Effect of a 20-day ski trek on fuel selection during prolonged exercise at low workload with ingestion of 13C-glucose.

Fuel selection was measured in five subjects (36.0 +/- 10.5 years old; 87.3 +/- 12.5 kg; mean +/- SD) during a 120-min tethered walking with ski poles (1.12 l O(2) min(-1)) with ingestion of (13)C-glucose (1.5 g kg(-1)), before and after a 20-day 415-km ski trek [physical activity level (PAL) approximately 3], using respiratory calorimetry, urea excretion, and (13)C/(12)C in expired CO(2) and in plasma glucose. Before the ski trek, protein oxidation contributed 9.7 +/- 1.6% to the energy yield (%En) while fat and carbohydrate (CHO) oxidation provided 73.5 +/- 5.5 and 16.7 +/- 6.5%En. Plasma glucose was the main source of CHO (52.9 +/- 9.5%En) with similar contributions from exogenous glucose (27.2 +/- 3.1%En), glucose from the liver (25.6 +/- 8.3%En) and muscle glycogen (20.9 +/- 4.0%En). Endogenous CHO contributed 46.6 +/- 3.9%En. Following the ski trek %En from protein, fat, CHO, exogenous glucose and endogenous CHO were not significantly modified (10.1 +/- 1.3, 15.8 +/- 6.7, 74.1 +/- 6.5, 28.7 +/- 3.0 and 45.5 +/- 7.5%En, respectively) but the %En from plasma glucose and glucose from the liver (41.1 +/- 3.6 and 12.4 +/- 4.0%En) were reduced, while that from muscle glycogen increased (33.0 +/- 4.5%En). These results show that in subjects in the fed state with glucose ingestion during exercise, CHO is the main substrate oxidized, with major contributions from both exogenous and endogenous CHO. Following a ~3-week period of prolonged low intensity exercise, the %En from protein, fat, CHO, exogenous glucose and endogenous CHO were not modified. However, the %En from glucose released from the liver was reduced (possibly due to an increased insulin sensitivity of the liver) while that from muscle glycogen was increased.

Muscle glycogen oxidation during prolonged exercise measured with oral [13C]glucose: comparison with changes in muscle glycogen content.

Plasma glucose and muscle glycogen oxidation during prolonged exercise [75-min at 48 and 76% maximal O(2) uptake (Vo(2 max))] were measured in eight well-trained male subjects [Vo(2 max) = 4.50 l/min (SD 0.63)] using a simplified tracer technique in which a small amount of glucose highly enriched in (13)C was ingested: plasma glucose oxidation was computed from (13)C/(12)C in plasma glucose (which was stable beginning at minute 30 and minute 15 during exercise at 48 and 76% Vo(2 max), respectively) and (13)CO(2) production, and muscle glycogen oxidation was estimated by subtracting plasma glucose oxidation from total carbohydrate oxidation. Consistent data from the literature suggest that this small dose of exogenous glucose does not modify muscle glycogen oxidation and has little effect, if any, on plasma glucose oxidation. The percent contributions of plasma glucose and muscle glycogen oxidation to the energy yield at 48% Vo(2 max) [15.1% (SD 3.8) and 45.9% (SD 5.8)] and at 76% Vo(2 max) [15.4% (SD 3.6) and 59.8% (SD 9.2)] were well in line with data previously reported for similar work loads and exercise durations using conventional tracer techniques. The significant reduction in glycogen concentration measured from pre- and postexercise vastus lateralis muscle biopsies paralleled muscle glycogen oxidation calculated using the tracer technique and was larger at 76% than at 48% Vo(2 max). However, the correlation coefficients between these two estimates of muscle glycogen utilization were not different from zero at each of the two work loads. The simplified tracer technique used in the present experiment appears to be a valid alternative approach to the traditional tracer techniques for computing plasma glucose and muscle glycogen oxidation during prolonged exercise.

Substrate source utilization during moderate intensity exercise with glucose ingestion in Type 1 diabetic patients.

Substrate oxidation and the respective contributions of exogenous glucose, glucose released from the liver, and muscle glycogen oxidation were measured by indirect respiratory calorimetry combined with tracer technique in eight control subjects and eight diabetic patients (5 men and 3 women in both groups) of similar age, height, body mass, and maximal oxygen uptake, over a 60-min exercise period on cycle ergometer at 50.8% (SD 4.0) maximal oxygen uptake [131.0 W (SD 38.2)]. The subjects and patients ingested a breakfast (containing approximately 80 g of carbohydrates) 3 h before and 30 g of glucose (labeled with 13C) 15 min before the beginning of exercise. The diabetic patients also received their usual insulin dose [Humalog = 9.1 U (SD 0.9); Humulin N = 13.9 U (SD 4.4)] immediately before the breakfast. Over the last 30 min of exercise, the oxidation of carbohydrate [1.32 g/min (SD 0.48) and 1.42 g/min (SD 0.63)] and fat [0.33 g/min (SD 0.10) and 0.30 g/min (SD 0.10)] and their contribution to the energy yield were not significantly different in the control subjects and diabetic patients. Exogenous glucose oxidation was also not significantly different in the control subjects and diabetic patients [6.3 g/30 min (SD 1.3) and 5.2 g/30 min (SD 1.6), respectively]. In contrast, the oxidation of plasma glucose and oxidation of glucose released from the liver were significantly lower in the diabetic patients than in control subjects [14.5 g/30 min (SD 4.3) and 9.3 g/30 min (SD 2.8) vs. 27.9 g/30 min (SD 13.3) and 21.6 g/30 min (SD 12.8), respectively], whereas that of muscle glycogen was significantly higher [28.1 g/30 min (SD 15.5) vs. 11.6 g/30 min (SD 8.1)]. These data indicate that, compared with control subjects, in diabetic patients fed glucose before exercise, substrate oxidation and exogenous glucose oxidation overall are similar but plasma glucose oxidation is lower; this is associated with a compensatory higher utilization of muscle glycogen.

Intuitive wireless control of a robotic arm for people living with an upper body disability.

Assistive Technologies (ATs) also called extrinsic enablers are useful tools for people living with various disabilities. The key points when designing such useful devices not only concern their intended goal, but also the most suitable human-machine interface (HMI) that should be provided to users. This paper describes the design of a highly intuitive wireless controller for people living with upper body disabilities with a residual or complete control of their neck and their shoulders. Tested with JACO, a six-degree-of-freedom (6-DOF) assistive robotic arm with 3 flexible fingers on its end-effector, the system described in this article is made of low-cost commercial off-the-shelf components and allows a full emulation of JACO's standard controller, a 3 axis joystick with 7 user buttons. To do so, three nine-degree-of-freedom (9-DOF) inertial measurement units (IMUs) are connected to a microcontroller and help measuring the user's head and shoulders position, using a complementary filter approach. The results are then transmitted to a base-station via a 2.4-GHz low-power wireless transceiver and interpreted by the control algorithm running on a PC host. A dedicated software interface allows the user to quickly calibrate the controller, and translates the information into suitable commands for JACO. The proposed controller is thoroughly described, from the electronic design to implemented algorithms and user interfaces. Its performance and future improvements are discussed as well.

Metabolic availability of oral glucose during exercise: a reassessment.

The purpose of this study was to reassess the metabolic availability of oral glucose during prolonged exercise in man, using 13C-labeling and a computation procedure (J Appl Physiol 69:1047-1052, 1990) that correctly takes into account changes in isotopic composition of CO2 arising from oxidation of endogenous substrates (Rendo). These changes are due to glucose ingestion associated with exercise. Each of the seven subjects completed three 2-hour periods of exercise at 67% maximum oxygen consumption (VO2max) on an ergocycle, with ingestion of water (1,000 mL) or 60 g (in 1,000 mL water) of 13C-labeled glucose at two levels of enrichment (13C/12C = 1.11482% and 1.13303%). As expected, Rendo significantly increased from rest to exercise with water ingestion (1.09888% +/- .00196% to 1.09970% +/- .00175%) and with glucose ingestion (1.10002% +/- .00159%) due to changes in the respective contributions of endogenous carbohydrates and fat to energy requirements as assessed by the respiratory exchange ratio (RER). When changes in Rendo were taken into account, the estimated amount of exogenous glucose oxidized was 38.8 +/- 10.3 g. Much higher values were found when Rendo at rest or during exercise with water ingestion were used in the computation (42.3 +/- 10.3 to 65.1 +/- 20.5 g) according to the commonly used method. Examination of data in the literature indicates that the reported oxidation rate of exogenous glucose (g/min) is significantly related to oxygen consumption (VO2) (L/min; r = .592) and that exogenous glucose contributes approximately 14% to 17% to the energy requirement.(ABSTRACT TRUNCATED AT 250 WORDS)

Increase in blood bradykinin concentration after eccentric weight-training exercise in men.

The purpose of this study was to verify the possible appearance in the blood of bradykinin (BK) and des-Arg(9)-bradykinin (des-Arg(9)-BK) after eccentric exercise in 13 male subjects. Eccentric exercise (5 x 10 leg presses at 120% maximal voluntary concentric contraction) resulted in muscle damage and inflammation, as suggested by the significant increase in serum creatine kinase activity (from 204 +/- 41 to 322 +/- 63 U/l 12 h postexercise) and by severe lasting pain, which also peaked at 12 h postexercise. Blood BK and des-Arg(9)-BK concentrations were measured by competitive enzyme immunoassays using highly specific polyclonal rabbit IgG. Des-Arg(9)-BK concentration was not modified (preexercise: 44 +/- 14 pmol/l; pooled postexercise: 47 +/- 4 pmol/l). In contrast, BK concentration significantly increased immediately after the exercise session (68 +/- 9 vs. 42 +/- 3 pmol/l preexercise) and returned to basal values at 12, 24, and 48 h (pooled value: 40 +/- 4 pmol/l). This observation suggests that the inflammatory process due to eccentric exercise-induced muscle damage could be mediated in part by BK.

Use of 13C substrates for metabolic studies in exercise: methodological considerations.

The purpose of this study is to outline a common mistake made when the rate of oxidation of exogenous substrates during prolonged exercise is computed using 13C naturally labeled substrates. The equation proposed and commonly used in the computation does not take into account that exercise and/or exogenous substrate ingestion modifies the composition of the mixture of endogenous substrates oxidized and, consequently, the isotopic composition of CO2 arising from oxidation of endogenous substrates. The recovery of 13C and the amount of exogenous substrate oxidized are thus overestimated. An adequate procedure for the computation of exogenous substrate oxidation taking into account changes in isotopic composition of CO2 arising from oxidation of endogenous substrates is suggested. Results from a pilot experiment (4 subjects) using this procedure indicate that over 2 h of exercise (66% of maximal O2 uptake), with ingestion of 60 g of glucose, 39 +/- 4 g of glucose were oxidized. Estimates made without taking into account changes in isotopic composition of CO2 arising from oxidation of endogenous substrates range between 70 +/- 8 and 44 +/- 3 g depending on 1) the isotopic composition of exogenous glucose and 2) the isotopic composition of expired CO2 taken as reference (rest or exercise without glucose ingestion). These observations suggest that results from previous studies of exogenous substrate oxidation during exercise using 13C labeling should be used with caution.

Oxidation of a glucose polymer during exercise: comparison with glucose and fructose.

The purpose of this study was to compare the oxidation of 13C-labeled glucose, fructose, and glucose polymer ingested (1.33 g.kg-1 in 19 ml.kg-1 water) during cycle exercise (120 min, 53 +/- 2% maximal O2 uptake) in six healthy male subjects. Oxidation of exogenous glucose and glucose polymer (72 +/- 15 and 65 +/- 18%, respectively, of the 98.9 +/- 4.7 g ingested) was similar and significantly greater than exogenous fructose oxidation (54 +/- 13%). A transient rise in plasma glucose concentration was observed with glucose ingestion only. However, plasma insulin levels were similar with glucose and glucose polymer ingestions and significantly higher than with water or fructose ingestion. Plasma free fatty acid and glycerol responses to exercise were blunted with carbohydrate ingestion. However, fat utilization was not significantly different with water (82 +/- 14 g), glucose (60 +/- 3 g), fructose (59 +/- 11 g), or glucose polymer ingestion (60 +/- 8 g). Endogenous carbohydrate utilization was significantly lower with glucose (184 +/- 22 g), glucose polymer (187 +/- 31 g), and fructose (211 +/- 18 g) than with water (239 +/- 30 g) ingestion. Plasma volume slightly increased with water ingestion (7.4 +/- 4.5%), but the decrease was similar with glucose (-7.6 +/- 5.1%) and glucose polymer (-8.2 +/- 4.6%), suggesting that the rate of water delivery to plasma was similar with the two carbohydrates.(ABSTRACT TRUNCATED AT 250 WORDS)

Oxidation of exogenous medium-chain free fatty acids during prolonged exercise: comparison with glucose.

The purpose of this study was to compare the oxidation rate of exogenous 13C-labeled medium-chain triacylglycerols (MCT) with that of an isocaloric amount of exogenous [13C]glucose and to evaluate their respective effects on endocrine and metabolic responses to moderate prolonged exercise. To take into account changes in isotopic composition of 13CO2 arising from oxidation of endogenous substrates because of exercise and/or substrate ingestion that overestimates the oxidation rate of exogenous substrates, two levels of 13C enrichment were used for each substrate. Six young healthy males (20-26 yr of age) completed five 2-h periods of exercise at 65 +/- 3% maximal O2 uptake (VO2max) on a cycle ergometer at 7-day intervals: one control exercise with water ingestion, two trials with ingestion of 25 g of [13C]MCT (trioctanoate) 1 h before exercise, and two trials with 57 g of [13C]glucose (dissolved in 1,000 ml of water) ingested during exercise. Exogenous MCT and glucose began to be oxidized within the first 30 min of exercise, and the oxidation rate increased progressively until the end of exercise for both substrates. Over the 2-h period of exercise, 13.6 +/- 3.5 g of ingested MCT and 36.4 +/- 8.2 g of exogenous glucose were oxidized, which represent 54 and 64%, respectively, of the total amount ingested. The contribution of MCT (119 +/- 31 kcal) and glucose (140 +/- 36 kcal) was not significantly different and represented 7 and 8.5%, respectively, of the total energy expenditure.(ABSTRACT TRUNCATED AT 250 WORDS)

Breath [13CO2] recovery from an oral glucose load during exercise: comparison between [U-13C] and [1,2-13C]glucose.

The purpose of the present experiment was to compare 13CO2 recovery at the mouth, and the corresponding exogenous glucose oxidation computed, during a 100-min exercise at 63 +/- 3% maximal O2 uptake with ingestion of glucose (1.75 g/kg) in six active male subjects, by use of [U-13C] and [1,2-13C]glucose. We hypothesized that 13C recovery and exogenous glucose oxidation could be lower with [1,2-13C] than [U-13C]glucose because both tracers provide [13C]acetate, with possible loss of 13C in the tricarboxylic acid (TCA) cycle, but decarboxylation of pyruvate from [U-13C]glucose also provides 13CO2, which is entirely recovered at the mouth during exercise. The recovery of 13C (25.8 +/- 2.3 and 27.4 +/- 1.2% over the exercise period) and the amounts of exogenous glucose oxidized computed were not significantly different with [1,2-13C] and [U-13C]glucose (28.9 +/- 2.6 and 30.7 +/- 1.3 g, between minutes 40 and 100), suggesting that no significant loss of 13C occurred in the TCA cycle. This stems from the fact that, during exercise, the rate of exogenous glucose oxidation is probably much larger than the flux of the metabolic pathways fueled from TCA cycle intermediates. It is thus unlikely that a significant portion of the 13C entering the TCA cycle could be diverted to these pathways. From a methodological standpoint, this result indicates that when a large amount of [13C]glucose is ingested and oxidized during exercise, 13CO2 production at the mouth accurately reflects the rate of glucose entry in the TCA cycle and that no correction factor is needed to compute the oxidative flux of exogenous glucose.

Respective oxidation of 13C-labeled lactate and glucose ingested simultaneously during exercise.

The purpose of this experiment was to measure, by using 13C labeling, the oxidation rate of exogenous lactate (25 g, as Na+, K+, Ca2+, and Mg2+ salts) and glucose (75 g) ingested simultaneously (in 1,000 ml of water) during prolonged exercise (120 min, 65 +/- 3% maximum oxygen uptake in 6 male subjects). The percentage of exogenous glucose and lactate oxidized were similar (48 +/-3 vs. 45 +/- 5%, respectively). However, because of the small amount of oral lactate that could be tolerated without gastrointestinal discomfort, the amount of exogenous lactate oxidized was much smaller than that of exogenous glucose (11.1 +/- 0.5 vs. 36.3 +/- 1.3 g, respectively) and contributed to only 2.6 +/- 0.4% of the energy yield (vs. 8.4 +/- 1.9% for exogenous glucose). The cumulative amount of exogenous glucose and lactate oxidized was similar to that observed when 100 g of [13C]glucose were ingested (47.3 +/- 1.8 vs. 50.9 +/- 1.2 g, respectively). When [13C]glucose was ingested, changes in the plasma glucose 13C/12C ratio indicated that between 39 and 61% of plasma glucose derived from exogenous glucose. On the other hand, the plasma glucose 13C/12C ratio remained unchanged when [13C]lactate was ingested, suggesting no prior conversion into glucose before oxidation.

Oral [13C]glucose oxidation during prolonged exercise after high- and low-carbohydrate diets.

The effect of a diet either high or low in carbohydrates (CHO) on exogenous 13C-labeled glucose oxidation (200 g) during exercise (ergocycle: 120 min at 64.0 +/- 0.5% maximal oxygen uptake) was studied in six subjects. Between 40 and 80 min, exogenous glucose oxidation was significantly higher after the diet low in CHO (0.63 +/- 0.05 vs. 0.52 +/- 0.04 g/min), but this difference disappeared between 80 and 120 min (0.71 +/- 0.03 vs. 0.69 +/- 0.04 g/min). The oxidation rate of plasma glucose, computed from the volume of 13CO2 produced the 13C-to-12C ratio in plasma glucose at 80 min, and of glucose released from the liver, computed from the difference between plasma glucose and exogenous glucose oxidation, was higher after the diet low in CHO (1.68 +/- 0.26 vs. 1.41 +/- 0.17 and 1.02 +/- 0.20 vs. 0.81 +/- 0.14 g/min, respectively). In contrast the oxidation rate of glucose plus lactate from muscle glycogen (computed from the difference between total CHO oxidation and plasma glucose oxidation) was lower (0.31 +/- 0.35 vs. 1.59 +/- 0.20 g/min). After a diet low in CHO, the oxidation of exogenous glucose and of glucose released from the liver is increased and partly compensates for the reduction in muscle glycogen availability and oxidation.

Prolactinotrophic effect of endogenous and exogenous heat loads in human male adults.

Factors associated with heat-induced increase in blood prolactin (PRL) were investigated. Ten male volunteers (23.7 +/- 2.2 yr) were exposed to exogenous heating (head-out immersion) in 41 degrees C water (control 37 degrees C) for 30 min with and without face fanning and cooling. In seven of the subjects, endogenous heating was produced by a 45-min exercise in a warm environment (41 degrees C; control 10 degrees C) with and without selective face fanning. Venous blood was collected before and after each trial; blood hormones were analyzed by radioimmunologic techniques. Heat loading, whether exogenous or endogenous in origin, induced significant increases in blood PRL, beta-endorphin, and vasoactive intestinal peptide (VIP) levels. Blood thyrotropin (TSH) level decreased significantly during water immersion and more significantly with face cooling. From measurement in peripheral blood, the differential beta-endorphin, VIP, and TSH responses to selective face ventilation during exogenous and endogenous heat exposures suggest that blood PRL released in heat derives from secretory stimuli that are independent of these prolactinotropic factors.

Oxidation of ethanol at rest and during prolonged exercise in men.

The purpose of this study was to measure the oxidation of ethanol at rest and during prolonged moderate exercise with use of 13C labeling. Five healthy young males (22.4 +/- 2.7 yr; maximal O2 uptake = 56 +/- 6.6 ml.kg-1.min-1) performed three exercises (68.4 +/- 6.7% maximal O2 uptake; 90 min) on a cycle ergometer with ingestion of 0.4 (trial A) and 0.8 (trial B) g/kg body wt of [13C]ethanol (diluted in 770 +/- 72 ml of water) or water only (trial C). The subjects were also studied during a 90-min rest period after the ingestion of 0.8 g/kg body wt of [13C]ethanol (trial D). At rest, over the 90-min observation period, only 2.1 +/- 0.3 g of the 61.6 +/- 5.7 g of ethanol ingested were oxidized, providing 11.1 +/- 1.9% of the total energy expenditure. Over the 90 min of exercise, the amounts of ethanol oxidized were similar in trials A (9.5 +/- 2.0 g) and B (8.5 +/- 2.5 g). The contribution of ethanol represented 5.2 +/- 1.0% of the total energy expenditure, which is much lower than that previously reported for exogenous carbohydrates (8-18%) or medium-chain free fatty acids (7-14%). The small contribution of ethanol to energy metabolism did not significantly modify endogenous substrate oxidation.

Method for computing the oxidation of two 13C-substrates ingested simultaneously during exercise.

This study presents a method for computing the respective amounts of two simultaneously ingested exogenous substrates (A and B) that are oxidized during a period of prolonged exercise by use of 13C labeling. This method is based on the observation that the total volume of 13CO2 produced (V13CO2tot) is the sum of 1) V13CO2 arising from the oxidation of endogenous substrates (V13CO2endo), 2) V13CO2 arising from the oxidation of substrate A (V13CO2A), and 3) V13CO2 arising from the oxidation of substrate B (V13CO2B). The equation, V13CO2tot = V13CO2endo+V13CO2A+V13CO2B, with three unknowns, can be solved from the results of three experiments conducted under the same conditions but with at least two values for the isotopic composition of A and B. This method has been used on five healthy male subjects to compute the amounts of glucose and fructose oxidized when a mixture of 15 g of glucose and 15 g of fructose is ingested (in 300 ml of water) over 60 min of cycle ergometer exercise at 65% of maximal O2 uptake. Results from three experiments indicated that 9.8 +/- 3.1 and 5.7 +/- 2.1 g of glucose and fructose, respectively, were oxidized. The total amount of exogenous carbohydrates oxidized (15.5 +/- 4.3 g) is in agreement with the oxidation rates of exogenous glucose computed in similar conditions when 30 g of glucose were ingested (13 g; Péronnet et al. Med. Sci. Sports Exercise 25: 297-302, 1993). The difference between the oxidation rates of exogenous glucose and fructose is also in line with data from the literature.

Respective oxidation of exogenous glucose and fructose given in the same drink during exercise.

We computed the respective amounts of exogenous glucose (G) and fructose (F), which are oxidized during exercise when ingested simultaneously, with the use of 13C labeling. Six subjects exercised for 2 h at 60.7 +/- 2.9% of maximal O2 uptake on a cycle ergometer while ingesting 50 or 100 g of G or F or a mixture of 50 g each of G and F in 500 ml of water. The amount of exogenous G oxidized increased from 37.8 +/- 2.2 to 58.3 +/- 8.1 g when the total amount ingested increased from 50 to 100 g. The amount of F oxidized was significantly lower (32.2 +/- 1.2 and 45.8 +/- 2.6 g for the 50 and 100 g ingested, respectively). When 50 g each of G and F were simultaneously ingested in the same drink, the amounts oxidized (39.5 +/- 4.8 and 34.1 +/- 1.5 g, respectively) were similar to those observed when 50 g of G or F were ingested separately. The cumulative amount of exogenous hexoses oxidized (73.6 +/- 6.6 g) was 21% larger than when 100 g of G were ingested. This finding could be due to the fact that the routes for absorption and metabolism of exogenous G and F are at least partly different, resulting in less competition for oxidation when a mixture of these two hexoses is ingested than when an isocaloric amount of G is ingested. From a practical point of view, these data may provide experimental support for using mixtures of carbohydrates in the energy supplements for endurance athletes.

Metabolic response to [13C]glucose and [13C]fructose ingestion during exercise.

Seven healthy male volunteers exercised on a cycle ergometer at 50 +/- 5% VO2max for 180 min, on three occasions during which they ingested either water only (W), [13C]glucose (G), or [13C]fructose (F) (140 +/- 12 g, diluted at 7% in water, and evenly distributed over the exercise period). Blood glucose concentration (in mM) significantly decreased during exercise with W (5.1 +/- 0.4 to 4.2 +/- 0.1) but remained stable with G (5.0 +/- 0.4 to 5.3 +/- 0.6) or F ingestion (5.4 +/- 0.5 to 5.1 +/- 0.4). Decreases in plasma insulin concentration (microU/ml) were greater (P less than 0.05) with W (11 +/- 3 to 3 +/- 1) and F (12 +/- 4 to 5 +/- 1) than with G ingestion (11 +/- 2 to 9 +/- 5), and fat utilization was greater with F (103 +/- 11 g) than with G ingestion (82 +/- 9 g) and lower than with W ingestion (132 +/- 14 g). However F was less readily available for combustion than G; over the 3-h period 75% (106 +/- 11 g) of ingested G was oxidized, compared with 56% (79 +/- 8 g) of ingested fructose. As a consequence, carbohydrate store utilizations were similar in the two conditions (G, 174 +/- 20 g; F, 173 +/- 17 g; vs. W, 193 +/- 22 g). These observations suggest that, during prolonged moderate exercise, F ingestion maintains blood glucose as well as G ingestion, and increases fat utilization when compared to G ingestion. However, due to a slower rate of utilization of F, carbohydrate store sparing is similar with G and F ingestions.

Oxidation of [(13)C]glycerol ingested along with glucose during prolonged exercise.

The respective oxidation of glycerol and glucose (0.36 g/kg each) ingested simultaneously immediately before exercise (120 min at 68 +/- 2% maximal oxygen uptake) was measured in six subjects using (13)C labeling. Indirect respiratory calorimetry corrected for protein and glycerol oxidation was used to evaluate the effect of glucose + glycerol ingestion on the oxidation of glucose and fat. Over the last 80 min of exercise, 10.0 +/- 0.8 g of exogenous glycerol were oxidized (43% of the load), while exogenous glucose oxidation was 21% higher (12.1 +/- 0.7 g or 52% of the load). However, because the energy potential of glycerol is 18% higher than that of glucose (4.57 vs. 3.87 kcal/g), the contribution of both exogenous substrates to the energy yield was similar (4.0-4.1%). Total glucose and fat oxidation were similar in the placebo (144.4 +/- 13.0 and 60.5 +/- 4.2 g, respectively) and the glucose + glycerol (135.2 +/- 12.0 and 59.4 +/- 6.5 g, respectively) trials, whereas endogenous glucose oxidation was significantly lower than in the placebo trial (123.7 +/- 11.7 vs. 144.4 +/- 13.0 g). These results indicate that exogenous glycerol can be oxidized during prolonged exercise, presumably following conversion into glucose in the liver, although direct oxidation in peripheral tissues cannot be ruled out.

Differential metabolic fate of the carbon skeleton and amino-N of [13C]alanine and [15N]alanine ingested during prolonged exercise.

The decarboxylation/oxidation and the deamination of 13C- and [15N]alanine ingested (1 g/kg or 73.7 +/- 2 g) during prolonged exercise at low workload (180 min at 53 +/- 2% maximal O2 uptake) was measured in six healthy male subjects from V13CO2 at the mouth and [15N]urea excretion in urine and sweat. Over the exercise period, 50.6 +/- 3.5 g of exogenous alanine were oxidized (68.7 +/- 4.5% of the load), providing 10.0 +/- 0.6% of the energy yield vs. 4.8 +/- 0.4, 47.6 +/- 4.3, and 37.4 +/- 4.7% for endogenous proteins, glucose, and lipids, respectively. Alanine could have been oxidized after conversion into glucose in the liver and/or directly in peripheral tissues. In contrast, only 13.0 +/- 3.2 mmol of [(15)N]urea were excreted in urine and sweat (10.6 +/- 0.4 and 2.4 +/- 0.5 mmol, respectively), corresponding to the deamination of 2.3 +/- 0.3 g of exogenous alanine (3.1 +/- 0.4% of the load). These results confirm that the metabolic fate of the carbon skeleton and the amino-N moiety of exogenous alanine ingested during prolonged exercise at low workload are markedly different. The large positive nitrogen balance (8.5 +/- 0.3 g) suggests that in this situation protein synthesis could be increased when a large amount of a single amino acid is ingested.

Oxidation of an oral [13C]glucose load at rest and prolonged exercise in trained and sedentary subjects.

The purpose of this study was to compare the oxidation of [13C]glucose (100 g) ingested at rest or during exercise in six trained (TS) and six sedentary (SS) male subjects. The oxidation of plasma glucose was also computed from the volume of 13CO2 and 13C/12C in plasma glucose to compute the oxidation rate of glucose released from the liver and from glycogen stores in periphery (mainly muscle glycogen stores during exercise). At rest, oxidative disposal of both exogenous (8.3 +/- 0.3 vs. 6.6 +/- 0.8 g/h) and liver glucose (4.4 +/- 0.5 vs. 2.6 +/- 0.4 g/h) was higher in TS than in SS. This could contribute to the better glucose tolerance observed at rest in TS. During exercise, for the same absolute workload [140 +/- 5 W: TS = 47 +/- 2.5; SS = 68 +/- 3 %maximal oxygen uptake (VO2 max)], [13C]glucose oxidation was higher in TS than in SS (39.0 +/- 2.6 vs. 33.6 +/- 1.2 g/h), whereas both liver glucose (16.8 +/- 2.4 vs. 24.0 +/- 1.8 g/h) and muscle glycogen oxidation (36.0 +/- 3.0 vs. 51.0 +/- 5.4 g/h) were lower. For the same relative workload (68 +/- 3% VO2 max: TS = 3.13 +/- 0.96; SS = 2.34 +/- 0.60 l O2/min), exogenous glucose (44.4 +/- 1.8 vs. 33.6 +/- 1.2 g/h) and muscle glycogen oxidation (73.8 +/- 7.2 vs. 51.0 +/- 5.4 g/h) were higher in TS. However, despite a higher energy expenditure in TS, liver glucose oxidation was similar in both groups (22.2 +/- 3.0 vs. 24.0 +/- 1.8 g/h). Thus exogenous glucose oxidation was selectively favored in TS during exercise, reducing both liver glucose and muscle glycogen oxidation.