The aim of this study was to investigate, in markedly obese children, the effect of puberty on substrate oxidation during an acute bout of exercise. Two groups of markedly obese boys (7 pre pubertal, 8 post pubertal, matched for adiposity) performed an exercise-test designed for measuring carbohydrate and fat oxidation with indirect calorimetry, and consisting of five six-minute steady-state workloads at 20, 30, 40, 50, and 60 % of the theoretical maximal aerobic power. Fat oxidation (mg . min (-1)) is correlated to fat free mass (FFM) (r = 0.7, p = 0.02). When expressed in crude flow rate units, fat oxidation is slightly higher in PostP than PreP children (p < 0.05). However, when expressed per unit of FFM or as a percentage of total fuel oxidation, fat oxidation is lower in PostP than PreP children (p < 0.05). Multivariable analysis shows that the influence of age on the ability to oxidize fat at exercise is explained by the pubertal increase in FFM. In markedly obese children during puberty, the ability of each kg of FFM to oxidize fat at exercise decreases (- 28% at 20%Wmax th), but the pubertal increase in FFM overcomes this effect, resulting in an increase in whole body ability to oxidize fat at exercise (+ 17,3% at 20%Wmax th).
This study evaluated the accuracy of surrogate indexes of insulin sensitivity (SI) in children. Surrogates (homeostasis model assessment index of insulin resistance, quick insulin sensitivity index, and 40/insulin ratio index) were cross-sectionally investigated in 66 obese and lean children (17 Tanner stage I, 19 Tanner stage II-III, and 30 Tanner stage IV-V) as indexes of insulin resistance in comparison with the minimal model. The pubertal decrease in SI was found with the minimal model (-47%; P = 0.01), but not with surrogates, which were not correlated to SI. Baseline insulin (Ib) did not mirror the decrease in SI, did not significantly change when plotted against pubertal stage or age, and was not correlated to SI. Ib and surrogates were positively correlated with the body mass index. The disposition index, which quantifies the feedback between SI and insulin release, was widely scattered and decreased during puberty (P = 0.05). The specificity and sensitivity of surrogates as predictors of insulin resistance were poor (e.g. 81.1% and 30.7%, respectively, for the homeostasis model assessment index of insulin resistance). Thus, during puberty, surrogates are not accurate predictors of insulin resistance. Because reference methods are rather expensive and invasive, additional studies of alternative techniques for evaluating SI are needed to allow accurate measurement of insulin resistance in children.
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