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Biomedical subjects

F Pirnay

Publications and source records attributed to F Pirnay.

At least 37 records · Page 2Linked to original sources
PubMed1986

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)

3-Hydroxybutyric Acid↗
PubMed1986

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)

Acarbose↗
PubMed1984

Energy expenditure of ambulation in paraplegics: effects of long term use of bracing.

Energy metabolism data were collected in a series of seven male paraplegic patients with complete spinal cord lesions (T9 to L1). Among these four had just been rehabilitated and three had been using their bilateral long leg braces for more than 4 years. A group of five healthy volunteers was used as a control. All the subjects ambulated on a treadmill between parallel bars and in a second trial they ambulated on the floor using forearm crutches. Mean O2 consumption was 1.46 ml O2/kg/m for the unaccustomed paraplegics who had never used long-leg braces before, 0.61 for paraplegics used to walking with braces, and 0.83 for the healthy subjects walking between parallel bars with a swing-through gait. The second trial (on the floor), showed a mean O2 consumption of 0.73 ml O2/kg/m for the paraplegic brace-user with a high heart rate (156/min). This mean O2 consumption was much lower than the values of the paraplegic non-user and slightly higher than the normal subjects.

Adolescent↗
PubMed1984

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.

Administration, Oral↗
PubMed1984

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.

Administration, Oral↗
PubMed1984

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)

Adult↗
PubMed1983

Metabolic adaptation to prolonged exercise in severely obese subjects.

In investigating the metabolic adaptation to prolonged exercise in markedly obese subjects, we compared blood glucose, plasma lactate, free fatty acids, insulin and glucagon concentrations during 3 h of treadmill exercise in nine severely obese male patients (OB) (weight excess 84 +/- 7 per cent of their ideal body weight) and in nine healthy controls (C). Speed and slope of treadmill were selected to give a similar oxygen consumption in both groups (OB: 1.61 +/- 0.08 1/min; C: 1.72 +/- 0.07 1/min). Under these conditions, heart rate was similar in both groups, whereas ventilation was significantly lower in overweight subjects. In obese patients, plasma free fatty acid (FFA) levels were higher in the basal state (OB: 740 +/- 43 mumol/l; C: 602 +/- 40 mumol/l, 2 P less than 0.05) but showed a lower increase during the exercise period (OB: + 576 +/- 135 mumol/l; C: + 1071 +/- 100 mumol/l, 2 P less than 0.02). This impaired FFA mobilization was related to significantly higher insulin (IRI) levels throughout the exercise period as shown by the regression line of exercise-induced FFA increase (y, mumol/l) vs mean plasma IRI during exercise (x, microU/ml): y = 1238 - 60 x, r = -0.709, 2 P less than 0.001. Lack of glucagon increase could also contribute to the lower rise of FFA in obese subjects. A correspondingly increased contribution of carbohydrates to the energy supply is suggested by a significant decline in blood glucose and higher lactate plasma concentrations during the second half of the exercise period in overweight patients. These abnormalities could represent a metabolic limitation for performing prolonged exercise in markedly obese patients.

Blood Glucose↗
PubMed1982

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.

Adaptation, Physiological↗
PubMed1982

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.

Adult↗
PubMed1981

Anaerobic and aerobic power of top athletes.

In this study the alactic anaerobic and aerobic power of top level sprinters, long-distance runners, and untrained students were compared. Maximal oxygen uptake was measured during the progressive test on a treadmill. The anaerobic power was estimated according to a newly developed bicycle ergometer technique. As reported elsewhere, the maximal oxygen uptake is very high in twelve long-distance runners (77.6 +/- 2.7 ml/kg . min-1) whereas the maximal oxygen uptake of six sprinters amounts to 60.1 +/- 5.9 ml/kg . min-1. The average alactic anaerobic power of a control group of 32 students was 710 W or 10.1 +/- 1.2 W/kg. Significantly lower results were obtained by long-distance runners (551 W or 8.93 W/kg) whereas significantly higher results were obtained by sprinters (1,021 W or 14.16 W/kg). In top level athletes, but not in the control group, a negative relation was found between aerobic power and anaerobic power.

Adolescent↗
PubMed1981

Glucose oxidation in relation to the size of the oral glucose loading dose.

Using "naturally labeled 13C-glucose" the conversion to expired air CO2 of 100, 66 and 33 g oral glucose loads was evaluated, during 7 hr, in 6 male healthy volunteers. The total amounts of exogenous glucose converted to expired air CO2 were proportional to the loading doses and averaged, in g/7 hr, 14.6 +/- 2.1 for 33 g, 20.8 +/- 2.1 for 66 g and 31.2 +/- 1.6 for 100 g. In contrast total glucose oxidation, evaluated by indirect calorimetry, was similar in the three groups and was not correlated with the dose of glucose given. The plasma insulin response was significantly correlated with the load of glucose (r = 0.86; p less than 0.001) whereas such correlation was not observed with the blood glucose response. Comparison with data available in the literature on the influence of the size of the oral glucose load on endogenous glucose production and on splanchnic glucose output suggests that the greater oxidation of exogenous glucose seen when the oral load of glucose is increased essentially results from a greater enrichment of the systemic glucose pool with exogenous glucose.

Adult↗