Changes in breath 13CO2/12CO2 during exercise of different intensities.

The measurement of breath 13CO2/12CO2 is commonly used during exercise to evaluate the oxidation rate of exogenous carbohydrates enriched in 13C. The aim of this study was to investigate whether exercise itself affects the 13C/12C ratio in expired air CO2 in relation to exercise intensity. The relative abundance of 13C and 12C in expired air CO2 was determined by isotoperatio mass spectrometry and expressed as delta 13C (in %o) by using Craig's formula and calibrated standards. Five healthy young men exercised on a treadmill after an overnight fast during > or = 105 min on four occasions and in a randomized order. Work rates were performed at approximately 30, 45, 60, and 75% of their maximal O2 uptake (VO2max). Delta 13C in expired air CO2 and respiratory exchange ratio (RER) were determined every 15 or 30 min during exercise. At 30 and 45% VO2max, a slight and not statistically significant increase in delta 13C was observed at 30 min. In contrast, at 60 75% VO2max, the rise was statistically significant and averaged 0.83 and 0.99%o, respectively. Average delta 13C (between 0 and 105 min) progressively increased with the intensity of exercise. Individual values of delta 13C and RER were positively correlated (r = 0.653, P = 0.002) as were values of delta 13C and endogenous carbohydrates utilized (r = 0.752, P < 0.001). Factitious or "pseudooxidation" of a 13C-enriched exogenous glucose load (indeed noningested) was calculated from the changes in expired air delta 13C. Over the whole period of exercise it was not statistically significant at 30 and 40% VO2max. However, over the first 60 min of exercise, such pseudooxidation of exogenous glucose was significant at 30 and 45% VO2max. In conclusion, by modifying the mix of endogenous substrates oxidized, exercise at 60% VO2max and above significantly increases the 13C/12C ratio in expired air CO2. At these intensities, this could lead to overestimation of the oxidation of 13C-labeled substrates given orally. At lower intensities of exercise, such overestimation is much smaller an affects mainly the values recorded during the initial part of the exercise bout.

Exogenous glucose oxidation during exercise in relation to the power output.

In order to study the influence of the power output on the oxidation rate of exogenous glucose and on the contribution of the various substrates to the energy demand, we combined the use of artificially enriched 13C-glucose with classical indirect calorimetry during uphill treadmill exercise. Six young male healthy subjects underwent three exercise bouts, in a randomized order and at least two weeks apart, at a low (45% VO2max, 1822 +/- 194 ml O2/min for 4 hours), moderate (60% VO2max, 2582 +/- 226 ml O2/min for 3 hours), and high intensity (75% VO2max, 3036 +/- 287 ml O2/min for 2 hours). After 10 min of exercise, each subject ingested 100 g of artificially 13C-labelled glucose dissolved in 400 ml of water. Over the four hours of the exercise at 45% VO2max, the amount of exogenous glucose oxidized was 89.5 +/- 5.9 g from the 100 g ingested. In all exercise bouts, the oxidation of exogenous glucose already began during the first 30 min after ingestion and peaked at 120 min. The maximum oxidation rates averaged 0.64 +/- 0.07, 0.75 +/- 0.04, and 0.63 +/- 0.08 g/min, and the mean amounts of exogenous glucose oxidized over the first two hours averaged 51.7 +/- 8.0, 61.5 +/- 6.6 and 50.9 +/- 8.45 g, at 45, 60 and 75% VO2max respectively. The contribution of the oxidation of exogenous glucose to the total energy supply progressively decreased when the power output increased, from 19.6 to 12.2%. In the meantime, the contribution of total carbohydrates (exogenous+endogenous) progressively increased from 55.1 to 77.8% while the contribution of lipids decreased from 35.5 to 16.6%. In conclusion, exogenous glucose ingested during exercise is largely oxidized and strongly contributes to the energy supply. The oxidation rate first increases with the power output, but levels off or even decreases at high intensity exercise.

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)

Modelling the arterial wall by finite elements.

The mechanical behaviour of the arterial wall was determined theoretically utilizing some parameters of blood flow measured in vivo. Continuous experimental measurements of pressure and diameter were recorded in anesthetized dogs on the thoracic ascending and midabdominal aorta. The pressure was measured by using a catheter, and the diameter firstly, at the same site, by a plethysmograph with mercury gauge and secondly, by a sonomicrometer with ferroelectric ceramic transducers. The unstressed radius and thickness were measured at the end of each experiment in situ. Considering that the viscous component is not important relatively to the nonlinear component of the elasticity and utilizing several equations for Young modulus calculation (thick and thin wall circular cylindrical tube formulas and Bergel's equation) the following values were obtained for this parameter: 0.6 MPa-2 MPa in midabdominal aorta and 2 MPa-6.5 MPa in thoracic ascending aorta. The behaviour of the aorta wall was modelled considering an elastic law and using the finite element program "Lagamine" working in large deformations. The discretized equilibrium equations are non-linear and a unique axi-symmetric, iso-parametric element of 1 cm in length with 8 knots was used for this bi-dimensional problem. The theoretical estimation of radius vessel, utilizing a constant 5 MPa Young modulus and also a variable one, are in good agreement with the experimental results, showing that this finite element model can be applied to study mechanical properties of the arteries in physiological and pathological conditions.

Fructose utilization during exercise in men: rapid conversion of ingested fructose to circulating glucose.

The aim of the present study was to compare the metabolic fate of repeated doses of fructose or glucose ingested every 30 min during long-duration moderate-intensity exercise in men. Healthy volunteers exercised for 3 h on a treadmill at 45% of their maximal oxygen consumption rate. "Naturally labeled" [13C]glucose or [13C]fructose was given orally at 25-g doses every 30 min (total feeding: 150 g; n = 6 in each group). Substrate utilization was evaluated by indirect calorimetry, and exogenous sugar oxidation was measured by isotope ratio mass spectrometry on expired CO2. Results were corrected for baseline drift in 13C/12C ratio in expired air due to exercise alone. Fructose conversion to plasma glucose was measured combining gas chromatography and isotope ratio mass spectrometry. Most of the ingested glucose was oxidized: 81 +/- 4 vs. 57 +/- 2 g/3 h for fructose (2P < 0.005). Exogenous glucose covered 20.8 +/- 1.4% of the total energy need (+/- 6.7 MJ) compared with 14.0 +/- 0.6% for fructose (2P < 0.005). The contribution of total carbohydrates was significantly higher and that of lipids significantly lower with glucose than with fructose. The blood glucose response was similar in both protocols. From 90 to 180 min, 55-60% of circulating glucose was derived from ingested fructose. In conclusion, when ingested repeatedly during moderate-intensity prolonged exercise, fructose is metabolically less available than glucose, despite a high rate of conversion to circulating glucose.

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.

Effect of osmolality on availability of glucose ingested during prolonged exercise in humans.

The aim of this study was to investigate whether the osmolality of a glucose solution, ingested at the beginning of a prolonged exercise bout, affects exogenous glucose disposal. We investigated the hormonal and metabolic response to a 50-g glucose load dissolved in either 200 (protocol A), 400 (protocol B), or 600 (protocol C) ml of water and given orally 15 min after adaptation to exercise in five healthy male volunteers. Naturally labeled [13C]glucose was used to follow the conversion of the ingested glucose to expired-air CO2. Total carbohydrate oxidation (indirect calorimetry) was similar in the three protocols (A, 237 +/- 20; B, 258 +/- 17; C, 276 +/- 20 g/4 h), as was lipid oxidation (A, 128 +/- 4; B, 132 +/- 15; C, 124 +/- 12 g/4 h). Exogenous glucose oxidation rates were similar under the three experimental conditions, and the total amount of exogenous glucose utilized was slightly, but not significantly, increased with the more diluted solution (A, 42.6 +/- 4.4; B, 43.4 +/- 4.1; C, 48.7 +/- 7.2 g/4 h). The blood glucose response was similar in the three protocols. Thus, within the range investigated, the osmolality of the glucose solution ingested had no significant influence either on its oxidation (which was 86-98% of the load ingested) or on the utilization of endogenous carbohydrate, lipid, or protein stores.

[A new approach to the biomechanics of the normal and pathologic lumbar disk using the finite element method]. / Une nouvelle approche de la biomécanique du disque lombaire normal et pathologique à l'aide de la méthode des éléments finis.

The model was created based on the L2-L3 intervertebral disc considering it to be symmetrical on a longitudinal axis and a mid-transverse plane and could be subjected to a longitudinal load of 400 N in compression. The analysis of this two-dimensional problem by using the finite element program S.A.M.C.E.F. utilizes a quadrangular isoparametric and axi-symmetric element. The results took into account the vertical deflection and radial displacement of the nodal points and also the deformation diagram and stress distribution (Von Mises comparison) of the three regions studied: nucleus pulposus, annulus fibrosus and the end plate. This model has been applied to three pathological states: fissuring of the annulus and nucleus herniation, simulation of an enucleation, and a fracture of the central area of end plate with Schmörl's nodule formation. In each case, a deformation and a stress distribution modified relatively to those observed in normal discs were obtained. For instance, in the case of herniation the maximum stress equals 3.700 N/mm2 in comparison with 1.350 N/mm2 found in normal cases. This simplified model is one of the first which reproduces some pathological states of intervertebral discs and facilitates the understanding of the biomechanics of these states.

Utilization of oral sucrose load during exercise in humans. Effect of the alpha-glucosidase inhibitor acarbose.

We investigated the hormonal and metabolic response to a 100-g sucrose load given 15 min after adaptation to moderate-intensity (50% VmaxO2) long-duration (4-h) exercise in healthy volunteers. The effect of a 100-mg dose of the alpha-glucosidase inhibitor Acarbose ingested with the sucrose load was also investigated. "Naturally labeled [13C] sucrose" was used to follow the conversion to expired-air CO2 of the sugar ingested by isotope-ratio mass spectrometry. Circulating hormone and metabolite data were obtained in nine subjects, and indirect calorimetry and stable isotope methodology were applied to six of them. Under placebo, 93 +/- 4 g sucrose were entirely oxidized during the 4 h of exercise, total carbohydrate utilization was 235 +/- 14 g, endogenous carbohydrate utilization was 142 +/- 13 g, and total lipid oxidation was 121 +/- 7 g. A single oral dose of 100 mg Acarbose ingested with the sucrose load did not significantly modify total carbohydrate (239 +/- 2 g/4 h) or lipid (122 +/- 6 g/4 h) oxidation. In contrast, sucrose oxidation was reduced to 53 +/- 6 g/4 h and endogenous carbohydrate utilization increased to 186 +/- 7 g/4 h. Reduction of the rises in blood glucose and fructose and of the increases in plasma insulin and C peptide under Acarbose confirmed these effects, whereas lower circulating levels of alanine suggested a higher rate of gluconeogenesis. These data show that a 100-g glucose load ingested soon after initiation of exercise is a perfect available metabolic substrate.(ABSTRACT TRUNCATED AT 250 WORDS)

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)

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)

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.

Effect of physical training on the oxidation of an oral glucose load at rest: a naturally labeled 13C-glucose study.

UNLABELLED: This study aimed at investigating, in six healthy, non obese, young (25 +/- 1 years) male volunteers, with strictly normal oral glucose tolerance, the influence of a six week physical training period (60 min bicycling 5 days/week at 30-40% of their individual VO2 max) on the hormonal and metabolic response to a 100 g oral 13C-naturally labeled glucose load given at rest before and 36 h after the last training session. Exogenous glucose oxidation was derived from 13CO2 measurements on expired air. Training resulted in: a 29% increase in VO2 max (2 p less than 0.002), a 27% decrease in plasma triglycerides (2 p less than 0.02). No changes were observed concerning weight, total body K, skinfold tolerance, which was strictly normal before training, remained unchanged, but the insulin response to the oral glucose load decreased by 24% (2 p less than 0.025). Exogenous glucose oxidation was similar before and after training, averaging 35.9 +/- 2.1 and 37.4 +/- 2.0 g/7 h respectively. IN CONCLUSION: a 6 week training period, performed on strictly healthy young males, studied at rest, induced an increase in VO2 max, a decrease in plasma triglycerides and a lower insulin response to oral glucose while glucose tolerance and exogenous glucose oxidation remained unchanged.

Fate of exogenous glucose during exercise of different intensities in humans.

The extent to which an oral load of glucose is absorbed from the gut and oxidized during prolonged exercise is a matter of controversy. Four healthy volunteers, 18-28 yr, were submitted on 4 different days to a 105-min treadmill exercise at 22, 39, 51, and 64% of their individual VO2max. After 15 min adaptation to exercise, they received orally 100 g naturally labeled [13C]glucose. Oxidation of the exogenous glucose was followed by 13CO2 measurements in the expired air; total carbohydrate and lipid oxidation were evaluated by indirect calorimetry. Between 22 and 51% VO2 max, total carbohydrate, lipid oxidation, and exogenous glucose oxidation were linearly correlated with the relative work load (r = 0.81; P less than 0.01). Between 51 and 64% VO2 max, exogenous glucose oxidation and lipid oxidation tended to level off, whereas endogenous carbohydrate oxidation was markedly enhanced. The lesser contribution of exogenous glucose during the most intense exercise might be due to a decrease in the oxidation in the muscles or to a lesser availability of this exogenous glucose.

Metabolic adaptations in post-exercise recovery.

To investigate further the hormonal and metabolic adaptations occurring when carbohydrates are ingested after prolonged exercise, we have compared the fate of a 100-g oral glucose load (using 'naturally labelled' 13C-glucose) in healthy volunteers after an overnight fast at rest either without previous exercise or after a 3-h exercise performed on a treadmill at about 50% of the individual VO2 max. In comparison to the control conditions, the oral glucose tolerance test (OGTT) performed in the post-exercise recovery period was characterized by a greater rise in peripheral blood glucose levels and delayed insulin response. Plasma glucagon values were significantly elevated at the time glucose was given (+48 +/- 13 pg ml-1) and at the end of the OGTT. Plasma-free fatty acid (FFA) levels were 1675 +/- 103 microEq 1-1 when glucose was given, and subsequently reduced to values similar to those observed in the control conditions. Indirect calorimetry indicated that OGTT in post-exercise recovery was associated with decreased carbohydrate and increased lipid oxidation when compared to control conditions. Exogenous glucose oxidation was also significantly reduced: 21.1 +/- 2.6 vs. 35.9 +/- 1.9 g per 7 h. We suggest that the higher plasma glucagon levels and the delayed insulin response played a role in the decreased hepatic glucose retention previously described by others in post-exercise recovery. Our data also suggest that the higher lipid oxidation rate observed at the time glucose was given in the post-exercise period could explain, according to the Randle 'glucose-fatty acid cycle', the decreased carbohydrate oxidation and the preferential muscle glycogen repletion already well documented. The reason why the lipid oxidation rate remains increased 3-7 h after glucose ingestion in spite of the fact that FAA levels at that time are similar to those observed in control conditions is still unknown; further kinetic studies are needed to clarify this point.