Linewidths from sum rules in mixed crystals.
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Biomedical subjects
Publications and source records attributed to A Tremblay.
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The purpose of this experiment was to assess the effects of short-term overfeeding (mixed diet) on the thermic effect of a meal (TEM) and associated hormonal changes and to investigate the role of the genotype in the observed changes. Six pairs of male sedentary monozygotic (MZ) twins consumed an extra 1,000 kcal per day over their individual level of energy expenditure while maintaining a sedentary existence. Resting metabolic rate (RMR) and TEM following a 4.2 MJ meal challenge was measured before and after 22 days of overfeeding. RMR did not change significantly (7% elevation) in response to the positive caloric stimulus, whereas significant increases (P less than 0.01) in TEM were observed. Moreover, postprandial insulin and glucose responses were not modified. Overfeeding did not significantly alter catecholamine levels but induced significant elevations in plasma levels of T3 and T4 (P less than 0.05). Changes in RMR exhibited moderate but nonsignificant within twin pair resemblance in response whereas significant within pair resemblance was noted in the magnitude of TEM changes induced by overfeeding (P less than 0.05). Hormonal responses exhibited a weaker genotype dependency. These results suggest that short-term overfeeding can induce an elevation in TEM with accompanying increases in T3 and T4. Large individual response variation in metabolic and hormonal measures were observed. The similarity of response within twin pairs suggests that sensitivity to change in TEM induced by short-term overfeeding is genetically influenced.
This study investigated the effects of overfeeding on the body composition and fat morphology characteristics of 6 pairs of male monozygotic twins. Each participant was submitted to a 22-day overfeeding period, supplemented by an additional 1000 kcal/day. Significant changes were observed in body composition and fat morphology as shown by increases in body weight, fat mass, sum of 9 skinfolds, and fat cell diameter. Significant within-pair resemblance for absolute changes was observed for body weight, percent body fat, fat mass, sum of skinfolds, trunk skinfolds, and extremity skinfolds, suggesting a role for the genotype in determining the sensitivity of the response to an energy surplus. Significant within-pair resemblance was noted for the biceps, triceps, and thigh with less resemblance noted in the subscapular, abdomen, suprailiac, calf, axillary, and chest sites, suggesting a variation in genotype dependency for subcutaneous fat. The results suggest that changes in body fat following short-term overfeeding appear to have a genetic basis.
The present study investigated the interaction of genotype and short-term overfeeding on adipose tissue metabolism of six pairs of male monozygotic twins. The sedentary nonobese twins were submitted to a 22-day overfeeding period in which their normal daily intake was supplemented by an additional 1,000 kcal/day. A fat tissue biopsy was performed in the suprailiac region before and after overfeeding to determine fat cell diameter and basal and maximal stimulated epinephrine, norepinephrine, and isoproterenol lipolysis from collagenase-isolated fat cells. Fat cell basal and maximal insulin-stimulated glucose conversion into triglycerides (basal and stimulated lipogenesis) were measured using [14C]glucose. Adipose tissue heparin-releasable lipoprotein lipase activity (LPL) was also determined. A repeated measures analysis of variance revealed overfeeding induced significant elevations in basal lipogenesis (P less than 0.05) and fat cell diameter (P less than 0.05). No significant group changes were noted in basal, epinephrine-, norepinephrine-, and isoproterenol-stimulated lipolysis, insulin-stimulated lipogenesis, and LPL activity due to large individual variation in the response to overfeeding. However, significant intrapair resemblance was noted in the changes of the aforementioned variables, suggesting a coherent within-twin pair response, despite large between-pair variation in response. Less within-pair similarity was noted in changes in basal lipogenesis and fat cell diameter. The results of the present study suggest that overfeeding induced a large range of adipose tissue metabolic responses and that the genotype plays a role in determining the sensitivity of adipose tissue adaptation to caloric affluence.
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.
Two experiments have been performed to establish whether exercise-training has an influence on resting metabolic rate (RMR). In a first study, RMR was measured in a cohort of 59 individuals comprising 20 trained and 39 non-trained subjects. The absolute level of RMR in trained subjects exceeded by 11 percent that observed in the non-trained individuals (P less than 0.01). When comparing regression lines of RMR versus FFM between the two groups, the intercept with the Y axis (RMR values) was also significantly higher in trained subjects (P less than 0.01). The second experiment was conducted to find out whether the trend for an elevated RMR noted in athletes could be reproduced in obese persons engaging in an exercise-training program. Eight moderately obese women were submitted to an 11-week training programme, including 5 hours of aerobic exercise per week performed at a mean intensity of about 50 percent VO2 max. The results showed that exercise-training induced a significant rise in RMR which corresponded to 8 percent of pretraining value in kcal/kg FFM/min (P less than 0.01). Thus, data reported here suggest that aerobic exercise-training is associated with an elevated RMR per unit of fat free mass in both lean and moderately obese individuals.
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.
Twenty-four male black African (25.5 +/- 3.0, mean +/- s.d., years of age) and 24 male Caucasian (21.5 +/- 3.6) subjects, ascertained as sedentary individuals, participated in this study designed to determine whether there were racial differences in fat distribution and adipose tissue metabolism while controlling the differences in body fat. An adipose tissue biopsy was obtained from the suprailiac region for the determination of basal (BL), epinephrine submaximal 10(-4) M (ESML) and maximal 10(-3) M (EML) stimulated lipolysis, basal (BLG) and maximal insulin 9 microU/ml (ILG) stimulated lipogenesis and heparin releasable lipoprotein lipase (LPL) activity. Body density was determined through underwater weighing procedures and body fat derived with the Siri equation. The following skinfolds were also measured: triceps, biceps, subscapular, abdomen, suprailiac, front thigh and medial calf. Caucasians were matched with the black Africans for age, body weight and body density. Results indicated that when Caucasians and black Africans of similar percentage body fat were compared, no significant differences were observed in the total amount of subcutaneous fat, fat distribution and suprailiac mean fat cell size. Moreover, no significant differences were observed between the two groups for BL, BLG, and ILG of adipose tissue. However, black Africans had higher (P less than 0.01) epinephrine stimulated lipolytic values (ESML and EML) and LPL activity (P less than 0.01) than the Caucasian subjects. These results suggest that for a comparable level of fatness and similar fat morphology and distribution, there are racial differences in adipose tissue metabolism.
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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.
In order to study the effect of alterations in fat morphology and metabolism induced by exercise-training on plasma lipids, 13 healthy young men were subjected to a 20-week aerobic training program on bicycle. Training significantly increased maximal aerobic power (VO2 max) (P less than 0.001) and decreased per cent body fat (P less than 0.001). A significant reduction of mean adipocyte diameter and an increase in isolated fat cell epinephrine-stimulated lipolysis were also observed following training. However, with the exception of total cholesterol, no changes were noted in plasma lipids. Neither before nor after training were triglycerides and high density lipoprotein cholesterol (HDL-C) correlated with VO2 max, fat cell diameter and adipocyte-stimulated lipolysis. The present study demonstrates that an important fat loss (mean loss of fat = 3 kg) and a significant gain in VO2 max induced by endurance training do not necessarily produce an increase in HDL-C levels in normal male subjects. Moreover, changes in VO2 max, body fatness and in fat cell epinephrine-stimulated lipolysis produced by endurance training are not related to modifications in plasma lipids in healthy men.