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.

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.

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.

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 utilization during prolonged exercise with ingestion of (13)C-glucose in acute hypobaric hypoxia (4,300 m).

Energy substrate oxidation was measured using indirect respiratory calorimetry combined with tracer technique in five healthy young male subjects, during a 80-min exercise period on ergocycle with ingestion of 140 g of (13)C-labelled glucose, in normoxia and acute hypobaric hypoxia (445 mmHg or 4,300 m), at the same relative [77% V(.-)((O)(2)(max))] and absolute workload (161+/-8 W, corresponding to 77 and 54% V(.-)((O)(2)(max)) in hypoxia and normoxia). The oxidation rate of exogenous glucose was not significantly different in the three experimental situations: 21.4+/-2.9, 20.2+/-1.2 and 17.2+/-0.6 g over the last 40 min of exercise at approximately 77 and approximately 54% V(.-)((O)(2)(max)) in normoxia and in hypoxia, respectively, providing 12.5+/-1.5, 16.8+/-1.1 and 14.9+/-1.1% of the energy yield, although ingestion of glucose during exercise resulted in a higher plasma glucose concentration in hypoxia than normoxia. The contribution of carbohydrate (CHO) oxidation to the energy yield was significantly higher in hypoxia (92.0+/-2.1%) than in normoxia for both a given absolute (75.3+/-5.2%) and relative workload (78.1+/-1.8%). This greater reliance on CHO oxidation in hypoxia was entirely due to the significantly larger contribution of endogenous glucose oxidation to the energy yield: 75.9+/-1.7% versus 66.6+/-3.3 and 55.2+/-3.7% in normoxia at the same relative and absolute workload.

Metabolic fate of a large amount of 13C-glycerol ingested during prolonged exercise.

We have shown that the oxidation rate of exogenous glycerol and glucose during prolonged exercise were similar when ingested in small amounts (0.36 g/kg) (J Appl Physiol 90:1685,2001). The oxidation rate of exogenous carbohydrate increases with the amount ingested. We, thus, hypothesized that the oxidation rate of exogenous glycerol would also be larger when ingested in large amount. The study was conducted on six male subjects exercising for 120 min at 64 (2)% VO(2)max while ingesting 1 g/kg of (13)C-glycerol. Substrate oxidation was measured using indirect respiratory calorimetry corrected for protein oxidation, and from V(13)CO(2) at the mouth. The (13)C enrichment of plasma glucose was also measured in order to follow the possible conversion of (13)C-glycerol into glucose. In spite of the large amount of glycerol ingested and absorbed (plasma glycerol concentration = 8.0 (0.3) mmol/l at min 100), exogenous glycerol oxidation over the last 80 min of exercise [8.8 (1.6) g providing 4.1 (0.7)% of the energy yield] was similar to that observed when 0.36 g/kg was ingested. The comparison between the (13)C enrichment of plasma glucose and the oxidation rate of (13)C-glycerol showed that a portion of exogenous glycerol was converted into glucose before being oxidized, but also suggested that another portion could have been directly oxidized in peripheral tissues.

Metabolic response to a large starch meal after rest and exercise: comparison between men and women.

BACKGROUND: Net whole-body and hepatic de novo lipogenesis could be more active in women than in men, but no comparison has been made between men and women in the two phases of the ovarian cycle after ingestion of a large carbohydrate meal. OBJECTIVE: We hypothesized that net whole-body de novo lipogenesis could be larger in women than men, and that glycogen and fat balance could be, respectively, lower and higher, following a large pasta meal ingested after rest or exercise. DESIGN: The metabolic response to a pasta meal (5 g dry weight/kg body mass) was studied in six men and six women (matched for age and BMI) in the follicular and luteal phases, following rest or exercise (90 min at 50% VO(2max)). Protein, glucose, and fat oxidation, and net whole-body de novo lipogenesis were computed for 10 h following ingestion of the meal using indirect respiratory calorimetry corrected for urea excretion. RESULTS: No net whole-body de novo lipogenesis was observed in any group in any situation (postrest and postexercise). When the meal was ingested following exercise, fat oxidation was significantly higher and glucose oxidation was significantly lower (P<0.05) than following the period of rest, and in a given experimental situation, the respective contributions of protein, fat, and glucose oxidation to the energy yield were similar in men and women in both phases of the cycle. CONCLUSIONS: The contribution of substrate oxidation to the energy expenditure as well as fat and glycogen balance, and the effect of a previous exercise period, were similar in men and women in both phases of the cycle following ingestion of the large carbohydrate meal.

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.

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.

Use of an alpha-glucosidase inhibitor to maintain glucose homoeostasis during postprandial exercise in intensively treated Type 1 diabetic subjects.

AIM: We evaluated the effects of an alpha-glucosidase inhibitor, acarbose, on glucose homoeostasis during postprandial exercise in Type 1 diabetic subjects. METHODS: Seven Type 1 diabetic subjects with good glycaemic control on ultralente-regular insulin were randomized in a single blind cross-over study to acarbose 100 mg or placebo taken with a mixed meal (600 kcal, 75 g carbohydrates), followed 90 min later by 30 min of exercise at 50% maximum aerobic capacity. Glucose turnover was measured by tracer (d-[6,6,2H2]glucose) methodology, and intestinal glucose absorption was quantified using carbohydrate polymers labelled with [13C]glucose. RESULTS: Acarbose resulted in a significant decrease in the postprandial glycaemic rise (mean +/- SEM 2.9 +/- 0.6 vs. 5.0 +/- 0.7 mmol/l; P < 0.005) and in the glycaemic nadir during exercise (- 0.8 +/- 0.6 vs. 0.9 +/- 1.3 mmol/l below baseline; P < 0.05). Total glucose appearance increased similarly under the two treatments during the postprandial (27.0 vs. 27.9 micromol per kg per min) and exercise (33.9 vs. 33.5 micromol per kg per min) periods. Mean glucose absorption was significantly delayed by acarbose (7.8 vs. 10.2 micromol per kg per min; P < 0.02), but was compensated by the lack of postprandial suppression of hepatic glucose production (106% of basal hepatic glucose production vs. 81%; P < 0.006). Episodes of hypoglycaemia were no different (three vs. six). CONCLUSION: These results indicate that, in Type 1 diabetic subjects, acarbose results in a better glycaemic profile during postprandial exercise and suggest that it could lead to a lower risk of exercise-induced hypoglycaemia due to delayed glucose absorption and less suppression of hepatic glucose production.

Metabolic response to small and large 13C-labelled pasta meals following rest or exercise in man.

The metabolic response to a 150 or 400 g 13C-labelled pasta meal was studied for 8 h following rest or exercise at low or moderate workload (n 6). Following rest, the 400 g meal totally suppressed fat oxidation (v. 14.1 g following the 150 g meal) and a small amount of glucose was converted into fat (4.6 g), but fat oxidation remained high in subjects who had exercised following both the small (21.8 and 34.1 g) and large meal (14.1 and 32.3 g). Exogenous glucose oxidation was significantly higher in subjects who had remained at rest both following the small (67.6 g v. 60.4 and 51.3 g in subjects who exercised at low and moderate workloads) and large meal (152.2 v. 123.0 and 127.2 g). Endogenous glucose oxidation was similar in the three groups following the 150 g meal (42.3-58.0 g), but was significantly lower following the 400 g meal in subjects who had exercised at low workload (24.2 v. 72.2 g following rest; and was totally suppressed in those who had exercised at moderate workload. As a consequence, a larger positive glycogen balance was observed in subjects who exercised before the large meal (182.8-205.1 g v. 92.4 g following rest; Total fat oxidation calculated from 08.00 hours to 20.00 hours was similar in subjects who exercised at low and moderate workloads. These results indicate that: (1) de novo lipogenesis, which plays only a minor role for the disposal of an acute dietary carbohydrate load, is totally suppressed following exercise, even when a very large carbohydrate load is ingested; (2) the reduction in glycogen turnover as well as a preferential conversion of glucose into glycogen are responsible for the increase in glycogen stores following exercise; (3) for a similar energy expenditure, exercise at low workload for a longer period does not favour fat oxidation when the post-exercise period is taken into account.

Ultrasonic inspection of composite hydrogen reservoirs using frequency diversity techniques.

The use of the signal processing techniques based on the principle of quasi-frequency diversity can be a suitable solution for the ultrasonic inspection of liquid hydrogen tanks manufactured out of composite materials. Nevertheless, the algorithms developed up to now suffer from limitations that restrict their large-scale use. The split-spectrum processing requires preliminary adjustments that are not always accessible to the user, while the cut-spectrum processing is not sensitive enough to eliminate the noise. We have thus developed an interesting alternative to these two filters. Based on the use of progressive low-pass filters, this algorithm, called low-spectrum processing, takes into account the physical characteristics of the ultrasonic wave propagation in a composite material. Its use in the inspection of tanks made in composites showed better performances.

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.

Increased density of glucagon receptors in liver from endurance-trained rats.

The binding properties of glucagon receptors were determined in plasma membranes isolated from liver of untrained (n = 6) and swimming endurance-trained Sprague-Dawley male rats (n = 7; 3 h/day, 5 days/wk, for 8 wk). Plasma membranes were purified from liver by aqueous two-phase affinity partitioning, and saturation kinetics were obtained by incubation of plasma membranes (10 microg of proteins/150 microl) with (125)I-labeled glucagon at concentrations ranging from 0.15 to 3.0 nM for 30 min at 30 degrees C. Saturating curve analysis indicated no difference in the affinity of glucagon receptors (0.57 +/- 0.06 and 0.77 +/- 0.09 nM in untrained and trained groups, respectively) but a significant higher glucagon receptor density in liver from untrained vs. trained rats (3.09 +/- 0.12 vs. 4.28 +/- 0.19 pmol/mg proteins). These results suggest that the reported increase in liver glucagon sensitivity in endurance-trained subjects (Drouin R, Lavoie C, Bourque J, Ducros F, Poisson D, and Chiasson J-L. Am J Physiol Endocrinol Metab 274: E23-E28, 1998) could be partly due to an increased glucagon receptor density in response to training.

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.

Carbon isotope fractionation between blood and expired CO2 at rest and exercise.

Carbon isotope fractionation occurs between bicarbonates and gaseous CO2. Accordingly, expired CO2 could be impoverished in 13C vs. blood CO2 (approximately 90% bicarbonates). The ratio 13C/12C in expired and blood CO2 was measured in six healthy subjects at rest and at the end of exercise (90 min; 65+/-5% VO2max), with ingestion of water (300 ml) without or with glucose (30 g) naturally or artificially enriched in 13C, in order to study a range of 13C/12C in blood (-17.5+/-0.3 to 3.4+/-0.6% delta 13C PDB-1). At rest, 13C/12C in expired CO2 was 4.7+/-0.2% delta 13C PDB-1 lower than in blood CO2. This difference was not modified in response to exercise with ingestion of water or 13C-glucose (average difference 4.6+/-0.4 % delta 13C PDB-1). Carbon isotope fractionation across the lung was approximately 30% lower than predicted from the fractionation factor between bicarbonates and gaseous CO2 (1.00674 at 37 degrees C, or a approximately 6.6% delta 13C PDB-1 difference). This is consistent with the fact that approximately 40% of expired CO2 is released from carbamates and dissolved CO2. From a methodological point of view, these results indicate that 13C/12C in expired CO2 adequately tracks 13C/12C in blood CO2 with a constant approximately 4.6 % delta 13C PDB-1 difference.

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.

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.

Oxidation of 13C-glucose and 13C-fructose ingested as a preexercise meal: effect of carbohydrate ingestion during exercise.

The oxidation of 13C-labeled glucose and fructose ingested as a preexercise meal between 180 and 90 min before exercise was measured on 6 subjects when either a placebo or sucrose was ingested during the exercise period. Labeled hexose oxidation, which occurred mainly during the first hour of exercise, was not significantly modified when sucrose was ingested, but exogenous glucose oxidation was significantly higher than exogenous fructose oxidation in both situations. The results suggest that the absorption rate of exogenous hexoses was high when exercise was initiated but diminished thereafter, and that glucose and fructose released from sucrose ingested during exercise did not compete with glucose or fructose ingested before exercise for intestinal absorption, for conversion into glucose in the liver (for fructose), or for uptake and oxidation of glucose in peripheral tissues. However, as already shown, in terms of availability for oxidation of carbohydrates provided by the preexercise meal, glucose should be favored over fructose.

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.