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We determined whether cold water swimming for six consecutive months results in adaptive changes in body composition and insulin sensitivity. Thirty healthy subjects aged 50.2 ± 9.4 years were exposed to cold water at least twice a week. Body composition was determined and serum glucose and insulin served to calculate beta-cell function, insulin sensitivity, and resistance using HOMA2. Compared with control subjects, swimmers were overweight, and had greater percent body fat and beta cell function. Women had lower values of BMI, fat free mass, muscle mass, visceral adipose tissue level, and greater percent body fat than men. Increased insulin sensitivity and decreased insulin secretion and resistance from beginning to middle of swim season was observed in females and in lean subjects. Findings suggest that men and women differ in regard to body composition and response to repeated cold exposure. Cold water swimming may beneficially modulate insulin sensitivity in cold acclimated lean swimmers.

Pre-exercise carbohydrate feeding may result in rebound hypoglycemia in some but not all athletes. The aim of the present study was to examine whether insulin sensitivity in athletes who develop rebound hypoglycemia is higher compared with those who do not show rebound hypoglycemia. Twenty trained athletes (V̇O_2max of 61.8 ± 1.4 ml · kg⁻¹ · min⁻¹) performed an exercise trial on a cycle ergometer. Forty-five minutes before the start of exercise, subjects consumed 500 ml of a beverage containing 75 g of glucose. The exercise trial consisted of · 20 min of submaximal exercise at 74 ± 1% V̇O_2max immediately followed by a time trial. Based upon the plasma glucose nadir reached during submaximal exercise, subjects were assigned to a Hypo group (<3.5 mmol/L) and a Non-hypo group (≥3.5 mmol/L). An oral glucose tolerance test was performed to obtain an index of insulin sensitivity (ISI). The plasma glucose nadir during submaximal exercise was significantly lower (p < .01) in the Hypo-group (n = 10) compared with the Non-hypo group (n = 10) (2.7 ± 0.1 vs. 4.1 ± 0.2 mmol/L, respectively). No difference was found in ISI between the Hypo and the Non-hypo group (3.7 ± 0.4 vs. 3.8 ± 0.5, respectively). The present results suggest that insulin sensitivity does not play an important role in the occurrence of rebound hypoglycemia.

It is unclear whether long-term aerobic (AT) or resistance (RT) training can improve insulin sensitivity (IS) beyond the residual effect of the last training bout in older women (54–78 years). Therefore, a group of nonobese, healthy older women underwent 6 months of AT (n = 8) or RT (n = 10), and the authors measured IS 4 days after the last training bouts using the hyperinsulinemic-euglycemic clamp technique. Women trained 3 days/week. AT consisted of 25- to 60-min sessions of walking/jogging at 60–95% of maximal heart rate. RT consisted of three sets of nine exercises repeated 10 times at 80% of 1 repetition maximum. AT decreased fat mass, whereas both AT and RT increased fat-free mass. Neither training program, however, improved absolute or relative rates of glucose disposal. The authors therefore concluded that nonobese, healthy older women should perform AT or RT on a daily basis in order to improve IS and maintain the improvement.

Unaccustomed eccentric exercise using large muscle groups elicits soreness, decrements in physical function and impairs markers of whole-body insulin sensitivity; although these effects are attenuated with a repeated exposure. Eccentric exercise of a small muscle group (elbow flexors) displays similar soreness and damage profiles in response to repeated exposure. However, it is unknown whether damage to small muscle groups impacts upon whole-body insulin sensitivity. This pilot investigation aimed to characterize whole-body insulin sensitivity in response to repeated bouts of eccentric exercise of the elbow flexors. Nine healthy males completed two bouts of eccentric exercise separated by 2 weeks. Insulin resistance (updated homeostasis model of insulin resistance, HOMA2-IR) and muscle damage profiles (soreness and physical function) were assessed before, and 48 h after exercise. Matsuda insulin sensitivity indices (ISI_Matsuda) were also determined in 6 participants at the same time points as HOMA2-IR. Soreness was elevated, and physical function impaired, by both bouts of exercise (both p < .05) but to a lesser extent following bout 2 (time x bout interaction, p < .05). Eccentric exercise decreased ISI_Matsuda after the first but not the second bout of eccentric exercise (time x bout interaction p < .05). Eccentric exercise performed with an isolated upper limb impairs whole-body insulin sensitivity after the first, but not the second, bout.

Vanadium compounds have been shown to have insulin-like properties in rats and non-insulin-dependent diabetic humans. The purpose of the present study was to examine whether the effects of acute and short-term administration of vanadyl sulphate (VS) on insulin sensitivity also exist in healthy active individuals. Five male and 2 female participants (age: 24.9 ± 1.5 years; height: 176.1 ± 2.9 cm; body mass: 70.1 ± 2.9 kg) underwent 3 oral glucose tolerance tests (OGTT). The first OGTT was performed to obtain a baseline index of insulin sensitivity (ISI). On the night preceding the second OGTT, participants ingested 100 mg of VS, and the acute effects of VS on ISI were examined. For the next 6 days, participants were instructed to ingest 50 mg of VS twice daily, and a final OGTT was performed on day 7 to determine the short-term effects of VS on ISI. No differences were found in fasting plasma glucose and insulin concentrations after VS administration. Furthermore, ISI after 1 day and 7 days of VS administration was not different compared with baseline ISI (4.8±0.1 vs. 4.7±0.1 vs. 4.7 ± 0.1, respectively). These results demonstrate that there are no acute and short-term effects of VS administration on insulin sensitivity in healthy humans.

We initiated a pilot study to investigate the effects of 8 wks of aerobic exercise training (ET) on insulin sensitivity and inflammatory markers in obese and insulin-resistant minority adolescents. Eleven morbidly obese (BMI 41.4 ± 1.8 kg/m²) minority adolescents were entered into a supervised ET intervention (~180 min/wk at 40–55%VO_2PeakR [(VO_2Peak − VO_2Rest)/VO_2Rest]). The effects of training on insulin sensitivity (S_I), inflammation and other metabolic syndrome features were examined. Results: Insulin action improved in response to training, as indicated by a ~37% increase in S_I (p = .018). Plasma levels of several proinflammatory cytokines were reduced in response to ET, as indicated by significant decrements in sTNF-R, CCL2, MPO, IL-6, resistin, and leptin, with no significant changes in hsCRP. ET induced reductions in BMI and percent total body fat. Conclusions: The present study supports the efficacy of ET interventions on metabolic syndrome features in morbidly obese minority youth.

Nosotros iniciamos un estudio piloto para investigar los efectos de 8 semanas de entrenamiento con ejercicios aeróbicos (EA) sobre la sensibilidad insulinica y los marcadores inflamatorios en un grupo minoritario de adolescentes abesos con resistencia a lá insulina. Once adolescentes con obesidad mórbida (IMC 41, 4+1.8kg/m²) fueron asignados a un grupo de intervención que realizo un EA supervisado (~180 min/semana al 40-55%VO₂ picoR [(VO₂Pico − VO₂Reposo)/VO₂Reposo]). Se analizo el efecto del entrenamiento sobre la sensibilidad insulinica (IS), inflamación y otras características del síndrome metabòlico. RESULATDOS: El incremento del 37% en la SI (p = 0.018) indico que La acción de la insulina mejora en respuesta al entrenamiento. Como indican la disminución significativa de sTNF-R, CCL2, MPO, IL-6, resistina, and leptina, y la falta de cambios significativos en hsCR, los niveles plasmáticos de varias citoquinas proinflamatorias se redujeron en respuesta al EA. Además, el entrenamiento produjo una reducción del IMC y del porcentaje de grasa corporal. CONCLUSIONES: Los resultados del presente estudio apoyan la eficacia de una intervención con EA sobre las características del síndrome metabólico en un grupo minoritario de adolescentes con obesidad mórbida.

We determined the effect of a high-fat diet and carbohydrate (CHO) restoration on substrate oxidation and glucose tolerance in 7 competitive ultra-endurance athletes (peak oxygen uptake [V̇O_2peak] 68 ± 1 ml · kg⁻¹ · min⁻¹; mean±SEM). For 6 days, subjects consumed a random order of a high-fat (69% fat; FAT-adapt) or a high-CHO (70% CHO; HCHO) diet, each followed by 1 day of a high-CHO diet. Treatments were separated by an 18-day wash out. Substrate oxidation was determined during submaximal cycling (20 min at 65% V̇O_2peak) prior to and following the 6 day dietary interventions. Fat oxidation at baseline was not different between treatments (17.4 ± 2.1 vs. 16.1 ± 1.3 g · 20 min⁻¹ for FAT-adapt and HCHO, respectively) but increased 34% after 6 days of FAT-adapt (to 23.3 ± 0.9 g · 20 min⁻¹, p < .05) and decreased 30% after HCHO (to 11.3±1.4 g · 20 min⁻¹, p < .05). Glucose tolerance, determined by the area under the plasma [glucose] versus time curve during an oral glucose tolerance (OGTT) test, was similar at baseline (545±21 vs. 520±28 mmol · L⁻¹ · 90 min⁻¹), after 5-d of dietary intervention (563 ± 26 vs. 520 ± 18 mmol · L⁻¹ · 90 min⁻¹) and after 1 d of high-CHO (491 ± 28 vs. 489 ± 22 mmol · L⁻¹ · 90min⁻¹ for FAT- adapt and HCHO, respectively). An index of whole-body insulin sensitivity (S_I 10000/÷fasting [glucose] × fasting [insulin] × mean [glucose] during OGTT × mean [insulin] during OGTT) was similar at baseline (15 ± 2 vs. 17 ± 5 arbitrary units), after 5-d of dietary intervention (15 ± 2 vs. 15 ± 2) and after 24 h of CHO loading (17 ± 3 vs. 18 ± 2 for FAT- adapt and HCHO, respectively). We conclude that despite marked changes in the pattern of substrate oxidation during submaximal exercise, short-term adaptation to a high-fat diet does not alter whole-body glucose tolerance or an index of insulin sensitivity in highly-trained individuals.