma insulin levels observed in the physically trained subjects was significantly smaller than that note in the nontrained subjects, indicating reduced insulin requirements in physically-trained persons. During the period of exercise, glucose levels increased significantly in the trained subjects only. In the period that followed exercise, that is between 1:30 PM and 9:00 PM, the physically trained subjects had plasma glucose levels that were higher than those noted during the comparable hours not preceded by exercise; no comparable difference were found with insulin. Calculation of the total area for insulin indicated a reduction of insulin requirement of about 40% associated with physical training.

Adult↗
PubMed1983

Long-term changes in the diabetic state induced by different doses of streptozotocin in rats.

The long-term effects of different doses (0, 25, 35, 45, 55, 65 and 100 mg/kg) of streptozotocin (STZ) in male Wistar rats had been followed over a 16 week period. The weight-gain curve and the epididymal fat pad weight were significantly different (P less than 0.05) from control after 1 week with the 65 and 100 mg/kg doses and after 4 weeks with the 45 and 55 mg/kg doses; there were no significant changes with the 25 and 35 mg/kg doses even after 16 weeks. An i.v. glucose tolerance test (0.5 g/kg) was performed at 1, 4 or 16 weeks after the injection of STZ. The basal levels of glucose were significantly elevated (P less than 0.05) after 1 week with the greater than or equal to 55 mg/kg doses, and after 16 weeks with the greater than or equal to 45 mg/kg doses; there was also an overall increase in the basal glucose levels between 1 and 16 weeks in rats treated with the greater than or equal to 45 mg/kg doses. The basal insulin levels were significantly decreased (P less than 0.05) after 1 week with the greater than or equal to 65 mg/kg doses, after 4 weeks with the greater than or equal to 55 mg/kg doses and after 16 weeks with the greater than or equal to 35 mg/kg doses. The insulin peak 2 min after the glucose load was significantly less (P less than 0.05) after 1 week with the greater than or equal to 35 mg/kg doses and after 16 weeks with the greater than or equal to 25 mg/kg doses. The use of an insulinogenic index to assess the insulin secretory capacity showed a significant decrease (P less than 0.05) for the greater than or equal to 35 mg/kg doses at each tested time; with the 45 mg/kg dose, there was a further significant decrease (P less than 0.01) between the first and sixteenth week. The present long-term studies showed that there is a progressive deterioration in the glucose tolerance and insulin secretion after the injection of different doses of STZ. Furthermore, changes in glucose-insulin interrelationships over time suggest that the insulin insensitivity previously described in STZ diabetic rats might be only an early transient phenomenon.

Adipose Tissue↗
PubMed1982

Variations in plasma glucose, insulin, growth hormone and catecholamines in response to insulin in trained and non-trained subjects.

Previous studies have shown a reduced insulin secretion in trained subjects challenged by a glucose load. In the present study the response to insulin of 8 athletes was compared to that of 8 non-trained subjects. The disappearance of plasma insulin was not different between the two groups, but the level of hypoglycemia was greater in the trained subjects. The injection of insulin increased the plasma levels of epinephrine (E) and norepinephrine (NE) in both groups of subjects, but the raise in E was greater in the trained subjects. Similarly, the increase of growth hormone (GH) was greater in the trained subjects. These findings substantiate previous results showing a decreased insulinic index and an increased insulin binding to monocytes in trained subjects. It is also suggested that the enhanced E and GH secretion found in trained subjects injected with insulin, is possibly related to the greater fall in plasma glucose in the trained subjects compared to the non-trained subjects.

Adult↗
PubMed1982

Effects of physical training on beta-adrenergic receptors in rat myocardial tissue.

A diminished sympathetic activity has been related to training bradycardia seen at rest and during exercise. In order to evaluate if changes in heart adrenergic receptors can be one of the mechanisms by which the sympathetic responsiveness could be decreased by physical training, the number and affinity of beta-adrenergic receptors were determined in heart ventricular tissue of rats submitted to a 10-week running programme. Binding studies were done at different concentrations of (-)[3H] dihydroalprenolol (DHA) (0.5 to 14.4 nmol X litre-1) with ventricular membrane preparations from control and trained rats. Direct linear plot analysis revealed that physical training reduced the total number (1933 +/- 192 vs 2922 +/- 211 fmol X ventricles-1; P less than 0.01) density of beta-adrenergic receptors expressed either as fmol X mg-1 of membrane protein (34 +/- 3 vs 43 +/- 3; P less than 0.05) or as fmol X g-1 ventricle (1740 +/- 170 vs 2308 +/- 155; P less than 0.05). There was no significant change in the dissociation constant (3.11 +/- 0.14 vs 4.08 +/- 0.51 nmol X litre-1; P greater than 0.05). Basal plasma noradrenaline levels were not affected by training (116 +/- 18 vs 101 +/- 14 pg X cm-3; P greater than 0.10); however the adrenaline values were significantly higher in trained rats (91 +/- 16 vs 47 +/- 7 pg X cm-3; P less than 0.05). These data indicate that physical training induces changes at the level of beta-adrenergic receptors and this may partly explain the bradycardia seen in trained subjects and animals.

Animals↗
PubMed1982

Beneficial effects of physical training in rats with a mild streptozotocin-induced diabetes mellitus.

The present studies have been designed to evaluate the effects of physical training in rats with a diminished insulin reserve. Mild diabetes mellitus was induced in rats with 45 mg/kg streptozotocin. Physical training was done on a treadmill, with a progressive program, twice daily, 5 days per week, for 10 wk in control and diabetic rats. At the end of the training program, a significant diminution in body weight gain and in epididymal fat pad weight was observed in both trained groups, as compared with sedentary controls. Sixty-four hours after the last exercise, control (N = 16), control-trained (N = 14), diabetic (N = 17), and diabetic-trained (N = 15) rats were submitted to an intravenous glucose tolerance test (0.5 g/kg). Arterial blood samples were collected at -15, 0, 2, 4, 6, 10, 15, 30, 45, and 60 min during the test in unanesthetized and precannulated rats for plasma glucose and insulin determinations. In normal rats, physical training induced a sharp decrease in the basal insulin levels (36 +/- vs. 101 +/- 6 microunits/ml; P less than 0.001) without any significant changes in glucose levels (122 +/- 4 vs. 129 +/- 2 mg/dl; P less than 0.05). After the glucose loading there was no significant change in the glucose tolerance curve, although the insulin values remained lower throughout the test in the trained group. In the diabetic rats, the elevated basal glucose levels were significantly diminished in the trained group as compared with the untrained diabetic group (177 +/- 22 vs. 306 +/- 37 mg/dl; P less than 0.001), although the basal insulin values were similar in both groups (51 +/- 7 vs. 54 +/- 9 microunits/ml; P greater than 0.05). The improvement in the glucose tolerance of the diabetic-trained rats was further confirmed by the glucose disappearance rate constant that was significantly increased (3.6 0.4 vs. 2.0 +/- 0.3; P less than 0.01), although not fully restored to normal (6.3 +/- 0.2; P less than 0.001). These data clearly show that in rats with a diminished insulin reserve, a 10-wk running program greatly improved the glucose homeostasis. Measurements of circulating insulin suggest that, although an effect on insulin secretion cannot be totally excluded, the beneficial effect of physical training on diabetes mellitus is probably best explained by an increase in insulin sensitivity.

Animals↗
PubMed1981

Studies on the sparing effect of exercise on insulin requirements in human subjects.

The reduced insulin response of trained subjects in the presence of normal glucose tolerance has been confirmed. It was also found that this beneficial effect of exercise is greatly reduced if trained subjects are inactive for 3 days while eating ad libidum. During that period excessive food intake (3291 cal/day) was noted. However, when the subjects were on a restricted diet (2076 cal/day) the reduced insulin response to a glucose load was retained. The ratio of food intake with regard to caloric utilization is possibly the important modulator of the action of exercise on insulin requirements. The effect of exercise on insulin secretion was also found to be acquired rapidly since it was observed 18 hr after 1 hr of physical activity at 70% of V02 max in non-trained subjects. For all these studies a correlation (p less than 0.01) was found between the secretion of insulin in response to glucose challenge and both basal plasma glucose and insulin.

Adolescent↗
PubMed1979

Effects of physical training and adiposity on glucose metabolism and 125I-insulin binding.

Eighteen young male subjects, aged 18-30 yr, with maximal oxygen intake (VO2max) varying between 36 and 80 ml.kg-1.min-1, were studied. Between 20 and 120 min after injection, tolerance to iv glucose (20 g/m2) was not affected by VO2max but the insulin response was very significantly reduced in the better trained subjects. 125I-insulin binding to monocytes was found to be greater in the best trained subjects. Simple correlation analysis indicates that both VO2max and adiposity are related to plasma glucose and plasma insulin levels as well as to 125I-insulin binding. Because VO2max is negatively correlated to percent of body fat, a partial correlation analysis was made. Results indicate that the differences observed in athletes with regard to glucose and insulin levels and 125I-insulin binding are related to reduced adiposity rather than to enhanced VO2max.

Adipose Tissue↗
PubMed1977

Effect of somatostatin on thyrotropin, prolactin, growth hormone and insulin responses to thyrotropin releasing hormone and arginine in healthy, hypothyroid and acromegalic subjects.

The effect of somatostatin on the thyrotropin (TSH), prolactin, growth hormone (GH) and insulin responses to the combined administration of thyrotropin releasing hormone (TRH) and arginine was studied in six healthy subjects, three hypothyroid patients and three acromegalic patients. Similar inhibition by somatostatin of the TSH and insulin responses was observed in the three groups. While the tetradecapeptide had no significant effect on the prolactin response in the healthy and acromegalic subjects, it caused an unexpected inhibition of the prolactin response in two of the hypothyroid subjects. Contrary to the findings in the healthy and hypothyroid subjects, somatostatin did not inhibit the GH response in the acromegalic patients. Normal inhibition by somatostatin of the insulin response, followed by a rebound in insulin secretion, was observed in all subjects. These preliminary data indicate increased sensitivity of the prolactin-secreting cells to somatostatin in hypothyroidism and suggest that decreased responsiveness of the somatotrophs to somatostatin could play a role in the pathogenesis of acromegaly.

Acromegaly↗