Total Carbohydrate Oxidation Research Articles

Glucose kinetics during prolonged exercise in euglycaemic and hyperglycaemic subjects

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 (Rox) 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 (Ra), while unlabelled glucose (25% dextrose) was infused to maintain plasma glucose concentration at either 5 or 10 mM. During ET, endogenous liver glucose Ra (total Ra minus the rate of infusion) declined from 22.4 +/- 4.9 to 6.5 +/- 1.4 mumol/min per kg fat-free mass [FFM] (P < 0.05) and during HT it was completely suppressed. In contrast, Rox increased to 152 +/- 21 and 61 +/- 10 mumol/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 microU/ml) also increased total carbohydrate oxidation from 203 +/- 7 (ET) to 310 +/- 3 mumol/min per kg FFM (P < 0.0001) and suppressed fat oxidation from 51 +/- 3 (ET) to 18 +/- 2 mumol/min per kg FFM (P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Availability of glucose ingested during muscle exercise performed under acipimox-induced lipolysis blockade

This study investigated the percentage of carbohydrate utilization than can be accounted for by glucose ingested during exercise performed after the ingestion of the potent lipolysis inhibitor Acipimox. Six healthy male volunteers exercised for 3 h on a treadmill at about 45% of their maximal oxygen uptake, 75 min after having ingested 250 mg of Acipimox. After 15-min adaptation to exercise, they ingested either glucose dissolved in water, 50 g at time 0 min and 25 g at time 60 and 120 min (glucose, G) or sweetened water (control, C). Naturally labelled [13C]glucose was used to follow the conversion of the ingested glucose to expired-air CO2. Acipimox inhibited lipolysis in a similar manner in both experimental conditions. This was reflected by an almost complete suppression of the exercise-induced increase in plasma free fatty acid and glycerol and by an almost constant rate of lipid oxidation. Total carbohydrate oxidation evaluated by indirect calorimetry, was similar in both experimental conditions [C, 182, (SEM 21); G, 194 (SEM 16) g.3 h-1], as was lipid oxidation [C, 57 (SEM 6); G, 61 (SEM 3) g.3 h-1]. Exogenous glucose oxidation during exercise G, calculated by the changes in 13C:12C ratio of expired air CO2, averaged 66 (SEM 5) g.3 h-1 (19% of the total energy requirement). Consequently, endogenous carbohydrate utilization was significantly smaller after glucose than after placebo ingestion: 128 (SEM 18) versus 182 (SEM 21) g.3 h-1, respectively (P < 0.05). Symptoms of intense fatigue and leg cramps observed with intake of sweet placebo were absent with glucose ingestion.(ABSTRACT TRUNCATED AT 250 WORDS)

Metabolic Responses When Different Forms of Carbohydrate Energy Are Consumed during Cycling

This study examined the effects of consuming the same amount of carbohydrate in solid form, liquid form, or both on metabolic responses during 2 hrs of cycling at 70% peak VO2 and on cycling time-trial performance. Subjects consumed 0.4 g carbohydrate/kg body mass before and every 30 min during exercise. The liquid was a 7% carbohydrate-electrolyte beverage and the solid was a sports bar (1171 kJ) in which 76%, 18%, and 6% of total energy was derived from carbohydrate, fat, and protein, respectively. Blood obtained at baseline, before exercise, and every 30 min was analyzed for glucose, insulin, lactate, hemoglobin, hematocrit, and plasma volume. There were no differences among the treatments for the blood parameters. Total carbohydrate oxidation and time-trial performance were also similar among treatments. Under thermoneutral conditions with equal liquid ingestion, the metabolic and performance responses are similar when consuming carbohydrate as a liquid, solid, or in combination during prolonged, moderate intensity cycling.

Effects of preexercise candy bar ingestion on glycemic response, substrate utilization, and performance.

This study examined the effects of preexercise candy bar ingestion on glycemic response, substrate utilization, and performance in 8 trained male cyclists. The cyclists randomly ingested one large milk chocolate bar (1CB), two large milk chocolate bars (2CB), or a placebo (P) 30 min prior to a 90-min cycle ride at 70% VO2max followed by a 33-W increase every 2 min until exhaustion (approximately 10 min). Glucose decreased after 15 min of exercise but returned to preexercise values by 30 min of exercise. Glucose concentration for 2CB was significantly higher than for P and 1CB at exhaustion. Insulin concentration increased in response to 1CB and 2CB and returned to preexercise values within 15 min of exercise. No significant differences were noted for free fatty acid (FFA) concentrations, lactate concentrations, respiratory exchange ratio, total carbohydrate oxidation, or estimated fat and carbohydrate oxidation rates. Time to exhaustion was similar among the groups. The results suggest that the transient lowering of blood glucose observed with preexercise milk chocolate bar ingestion 30 min prior to exercise may not cause major metabolic perturbations that impair athletic performance in trained athletes performing moderately intense cycle exercise.

Endogenous substrate oxidation during exercise and variations in breath 13CO2/12CO2

This study attempted to induce a major shift in the utilization of endogenous substrates during exercise in men by the use of a potent inhibitor of adipose tissue lipolysis, Acipimox, and to see to what extent this affects the 13C/12C ratio in expired air CO2. Six healthy volunteers exercised for 3 h on a treadmill at approximately 45% of their maximum O2 uptake, 75 min after having ingested either a placebo or 250 mg Acipimox. The rise in plasma free fatty acids and glycerol was almost totally prevented by Acipimox, and no significant rise in the utilization of lipids, evaluated by indirect calorimetry, was observed. Total carbohydrate oxidation averaged 128 +/- 17 (placebo) and 182 +/- 21 g/3 h (Acipimox). Conversely, total lipid oxidation was 84 +/- 5 (placebo) and 57 +/- 6 g/3 h (Acipimox; P < 0.01). Under placebo, changes in expired air CO2 delta 13C were minimal, with only a 0.49/1000 significant rise at 30 min. In contrast, under Acipimox, the rise in expired air CO2 delta 13C averaged 1/1000 and was significant throughout the 3-h exercise bout; in these conditions calculation of a "pseudooxidation" of an exogenous sugar naturally or artificially enriched in 13C, but not ingested, would have given an erroneous value of 19.8 +/- 2.6 g/3 h. Thus under conditions of extreme changes in endogenous substrate utilization, an appropriate control experiment is mandatory when studying exogenous substrate oxidation by 13C-labeled substrates and isotope-ratio mass spectrometry measurements on expired air CO2.

Carbohydrate feeding during exercise.

During strenuous exercise (i.e. 70% maximal O2 consumption) there is a progressive shift from muscle glycogen to blood glucose oxidation with increasing duration of exercise. By maintaining blood glucose concentration and the rate of carbohydrate oxidation necessary to exercise strenuously, carbohydrate consumption throughout exercise delays fatigue by 30-60 min in endurance-trained subjects. This requires exogenous glucose supplementation at rates in excess of 1 gram/min (i.e., 16 mg/kg/min) as evidenced by the observation that intravenous glucose infusion at this rate is required to maintain blood glucose at 5 mM. Exogenous glucose must be infused at a rate of 2.6 gram/min (i.e., 37 mg/kg/min), which is similar to the total rate of carbohydrate oxidation, in order to maintain blood glucose at 10 mM after 2 h of exercise. However, carbohydrate supplementation during intense exercise does not spare muscle glycogen utilization in people. This suggests that over the course of 2-4 hours of exercise at 70% VO2max, muscle glycogen and blood glucose contribute equally to total carbohydrate oxidation. Furthermore, during the latter stages of prolonged exercise, exogenous blood glucose supplementation may be capable of supplying almost all of the carbohydrate requirements of exercise at intensities up to 70% VO2max.

Influence of dietary fat polyunsaturated to saturated ratio on energy substrate utilization in obesity

The effect of the polyunsaturated to saturated (P:S) ratio of dietary fat on preprandial and postprandial macronutrient oxidation was studied in normal-weight and obese individuals. Total thermogenic response and fat and carbohydrate oxidation rates were determined by duplicate respiratory gas exchange measurements after test breakfasts, in seven normal and eight overweight subjects who consumed self-selected diets containing fat of high or low P:S ratio. Dietary intake records and erythrocyte linoleic to oleic (L:O) acid ratio changes were used as indicators of compliance. No diet- or weight-related differences were observed in resting fat or carbohydrate oxidation rates, or in protein-free basal energy expenditure. Obese subjects consuming low P:S ratio diets exhibited reduced ( P < .05) contribution of fat oxidation to the thermogenic response, compared with lean individuals consuming high or low P:S ratio diets. However, total calories associated with the thermogenic response, and total fat and carbohydrate oxidation after the test breakfasts, did not differ significantly across groups. These findings suggest that, in obesity, whole-body postprandial disposal of dietary fat is influenced by the long-chain fatty acid composition.

Carbohydrate feedings 1 h before exercise improves cycling performance

The effects of consuming two different amounts of liquid carbohydrate 1 h before exercise on the metabolic responses during exercise and on exercise performance were determined. Subjects consumed either 1.1 g (LC) or 2.2 g (HC) carbohydrate/kg body mass or a placebo (P). Subjects cycled at 70% of maximal oxygen consumption (VO2max) for 90 min and then underwent a performance trial. Blood glucose and insulin responses during exercise were different among the three trials. Total carbohydrate oxidation was greater for the carbohydrate trials compared with P. Time-trial performance was significantly improved by LC and HC. Despite elevated insulin concentrations at the start of and during exercise, and despite an initial drop in blood glucose, consumption of between 1.1 and 2.2 g liquid carbohydrate/kg body mass 60 min before moderately intense prolonged exercise can improve performance, presumably via enhanced carbohydrate oxidation.

Effects of fat on insulin-stimulated carbohydrate metabolism in normal men.

We have examined the onset and duration of the inhibitory effect of an intravenous infusion of lipid/heparin on total body carbohydrate and fat oxidation (by indirect calorimetry) and on glucose disappearance (with 6,6 D2-glucose and gas chromatography-mass spectrometry) in healthy men during euglycemic hyperinsulinemia. Glycogen synthase activity and concentrations of acetyl-CoA, free CoA-SH, citrate, and glucose-6-phosphate were measured in muscle biopsies obtained before and after insulin/lipid and insulin/saline infusions. Lipid increased insulin-inhibited fat oxidation (+40%) and decreased insulin-stimulated carbohydrate oxidation (-63%) within 1 h. These changes were associated with an increase (+489%) in the muscle acetyl-CoA/free CoA-SH ratio. Glucose disappearance did not decrease until 2-4 h later (-55%). This decrease was associated with a decrease in muscle glycogen synthase fractional velocity (-82%). The muscle content of citrate and glucose-6-phosphate did not change. We concluded that, during hyperinsulinemia, lipid promptly replaced carbohydrate as fuel for oxidation in muscle and hours later inhibited glucose uptake, presumably by interfering with muscle glycogen formation.

Carbohydrate Feeding before Exercise: Effect of Glycemic Index

Low glycemic index (GI) foods may confer an advantage when eaten before prolonged strenuous exercise by providing a slow-release source of glucose to the blood without an accompanying insulin surge. To test this hypothesis, eight trained cyclists pedalled to exhaustion one hour after ingestion of equal carbohydrate portions of four test meals: lentils, a low GI food (LGI); potato, a high GI food (HGI), and glucose and water. Plasma glucose and insulin levels were lower after LGI than after HGI from 30 to 60 min after ingestion (p less than 0.05). Plasma free fatty acid (FFA) levels were highest after water (p less than 0.05) followed by LGI and then glucose and HGI. From 45 to 60 min after ingestion, plasma lactate was higher in the HGI trial than in the LGI trial (p less than 0.05) and remained higher throughout the period of exercise. The rank order from lowest to highest for total carbohydrate oxidation during exercise was water, lentils, glucose and potato. Endurance time was 20 min longer after LGI than after HGI (p less than 0.05). These findings suggest that a low GI pre-game meal may prolong endurance during strenuous exercise by inducing less post-prandial hyperglycemia and hyperinsulinemia, lower levels of plasma lactate before and during exercise, and by maintaining plasma glucose and FFA at higher levels during critical periods of exercise.

Severity, duration, and mechanisms of insulin resistance during acute infections.

Acute infections provoke insulin resistance. These experiments were designed to study the severity, duration, and mechanisms of insulin resistance caused by acute infections. First, we studied eight patients [mean age, 29 +/- 11 (+/- SD) yr; body mass index, 23 +/- 2 kg/m2] with acute viral or bacterial infections during the acute stage of their infection and 1-3 months after recovery. The rate of glucose infusion required to maintain normoglycemia during hyperinsulinemia (approximately 500 pmol/L) was used as a measure of insulin action. During infection, the glucose requirements in the patients [21 +/- 2 (+/- SE) mumol/kg.min] were 52% less than those in weight- and age-matched normal subjects (44 +/- 2 mumol/kg.min; P less than 0.001). Compared to data from a large group of normal subjects, the resistance to insulin during infection corresponded to that predicted for a weight-matched 84-yr-old normal person or an age-matched obese person with a body mass index of 37 kg/m2. One to 3 months after recovery, the patients' glucose requirements were still significantly lower (37 +/- 3 mumol/kg.min; P less than 0.02) than those in matched normal subjects. To assess the mechanism of insulin resistance, seven additional patients were studied during the acute stage of infection using a low dose insulin infusion (plasma insulin, 215 pmol/L) combined with a [3-3H]glucose infusion and indirect calorimetry. Again, the glucose requirements were 59% lower in the patients (14 +/- 2 mumol/kg.min) than in matched normal subjects (34 +/- 2 mumol/kg.min; P less than 0.001). This decrease was due to a defect in glucose utilization (18 +/- 2 vs. 37 +/- 1 mumol/kg.min; P less than 0.001, patients vs. normal subjects) rather than impaired suppression of glucose production (4 +/- 1 vs. 3 +/- 1 mumol/kg.min, respectively). Total carbohydrate oxidation rates were similar in both groups (16 +/- 2 vs. 14 +/- 1 mumol/kg.min, respectively), whereas the apparent glucose storage was neglible in the patients (2 +/- 1 mumol/kg.min) compared to that in normal subjects (22 +/- 2 mumol/kg.min; P less than 0.001). We conclude that acute infections induce severe and long-lasting insulin resistance, which is localized to glucose-utilizing pathways. The rate of carbohydrate oxidation is normal during infections, whereas the rate of nonoxidative glucose disposal, as determined by indirect calorimetry, is nearly zero. The apparent blockade in glucose storage could result from diminished glycogen synthesis, accelerated glycogenolysis, or both.

Effect of elevated free fatty acids on glucose oxidation in normal humans

In vitro studies indicating an inverse relationship between free fatty acid (FFA) availability and glucose oxidation led to proposal of the glucose-fatty acid cycle. In vivo studies have yielded conflicting results regarding the effect of FFA on glucose oxidation. In the present study the effect of FFA on glucose oxidation was determined in six normal volunteer subjects. The rate of glucose uptake was fixed by using a constant glucose infusion to suppress endogenous glucose production. Glucose was infused continuously overnight and during the four hour study at 8 mg/kg × min to ensure use of glucose as an energy substrate by virtually all tissues. Following a two-hour baseline glucose infusion, infusion of 20% IV fat emulsion at 1.0 mL/min plus heparin was added to the constant glucose infusion for two additonal hours. Total carbohydrate oxidation was determined by indirect calorimetry, and the direct oxidation of the infused (plasma) glucose was measured by the use of U- 13C-glucose. Glycogen oxidation was calculated as the difference between total carbohydrate oxidation and the oxidation of plasma glucose. Glucose uptake was calculated from the infusion rate, corrected for any changes in plasma and/or urine glucose concentration. Glucose uptake closely approximated the rate of IV glucose infusion and was unchanged by fat infusion. The percent of CO 2 production from U- 13C-glucose oxidation (74.5 ± 12.3, mean ± SD) was not affected by FFA, nor was the percent of glucose uptake oxidized (37.5 ± 4.0). Indirect calorimetry showed a decrease of total carbohydrate oxidation from 4.22 ± 1.12 mg/kg × min to 3.13 ± 1.65 mg/kg × min ( P < .05) during the final hour of fat infusion. The calculated value for glycogen oxidation (the oxidation of glucose which never entered the plasma pool) significantly decreased with increased FFA availability (0.97 ± 1.18 to 0.05 ± 1.54 mg/kg × min) ( P < .05). These data suggest that FFAs do not inhibit plasma glucose oxidation when the rate of glucose uptake is constant. Increases in circulating FFAs may affect total glucose oxidation, however, by suppressing the oxidation of glycogen.

Glucose carbon recycling and oxidation in human newborns.

Total carbohydrate oxidation, plasma glucose oxidation, and glucose carbon recycling were measured in 11 fasting newborns using a constant infusion of D-[U-13C]glucose combined with respiratory calorimetry. The "true" rate of glucose appearance (Ra) was quantified from the enrichment of the nonrecycling tracer species (m + 6), while the "apparent" rate of glucose appearance was quantified from the enrichment of glucose C - 1. The plasma glucose concentration remained constant at approximately 50 mg/dl (2.8 mM) throughout the study. The true rate of glucose production was 5.02 +/- 0.41 mg X kg-1 X min-1, (means +/- SD). Glucose was oxidized at a rate of 2.67 +/- 0.34 mg X kg-1 X min-1 and represented 53% of the glucose turnover. Recycling of glucose carbon represented 36% of the glucose production rate, or 1.87 +/- 0.74 mg X kg-1 X min-1. The oxidation of plasma glucose provided 15.8 +/- 2.0 kcal X kg-1 X day-1, whereas total carbohydrate oxidation (measured by respiratory calorimetry) provided 19.9 +/- 6.6 kcal X kg X day. The data indicate that 1) recycling of glucose carbon accounts for about one-third of glucose production, demonstrating active gluconeogenesis in the fasting newborn; 2) the oxidation of plasma glucose represents only 80% of total carbohydrate oxidation, the remaining 20% possibly representing the local oxidation of tissue glycogen stores; and 3) as the measured rate of glucose oxidation will be insufficient to supply the entire calculated cerebral metabolic requirements, these data suggest that fuels in addition to glucose may be important for cerebral metabolism in the fasting human newborn.

Remarkable metabolic availability of oral glucose during long-duration exercise in humans.

It was reported previously that glucose ingestion prior to or at the beginning of muscular exercise was a readily available metabolic substrate. The aim of this study was to see what percentage of carbohydrate utilization can be covered by glucose ingested regularly during exercise. Male healthy volunteers exercised for 285 min at approximately 45% of their individual maximal O2 uptake on a 10% uphill treadmill. After 15 min adaptation to exercise they received either 200 g (group G 200) or 400 g (group G 400) glucose (0.25 g X ml H2O-1) orally in eight equal doses repeated every 30 min (G 200 = 8 X 25 g, n = 4; G 400 = 8 X 50 g, n = 4). Indirect calorimetry was used to evaluate carbohydrate and lipid oxidation. Naturally labeled [13C]glucose was used to follow the oxidation of the exogenous glucose. Total carbohydrate oxidation was 341 +/- 22 and 332 +/- 32 g, lipid oxidation was 119 +/- 8 and 105 +/- 5 g, and exogenous glucose oxidation was 137 +/- 4 and 227 +/- 13 g (P less than 0.005) in groups G 200 and G 400, respectively. Endogenous glucose oxidation was about half in G 400 of what it was in G 200: 106 +/- 27 vs. 204 +/- 24 g (P less than 0.02). During the last hour of exercise, exogenous oxidation represented 55.3 and 87.5% of total carbohydrate oxidation for groups G 200 and G 400, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Carbohydrate (CHO) oxidation in patients with type B insulin resistance.

Total body carbohydrate (CHO) and fat oxidation rates, plasma glucose, free fatty acid, and insulin concentrations were determined in two patients with the type B syndrome of severe insulin resistance and in normal controls in response to insulin infusions (1-100 mU/kg/min) and to a test meal. In addition, insulin was infused at higher rates (10-1000 mU/kg/min) in one of the two patients while plasma glucose concentrations were clamped first at 195 and later at 244 mg/dl. During the postabsorptive state, resting metabolic rates (RMR) were 914 and 979 cal/min/1.73 m2 in the two patients (controls: 1018 +/- 85 cal/min/1.73 m2). Patients met 85% and 83% of their caloric requirements by oxidizing fat (controls: 63 +/- 7%). Protein oxidation accounted for 15% and 13% (controls: 14 +/- 3%) of energy requirements and CHO oxidation for 0% and 0%, respectively, in both patients (controls: 23 +/- 5%). Infusion of insulin at a rate of 10 mU/kg/min raised plasma insulin concentrations from 1400 and 440 microU/ml to 6000 and 2500 microU/ml, respectively, in patients 1 and 2 (controls: from 4 +/- 0.3 to 1288 +/- 50 microU/ml), but had no effects on rates of CHO, fat, or protein oxidation in either patient. By comparison, the rate of CHO oxidation in controls rose about sixfold from 40 +/- 8 to 234 +/- 12 mg/min/1.73 m2. Infusion of 1000 mU/kg/min in combination with an increase in plasma glucose from 195 +/- 1.1 to 244 +/- 1.9 mg/dl in patient 1, however, raised CHO oxidation from 0 to 36 mg/min/1.73 m2 and lowered fat oxidation from 105 to 69 mg/min/1.73 m2.(ABSTRACT TRUNCATED AT 250 WORDS)

Contribution of 500 g naturally labeled 13C dextrin maltose to total carbohydrate utilization and the effect of the antecedent diet, in man

Exogenous carbohydrate oxidation was studied for 24 h in 14 healthy young male volunteers after ingestion of 500 g naturally labeled 13C carbohydrate. Prior to the test, the antecedent diet was high in fat (4 subjects), mixed (4 subjects), or high in carbohydrate (6 subjects). The rate of exogenous carbohydrate oxidation was greater in the high carbohydrate and mixed diet groups than in the high fat group and endogenous carbohydrate continued to contribute to total carbohydrate oxidation for approximately 10 h after ingestion of the carbohydrate load in all groups. After 14 h, 178 +/- 5 g, 241 +/- 11 g and 260 +/- 9 g carbohydrate had been utilized of which 130 +/- 8 g, 155 +/- 6 g and 180 +/- 7 g was of exogenous origin in the high fat, mixed and high carbohydrate groups respectively. At the end of the test, postabsorptive glucose oxidation was of exogenous origin whatever the antecedent diet indicating that much of basal hepatic glucose production was covered by glycogenolysis of recently synthesized labeled glycogen.

Effect of physical training on utilization of a glucose load given orally during exercise.

The effect of a 6-wk training period on the oxidation of a 100-g glucose load given orally during exercise was investigated in six healthy male volunteers. The subjects were submitted before and 24 h after the training program to a 105-min exercise bout (performed at about 40% of the pretraining VO2max) followed by a 90-min resting period. Naturally labeled [13C]glucose was given 15 min after the beginning of exercise. Exogenous glucose oxidation was derived from 13CO2 measurements in expired air, and total glucose and lipid oxidation were evaluated by indirect calorimetry. Training (60-min bicycling 5 days a week at 30-40% VO2max) resulted in a 29% increase in VO2max. During the 15 min of exercise that preceded glucose ingestion, the rate of total carbohydrate oxidation was slightly decreased after training, whereas the rate of lipid oxidation was slightly increased. Training did not affect the response of blood glucose, plasma insulin, or plasma free fatty acids to the glucose ingested during exercise; in contrast, the circulating levels of epinephrine, glycerol, and lactate were significantly reduced after training. Substrate utilization measurements revealed similar oxidation rates of carbohydrates (106.9 +/- 2.7 before vs. 100.2 +/- 4.7 g/3 h after training) and of lipids. However, detailed analysis revealed a significant 17% increase in exogenous glucose oxidation, thus indicating a significant sparing of endogenous carbohydrates. In conclusion, physical training induces a modest but significant increase in the oxidation of an oral load of glucose given during subsequent exercise of moderate intensity, a phenomenon reinforcing the sparing of endogenous carbohydrate stores.

Metabolic availability of glucose ingested 3 h before prolonged exercise in humans.

The aim of the present study was to investigate the extent to which an oral load of glucose ingested 3 h before a 4-h exercise bout of moderate intensity represents an energy source readily available during that exercise. Therefore, five healthy male volunteers drank 100 g of naturally labeled [13C]glucose dissolved in 400 ml of water, rested for 3 h, and then exercised on a treadmill for the next 4 h at about 45% of their individual maximum O2 consumption. Total glucose oxidation was derived from nonprotein respiratory quotient and exogenous glucose oxidation evaluated by the 13C methodology as previously described. Total carbohydrate oxidation averaged 285 +/- 17 g during the 7 h of the test, the global amount of carbohydrate oxidized during the exercising period was 253.1 +/- 16.9 g/4 h. Exogenous glucose oxidation averaged 11.3 +/- 0.7 g during the 3-h period of rest and increased markedly after the beginning of exercise, reaching 18.9 +/- 2.2 g/30 min during the first 30 min of exercise; the total amount of exogenous glucose oxidized during the 4 h of exercise was 67.5 +/- 9.4 g. Throughout the whole period of exercise, blood glucose concentrations remained between 3.5 and 4.0 mmol/l. Exercise induced a major fall in plasma insulin levels that reached undetectable values after 3 and 4 h, whereas plasma glucagon levels tended to rise, but their level never significantly exceeded the basal values; plasma free fatty acids and glycerol increased markedly during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

OXIDATIVE METABOLISM OF 13C MEDIUM CHAIN TRIGLYCERIDE (MCT) FED TO PRETERM INFANTS (PT)

Fat malbsorption is frequent in preterm infants fed either breast or formula milk and improves when part of milk fat is replaced by MCT. The metabolic fate of MCT is not well known in PT. Five PT (BW: 1771 ± 100 g; GA: 34 ± 1 wks; age at study: 24 ± 4 d) fed a formula containing 50% of fat as MCT were given a known amount of 13C-trioctanoin on the second day of a 3 day balance. Continuous indirect calorimetry was performed during the 24 hours following the 13C-MCT ingestion and energy expenditure, total carbohydrate, lipid and protein oxidation were determined. Continuous sampling of expired CO2 allowed 13C/12C ratio measurements over the 24 hour period and the amount of MCT oxidized was then derived. Results are shown in the table (per kg/d, m ± s.d.): Elimination curves of 13C in expired CO2 were similar in all infants but were different in amplitude. Mean MCT oxidation was 27 ± 14% (range 6-43%) and accounted for 31% (range 7-47%) of the total fat oxidation. In conclusion, MCT oxidation shows considerable variations between PT infants. Furthermore no correlation with energy expenditure and with total fat oxidation is observed.

Availability of glucose given orally during exercise.

Adequate utilization of glucose given orally during prolonged muscular exercise remains a matter of controversy. The aim of the present study was to investigate whether the time when glucose is ingested during exercise affects exogenous glucose disposal. Nine healthy male volunteers were submitted to a 4-h period of treadmill exercise at about 45% of their maximum O2 consumption. A 100-g load of naturally labeled [13C]glucose was given orally after 120 min (5 subj, group A) or 15 min (4 subj, group B) of exercise. In the 2 h after glucose ingestion, total carbohydrate oxidation (indirect calorimetry) was similar in both groups (A: 147 +/- 12 g/2 h; B: 135 +/- 12 g/2 h) as was lipid oxidation (A: 51 +/- 4 g/2 h; B: 57 +/- 11 g/2 h). Exogenous glucose oxidation was 54 +/- 2 g/h in group A vs. 55 +/- 6 g/2 h in group B. The blood glucose response to oral glucose was similar in the two conditions, whereas the C-peptide response, already modest, was further blunted when glucose was ingested after 2 h of exercise compared with the response observed after 15 min. In conclusion, glucose ingestion during prolonged exercise of moderate intensity is effectively oxidized, 55% of the load given being recovered as expired CO2 within 2 h; utilization of glucose given orally is similar when ingestion takes place 15 or 120 min after initiation of exercise.