No abstract

-When previously sedentary men and women follow exercise training programs with ad libitum feeding, men lose body fat, but women do not. The purpose of this study was to evaluate whether this observation could be related to sex differences in the way energy-regulating hormones and appetite perception respond to exercise. Eighteen (9 men, 9 women) overweight/ obese individuals completed four bouts of exercise with energy added to the baseline diet to maintain energy balance (BAL), and four bouts without energy added to induce energy deficit (DEF). Concentrations of acylated ghrelin, insulin, and leptin, as well as appetite ratings were measured in response to a meal after a no-exercise baseline and both exercise conditions. In men, acylated ghrelin area under the curve (AUC) was not different between conditions. In women, acylated ghrelin AUC was higher after DEF (ϩ32%) and BAL (ϩ25%), and the change from baseline was higher than men (P Ͻ 0.05). In men, insulin AUC was reduced (Ϫ17%) after DEF (P Ͻ 0.05), but not BAL. In women, insulin AUC was lower (P Ͻ 0.05) after DEF (Ϫ28%) and BAL (Ϫ15%). Leptin concentrations were not different across conditions in either sex. In men, but not in women, appetite was inhibited after BAL relative to DEF. The results indicate that, in women, exercise altered energy-regulating hormones in a direction expected to stimulate energy intake, regardless of energy status. In men, the response to exercise was abolished when energy balance was maintained. The data are consistent with the paradigm that mechanisms to maintain body fat are more effective in women. acylated ghrelin; leptin; insulin; physical activity; body fat; food intake EVIDENCE FROM THE NATIONAL WEIGHT CONTROL REGISTRY shows the critical importance of regular aerobic exercise in maintaining lost body weight and body fat (25). On the basis of a strong body of data, the Institute of Medicine indicated that preventing body fat gain over time probably requires 60 min of physical activity per day (4). When previously sedentary individuals begin exercise training programs, however, fat loss is neither inevitable nor consistent across the sexes (11, 36). In general, men lose body fat when they undertake structured exercise training programs with ad libitum eating (9,22,36). In contrast, women do not lose body fat in identical protocols (9,22,36). For example, Donnelly et al. (11) reported that supervised aerobic exercise 5 days/wk for 16 mo lowered body fat and body weight in men who ate ad libitum. In contrast, there were no changes in body fat and body mass in women. These data are corroborated by similar studies showing sex differences in body fat loss or fat oxidation (19,20,36). Taken together, these data suggest that during exercise training, men do not sufficiently increase energy intake to balance their new higher energy expenditure. In contrast, women more precisely match intake with expenditure and therefore maintain body weight and body fat.Sex differences in body fat loss in response to aerobic exercise may result, a...

This study examined substrate use during exercise in early-pubertal (EP), mid-pubertal (MP), late-pubertal (LP), and young-adult (YA) males. Fuel use was calculated using the RER and VO2 response during cycling exercise at 30 to 70% of VO2speak. Significant group by intensity interactions were found for lactate, RER, percent CHO, and fat use, in addition to fat and CHO oxidation rates, which suggest a maturation effect on substrate use during exercise. While significance was not achieved at all intensities, post hoc analyses revealed greater fat use, lower CHO use, and lower lactate concentrations in EP and MP compared to LP or YA. No differences were noted between EP and MP or LP and YA at any intensity, suggesting the development of an adult-like metabolic profile occurs between mid- to late-puberty and is complete by the end of puberty.

Individually, exercise and the drug metformin have been shown to prevent or delay type 2 diabetes. Metformin mildly inhibits complex I of the electron transport system and may impact aerobic capacity in people exercising while tak ing metformin. The purpose of the study was to evaluate the effects of metformin on maximal aerobic capacity in healthy individuals without mitochondrial dysfunction. Seventeen healthy, normal-weight men (n = 11) and women (n = 6) partici pated in a double-blind, placebo-controlled, cross-over design. Peak aerobic capacity was measured twice using a continu ous, incrementally graded protocol; once after 7-9 d of metformin (final dose = 2000 mg/d) and once with placebo, with 1 week between tests. The order of the conditions was counterbalanced. Peak oxygen uptake (VO2 peak), heart rate (HR), ventilation (VE), respiratory exchange ratio (RER), rating of perceived exertion (RPE), and test duration were compared across conditions using paired t tests with the R statistical program. VO2 peak (-2.7%), peak heart rate (-2.0%), peak ven tilation (-6.2%), peak RER (-3.0%), and exercise duration (-4.1%) were all reduced slightly, but significantly, with metformin (all p < 0.05). There was no effect of metformin on RPE or ventilatory breakpoint. Correlations between the decrement in VO2 peak and any of the other outcome variables were weak (r 2 < 0.20) and not significant. Shortterm treatment with metformin has statistically significant, but physiologically subtle, effects that reduce key outcomes related to maximal exercise capacity. Whether this small but consistent effect is manifested in people with insulin re sistance or diabetes who already have some degree of mitochondrial dysfunction remains to be determined.Key words: pre-diabetes, type 2 diabetes, exercise, biguanide.Résumé : Isolément, l'exercice physique et un médicament, la metformine, préviennent ou retardent l'apparition du dia bète de type 2. La metformine inhibe légèrement le complexe I de la chaîne respiratoire et peut avoir un effet sur la capa cité aérobie des individus qui font de l'exercice physique. Le but de cette étude est d'évaluer l'effet de la metformine sur la puissance aérobie maximale d'individus en bonne santé et sans troubles mitochondriaux. Six femmes et 11 hommes en bonne santé et de poids normal participent à une étude expérimentale à double insu avec groupe témoin et inversion des groupes. On mesure deux fois la puissance aérobie de pointe au moyen d'un test d'effort continu d'intensité croissante, une fois après 7 à 9 jours de consommation de metformine (dose terminale, 2 000 mg par jour) et l'autre fois, à sept jours d'écart, après avoir pris un placebo. L'ordre des séances d'évaluation est contrebalancé. Au moyen du programme d'analyse statistique R, on compare par des tests t pour mesures appariées les variables suivantes observées dans les deux conditions : la consommation d'oxygène (VO 2 ) de pointe, la fréquence cardiaque (HR), le débit ventilatoire (VE), le ratio d'échanges gazeux (RER), la p...

Exercise and metformin may prevent or delay Type 2 diabetes by, in part, raising the capacity for fat oxidation. Whether the addition of metformin has additive effects on fat oxidation during and after exercise is unknown. Therefore, the purpose of this study was to evaluate the effect of metformin on substrate oxidation during and after exercise. Using a double-blind, counter-balanced crossover design, substrate oxidation was assessed by indirect calorimetry in 15 individuals taking metformin (2,000 mg/d) and placebo for 8-10 d. Measurements were made during cycle exercise at 5 submaximal cycle workloads, starting at 30% peak work (W(peak)) and increasing by 10% every 8 min to 70% W(peak). Substrate oxidation was also measured for 50 min postexercise. Differences between conditions were assessed using analysis of variance with repeated measures, and values are reported as M + or - SE. During exercise, fat oxidation (0.19 + or - 0.03 vs. 0.15 + or - 0.01 g/min, p < .01) and percentage of energy from fat (32% + or - 3% vs. 28% + or - 3%, p < .01) were higher with metformin than with placebo. Postexercise, metformin slightly lowered fat oxidation (0.12 + or - 0.02 to 0.10 + or - 0.02 g/min, p < .01) compared with placebo. There was an inverse relationship between postexercise fat oxidation and the rate of fat oxidation during exercise (r = -.68, p < .05). In healthy individuals, metformin has opposing actions on fat oxidation during and after exercise. Whether the same effects are evident in insulin-resistant individuals remains to be determined.