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Roy L.P.G. Jentjens and Asker E. Jeukendrup

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.

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Roy L.P.G. Jentjens and Asker E. Jeukendrup

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 (V̇O2max 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% V̇O2max 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.

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William M. Sherman, Julie M. Lash, John C. Simonsen, and Susan A. Bloomfield

Because muscle damage from eccentric exercise has been associated with alterations in muscle glycogen metabolism, this study determined the effects of exercise on the insulin and glucose responses to an oral glucose tolerance test (OGTT). In a repeated-measures design, 11 subjects undertook either no exercise, 2 min of isokinetic leg exercise, or 50 min of level or downhill running. No exercise was performed and diet was controlled during the 48 hrs after the treatments and before the OGTT. Ratings of muscle soreness and CK activity were significantly elevated 48 hrs after downhill running. Level running also increased CK activity but did not induce muscle soreness. Isokinetic exercise did not affect either one. Blood glucose responses to the OGTT were similar among the treatments. In contrast, the insulin responses to the OGTT following downhill running were significantly increased. These results suggest that eccentric exercise associated with downhill running that results in delayed muscle soreness is associated with the development of a mild insulin-resistant condition.

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Matthew David Cook, Stephen David Myers, John Stephen Michael Kelly, and Mark Elisabeth Theodorus Willems

Impaired glucose tolerance was shown to be present 48 hr following muscle-damaging eccentric exercise. We examined the acute effect of concentric and muscle-damaging eccentric exercise, matched for intensity, on the responses to a 2-hr 75-g oral glucose tolerance test (OGTT). Ten men (27 ± 9 years, 178 ± 7 cm, 75 ± 11 kg, VO2max: 52.3 ± 7.3 ml·kg-1·min-1) underwent three OGTTs after an overnight 12 hr fast: rest (control), 40-min (5 × 8-min with 2-min interbout rest) of concentric (level running, 0%, CON) or eccentric exercise (downhill running, –12%, ECC). Running intensity was matched at 60% of maximal metabolic equivalent. Maximal isometric force of m. quadriceps femoris of both legs was measured before and after the running protocols. Downhill running speed was higher (level: 9.7 ± 2.1, downhill: 13.8 ± 3.2 km·hr-1, p < .01). Running protocols had similar VO2max (p = .59), heart rates (p = .20) and respiratory exchange ratio values (p = .74) indicating matched intensity and metabolic demands. Downhill running resulted in higher isometric force deficits (level: 3.0 ± 6.7, downhill: 17.1 ± 7.3%, p < .01). During OGTTs, area-under-the-curve for plasma glucose (control: 724 ± 97, CON: 710 ± 77, ECC: 726 ± 72 mmol·L-1·120 min, p = .86) and insulin (control: 24995 ± 11229, CON: 23319 ± 10417, ECC: 21842 ± 10171 pmol·L-1·120 min, p = .48), peak glucose (control: 8.1 ± 1.3, CON: 7.7 ± 1.2, ECC: 7.7 ± 1.1 mmol·L-1, p = .63) and peak insulin levels (control: 361 ± 188, CON: 322 ± 179, ECC: 299 ± 152 pmol·L-1, p = .30) were similar. It was concluded that glucose tolerance and the insulin response to an OGTT were not changed immediately by muscle-damaging eccentric exercise.

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Michael S. Green, J. Andrew Doyle, Christopher P. Ingalls, Dan Benardot, Jeffrey C. Rupp, and Benjamin T. Corona

This study determined whether disrupted glucose and insulin responses to an oral glucose-tolerance test (OGTT) induced by eccentric exercise were attenuated after a repeated bout. Female participants (n = 10, age 24.7 ± 3.0 yr, body mass 64.9 ± 7.4 kg, height 1.67 ± 0.02 m, body fat 29% ± 2%) performed 2 bouts of downhill running (DTR 1 and DTR 2) separated by 14 d. OGTTs were administered at baseline and 48 hr after DTR 1 and DTR 2. Maximum voluntary isometric quadriceps torque (MVC), subjective soreness (100-mm visual analog scale), and serum creatine kinase (CK) were assessed pre-, post-, and 48 hr post-DTR 1 and DTR 2. Insulin and glucose area under the curve (38% ± 8% and 21% ± 5% increase, respectively) and peak insulin (44.1 ± 5.1 vs. 31.6 ± 4.0 μU/ml) and glucose (6.5 ± 0.4 vs. 5.5 ± 0.4 mmol/L) were elevated after DTR 1, with no increase above baseline 48 hr after DTR 2. MVC remained reduced by 9% ± 3% 48 hr after DTR 1, recovering back to baseline 48 hr after DTR 2. Soreness was elevated to a greater degree 48 hr after DTR 1 (48 ± 6 vs. 13 ± 3 mm), with a tendency for greater CK responses 48 hr after DTR 1 (813 ± 365 vs. 163 ± 43 U/L, p = .08). A novel bout of eccentric exercise confers protective effects, with subsequent bouts failing to elicit disruptions in glucose and insulin homeostasis.

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Heidi M. Staudacher, Andrew L. Carey, Nicola K. Cummings, John A. Hawley, and Louise M. Burke

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 [V̇O2peak] 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% V̇O2peak) 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 (SI 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.

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Loretta DiPietro, Catherine W. Yeckel, and James Dziura


Few studies have compared long-term moderate-intensity aerobic versus light-resistance training on serial improvements in glucose tolerance in older people.


Healthy, inactive older (74 ± 5 [SD] years) women (N = 20) were randomized into either a high-volume, moderate-intensity aerobic (ATM, n = 12) or a lower-intensity resistance training (RTL, n = 8) group. Both groups exercised under supervision 4 times per week for 45- to 60-minute sessions over 9 months. Measurements of plasma glucose, insulin, and free fatty acid (FFA) responses to an oral glucose tolerance test (OGTT) were performed at baseline and at 3, 6, and 9 months 48 hours after the last exercise session.


We observed significant improvements in 2-hour glucose concentrations at 3, 6, and 9 months among women in the RTL (152 ± 42 vs 134 ± 33 vs 134 ± 24 vs 130 ± 27 mg · dL−1; P < .05), but not the ATM (151 ± 25 vs 156 ± 37 vs 152 ± 40 vs 155 ± 39 mg · dL−1) group. These improvements were accompanied by an 18% (P < .07) decrease in basal FFA concentrations in the RTL group, whereas basal and 30-minute FFA concentrations increased (P < .05) after training in the ATM group.


These findings suggest that the net physiological benefits of exercise might have been blunted in the ATM group, owing to higher circulating levels of FFA, which might have temporarily interfered with insulin action.

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Karen Van Proeyen, Monique Ramaekers, Ivo Pischel, and Peter Hespel

The purpose of this study was to investigate the effect of Opuntia ficus-indica (OFI) cladode and fruit-skin extract on blood glucose and plasma insulin increments due to high-dose carbohydrate ingestion, before and after exercise. Healthy, physically active men (n = 6; 21.0 ± 1.6 years, 78.1 ± 6.0 kg) participated in a doubleblind placebo-controlled crossover study involving 2 experimental sessions. In each session, the subjects successively underwent an oral glucose tolerance test at rest (OGTTR), a 30-min cycling bout at ~75% VO2max, and another OGTT after exercise (OGTTEX). They received capsules containing either 1,000 mg OFI or placebo (PL) 30 min before and immediately after the OGTTR. Blood samples were collected before (t 0) and at 30-min intervals after ingestion of 75 g glucose for determination of blood glucose and serum insulin. In OGTTEX an additional 75-g oral glucose bolus was administered at t 60. In OGTTR, OFI administration reduced the area under the glucose curve (AUCGLUC) by 26%, mainly due to lower blood glucose levels at t 30 and t 60 (p < .05). Furthermore, a higher serum insulin concentration was noted after OFI intake at baseline and at t 30 (p < .05). In OGTTEX, blood glucose at t 60 was ~10% lower in OFI than in PL, which resulted in a decreased AUCGLUC (–37%, p < .05). However, insulin values and AUCINS were not different between OFI and PL. In conclusion, the current study shows that OFI extract can increase plasma insulin and thereby facilitate the clearance of an oral glucose load from the circulation at rest and after endurance exercise in healthy men.

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Emma L. Sweeney, Daniel J. Peart, Irene Kyza, Thomas Harkes, Jason G. Ellis, and Ian H. Walshe

seated position. After the recovery period, a 2-hr oral glucose tolerance test (OGTT) was conducted, and blood samples were drawn at regular intervals. The OGTT consisted of 82.5-g dextrose (MyProtein, Northwich, United Kingdom) mixed with 300-ml water, consumed within 5 min. During the OGTT

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Christopher C. Webster, Kathryn M. van Boom, Nur Armino, Kate Larmuth, Timothy D. Noakes, James A. Smith, and Tertius A. Kohn

days: (a) a peak power output test; (b) an exercise familiarization trial; (c) an experimental trial to measure EGP, muscle glycogen usage, and substrate oxidation; and (d) an oral glucose tolerance test (OGTT). Data from muscle samples collected at rest before the experimental trial and from the OGTT