Oral [13C]glucose and endogenous energy substrate oxidation during prolonged treadmill running

2002 ◽  
Vol 92 (3) ◽  
pp. 1255-1260 ◽  
Author(s):  
Stéphane Couture ◽  
Denis Massicotte ◽  
Carole Lavoie ◽  
Claude Hillaire-Marcel ◽  
François Péronnet

Six male subjects were studied during running exercise (120 min, 69% maximal oxygen consumption) with ingestion of a placebo or 3.5 g/kg of [13C]glucose (∼2 g/min). Indirect respiratory calorimetry corrected for urea excretion in urine and sweat, production of 13CO2 at the mouth, and changes in plasma glucose 13C/12C were used to compute energy substrate oxidation. The oxidation rate of exogenous glucose increased from 1.02 at minute 60 to 1.22 g/min at minute 120 providing ∼24 and 33% of the energy yield (%En). Glucose ingestion did not modify protein oxidation, which provided ∼4–5%En, but significantly increased glucose oxidation by ∼7%, reduced lipid oxidation by ∼16%, and markedly reduced endogenous glucose oxidation (1.25 vs. 2.21 g/min between minutes 80 and 120, respectively). The oxidation rate of glucose released from the liver (0.38 and 0.47 g/min, or 10–13%En at minutes 60 and 120, respectively), and of plasma glucose (1.30–1.69 g/min, or 34 and 45%En and 50 and 75% of glucose oxidation) significantly increased from minutes 60 to 120, whereas the oxidation of muscle glycogen significantly decreased (1.28 to 0.58 g of glucose/min, or 34 and 16%En and 50 and 25% of glucose oxidation). These results indicate that, during moderate prolonged running exercise, ingestion of a very large amount of glucose significantly reduces endogenous glucose oxidation, thus sparing muscle and/or liver glycogen stores.

2002 ◽  
Vol 92 (4) ◽  
pp. 1562-1572 ◽  
Author(s):  
Roy L. P. G. Jentjens ◽  
Anton J. M. Wagenmakers ◽  
Asker E. Jeukendrup

The aim of the present study was to test the hypothesis that the oxidation rate of ingested carbohydrate (CHO) is impaired during exercise in the heat compared with a cool environment. Nine trained cyclists (maximal oxygen consumption 65 ± 1 ml · kg body wt−1 · min−1) exercised on two different occasions for 90 min at 55% maximum power ouptput at an ambient temperature of either 16.4 ± 0.2°C (cool trial) or 35.4 ± 0.1°C (heat trial). Subjects received 8% glucose solutions that were enriched with [U-13C]glucose for measurements of exogenous glucose, plasma glucose, liver-derived glucose and muscle glycogen oxidation. Exogenous glucose oxidation during the final 30 min of exercise was significantly ( P < 0.05) lower in the heat compared with the cool trial (0.76 ± 0.06 vs. 0.84 ± 0.05 g/min). Muscle glycogen oxidation during the final 30 min of exercise was increased by 25% in the heat (2.07 ± 0.16 vs. 1.66 ± 0.09 g/min; P < 0.05), and liver-derived glucose oxidation was not different. There was a trend toward a higher total CHO oxidation and a lower plasma glucose oxidation in the heat although this did not reach statistical significance ( P = 0.087 and P = 0.082, respectively). These results demonstrate that the oxidation rate of ingested CHO is reduced and muscle glycogen utilization is increased during exercise in the heat compared with a cool environment.


2007 ◽  
Vol 17 (3) ◽  
pp. 232-243 ◽  
Author(s):  
Neil M. Johannsen ◽  
Rick L. Sharp

The purpose of this study was to investigate differences in substrate oxidation between dextrose (DEX) and unmodified (UAMS) and acid/alcohol-modified (MAMS) cornstarches. Seven endurance-trained men (VO2peak = 59.1 ± 5.4 mL·kg−1·min−1) participated in 2 h of exercise (66.4% ± 3.3% VO2peak) 30 min after ingesting 1 g/kg body weight of the experimental carbohydrate or placebo (PLA). Plasma glucose and insulin were elevated after DEX (P < 0.05) compared with UAMS, MAMS, and PLA. Although MAMS and DEX raised carbohydrate oxidation rate through 90 min of exercise, only MAMS persisted throughout 120 min (P < 0.05 compared with all trials). Exogenous-carbohydrate oxidation rate was higher in DEX than in MAMS and UAMS until 90 min of exercise. Acid/alcohol modification resulted in augmented carbohydrate oxidation with a small, sustained increase in exogenous-carbohydrate oxidation rate. MAMS appears to be metabolizable and available for oxidation during exercise.


2007 ◽  
Vol 103 (1) ◽  
pp. 119-124 ◽  
Author(s):  
M. Robitaille ◽  
M.-C. Dubé ◽  
S. J. Weisnagel ◽  
D. Prud'homme ◽  
D. Massicotte ◽  
...  

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 ∼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.


2006 ◽  
Vol 290 (4) ◽  
pp. E708-E715 ◽  
Author(s):  
Gareth A. Wallis ◽  
Ruth Dawson ◽  
Juul Achten ◽  
Jonathan Webber ◽  
Asker E. Jeukendrup

The present study investigated potential sex-related differences in the metabolic response to carbohydrate (CHO) ingestion during exercise. Moderately endurance-trained men and women ( n = 8 for each sex) performed 2 h of cycling at ∼67% V̇o2 max with water (WAT) or CHO ingestion (1.5 g of glucose/min). Substrate oxidation and kinetics were quantified during exercise using indirect calorimetry and stable isotope techniques ([13C]glucose ingestion, [6,6-2H2]glucose, and [2H5]glycerol infusion). In both sexes, CHO ingestion significantly increased the rates of appearance (Ra) and disappearance (Rd) of glucose during exercise compared with WAT ingestion [males: WAT, ∼28–29 μmol·kg lean body mass (LBM)−1·min−1; CHO, ∼53 μmol·kg LBM−1·min−1; females: WAT, ∼28–29 μmol·kg LBM−1·min−1; CHO, ∼61 μmol·kg LBM−1·min−1; main effect of trial, P < 0.05]. The contribution of plasma glucose oxidation to the energy yield was significantly increased with CHO ingestion in both sexes (from ∼10% to ∼20% of energy expenditure; main effect of trial, P < 0.05). Liver-derived glucose oxidation was reduced, although the rate of muscle glycogen oxidation was unaffected with CHO ingestion (males: WAT, 108 ± 12 μmol·kg LBM−1·min−1; CHO, 108 ± 11 μmol·kg LBM−1·min−1; females: WAT, 89 ± 10 μmol·kg LBM−1·min−1; CHO, 93 ± 11 μmol·kg LBM−1·min−1). CHO ingestion reduced fat oxidation and lipolytic rate (Ra glycerol) to a similar extent in both sexes. Finally, ingested CHO was oxidized at similar rates in men and women during exercise (peak rates of 0.70 ± 0.08 and 0.65 ± 0.06 g/min, respectively). The present investigation suggests that the metabolic response to CHO ingestion during exercise is largely similar in men and women.


2002 ◽  
Vol 93 (1) ◽  
pp. 77-84 ◽  
Author(s):  
François Haman ◽  
François Péronnet ◽  
Glen P. Kenny ◽  
Denis Massicotte ◽  
Carole Lavoie ◽  
...  

The relative roles of circulatory glucose, muscle glycogen, and lipids in shivering thermogenesis are unclear. Using a combination of indirect calorimetry and stable isotope methodology ([U-13C]glucose ingestion), we have quantified the oxidation rates of these substrates in men acutely exposed to cold for 2 h (liquid conditioned suit perfused with 10°C water). Cold exposure stimulated heat production by 2.6-fold and increased the oxidation of plasma glucose from 39.4 ± 2.4 to 93.9 ± 5.5 mg/min (+138%), of muscle glycogen from 126.6 ± 7.8 to 264.2 ± 36.9 mg glucosyl units/min (+109%), and of lipids from 46.9 ± 3.2 to 176.5 ± 17.3 mg/min (+376%). Despite the observed increase in plasma glucose oxidation, this fuel only supplied 10% of the energy for heat generation. The major source of carbohydrate was muscle glycogen (75% of all glucose oxidized), and lipids produced as much heat as all other fuels combined. During prolonged, low-intensity shivering, we conclude that total heat production is unequally shared among lipids (50%), muscle glycogen (30%), plasma glucose (10%), and proteins (10%). Therefore, future research should focus on lipids and muscle glycogen that provide most of the energy for heat production.


2006 ◽  
Vol 290 (6) ◽  
pp. E1198-E1204 ◽  
Author(s):  
Vincent Rigalleau ◽  
Marie-Christine Beauvieux ◽  
Jean-Louis Gallis ◽  
Henri Gin ◽  
Phillippe Schneiter ◽  
...  

The plasma glucose excursion may influence the metabolic responses after oral glucose ingestion. Although previous studies adressed the effects of hyperglycemia in conditions of hyperinsulinemia, it has not been evaluated whether the route of glucose administration (oral vs. intravenous) plays a role. Our aim was to determine the effects of moderately controlled hyperglycemia on glucose metabolism before and after oral glucose ingestion. Eight normal men underwent two oral glucose clamps at 6 and 10 mmol/l plasma glucose. Glucose turnover and cycling rates were measured by infusion of [2H7]glucose. The oral glucose load was labeled by d-[6,6-2H2]glucose to monitor exogenous glucose appearance, and respiratory exchanges were measured by indirect calorimetry. Sixty percent of the oral glucose load appeared in the systemic circulation during both the 6 and 10 mmol/l plasma glucose tests, although less endogenous glucose appeared during the 10 mmol/l tests before glucose ingestion ( P < 0.05). This inhibitory effect of hyperglycemia was not detectable after oral glucose ingestion, although glucose utilization was increased (+28%, P < 0.05) due to increased nonoxidative glucose disposal [10 vs. 6 mmol/l: +20%, not significant (NS) before oral glucose ingestion; +40%, P < 0.05 after oral glucose ingestion]. Glucose cycling rates were increased by hyperglycemia (+13% before oral glucose ingestion, P < 0.001; +31% after oral glucose ingestion, P < 0.05) and oral glucose ingestion during both the 6 (+10%, P < 0.05) and 10 mmol/l (+26%, P < 0.005) tests. A moderate hyperglycemia inhibits endogenous glucose production and contributes to glucose tolerance by enhancing nonoxidative glucose disposal. Hyperglycemia and oral glucose ingestion both stimulate glucose cycling.


1998 ◽  
Vol 85 (2) ◽  
pp. 723-730 ◽  
Author(s):  
F. Péronnet ◽  
N. Rhéaume ◽  
C. Lavoie ◽  
C. Hillaire-Marcel ◽  
D. Massicotte

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 of13CO2produced the13C-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.


2004 ◽  
Vol 96 (1) ◽  
pp. 32-40 ◽  
Author(s):  
François Haman ◽  
François Péronnet ◽  
Glen P. Kenny ◽  
Éric Doucet ◽  
Denis Massicotte ◽  
...  

Carbohydrates (CHO) can play an important thermogenic role during shivering, but the effect of their availability on the use of other oxidative fuels is unclear. Using indirect calorimetry and tracer methods ([U-13C]glucose ingestion), we have determined the specific contributions of plasma glucose, muscle glycogen, proteins, and lipids to total heat production (Ḣprod) in men exposed to cold for 2-h (liquid-conditioned suit perfused with 10°C water). Measurements were made after low-CHO diet and exercise (Lo) and high-CHO diet without exercise (Hi). The size of CHO reserves had no effect on Ḣprod but a major impact on fuel selection before and during shivering. In the cold, a complete shift from lipid oxidation for Lo (53, 28, and 19% Ḣprod for lipids, CHO, and proteins, respectively) to CHO-based metabolism for Hi (23, 65, and 12% Ḣprod for lipids, CHO, and proteins, respectively) was observed. Plasma glucose oxidation remains a minor fuel under all conditions (<13% Ḣprod), falling to 7% Ḣprod for Lo. Therefore, adjusting plasma glucose oxidation to compensate for changes in muscle glycogen oxidation is not a strategy used for maintaining heat production. Instead, proteins and lipids share responsibility for this compensation. We conclude that humans can show remarkable flexibility in oxidative fuel selection to ensure that heat production is not compromised during sustained cold exposure.


2008 ◽  
Vol 295 (5) ◽  
pp. H2098-H2105 ◽  
Author(s):  
Khaled Qanud ◽  
Mohammed Mamdani ◽  
Martino Pepe ◽  
Ramzi J. Khairallah ◽  
John Gravel ◽  
...  

When recovering from heart failure (HF), the myocardium displays a marked plasticity and can regain normal gene expression and function; however, recovery of substrate oxidation capacity has not been explored. We tested whether cardiac functional recovery is matched by normalization of energy substrate utilization during post-HF recovery. HF was induced in dogs by pacing the left ventricle (LV) at 210–240 beats/min for 4 wk. Tachycardia was discontinued, and the heart was allowed to recover. An additional group was studied in HF, and healthy dogs served as controls ( n = 8/group). Cardiac free fatty acids (FFAs) and glucose oxidation were measured with [3H]oleate and [14C]glucose. At 10 days of recovery, hemodynamic parameters returned to control values; however, the contractile response to dobutamine remained depressed, LV end-diastolic volume was 28% higher than control, and the heart mass-to-body mass ratio was increased (9.8 ± 0.4 vs. 7.5 ± 0.2 g/kg, P < 0.05). HF increased glucose oxidation (76.8 ± 19.7 nmol·min−1·g−1) and decreased FFA oxidation (20.7 ± 6.4 nmol·min−1·g−1), compared with normal dogs (24.5 ± 6.3 and 51.7 ± 9.6 nmol·min−1·g−1, respectively), and reversed to normal values at 10 days of recovery (25.4 ± 6.0 and 46.6 ± 6.7 nmol·min−1·g−1, respectively). However, similar to HF, the recovered dogs failed to increase glucose and fatty acid uptake in response to pacing stress. The activity of myocardial citrate synthase and aconitase was significantly decreased during recovery compared with that in control dogs (58 and 27% lower, respectively, P < 0.05), indicating a persistent reduction in mitochondrial oxidative capacity. In conclusion, cardiac energy substrate utilization is normalized in the early stage of post-HF recovery at baseline, but not under stress conditions.


Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 246-OR
Author(s):  
MARIAM ALATRACH ◽  
CHRISTINA AGYIN ◽  
NITCHAKARN LAICHUTHAI ◽  
JOHN M. ADAMS ◽  
MUHAMMAD ABDUL-GHANI ◽  
...  

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