Effect of carbohydrate ingestion on metabolism during running and cycling.

The effects of carbohydrate or water ingestion on metabolism were investigated in seven male subjects during two running and two cycling trials lasting 60 min at individual lactate threshold using indirect calorimetry, U-14C-labeled tracer-derived measures of the rates of oxidation of plasma glucose, and direct determination of mixed muscle glycogen content from the vastus lateralis before and after exercise. Subjects ingested 8 ml/kg body mass of either a 6.4% carbohydrate-electrolyte solution (CHO) or water 10 min before exercise and an additional 2 ml/kg body mass of the same fluid after 20 and 40 min of exercise. Plasma glucose oxidation was greater with CHO than with water during both running (65 +/- 20 vs. 42 +/- 16 g/h; P < 0.01) and cycling (57 +/- 16 vs. 35 +/- 12 g/h; P < 0.01). Accordingly, the contribution from plasma glucose oxidation to total carbohydrate oxidation was greater during both running (33 +/- 4 vs. 23 +/- 3%; P < 0.01) and cycling (36 +/- 5 vs. 22 +/- 3%; P < 0.01) with CHO ingestion. However, muscle glycogen utilization was not reduced by the ingestion of CHO compared with water during either running (112 +/- 32 vs. 141 +/- 34 mmol/kg dry mass) or cycling (227 +/- 36 vs. 216 +/- 39 mmol/kg dry mass). We conclude that, compared with water, 1) the ingestion of carbohydrate during running and cycling enhanced the contribution of plasma glucose oxidation to total carbohydrate oxidation but 2) did not attenuate mixed muscle glycogen utilization during 1 h of continuous submaximal exercise at individual lactate threshold.     

Effects of pre-exercise carbohydrate feedings on muscle glycogen use during exercise in well-trained runners

The purpose of this study was to examine the effects of pre-exercise glucose and fructose feedings on muscle glycogen utilization during exercise in six well-trained runners (VO2max = 68.2 +/- 3.4 ml X kg-1 X min-1). On three separate occasions, the runners performed a 30 min treadmill run at 70% VO2max. Thirty minutes prior to exercise each runner ingested 75 g of glucose (trial G), 75 g of fructose (trial F) or 150 ml of a sweetened placebo (trial C). During exercise, no differences were observed between any of the trials for oxygen uptake, heart rate or perceived exertion. Serum glucose levels were elevated as a result of the glucose feeding (P less than 0.05) reaching peak levels at 30 min post-feeding (7.90 +/- 0.24 mmol X l-1). With the onset of exercise, glucose levels dropped to a low of 5.89 +/- 0.85 mmol X l-1 at 15 min of exercise in trial G. Serum glucose levels in trials F and C averaged 6.21 +/- 0.31 mmol X l-1 and 5.95 +/- 0.23 mmol X l-1 respectively, and were not significantly different (P less than 0.05). There were also no differences in serum glucose levels between any of the trials at 15 and 30 min of exercise.     

Oxidation of combined ingestion of glucose and fructose during exercise.

The purpose of the present study was to examine whether combined ingestion of a large amount of fructose and glucose during cycling exercise would lead to exogenous carbohydrate oxidation rates >1 g/min. Eight trained cyclists (maximal O(2) consumption: 62 +/- 3 ml x kg(-1) x min(-1)) performed four exercise trials in random order. Each trial consisted of 120 min of cycling at 50% maximum power output (63 +/- 2% maximal O(2) consumption), while subjects received a solution providing either 1.2 g/min of glucose (Med-Glu), 1.8 g/min of glucose (High-Glu), 0.6 g/min of fructose + 1.2 g/min of glucose (Fruc+Glu), or water. The ingested fructose was labeled with [U-(13)C]fructose, and the ingested glucose was labeled with [U-(14)C]glucose. Peak exogenous carbohydrate oxidation rates were approximately 55% higher (P < 0.001) in Fruc+Glu (1.26 +/- 0.07 g/min) compared with Med-Glu and High-Glu (0.80 +/- 0.04 and 0.83 +/- 0.05 g/min, respectively). Furthermore, the average exogenous carbohydrate oxidation rates over the 60- to 120-min exercise period were higher (P < 0.001) in Fruc+Glu compared with Med-Glu and High-Glu (1.16 +/- 0.06, 0.75 +/- 0.04, and 0.75 +/- 0.04 g/min, respectively). There was a trend toward a lower endogenous carbohydrate oxidation in Fruc+Glu compared with the other two carbohydrate trials, but this failed to reach statistical significance (P = 0.075). The present results demonstrate that, when fructose and glucose are ingested simultaneously at high rates during cycling exercise, exogenous carbohydrate oxidation rates can reach peak values of approximately 1.3 g/min.     

Effects of prior exercise on the thermic effect of glucose and fructose

It has been previously observed that the thermic effect of a glucose load is potentiated by prior exercise. To determine whether this phenomenon is observed when different carbohydrates are used and to ascertain the role of insulin, the thermic effects of fructose and glucose were compared during control (rest) and postexercise trials. Six male subjects ingested 100 g fructose or glucose at rest or after recovery from 45 min of treadmill exercise at 70% of maximal O2 consumption. Measurements of O2 consumption, respiratory exchange ratio, and plasma concentrations of glucose, insulin, glycerol, and lactate were measured for 3 h postingestion. Although glucose and fructose increased net energy expenditure by 44 and 51 kcal, respectively, over baseline during control trials, exercise increased the thermic effect of both carbohydrate challenges an additional 20-25 kcal (P less than 0.05). Glucose ingestion was associated with large (P less than 0.05) increases in plasma insulin concentration during control and exercise trials, in contrast to fructose ingestion. Because fructose, which is primarily metabolized by liver, and glucose elicited a similar postexercise potentiation of thermogenesis, the results indicate that the thermogenic phenomenon is not limited to skeletal muscle. These results also demonstrate that carbohydrate-induced postexercise thermogenesis is not related to an incremental increase in plasma insulin concentration.     

Effect of carbohydrate ingestion on glucose kinetics and muscle metabolism during intense endurance exercise.

There has been recent interest in the potential performance and metabolic effects of carbohydrate ingestion during exercise lasting approximately 1 h. In this study, 13 well-trained men ingested in randomized order either a 6% glucose solution (CHO trial) or a placebo (Con trial) during exercise to exhaustion at 83+/-1% peak oxygen uptake. In six subjects, vastus lateralis muscle was sampled at rest, at 32 min, and at exhaustion, and in six subjects, glucose kinetics was determined by infusion of [6,6-(2)H]glucose in both trials and ingestion of [6-(3)H]glucose in the CHO trial. Of the 84 g of glucose ingested during exercise in the CHO trial, only 22 g appeared in the peripheral circulation. This resulted in a small (12 g) but significant (P<0.05) increase in glucose uptake without influencing carbohydrate oxidation, muscle glycogen use, or time to exhaustion (CHO: 68.1+/-4.1 min; Con: 69.6+/-5.5 min). Decreases in muscle phosphocreatine content and increases in muscle inosine monophosphate and lactate content during exercise were similar in the two trials. Although endogenous glucose production during exercise was partially suppressed in the CHO trial, it remained significantly above preexercise levels throughout exercise. In conclusion, only 26% of the ingested glucose appeared in the peripheral circulation. Glucose ingestion increased glucose uptake and partially reduced endogenous glucose production but had no effect on carbohydrate oxidation, muscle metabolism, or time to exhaustion during exercise at 83% peak oxygen uptake.     

Validation of two running tests as estimates of maximal aerobic power in children

In order to validate the "Maximal Multistage 20 Meter Shuttle Run Test" by Leger and Lambert (1982) (20-MST) as an estimate of maximal aerobic power (VO2max) and to compare the results of this test with the results of a 6 min endurance run, 82 subjects (41 boys and 41 girls) aged 12-14 performed the 20-MST and the 6 min endurance run, and had their VO2max directly measured during maximal treadmill running. The 20-MST is a maximal running test starting at a running speed of 8.0 km X h-1, which is increased every minute and in which the pace is set by an audio signal. Performing the test, one runs a 20-meter course back and forth. The test result is expressed as "palier" (one palier is approximately one minute). The mean results of the 20-MST were, for boys, 8.0 palier (+/- 1.7) and for girls, 6.4 palier (+/- 1.5). The mean results of the 6 min endurance run were for boys, 1264.4 meters (+/- 160.8), and for girls, 1103.9 meters (+/- 144.7). The mean VO2max for boys was 53.2 ml X kg-1 X min-1 (+/- 5.4) and for girls, 44.1 (+/- 4.8) ml X kg-1 X min-1. The correlation coefficient between VO2max and the 20-MST was found to be 0.68 (+/- 3.9) for boys, 0.69 (+/- 3.4) for girls and 0.76 (+/- 4.4) for both sexes, and that of VO2max with the 6 min endurance run was 0.51 (+/- 4.6) for boys, 0.45 (+/- 4.3) for girls and 0.63 (+/- 5.3) for both sexes. The conclusion is that the 20-MST is a suitable tool for the evaluation of maximal aerobic power. Although the differences in validity between the 20-MST and the 6 minutes endurance run were statistically not significant (p greater than 0.05), for reasons of practicability the 20-MST should be preferred to the 6 minutes endurance run when used in physical education classes.     

Effects of fructose on hepatic glucose metabolism in humans

Hepatic and extrahepatic insulin sensitivity was assessed in six healthy humans from the insulin infusion required to maintain an 8 mmol/l glucose concentration during hyperglycemic pancreatic clamp with or without infusion of 16.7 micromol. kg(-1). min(-1) fructose. Glucose rate of disappearance (GR(d)), net endogenous glucose production (NEGP), total glucose output (TGO), and glucose cycling (GC) were measured with [6,6-(2)H(2)]- and [2-(2)H(1)]glucose. Hepatic glycogen synthesis was estimated from uridine diphosphoglucose (UDPG) kinetics as assessed with [1-(13)C]galactose and acetaminophen. Fructose infusion increased insulin requirements 2.3-fold to maintain blood glucose. Fructose infusion doubled UDPG turnover, but there was no effect on TGO, GC, NEGP, or GR(d) under hyperglycemic pancreatic clamp protocol conditions. When insulin concentrations were matched during a second hyperglycemic pancreatic clamp protocol, fructose administration was associated with an 11.1 micromol. kg(-1). min(-1) increase in TGO, a 7.8 micromol. kg(-1). min(-1) increase in NEGP, a 2.2 micromol. kg(-1). min(-1) increase in GC, and a 7.2 micromol. kg(-1). min(-1) decrease in GR(d) (P < 0. 05). These results indicate that fructose infusion induces hepatic and extrahepatic insulin resistance in humans.     

Effects of fluid, electrolyte and substrate ingestion on endurance capacity

The availability of carbohydrate (CHO) as a substrate for the exercising muscles is known to be a limiting factor in the performance of prolonged cycle exercise, and provision of exogenous CHO in the form of glucose can increase endurance capacity. The present study examined the effects of ingestion of fluids and of CHO in different forms on exercise performance. Six male volunteers exercised to exhaustion on a cycle ergometer at a workload which required approximately 70% of Vo2max. After one preliminary trial, subjects performed this exercise test on six occasions, one week apart. Immediately before exercise, and at 10-min intervals throughout, subjects ingested 100 ml of one of the following: control (no drink), water, glucose syrup, fructose syrup, glucose-fructose syrup or a dilute glucose-electrolyte solution. Each of the syrup solutions contained approximately 36 g CHO per 100 ml; the isotonic glucose-electrolyte solution contained 4 g glucose per 100 ml. A randomised Latin square order of administration of trials was employed. Expired air samples for determination of Vo2, respiratory exchange ratio and rate of CHO oxidation were collected at 15-min intervals. Venous blood samples were obtained before and after exercise. Subjects drinking the isotonic glucose-electrolyte solution exercised longer (90.8 (12.4) min, mean (SEM] than on the control test (70.2 (8.3) min; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Fructose and glucose ingestion and muscle glycogen use during submaximal exercise

Substrate utilization after fructose, glucose, or water ingestion was examined in four male and four female subjects during three treadmill runs at approximately 75% of maximal O2 uptake. Each test was preceded by three days of a carbohydrate-rich diet. The runs were 30 min long and were spaced at least 1 wk apart. Exercise began 45 min after ingestion of 300 ml of randomly assigned 75 g fructose (F), 75 g glucose (G), or control (C). Muscle glycogen depletion determined by pre- and postexercise biopsies (gastrocnemius muscle) was significantly (P less than 0.05) less during the F trial than during C or G. Venous blood samples revealed a significant increase in serum glucose (P less than 0.05) and insulin (P less than 0.01) within 45 min after the G drink, followed by a decrease (P less than 0.05) in serum glucose during the first 15 min of exercise, changes not observed in the C or F trials. Respiratory exchange ratio was higher (P less than 0.05) during the G than C or F trials for the first 5 min of exercise and lower (P less than 0.05) during the C trial compared with G or F for the last 15 min of exercise. These data suggest that fructose ingested before 30 min of submaximal exercise maintains stable blood glucose and insulin concentrations, which may lead to the observed sparing of muscle glycogen.     

Effect of training status on fuel selection during submaximal exercise with glucose ingestion.

In this study, an oral glucose load was enriched with a [U-(13)C]glucose tracer to determine differences in substrate utilization between endurance-trained (T) and untrained (UT) subjects during submaximal exercise at the same relative and absolute workload when glucose is ingested. Six highly trained cyclists/triathletes [maximal workload (Wmax), 400 +/- 9 W] and seven UT subjects (Wmax, 296 +/- 8 W) were studied during 120 min of cycling exercise at 50% Wmax ( approximately 55% maximal O(2) consumption). The T subjects performed a second trial at the mean workload of the UT group (148 +/- 4 W). Before exercise, 8.0 ml/kg of a (13)C-enriched glucose solution (80 g/l) was ingested. During exercise, boluses of 2.0 ml/kg of the same solution were administered every 15 min. Measurements were made in the 90- to 120-min period when a steady state was present in breath (13)CO(2) and plasma glucose (13)C enrichment. Energy expenditure was higher in T than in UT subjects (58 vs. 47 kJ/min, respectively; P < 0.001) at the same relative intensity. This was completely accounted for by an increased fat oxidation (0.57 vs. 0.40 g/min; P < 0.01). At the same absolute intensity, fat oxidation contributed more to energy expenditure in the T compared with the UT group (44 vs. 33%, respectively; P < 0.01). The reduction in carbohydrate oxidation in the T group was explained by a diminished oxidation rate of muscle glycogen (indirectly assessed by using tracer methodology at 0.72 +/- 0.1 and 1.03 +/- 0.1 g/min, respectively; P < 0.01) and liver-derived glucose (0.15 +/- 0.03 and 0.22 +/- 0.02 g/min, respectively; P < 0.05). Exogenous glucose oxidation rates were similar during all trials (+/-0.70 g/min).     

Effect of carbohydrate ingestion on glucose kinetics during exercise in the heat.

Six endurance-trained men [peak oxygen uptake (V(O(2))) = 4.58 +/- 0.50 (SE) l/min] completed 60 min of exercise at a workload requiring 68 +/- 2% peak V(O(2)) in an environmental chamber maintained at 35 degrees C (<50% relative humidity) on two occasions, separated by at least 1 wk. Subjects ingested either a 6% glucose solution containing 1 microCi [3-(3)H]glucose/g glucose (CHO trial) or a sweet placebo (Con trial) during the trials. Rates of hepatic glucose production [HGP = glucose rate of appearance (R(a)) in Con trial] and glucose disappearance (R(d)), were measured using a primed, continuous infusion of [6,6-(2)H]glucose, corrected for gut-derived glucose (gut R(a)) in the CHO trial. No differences in heart rate, V(O(2)), respiratory exchange ratio, or rectal temperature were observed between trials. Plasma glucose concentrations were similar at rest but increased (P < 0.05) to a greater extent in the CHO trial compared with the Con trial. This was due to the absorption of ingested glucose in the CHO trial, because gut R(a) after 30 and 50 min (16 +/- 5 micromol. kg(-1). min(-1)) was higher (P < 0.05) compared with rest, whereas HGP during exercise was not different between trials. Glucose R(d) was higher (P < 0.05) in the CHO trial after 30 and 50 min (48.0 +/- 6.3 vs 34.6 +/- 3.8 micromol. kg(-1). min(-1), CHO vs. Con, respectively). These results indicate that ingestion of carbohydrate, at a rate of approximately 1.0 g/min, increases glucose R(d) but does not blunt the rise in HGP during exercise in the heat.     

Effects of dynamic stretching on energy cost and running endurance performance in trained male runners

The purpose of this study was to examine the effects of dynamic stretching on running energy cost and endurance performance in trained male runners. Fourteen male runners performed both a 30-minute preload run at 65% VO2max and a 30-minute time trial to assess running energy cost and performance, respectively. The subjects repeated both the trials after either 15 minutes of dynamic stretching (i.e., experimental condition) or quiet sitting (i.e., control condition) while the order was balanced between the subjects to avoid any order effect. The total calories expended were determined for the 30-minute preload run, whereas the distance covered was measured in the time trial. Average resting VO2 increased significantly (p < 0.05) after dynamic stretching (prestretch: 6.2 ± 1.7 vs. poststretch: 8.4 ± 2.1 ml·kg(-1)·min(-1)) but not during the quiet-sitting condition. Caloric expenditure was significantly higher during the 30-minute preload run for the stretching (416.3 ± 44.9 kcal) compared with that during the quiet sitting (399.3 ± 50.4 kcal) (p < 0.05). There was no difference in the distance covered after quiet sitting (6.3 ± 1.1 km) compared with that for the stretching condition (6.1 ± 1.3 km). These findings suggest that dynamic stretching does not affect running endurance performance in trained male runners.     

Exogenous carbohydrate oxidation from drinks ingested during prolonged exercise in a cold environment in humans.

Six healthy male volunteers performed four rides to exhaustion on a cycle ergometer at approximately 80% of maximal oxygen consumption. Subjects ingested a bolus volume of fluid (7.14 ml/kg) immediately before exercise and additional fluid volumes (1.43 ml/kg) every 10 min during exercise. The fluids ingested were either a flavored water control or glucose-electrolyte beverages with glucose concentrations of 2, 6, or 12%. The beverages were labeled with [U-(13)C]glucose (99.2%: 0.05 g/l). Exercise capacity was not different (P = 0.13) between trials; median (range) exercise time was 83.52 (79.85--89.68), 103.19 (78.82--108.22), 100.37 (80.60--124.07), and 94.76 (76.78--114.25) min in the 0, 2, 6, and 12% trials, respectively. The oxidation of exogenous glucose in each 15-min period was significantly lower in the 2% trial (P = 0.02) than in the 6 and 12% trials where oxidation rates were between 0.5 and 0.7 g/min. No difference in endogenous glucose oxidation was observed between trials (P = 0.71). These findings indicate that the oxidation of exogenous glucose during exercise of this intensity and duration in a cold environment is similar to that observed in warmer conditions. Thus a low oxidation of exogenous substrate is unlikely to be a factor limiting the effectiveness of carbohydrate-electrolyte drink ingestion on exercise capacity in a cold environment.     

Konstitutive Glucose-6-phosphat-Dehydrogenase bei Glucose verwertenden Mutanten von einem kryptischen Wildstamm

Zusammenfassung Von Wildtyppopulationen von Hydrogenomonas H 16 und anderen Stämmen, die lediglich Fructose, aber nicht Glucose zu verwerten vermögen, wurden Glucose verwertende Mutanten isoliert. Sämtliche Mutanten stimmen in zwei Merkmalen überein: 1. sie bilden Glucose-6-phosphat-Dehydrogenase konstitutiv und 2. die Substratsättigungskurve der Veratmung von Glucose verläuft flacher als die für Fructose. Während die Atmungsrate bei 1,66 mM Fructose schon maximal ist, erreicht die Veratmung von Glucose bei 1,66 mM Glucose erst 15 bis 55%. Die Beziehungen zwischen diesen pleiotropen Effekten (Glucoseverwertung und konstitutive Bildung der Glucose-6-phosphat-Dehydrogenase) sind unbekannt.

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Constitutive glucose-6-phosphate dehydrogenase in mutants utilizing glucose, which are derived from cryptic wildtype strains

Summary Wildtype cells of Hydrogenomonas H 16 and of similar strains of Hydrogenomonas utilize only fructose; they are unable to use glucose as a carbon source. Mutants were isolated which are able to grow on glucose. Ten of these mutants were investigated and found to be similar with regard to the following properties: 1. they are constitutively derepressed for the formation of glucose-6-phosphate dehydrogenase, 2. the substrate saturation curve of the respiration of glucose is unlike of the fructose curve. While the respiratory rate with fructose as a substrate is already maximal at 1.66 mM fructose, the respiratory rate for glucose as a substrate (at 1.66 mM) amounts only to 15 to 55% of the maximal rate (substrate saturation). The relationships between these pleiotropic effects (glucose utilization and constitutive glucose-6-phosphate dehydrogenase) are unknown.

     

Fructose transport in Neurospora crassa.

A specific fructose uptake system (Km = 0.4 mM) appeared in Neurospora crassa when glucose-grown mycelia were starved. Fructose uptake had kinetics different from those of intramycelial fructose phosphorylation, and uptake appeared to be carrier mediated. The only sugar which competitively inhibited fructose uptake was L-sorbose (Ki = 9 mM). Glucose, 2-deoxyglucose, mannose, and 3-O-methyl glucose were noncompetitive inhibitors of fructose uptake. Incubation of glucose-grown mycelia with glucose, 2-deoxyglucose, or mannose prevented derepression of the fructose transport system, whereas incubation with 3-O-methyl glucose caused the appearance of five times as much fructose uptake activity as did starvation conditions.     

Gastrointestinal permeability during exercise: effects of aspirin and energy-containing beverages.

The purpose of this study was to determine whether aspirin (A) ingestion combined with prolonged exercise increases gastrointestinal permeability and whether consumption of a carbohydrate-containing (CHO) or a CHO + glutamine-containing (CHO+G) beverage would reduce this effect. Seventeen subjects completed six experiments. They ingested A (1,300 mg) or placebo (P) pills the evening before and before running 60 min at 70% maximal oxygen uptake. Also, before running they ingested a solution containing 5 g lactulose (L), 5 g sucrose (S), and 2 g rhamnose (R). During each trial, either a 6% CHO beverage, a 6% CHO+G (0.6%; 41 mM) beverage, or a water placebo (WP) was consumed. For 4 h after a run, all urine was collected to measure urinary excretion of L, R, and S. S excretion (percentage of dose ingested; measure of gastroduodenal permeability) was significantly greater (P < 0.05) during the A trial while the subjects drank the WP compared with all other trials. Administration of A also significantly increased L/R (measure of intestinal permeability) for the CHO and WP trials compared with all P trials. Ingestion the CHO or CHO+G beverages significantly reduced S excretion and L excretion when A was administered, but it did not reduce L/R. These results indicate that gastroduodenal and intestinal permeability increase after A ingestion during prolonged running and that ingestion of a CHO beverage attenuates the gastroduodenal effect but not the intestinal effect. Furthermore, addition of G to the CHO beverage provided no additional benefit in reducing gastroduodenal or intestinal permeability.     

Carbohydrate ingestion and muscle glycogen depletion during marathon and ultramarathon racing

Two studies were undertaken to characterize the effects of carbohydrate ingestion on fuel/hormone response to exercise and muscle glycogen utilization during prolonged competitive exercise. In study 1, eighteen subjects were divided into three groups, matched for maximum oxygen consumption (VO2max) and blood lactate turnpoint. All subjects underwent a 3-day carbohydrate (CHO) depletion phase, followed by 3 days of CHO loading (500-600 g.day-1). During the race, the groups drank either 2% glucose (G), 8% glucose polymer (GP), or 8% fructose (F). Muscle biopsies were performed before and after the race and venous blood was sampled before and at regular intervals during the race. In study 2, eighteen subjects divided into 2 matched groups ingested either a 4% G or 10% GP solution during a 56 km race. Despite significantly greater CHO ingestion by GP and F in study 1 and by GP in study 2, blood glucose, free fatty acids and insulin concentrations, muscle glycogen utilization and running performance were not different between groups. These studies show (i) that hypoglycaemia is uncommon in athletes competing in races of up to 56 km provided they CHO-load before and ingest a minimum of 10 g CHO.h-1 during competition; (ii) that neither the amount (10 g vs 40 g.h-1) nor the type of carbohydrate (G vs GP vs F) has any effect on the extent of muscle glycogen depletion or running performance in matched subjects racing over distances up to 56 km.     

Higher dietary carbohydrate content during intensified running training results in better maintenance of performance and mood state.

The aim of this study was to determine whether consumption of a diet containing 8.5 g carbohydrate (CHO) x kg(-1) x day(-1) (high CHO; HCHO) compared with 5.4 g CHO x kg(-1) x day(-1) (control; Con) during a period of intensified training (IT) would result in better maintenance of physical performance and mood state. In a randomized cross-over design, seven trained runners [maximal O(2) uptake (Vo(2 max)) 64.7 +/- 2.6 ml x kg(-1) x min(-1)] performed two 11-day trials consuming either the Con or the HCHO diet. The last week of both trials consisted of IT. Performance was measured with a preloaded 8-km all-out run on the treadmill and 16-km all-out runs outdoors. Substrate utilization was measured using indirect calorimetry and continuous [U-(13)C]glucose infusion during 30 min of running at 58 and 77% Vo(2 max). Time to complete 8 km was negatively affected by the IT: time significantly increased by 61 +/- 23 and 155 +/- 38 s in the HCHO and Con trials, respectively. The 16-km times were significantly increased (by 8.2 +/- 2.1%) during the Con trial only. The Daily Analysis of Life Demands of Athletes questionnaire showed significant deterioration in mood states in both trials, whereas deterioration in global mood scores, as assessed with the Profile of Mood States, was more pronounced in the Con trial. Scores for fatigue were significantly higher in the Con compared with the HCHO trial. CHO oxidation decreased significantly from 1.7 +/- 0.2 to 1.2 +/- 0.2 g/min over the course of the Con trial, which was completely accounted for by a decrease in muscle glycogen oxidation. These findings indicate that an increase in dietary CHO content from 5.4 to 8.5 g CHO x kg(-1)x day(-1) (41 vs. 65% total energy intake, respectively) allowed better maintenance of physical performance and mood state over the course of training, thereby reducing the symptoms of overreaching.     

Effects of fructose and/or fat in the diet on developing the type 2 diabetic-like syndrome in CD-1 mice

The aim of the present study was to examine the interactions of fructose and fat on glucose regulation and lipid metabolism in CD-1 mice. Mice were assigned in five groups. The control group was provided with tap water and a gavage of vehicle; four experimental groups were treated with 150 g/l fructose solution (FS1), fat emulsion (FE), 150 g/l fructose solution and fat emulsion (FS1+FE), or 70 g/l fructose solution and fat emulsion (FS2+FE) for 12 weeks. At the end of the 8th week, both oral glucose tolerance test and insulin tolerance test were conducted. Lipid profiles in serum, liver, and red gastrocnemius muscle, and serum insulin and glucose concentrations were assessed. The FS1+FE group showed combined glucose intolerance (CGI) and decrease of insulin sensitivity. The low-density lipoprotein cholesterol (LDL-C) concentrations were elevated in all experimental groups (p<0.05). The combined diet groups showed statistically significant (p<0.01) increase in total cholesterol (TC) level in comparison with the control FE (p<0.05), or FS1 (p<0.05) group. Triglyceride levels in liver and red gastrocnemius muscle were significantly increased in FE and combined groups. In conclusion, combination of FE and 150 g/l fructose solution for 8 weeks led to CGI. Fructose enhanced the adverse effect of FE on glucose regulation with increasing percentage in the diet. Furthermore, there was a synergistic effect of fructose and fat on elevating the serum TC level.     

Oxidation of exogenous glucose, sucrose, and maltose during prolonged cycling exercise.

The purpose of the present study was to investigate whether combined ingestion of two carbohydrates (CHO) that are absorbed by different intestinal transport mechanisms would lead to exogenous CHO oxidation rates of >1.0 g/min. Nine trained male cyclists (maximal O(2) consumption: 64 +/- 2 ml x kg body wt(-1) x min(-1)) performed four exercise trials, which were randomly assigned and separated by at least 1 wk. Each trial consisted of 150 min of cycling at 50% of maximal power output (60 +/- 1% maximal O(2) consumption), while subjects received a solution providing either 1.8 g/min of glucose (Glu), 1.2 g/min of glucose + 0.6 g/min of sucrose (Glu+Suc), 1.2 g/min of glucose + 0.6 g/min of maltose (Glu+Mal), or water. Peak exogenous CHO oxidation rates were significantly higher (P < 0.05) in the Glu+Suc trial (1.25 +/- 0.07 g/min) compared with the Glu and Glu+Mal trials (1.06 +/- 0.08 and 1.06 +/- 0.06 g/min, respectively). No difference was found in (peak) exogenous CHO oxidation rates between Glu and Glu+Mal. These results demonstrate that, when a mixture of glucose and sucrose is ingested at high rates (1.8 g/min) during cycling exercise, exogenous CHO oxidation rates reach peak values of approximately 1.25 g/min.