Ingestion of a high-glycemic index meal increases muscle glycogen storage at rest but augments its utilization during subsequent exercise.

The aim of this study was to compare the effect of preexercise breakfast containing high- and low-glycemic index (GI) carbohydrate (CHO) (2.5g CHO/kg body mass) on muscle glycogen metabolism. On two occasions, 14 days apart, seven trained men ran at 71% maximal oxygen uptake for 30 min on a treadmill. Three hours before exercise, in a randomized order, subjects consumed either isoenergetic high- (HGI) or low-GI (LGI) CHO breakfasts that provided (per 70 kg body mass) 3.43 MJ energy, 175 g CHO, 21 g protein, and 4 g fat. The incremental areas under the 3-h plasma glucose and serum insulin response curves after the HGI meal were 3.9- (P < 0.05) and 1.4-fold greater (P < 0.001), respectively, than those after the LGI meal. During the 3-h postprandial period, muscle glycogen concentration increased by 15% (P < 0.05) after the HGI meal but remained unchanged after the LGI meal. Muscle glycogen utilization during exercise was greater in the HGI (129.1 +/- 16.1 mmol/kg dry mass) compared with the LGI (87.9 +/- 15.1 mmol/kg dry mass; P < 0.01) trial. Although the LGI meal contributed less CHO to muscle glycogen synthesis in the 3-h postprandial period compared with the HGI meal, a sparing of muscle glycogen utilization during subsequent exercise was observed in the LGI trial, most likely as a result of better maintained fat oxidation.     

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.     

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.     

Glucose kinetics and exercise performance during phases of the menstrual cycle: effect of glucose ingestion

To study the effect of menstrual cycle phase and carbohydrate ingestion on glucose kinetics and exercise performance, eight healthy, moderately trained, eumenorrheic women cycled at 70% of peak O(2) consumption for 2 h and then performed a 4 kJ/kg body wt time trial. A control (C) and a glucose ingestion (G) trial were completed during the follicular (F) and luteal (L) phases of the menstrual cycle. Plasma substrate concentrations were similar before the commencement of exercise. Glucose rates of appearance and disappearance were higher (P < 0.05) during the 2nd h of exercise in FC than in LC. The percent contribution of carbohydrate to total energy expenditure was greater in FC than in LC, and subjects performed better (13%, P < 0.05) in FC. Performance improved (19% and 26% in FG and LG compared with FC and LC, respectively, P < 0.05) with the ingestion of glucose throughout exercise. These data demonstrate that substrate metabolism and exercise performance are influenced by the menstrual cycle phase, but ingestion of glucose minimizes these effects.     

Carbohydrate feedings before, during, or in combination improve cycling endurance performance.

This study examined the effects of no carbohydrate (PP), preexercise carbohydrate feeding (CP), carbohydrate feedings during exercise (PC), and the combination of carbohydrate feedings before and during exercise (CC) on the metabolic responses during exercise and on exercise performance. Nine well-trained cyclists exercised at 70% of maximal O2 uptake until exhaustion. Blood glucose peaked 30 min after the preexercise carbohydrate feeding and at the start of exercise was 25% below the prefeeding concentration (4.76 mM). At exhaustion, glucose had declined to 3.8 (PP), 4.0 (CP), 4.6 (PC), and 5.0 mM (CC). Insulin was 300% above basal (7 microU/ml) at the start of exercise for CC and CP and returned to baseline by 120 min of exercise. When carbohydrates were consumed, the rate of carbohydrate oxidation was significantly higher throughout exercise than during PP. Total work produced during exercise was 19-46% (P less than 0.05) higher when carbohydrates were consumed. Time to exhaustion was 44% (CC), 32% (PC), and 18% (CP) greater than PP (201 min; P less than 0.05). Performance was improved by ingestion of carbohydrates before and/or during exercise; performance was further improved by their combination. This is probably the result of enhanced carbohydrate oxidation, especially during the later stages of exercise.     

Exogenous carbohydrate oxidation rates are elevated after combined ingestion of glucose and fructose during exercise in the heat.

The first purpose of this study was to investigate whether a glucose (GLU)+fructose (FRUC) beverage would result in a higher exogenous carbohydrate (CHO) oxidation rate and a higher fluid availability during exercise in the heat compared with an isoenergetic GLU beverage. A second aim of the study was to examine whether ingestion of GLU at a rate of 1.5 g/min during exercise in the heat would lead to a reduced muscle glycogen oxidation rate compared with ingestion of water (WAT). Eight trained male cyclists (maximal oxygen uptake: 64+/-1 ml.kg-1.min-1) cycled on three different occasions for 120 min at 50% maximum power output at an ambient temperature of 31.9+/-0.1 degrees C. Subjects received, in random order, a solution providing either 1.5 g/min of GLU, 1.0 g/min of GLU+0.5 g/min of FRUC, or WAT. Exogenous CHO oxidation during the last hour of exercise was approximately 36% higher (P<0.05) in GLU+FRUC compared with GLU, and peak oxidation rates were 1.14+/-0.05 and 0.77+/-0.08 g/min, respectively. Endogenous CHO oxidation was significantly lower (P<0.05) in GLU+FRUC compared with WAT. Muscle glycogen oxidation was not different after ingestion of GLU or WAT. Plasma deuterium enrichments were significantly higher (P<0.05) in WAT and GLU+FRUC compared with GLU. Furthermore, at 60 and 75 min of exercise, plasma deuterium enrichments were higher (P<0.05) in WAT compared with GLU+FRUC. Ingestion of GLU+FRUC during exercise in the heat resulted in higher exogenous CHO oxidation rates and fluid availability compared with ingestion of GLU and reduced endogenous CHO oxidation compared with ingestion of WAT.     

Suppressing lipolysis increases interleukin-6 at rest and during prolonged moderate-intensity exercise in humans.

IL-6 induces lipolysis when administered to humans. Consequently, it has been hypothesized that IL-6 is released from skeletal muscle during exercise to act in a "hormonelike" manner and increase lipolysis from adipose tissue to supply the muscle with substrate. In the present study, we hypothesized that suppressing lipolysis, and subsequent free fatty acid (FFA) availability, would result in a compensatory elevation in IL-6 at rest and during exercise. First, we had five healthy men ingest nicotinic acid (NA) at 30-min intervals for 120 min at rest [10 mg/kg body mass (initial dose), 5 mg/kg body mass (subsequent doses)]. Plasma was collected and analyzed for FFA and IL-6. After 120 min, plasma FFA concentration was attenuated (0 min: 0.26 +/- 0.05 mmol/l; 120 min: 0.09 +/- 0.02 mmol/l; P < 0.01), whereas plasma IL-6 was concomitantly increased approximately eightfold (0 min: 0.75 +/- 0.18 pg/ml; 120 min: 6.05 +/- 0.89 pg/ml; P < 0.001). To assess the effect of lipolytic suppression on the exercise-induced IL-6 response, seven active, but not specifically trained, men performed two experimental exercise trials with (NA) or without [control (Con)] NA ingestion 60 min before (10 mg/kg body mass) and throughout (5 mg/kg body mass every 30 min) exercise. Blood samples were obtained before ingestion, 60 min after ingestion, and throughout 180 min of cycling exercise at 62 +/- 5% of maximal oxygen consumption. IL-6 gene expression, in muscle and adipose tissue sampled at 0, 90, and 180 min, was determined by using semiquantitative real-time PCR. IL-6 mRNA increased in Con (rest vs. 180 min; P < 0.01) approximately 13-fold in muscle and approximately 42-fold in fat with exercise. NA increased (rest vs. 180 min; P < 0.01) IL-6 mRNA 34-fold in muscle, but the treatment effect was not statistically significant (Con vs. NA, P = 0.1), and 235-fold in fat (Con vs. NA, P < 0.01). Consistent with the study at rest, NA completely suppressed plasma FFA (180 min: Con, 1.42 +/- 0.07 mmol/l; NA, 0.10 +/- 0.01 mmol/l; P < 0.001) and increased plasma IL-6 (180 min: Con, 9.81 +/- 0.98 pg/ml; NA, 19.23 +/- 2.50 pg/ml; P < 0.05) during exercise. In conclusion, these data demonstrate that circulating IL-6 is markedly elevated at rest and during prolonged moderate-intensity exercise when lipolysis is suppressed.     

Effects of carbohydrate ingestion before and during exercise on glucose kinetics and performance.

We investigated the effect of carbohydrate (CHO) ingestion before and during exercise and in combination on glucose kinetics, metabolism and performance in seven trained men, who cycled for 120 min (SS) at approximately 63% of peak power output, followed by a 7 kJ/kg body wt time trial (TT). On four separate occasions, subjects received either a placebo beverage before and during SS (PP); placebo 30 min before and 2 g/kg body wt of CHO in a 6.4% CHO solution throughout SS (PC); 2 g/kg body wt of CHO in a 25.7% CHO beverage 30 min before and placebo throughout SS (CP); or 2 g/kg body wt of CHO in a 25.7% CHO beverage 30 min before and 2 g/kg of CHO in a 6.4% CHO solution throughout SS (CC). Ingestion of CC and CP markedly (>8 mM) increased plasma glucose concentration ([glucose]) compared with PP and PC (5 mM). However, plasma [glucose] fell rapidly at the onset of SS so that after 80 min it was similar (6 mM) between all treatments. After this time, plasma [glucose] declined in both PP and CP (P < 0.05) but was well maintained in both CC and PC. Ingestion of CC and CP increased rates of glucose appearance (R(a)) and disappearance (R(d)) compared with PP and PC at the onset of, and early during, SS (P < 0.05). However, late in SS, both glucose R(a) and R(d) were higher in CC and PC compared with other trials (P < 0.05). Although calculated rates of glucose oxidation were different when comparing the four trials (P < 0.05), total CHO oxidation and total fat oxidation were similar. Despite this, TT was improved in CC and PC compared with PP (P < 0.05). We conclude that 1) preexercise ingestion of CHO improves performance only when CHO ingestion is maintained throughout exercise, and 2) ingestion of CHO during 120 min of cycling improves subsequent TT performance.     

Effect of carbohydrate ingestion on ammonia metabolism during exercise in humans.

The present study was undertaken to examine the effect of carbohydrate ingestion on plasma and muscle ammonia (NH(3) denotes ammonia and ammonium) accumulation during prolonged exercise. Eleven trained men exercised for 2 h at 65% peak pulmonary oxygen consumption while ingesting either 250 ml of an 8% carbohydrate-electrolyte solution every 15 min (CHO) or an equal volume of a sweet placebo. Blood glucose and plasma insulin levels during exercise were higher in CHO, but plasma hypoxanthine was lower after 120 min (1.7 +/- 0.3 vs. 2.6 +/- 0.1 micromol/l; P < 0. 05). Plasma NH(3) levels were similar at rest and after 30 min of exercise in both trials but were lower after 60, 90, and 120 min of exercise in CHO (62 +/- 9 vs. 76 +/- 9 micromol/l; P < 0.05). Muscle NH(3) levels were similar at rest and after 30 min of exercise but were lower after 120 min of exercise in CHO (1.51 +/- 0.21 vs. 2.07 +/- 0.23 mmol/kg dry muscle; P < 0.05; n = 5). These data are best explained by carbohydrate ingestion reducing muscle NH(3) production from amino acid degradation, although a small reduction in net AMP catabolism within the contracting muscle may also make a minor contribution to the lower tissue NH(3) levels.     

Carbohydrate intake during prolonged cycling minimizes effect of glycemic index of preexercise meal

We studied the effects of the glycemicindex (GI) of preexercise meals on metabolism and performance whencarbohydrate (CHO) was ingested throughout exercise. Six well-trainedcyclists performed three counterbalanced trials of 2-h cycling at~70% of maximal oxygen uptake, followed by a performance ride of 300 kJ. Meals consumed 2 h before exercise consisted of 2 g CHO/kg bodymass of either high-GI potato (HGI trial) or low-GI pasta (LGI trial), or of a low-energy jelly (Con trial). Immediately before and throughout exercise, subjects ingested a 10 g/100 ml[U-¹⁴C]glucosesolution for a total of 24 ml/kg body mass. Despite differences inpreexercise glucose, insulin, and free fatty acids concentrations amongtrials, both total CHO oxidation for HGI, LGI, and Con trials,respectively, during steady-state exercise [403 ± 16, 376 ± 29, and 373 ± 24 (SE) g/2 h] andoxidation of the ingested CHO (65 ± 6, 57 ± 6, and 63 ± 5 g/2 h) were similar. There was no difference in time tocomplete the subsequent performance ride (946 ± 23, 954 ± 35, and 970 ± 26 s for HGI, LGI, and Con trials, respectively). WhenCHO is ingested during exercise in amounts presently recommended bysports nutrition guidelines, preexercise CHO intake has little effecton metabolism or on subsequent performance during prolonged cycling(~2.5 h).

     

Glucose infusion attenuates endogenous glucose production and enhances glucose use of horses during exercise.

We examined the effects of increased glucose availability on glucose kinetics and substrate utilization in horses during exercise. Six conditioned horses ran on a treadmill for 90 min at 34 +/- 1% of maximum oxygen uptake. In one trial [glucose (Glu)], glucose was infused at a mean rate of 34.9 +/- 1.1 micromol. kg(-1). min(-1), whereas in the other trial [control (Con)] an equivalent volume of isotonic saline was infused. Plasma glucose increased during exercise in Glu (90 min: 8.3 +/- 1.7 mM) but was largely unchanged in Con (90 min: 5.1 +/- 0.4 mM). In Con, hepatic glucose production (HGP) increased during exercise, reaching a peak of 38.6 +/- 2.7 micromol. kg(-1). min(-1) after 90 min. Glucose infusion partially suppressed (P < 0.05) the rise in HGP (peak value 25.8 +/- 3.3 micromol. kg(-1). min(-1)). In Con, glucose rate of disappearance (R(d)) rose to a peak of 40.4 +/- 2.9 micromol. kg(-1). min(-1) after 90 min; in Glu, augmented glucose utilization was reflected by values for glucose R(d) that were twofold higher (P < 0.001) than in Con between 30 and 90 min. Total carbohydrate oxidation was higher (P < 0.05) in Glu (187.5 +/- 8.5 micromol. kg(-1). min(-1)) than in Con (159.2 +/- 7.3 micromol. kg(-1).min(-1)), but muscle glycogen utilization was similar between trials. We conclude that an increase in glucose availability in horses during low-intensity exercise 1) only partially suppresses HGP, 2) attenuates the decrease in carbohydrate oxidation during such exercise, but 3) does not affect muscle glycogen utilization.     

Muscle metabolism during prolonged exercise in humans: influence of carbohydrate availability.

Eight endurance-trained men cycled to volitional exhaustion at 69 +/- 1% peak oxygen uptake on two occasions to examine the effect of carbohydrate supplementation during exercise on muscle energy metabolism. Subjects ingested an 8% carbohydrate solution (CHO trial) or a sweet placebo (Con trial) in a double-blind, randomized order, with vastus lateralis muscle biopsies (n = 7) obtained before and immediately after exercise. No differences in oxygen uptake, heart rate, or respiratory exchange ratio during exercise were observed between the trials. Exercise time to exhaustion was increased by approximately 30% when carbohydrate was ingested [199 +/- 21 vs. 152 +/- 9 (SE) min, P < 0.05]. Plasma glucose and insulin levels during exercise were higher and plasma free fatty acids lower in the CHO trial. No differences between trials were observed in the decreases in muscle glycogen and phosphocreatine or the increases in muscle lactate due to exercise. Muscle ATP levels were not altered by exercise in either trial. There was a small but significant increase in muscle inosine monophosphate levels at the point of exhaustion in both trials, and despite the subjects in CHO trial cycling 47 min longer, their muscle inosine monophosphate level was significantly lower than in the Con trial (CHO: 0.16 +/- 0.08, Con: 0.23 +/- 0.09 mmol/kg dry muscle). These data suggest that carbohydrate ingestion may increase endurance capacity, at least in part, by improving muscle energy balance.     

Effect of a single bout of resistance exercise on postprandial glucose and insulin response the next day in healthy, strength-trained men

Postprandial blood glucose and insulin levels are both risk factors for developing obesity, type-2 diabetes, and coronary heart diseases. To date, research has shown that a single bout of moderate- to high-intensity aerobic exercise performed 相似文献   

A moderate glycemic meal before endurance exercise can enhance performance

Kirwan, John P., Donal O'Gorman, and William J. Evans.A moderate glycemic meal before endurance exercise can enhance performance. J. Appl. Physiol. 84(1):53-59, 1998.The purpose of this study was to determine whetherpresweetened breakfast cereals with various fiber contents and amoderate glycemic index optimize glucose availability and improveendurance exercise performance. Six recreationally active women ate 75 g of available carbohydrate in the form of breakfast cereals: sweetenedwhole-grain rolled oats (SRO, 7 g of dietary fiber) or sweetenedwhole-oat flour (SOF, 3 g of dietary fiber) and 300 ml of water orwater alone (Con). The meals were provided 45 min before semirecumbentcycle ergometer exercise to exhaustion at 60% of peakO₂ consumption (O_{2 peak}). Diet andphysical activity were controlled by having the subjects reside in theGeneral Clinical Research Center for 2 days before each trial. Bloodsamples were drawn from an antecubital vein for glucose, free fattyacid (FFA), glycerol, insulin, epinephrine, and norepinephrinedetermination. Breath samples were obtained at 15-min intervals aftermeal ingestion and at 30-min intervals during exercise. Muscle glycogenconcentration was determined from biopsies taken from the vastuslateralis muscle before the meal and immediately after exercise. PlasmaFFA concentrations were lower (P < 0.05) during the SRO and SOF trials for the first 60 and 90 min ofexercise, respectively, than during the Con trial. Respiratory exchangeratios were higher (P < 0.05) at 90 and 120 min of exercise for the SRO and SOF trials, respectively, than for the Con trial. At exhaustion, glucose, insulin, FFA, glycerol, epinephrine, and norepinephrine concentrations, respiratory exchange ratio, and muscle glycogen use in the vastus lateralis muscle weresimilar for all trials. Exercise time to exhaustion was 16% longer(P < 0.05) during the SRO thanduring the Con trial: 266.5 ± 13 and 225.1 ± 8 min,respectively. There was no difference in exercise time for the SOF(250.8 ± 12) and Con trials. We conclude that eating ameal with a high dietary fiber content and moderate glycemic index 45 min before prolonged moderately intense exercise significantly enhancesexercise capacity.

     

Intramyocellular lipid content and insulin sensitivity are increased following a short-term low-glycemic index diet and exercise intervention

The relationship between intramyocellular (IMCL) and extramyocellular lipid (EMCL) accumulation and skeletal muscle insulin resistance is complex and dynamic. We examined the effect of a short-term (7-day) low-glycemic index (LGI) diet and aerobic exercise training intervention (EX) on IMCL and insulin sensitivity in older, insulin-resistant humans. Participants (66 ± 1 yr, BMI 33 ± 1 kg/m(2)) were randomly assigned to a parallel, controlled feeding trial [either an LGI (LGI/EX, n = 7) or high GI (HGI/EX, n = 8) eucaloric diet] combined with supervised exercise (60 min/day, 85% HR(max)). Insulin sensitivity was determined via 40 mU·m(-2)·min(-1) hyperinsulinemic euglycemic clamp and soleus IMCL and EMCL content was assessed by (1)H-MR spectroscopy with correction for fiber orientation. BMI decreased (kg/m(2) -0.6 ± 0.2, LGI/EX; -0.7 ± 0.2, HGI/EX P < 0.0004) after both interventions with no interaction effect of diet composition. Clamp-derived insulin sensitivity increased by 0.91 ± 0.21 (LGI/EX) and 0.17 ± 0.55 mg·kg(-1)·min(-1) (HGI/EX), P = 0.04 (effect of time). HOMA-IR was reduced by -1.1 ± 0.4 (LGI/EX) and -0.1 ± 0.2 (HGI/EX), P = 0.007 (effect of time), P = 0.02 (time × trial). Although both interventions increased IMCL content, (Δ: 2.3 ± 1.3, LGI/EX; 1.4 ± 0.9, HGI/EX, P = 0.03), diet composition did not significantly effect the increase. However, the LGI/EX group showed a robust increase in the [IMCL]/[EMCL] ratio compared with the HGI/EX group (Δ: 0.5 ± 0.2 LGI/EX vs. 0.07 ± 0.1, P = 0.03). The LGI/EX group also demonstrated greater reductions in [EMCL] than the HGI/EX group (Δ: -5.8 ± 3.4, LGI/EX; 2.3 ± 1.1, HGI/EX, P = 0.03). Changes in muscle lipids and insulin sensitivity were not correlated; however, the change in [IMCL]/[EMCL] was negatively associated with the change in FPI (r = -0.78, P = 0.002) and HOMA-IR (r = -0.61, P = 0.03). These data suggest that increases in the IMCL pool following a low glycemic diet and exercise intervention may represent lipid repartitioning from EMCL. The lower systemic glucose levels that prevail while eating a low glycemic diet may promote redistribution of lipid stores in the muscle.     

Glucose ingestion during exercise blunts exercise-induced gene expression of skeletal muscle fat oxidative genes

Ingestion of carbohydrate during exercise may blunt the stimulation of fat oxidative pathways by raising plasma insulin and glucose concentrations and lowering plasma free fatty acid (FFA) levels, thereby causing a marked shift in substrate oxidation. We investigated the effects of a single 2-h bout of moderate-intensity exercise on the expression of key genes involved in fat and carbohydrate metabolism with or without glucose ingestion in seven healthy untrained men (22.7 +/- 0.6 yr; body mass index: 23.8 +/- 1.0 kg/m(2); maximal O(2) consumption: 3.85 +/- 0.21 l/min). Plasma FFA concentration increased during exercise (P < 0.01) in the fasted state but remained unchanged after glucose ingestion, whereas fat oxidation (indirect calorimetry) was higher in the fasted state vs. glucose feeding (P < 0.05). Except for a significant decrease in the expression of pyruvate dehydrogenase kinase-4 (P < 0.05), glucose ingestion during exercise produced minimal effects on the expression of genes involved in carbohydrate utilization. However, glucose ingestion resulted in a decrease in the expression of genes involved in fatty acid transport and oxidation (CD36, carnitine palmitoyltransferase-1, uncoupling protein 3, and 5'-AMP-activated protein kinase-alpha(2); P < 0.05). In conclusion, glucose ingestion during exercise decreases the expression of genes involved in lipid metabolism rather than increasing genes involved in carbohydrate metabolism.     

Reversal of fatigue during prolonged exercise by carbohydrate infusion or ingestion

Seven cyclists exercised at 70% of maximal O2 uptake (VO2max) until fatigue (170 +/- 9 min) on three occasions, 1 wk apart. During these trials, plasma glucose declined from 5.0 +/- 0.1 to 3.1 +/- 0.1 mM (P less than 0.001) and respiratory exchange ratio (R) fell from 0.87 +/- 0.01 to 0.81 +/- 0.01 (P less than 0.001). After resting 20 min the subjects attempted to continue exercise either 1) after ingesting a placebo, 2) after ingesting glucose polymers (3 g/kg), or 3) when glucose was infused intravenously ("euglycemic clamp"). Placebo ingestion did not restore euglycemia or R. Plasma glucose increased (P less than 0.001) initially to approximately 5 mM and R rose (P less than 0.001) to approximately 0.83 with glucose infusion or carbohydrate ingestion. Plasma glucose and R then fell gradually to 3.9 +/- 0.3 mM and 0.81 +/- 0.01, respectively, after carbohydrate ingestion but were maintained at 5.1 +/- 0.1 mM and 0.83 +/- 0.01, respectively, by glucose infusion. Time to fatigue during this second exercise bout was significantly longer during the carbohydrate ingestion (26 +/- 4 min; P less than 0.05) or glucose infusion (43 +/- 5 min; P less than 0.01) trials compared with the placebo trial (10 +/- 1 min). Plasma insulin (approximately 10 microU/ml) and vastus lateralis muscle glycogen (approximately 40 mmol glucosyl U/kg) did not change during glucose infusion, with three-fourths of total carbohydrate oxidation during the second exercise bout accounted for by the euglycemic glucose infusion rate (1.13 +/- 0.08 g/min).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of carbohydrate or carbohydrate plus medium-chain triglyceride ingestion on cycling time trial performance.

This study examined the effectiveness of ingesting a carbohydrate or carbohydrate + medium-chain triglycerides (MCT) on metabolism and cycling performance. Eight endurance-trained men [peak O(2) uptake = 4.71 +/- 0.09 (SE) l/min] completed 35 kJ/kg as quickly as possible [time trial (TT)] while consuming 250 ml/15 min of either a 6% (wt/vol) carbohydrate solution (C), a 6% carbohydrate + 4.2% MCT solution (C+M), or a sweet placebo (P). Time to complete the set amount of work was reduced in both C and C+M compared with P by 7 and 5%, respectively (C: 166 +/- 7 min; C+M: 169 +/- 7 min; P: 178 +/- 11 min; P < 0.01). Plasma glucose concentration was maintained at or above resting values throughout both C and C+M trials but decreased (P < 0.05) below resting values in P at the completion of the TT. The estimated rate of carbohydrate oxidation was not different during the first 90 min of exercise but thereafter was reduced (P < 0.05) in P and was maintained in both C and C+M. These data demonstrate that carbohydrate ingestion during exercise improves 100-km TT performance compared with a sweet placebo, but the addition of MCT does not provide any further performance enhancement.     

Effect of carbohydrate ingestion on exercise metabolism

Five male cyclists were studied during 2 h of cycle ergometer exercise (70% VO2 max) on two occasions to examine the effect of carbohydrate ingestion on muscle glycogen utilization. In the experimental trial (CHO) subjects ingested 250 ml of a glucose polymer solution containing 30 g of carbohydrate at 0, 30, 60, and 90 min of exercise; in the control trial (CON) they received an equal volume of a sweet placebo. No differences between trials were seen in O2 uptake or heart rate during exercise. Venous blood glucose was similar before exercise in both trials, but, on average, was higher during exercise in CHO [5.2 +/- 0.2 (SE) mmol/l] compared with CON (4.8 +/- 0.1, P less than 0.05). Plasma insulin levels were similar in both trials. Muscle glycogen levels were also similar in CHO and CON both before and after exercise; accordingly, there was no difference between trials in the amount of glycogen used during the 2 h of exercise (CHO = 62.8 +/- 10.1 mmol/kg wet wt, CON = 56.9 +/- 10.1). The results of this study indicate that carbohydrate ingestion does not influence the utilization of muscle glycogen during prolonged strenuous exercise.     

Plasma glucose kinetics during prolonged exercise in trained humans when fed carbohydrate

Nine endurance-trained men exercised on a cycle ergometer at approximately 68% peak O2 uptake to the point of volitional fatigue [232 +/- 14 (SE) min] while ingesting an 8% carbohydrate solution to determine how high glucose disposal could increase under physiological conditions. Plasma glucose kinetics were measured using a primed, continuous infusion of [6,6-2H]glucose and the appearance of ingested glucose, assessed from [3-3H]glucose that had been added to the carbohydrate drink. Plasma glucose was increased (P < 0.05) after 30 min of exercise but thereafter remained at the preexercise level. Glucose appearance rate (R(a)) increased throughout exercise, reaching its peak value of 118 +/- 7 micromol. kg(-1). min(-1) at fatigue, whereas gut R(a) increased continuously during exercise, peaking at 105 +/- 10 micromol. kg(-1). min(-1) at the point of fatigue. In contrast, liver glucose output never rose above resting levels at any time during exercise. Glucose disposal (R(d)) increased throughout exercise, reaching a peak value of 118 +/- 7 micromol. kg(-1). min(-1) at fatigue. If we assume 95% oxidation of glucose R(d), estimated exogenous glucose oxidation at fatigue was 1.36 +/- 0.08 g/min. The results of this study demonstrate that glucose uptake increases continuously during prolonged, strenuous exercise when carbohydrate is ingested and does not appear to limit exercise performance.