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  • 1
    Electronic Resource
    Electronic Resource
    Glucose kinetics during prolonged exercise in euglycaemic and hyperglycaemic subjects (1994)
    Springer
    Pflügers Archiv 426 (1994), S. 378-386 
    Details
    ISSN: 1432-2013
    Keywords: Glucose oxidation ; Glucose infusion ; Insulin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To determine the limits to oxidation of exogenous glucose by skeletal muscle, the effects of euglycaemia (plasma glucose 5 mM, ET) and hyperglycaemia (plasma glucose 10 mM, HT) on fuel substrate kinetics were evaluated in 12 trained subjects cycling at 70% of maximal oxygen uptake (VO2, max) for 2 h. During exercise, subjects ingested water labelled with traces of U-14C-glucose so that the rates of plasma glucose oxidation (R ox) could be determined from plasma 14C-glucose and expired 14CO2 radioactivities, and respiratory gas exchange. Simultaneously, 2-3H-glucose was infused at a constant rate to estimate rates of endogenous glucose turnover (R a), while unlabelled glucose (25% dextrose) was infused to maintain plasma glucose concentration at either 5 or 10 mM. During ET, endogenous liver glucose R a (total R a minus the rate of infusion) declined from 22.4±4.9 to 6.5±1.4 μmol/min per kg fat-free mass [FFM] (P〈0.05) and during HT it was completely suppressed. In contrast, R ox increased to 152±21 and 61±10 μmol/min per kg FFM at the end of HT and ET respectively (P〈0.05). HT (i. e., plasma glucose 10 mM) and hyperinsulinaemia (24.5±0.9 μU/ml) also increased total carbohydrate oxidation from 203±7 (ET) to 310±3 μmol/min per kg FFM (P〈0.0001) and suppressed fat oxidation from 51±3 (ET) to 18±2 μmol/min per kg FFM (P〈0.0001). As the rates of oxidation at more physiological euglycaemic concentrations of glucose were limited to 92±9 μmol/ min per kg FFM, and were similar to those reported when carbohydrate is ingested, the results of the current study suggest that the concentrations of glucose and insulin normally present during prolonged, intense exercise may limit the rate of muscle glucose uptake and oxidation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00388300
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  • 2
    Electronic Resource
    Electronic Resource
    Carbohydrate ingestion and muscle glycogen depletion during marathon and ultramarathon racing (1988)
    Springer
    European journal of applied physiology 57 (1988), S. 482-489 
    Details
    ISSN: 1439-6327
    Keywords: Carbohydrates ; Ultramarathon ; Glycogen ; Fructose ; Performance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 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 ( $$\dot V_{{\text{O}}_{{\text{2 max}}} } $$ ) 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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00417997
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of glucose ingestion or glucose infusion on fuel substrate kinetics during prolonged exercise (1994)
    Springer
    European journal of applied physiology 68 (1994), S. 381-389 
    Details
    ISSN: 1439-6327
    Keywords: Fat ; Glucose oxidation ; U-14C glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To determine if bypassing both intestinal absorption and hepatic glucose uptake by intravenous glucose infusion might increase the rate of muscle glucose oxidation above 1 g · min−1, ten endurance-trained subjects were studied during 125 min of cycling at 70% of peak oxygen uptake (VO2 peak). During exercise the subjects ingested either a 15 g · 100 ml−1 U-14C labelled glucose solution or H2O labelled with a U-14C glucose tracer for the determination of the rates of plasma glucose oxidation (Rox) and exogenous carbohydrate (CHO) oxidation from plasma14C glucose and14CO2 specific activities, and respiratory gas exchange. Simultaneously, 2-3H glucose was infused at a constant rate to measure glucose turnover, while unlabelled glucose (25% dextrose) was infused into those subjects not ingesting glucose to maintain plasma glucose concentration at 5 mmol · l−1. Despite similar plasma glucose concentrations [ingestion 5.3 (SEM 0.13) mmol · l−1; infusion 5.0 (0.09) mmol · l−1], compared to glucose infusion, CHO ingestion significantly increased plasma insulin concentrations [12.9 (1.0) vs 4.8 (0.5) mU · l−1;P〈0.05], raised total Rox values [9.5 (1.2) vs 6.2 (0.7) mmol · 125 min−1 kg fat free mass−1 (FFM);P〈0.05] and rates of CHO oxidation [37.2 (2.8)vs 24.1 (3.9) mmol · 125 min−1 kg FFM−1;P〈0.05]. An increased reliance on CHO metabolism with CHO ingestion was associated with a decrease in fat oxidation. Whereas the contribution from fat oxidation to energy production increased to 51 (10)% with glucose infusion, it only reached 18 (4)% with glucose ingestion (P〈0.05). Despite these differences in plasma insulin concentration and rates of fat oxidation, the rates of glucose oxidation by muscle were similar after 125 min of exercise for both trials [ingestion 93 (8); infusion 85 (5) μmol · min−1 kg FFM−1], suggesting that peak rates of muscle glucose oxidation were primarily dependent on blood glucose concentration which, in turn, regulated the hepatic appearance of ingested CHO.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00843733
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  • 4
    Electronic Resource
    Electronic Resource
    Dose-related elevations in venous pH with citrate ingestion do not alter 40-km cycling time-trial performance (2000)
    Springer
    European journal of applied physiology 83 (2000), S. 320-327 
    Details
    ISSN: 1439-6327
    Keywords: Key words Buffer ; Lactate ; Performance ; pH ; Sodium citrate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The purpose of the current investigation was to determine whether sodium citrate enhances endurance cycling performance and, if so, what dosage(s) produces this effect. Eight trained [peak power output: 362 (48) W; power:weight: 5.1 (0.4) W · kg−1, mean (SD)] male cyclists were requested to complete four, 40-km time-trials, each separated by 3–7 days, on their own bicycles, mounted on a Kingcycle ergometer. To mimic the stochastic nature of cycle road races, the time-trials included four 500-m, four 1-km and two 2-km sprints. The experimental conditions involved the ingestion of three dosages of sodium citrate dissolved in 400 ml water: 0.2 g · kg−1, 0.4 g · kg−1 and 0.6 g · kg−1 body mass (b.m.) and a placebo (calcium carbonate, 0.1 g · kg−1 b.m.). Subjects were asked to complete both the sprints and total distance in the fastest time possible. Venous blood samples were collected before, as well as at 10-km intervals during the trials for the analysis of plasma lactate and glucose concentrations and for the measurement of blood pH and PCO2 levels. Immediately before, as well as during exercise, pH was significantly higher in the group ingesting the highest citrate dose (range 7.36–7.45) compared to the placebo (range 7.31–7.39) and the two lower citrate dosages. Despite this, no significant differences in power output (P=0.886) or time taken to complete the 40 km (P=0.754) were measured between the four trials. The average performance times (in min:s, with SD in parentheses) and average power output (in W) for the 40-km time-trials were: 58:46 (5:06) [265 (62) W], 60:24 (6:07) [251 (59) W], 61:47 (5:07) [243 (44) W] and 60:02 (5.05) [255 (55) W] for the 0.2, 0.4, 0.6 g · kg−1 b.m. sodium citrate and placebo trials, respectively. There were also no significant differences measured between treatments in terms of time, power output, speed or heart rate during the 500-m, 1-km and 2-km sprints. The ingestion of increasing sodium citrate dosages before exercise produced dose-dependent changes in pH, base excess and HCO− 3 concentrations before and during the 40-km time-trial. However, these changes influenced neither the time-trial time nor the sprinting performance times.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004210000264
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