Preexercise glucose ingestion and glucose kinetics during exercise

1996 ◽  
Vol 81 (2) ◽  
pp. 853-857 ◽  
Author(s):  
N. Marmy-Conus ◽  
S. Fabris ◽  
J. Proietto ◽  
M. Hargreaves
Keyword(s):  
Glucose Uptake ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Placebo Control ◽  
O2 Uptake ◽  
Glucose Kinetics ◽  
Rapid Fall ◽  
Glucose Ingestion ◽  
Total Glucose ◽  
Glucose Output

The present study was undertaken to examine the effects of glucose ingestion before exercise on liver glucose output and muscle glucose uptake during exercise. On two occasions, at least 1 wk apart, six trained men (peak pulmonary O2 uptake = 5.11 +/- 0.17 l/min) ingested 400 ml of a solution containing either 75 g glucose [carbohydrate (CHO)] or a sweet placebo [control (Con)] 30 min before 60 min of exercise at 71 +/- 1% peak pulmonary O2 uptake. Glucose kinetics (rates of appearance and disappearance) were measured by a primed continuous infusion of [6,6–2H2]glucose. Liver glucose output was derived from total glucose appearance and the appearance of ingested glucose from the gut. After glucose ingestion, plasma glucose increased to 6.4 +/- 0.4 mmol/l immediately before exercise, fell to 4.2 +/- 0.5 mmol/l after 20 min of exercise, and then increased to a higher value than in the Con group (5.4 +/- 0.3 vs. 4.7 +/- 0.1 mmol/l; P < 0.05) after 60 min of exercise. In the CHO group, plasma insulin was higher immediately before exercise (P < 0.05) and, despite falling during exercise, remained higher than in the Con group after 60 min of exercise (57.0 +/- 11.4 vs. 24.8 +/- 1.7 pmol/l; P < 0.05). The rapid fall in plasma glucose in the CHO group was the result of a higher muscle glucose uptake with the onset of exercise (P < 0.05), which could not be matched by the glucose rate of appearance. Liver glucose output was decreased by glucose ingestion, and although it increased during the early stages of exercise in the CHO group, it did not rise above the basal values and was reduced by 62% over the 60 min of exercise compared with the Con group. In summary, preexercise glucose ingestion results in increased muscle glucose uptake and reduced liver glucose output during exercise.

Carbohydrate ingestion before exercise: comparison of glucose, fructose, and sweet placebo

1981 ◽  
Vol 51 (4) ◽  
pp. 783-787 ◽  
Author(s):  
V. A. Koivisto ◽  
S. L. Karonen ◽  
E. A. Nikkila
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Cycle Ergometer ◽  
Vo2 Max ◽  
Vigorous Exercise ◽  
Carbohydrate Ingestion ◽  
Rapid Fall ◽  
Ergometer Exercise ◽  
Glucose Ingestion ◽  
Response To Exercise

To examine the effect of various carbohydrates on the metabolic and hormonal response to exercise, 75 g glucose, fructose, or placebo were given to nine well-trained males (VO2 max 60 +/- 1 ml . kg-1 . min-1) 45 min before cycle ergometer exercise performed at 75% VO2 max for 30 min. After glucose ingestion, the rise in plasma glucose was 3-fold (P less than 0.005) in plasma insulin 2.5-fold (P less than 0.01) greater than after fructose. During exercise, after glucose administration plasma glucose fell from 5.3 +/- 0.3 to 2.5 +/- 0.2 mmol/l (P less than 0.001) and after fructose from 4.5 +/- 0.1 to 3.9 +/- 0.3 mmol/l (P less than 0.05). The fall in plasma glucose was closely related to the preexercise levels of plasma insulin (r = 0.82, P less than 0.001) and glucose (r = 0.81, P less than 0.001). Both glucose and fructose ingestion decreased the FFA levels by 40–50% (P less than 0.005) and during exercise they remained 30–40% lower after carbohydrate than placebo administration (P less than 0.02). This study suggests that glucose ingestion prior to exercise results in hypoglycemia during vigorous exercise, this rapid fall in plasma glucose is mediated, at least in part, by hyperinsulinemia, and fructose ingestion is associated with a modest rise in plasma insulin and does not result in hypoglycemia during exercise.

scholarly journals L-arabinose co-ingestion delays glucose absorption derived from sucrose in healthy men and women: a double-blind, randomized crossover trial

2021 ◽  
pp. 1-29
Author(s):  
Kenneth Pasmans ◽  
Ruth C.R. Meex ◽  
Jorn Trommelen ◽  
Joan M.G. Senden ◽  
Elaine E. Vaughan ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Glucose Production ◽  
Glucose Absorption ◽  
Endogenous Glucose Production ◽  
Dietary Interventions ◽  
Glucose Kinetics ◽  
Double Blind ◽  
Exogenous Glucose ◽  
Total Glucose ◽  
Glucose Output

Abstract Dietary interventions to delay carbohydrate digestion or absorption can effectively prevent hyperglycemia in the early postprandial phase. L-arabinose can specifically inhibit sucrase. It remains to be assessed whether co-ingestion of L-arabinose with sucrose delays sucrose digestion, attenuates subsequent glucose absorption, and impacts hepatic glucose output. In this double-blind, randomized crossover study, we assessed blood glucose kinetics following ingestion of a 200-mL drink containing 50 g sucrose with 7.5 g L-arabinose (L-ARA) or without L-arabinose (CONT) in twelve young, healthy participants (24±1 y; BMI: 22.2±0.5 kg/m2). Plasma glucose kinetics were determined by a dual stable isotope methodology involving ingestion of [U-13C6]-glucose-enriched sucrose, and continuous intravenous infusion of [6,6-2H2]-glucose. Peak glucose concentrations reached 8.18±0.29 mmol/L for CONT 30 min after ingestion. In contrast, the postprandial rise in plasma glucose was attenuated for L-ARA, because peak glucose concentrations reached 6.62±0.18 mmol/L only 60 min after ingestion. The rate of exogenous glucose appearance for L-ARA was 67 and 57% lower compared with CONT at t = 15 min and 30 min, respectively, whereas it was 214% higher at t = 150 min, indicating a more stable absorption of exogenous glucose for L-ARA compared with CONT. Total glucose disappearance during the first hour was lower for L-ARA compared with CONT (11±1 versus 17±1 g, p<0.0001). Endogenous glucose production was not differentially affected at any time point (p=0.27). Co-ingestion of L-arabinose with sucrose delays sucrose digestion, resulting in a slower absorption of sucrose-derived glucose without causing adverse effects in young, healthy adults.

Effect of carbohydrate ingestion on glucose kinetics during exercise

1994 ◽  
Vol 77 (3) ◽  
pp. 1537-1541 ◽  
Author(s):  
G. McConell ◽  
S. Fabris ◽  
J. Proietto ◽  
M. Hargreaves
Keyword(s):  
Oxygen Uptake ◽  
Glucose Uptake ◽  
Plasma Glucose ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Glucose Kinetics ◽  
Carbohydrate Ingestion ◽  
Pulmonary Oxygen Uptake ◽  
Hepatic Glucose ◽  
Total Glucose

Six well-trained men (peak pulmonary oxygen uptake = 5.03 +/- 0.11 l/min) were studied during 2 h of exercise at 69 +/- 1% peak pulmonary oxygen uptake to examine the effect of carbohydrate (CHO) ingestion on glucose kinetics. Subjects ingested 250 ml of either a 10% glucose solution containing 6-[3H]glucose (CHO) or a sweet placebo every 15 min during exercise. Glucose kinetics were assessed by 6,6-[2H]glucose infusion corrected for gut-derived glucose in CHO. Plasma glucose was higher (P < 0.05) in CHO from 20 min. Total glucose appearance was higher in CHO due to glucose delivery from the gut (68 +/- 7 g), since hepatic glucose production was reduced by 51% (29 +/- 5 vs. 59 +/- 5 g). Glucose uptake was higher in CHO (96 +/- 7 vs. 60 +/- 6 g) with the ingested glucose supplying 67 +/- 4 g and, with the assumption that it was fully oxidized, accounted for 14 +/- 1% of total energy expenditure. In conclusion, CHO ingestion during prolonged exercise results in suppression of hepatic glucose production and increased glucose uptake. These effects appear to be mediated mainly by increased plasma glucose and insulin levels.

scholarly journals Glucose ingestion and substrate utilization during exercise in boys with IDDM

2000 ◽  
Vol 88 (4) ◽  
pp. 1239-1246 ◽  
Author(s):  
M. C. Riddell ◽  
O. Bar-Or ◽  
M. Hollidge-Horvat ◽  
H. P. Schwarcz ◽  
G. J. F. Heigenhauser
Keyword(s):  
Energy Supply ◽  
Plasma Insulin ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Glucose Ingestion ◽  
Insulin Dependent ◽  
Plasma Insulin Levels ◽  
Endogenous Glucose ◽  
Total Fat ◽  
Total Glucose

This study was intended to compare exogenous [13C]glucose (Gluexo) oxidation in boys with insulin-dependent diabetes mellitus (IDDM) and healthy boys of similar age, weight, and maximal O2 uptake. In a control trial with water intake (CT) and in a 13C-enriched glucose trial (GT), subjects cycled for 60 min (58.8 ± 0.9% maximal O2 uptake) while the utilization of total glucose, total fat, and Gluexo was assessed. In CT, total glucose was 84.7 ± 9.2 vs. 91.3 ± 6.6 g/60 min (not significantly different) and total fat was 13.3 ± 2.2 vs. 11.1 ± 1.7 g/60 min (not significantly different) in IDDM vs. healthy boys, respectively. In GT, Gluexo was 10.4 ± 1.7 vs. 14.8 ± 1.1 g/60 min, corresponding to 9.0 ± 1.0 vs. 12.4 ± 0.5% of the total energy supply in IDDM and healthy boys, respectively ( P < 0.05). Endogenous glucose was spared in both groups by 12.6 ± 3.5% ( P < 0.05). Blood glucose and plasma insulin concentrations were two- to threefold higher in IDDM vs. healthy boys in both trials. In conclusion, Gluexo is impaired in exercising boys with IDDM, even when plasma insulin levels are elevated.

Estimation and kinetic analysis of insulin-independent glucose uptake in human subjects

1983 ◽  
Vol 244 (6) ◽  
pp. E632-E635 ◽  
Author(s):  
I. Gottesman ◽  
L. Mandarino ◽  
J. Gerich
Keyword(s):  
Glucose Uptake ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Human Subjects ◽  
Linear Regression Analysis ◽  
Increase Glucose Uptake ◽  
Glucose Transport System ◽  
Glucose Clamp Technique ◽  
Additional Support

Using the glucose clamp technique, glucose uptake was determined isotopically in normal human volunteers at plasma glucose concentrations of congruent to 60, 95, and 160 mg/dl during insulin infusions that increased plasma insulin to congruent to 20, 80, and 160 microU/ml. Because glucose uptake was found to be a linear function of plasma insulin at each plasma glucose concentration (r greater than 0.92, P less than 0.01), glucose uptake at 0 plasma insulin was estimated by linear regression analysis. The values thus derived (1.30, 1.62, and 2.59 mg . kg-1 . min-1 for plasma glucose concentrations of 60, 95, and 160 mg/dl, respectively) produced a linear Eadie-Hofstee plot, suggesting that insulin-independent glucose uptake followed Michaelis-Menten kinetics. The Km for glucose uptake at 0 plasma insulin (congruent to 10 mM) was similar to those observed for glucose uptake at the other plasma insulin concentrations studied (congruent to 9-12 mM), but its Vmax was less (5.2 vs. 6.4, 18.5, and 26.8 mg . kg-1 . min-1 for congruent to 20, 80, and 160 U/ml, respectively). These results indicate that in postabsorptive human subjects 75-85% of glucose uptake is noninsulin-mediated and provide additional support for the concept that insulin may increase glucose uptake merely by providing additional transport sites. The method described herein provides an assessment of insulin-independent glucose uptake in vivo that may prove useful in distinguishing between intrinsic defects of the glucose transport system and those due to defects in insulin action.

Plasma glucose kinetics during prolonged exercise in trained humans when fed carbohydrate

2002 ◽  
Vol 283 (3) ◽  
pp. E573-E577 ◽  
Author(s):  
Damien J. Angus ◽  
Mark A. Febbraio ◽  
Mark Hargreaves
Keyword(s):  
Plasma Glucose ◽  
Cycle Ergometer ◽  
Strenuous Exercise ◽  
Glucose Disposal ◽  
Glucose Kinetics ◽  
Exogenous Glucose ◽  
Appearance Rate ◽  
Volitional Fatigue ◽  
Glucose Output ◽  
Peak Value

Nine endurance-trained men exercised on a cycle ergometer at ∼68% peak O2 uptake to the point of volitional fatigue [232 ± 14 (SE) min] while ingesting an 8% carbohydrate solution to determine how high glucose disposal could increase under physiological conditions. Plasma glucose kinetics were measured using a primed, continuous infusion of [6,6-2H]glucose and the appearance of ingested glucose, assessed from [3-3H]glucose that had been added to the carbohydrate drink. Plasma glucose was increased ( P < 0.05) after 30 min of exercise but thereafter remained at the preexercise level. Glucose appearance rate (Ra) increased throughout exercise, reaching its peak value of 118 ± 7 μmol · kg−1 · min−1 at fatigue, whereas gut Ra increased continuously during exercise, peaking at 105 ± 10 μmol · kg−1 · min−1 at the point of fatigue. In contrast, liver glucose output never rose above resting levels at any time during exercise. Glucose disposal (Rd) increased throughout exercise, reaching a peak value of 118 ± 7 μmol · kg−1 · min−1 at fatigue. If we assume 95% oxidation of glucose Rd, estimated exogenous glucose oxidation at fatigue was 1.36 ± 0.08 g/min. The results of this study demonstrate that glucose uptake increases continuously during prolonged, strenuous exercise when carbohydrate is ingested and does not appear to limit exercise performance.

Effect of sequential infusions of glucagon and epinephrine on glucose turnover in the dog.

1978 ◽  
Vol 235 (3) ◽  
pp. E287 ◽  
Author(s):  
L Saccà ◽  
R Sherwin ◽  
P Felig
Keyword(s):  
Glucose Uptake ◽  
Plasma Glucose ◽  
Glucose Utilization ◽  
Glucose Production ◽  
Conscious Dogs ◽  
Glucose Turnover ◽  
Plasma Glucagon ◽  
Conscious Dog ◽  
Glucose Clearance ◽  
Glucose Output

Conscious dogs were infused with 1) glucagon (3 ng/kg.min) alone for 120 min followed by glucagon plus epinephrine (0.1 microgram/kg.min) for 60 min and 2) epinephrine alone (150 min) followed by epinephrine plus glucagon for 90 min. Glucagon alone caused a 10--15 mg/dl rise in plasma glucose and a 45% increase in glucose production that returned to baseline by 75--120 min. After addition of epinephrine, glucose production rose again by 80%. Infusion of epinephrine alone resulted in unchanged plasma glucagon levels, a 60--70 mg/dl rise in plasma glucose, and an 80--100% rise in glucose production that returned to baseline by 60--120 min. When glucagon was added, glucose output promptly rose again by 85%. When glucagon was infused alone, there was a rise in glucose uptake, whereas, with epinephrine, glucose uptake failed to rise and glucose clearance fell by 35--50%. We conclude that 1) hepatic refractoriness to persistent elevations of glucagon or epinephrine is specific for the hormone infused; 2) epinephrine stimulates glucose production in the conscious dog in the absence of a rise in plasma glucagon; 3) the hyperglycemic response to glucagon or epinephrine is determined in part by accompanying changes in glucose utilization.

Insulin as a mediator of hepatic glucose uptake in the conscious dog

1982 ◽  
Vol 242 (2) ◽  
pp. E97-E101 ◽  
Author(s):  
A. D. Cherrington ◽  
P. E. Williams ◽  
N. Abou-Mourad ◽  
W. W. Lacy ◽  
K. E. Steiner ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Plasma Insulin ◽  
Marked Effect ◽  
Glucose Infusion ◽  
Hepatic Glucose Output ◽  
Intravenous Glucose ◽  
Conscious Dog ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
Hepatic Glucose Uptake

The aim of this study was to determine whether a physiological increment in plasma insulin could promote substantial hepatic glucose uptake in response to hyperglycemia brought about by intravenous glucose infusion in the conscious dog. To accomplish this, the plasma glucose level was doubled by glucose infusion into 36-h fasted dogs maintained on somatostatin, basal glucagon, and basal or elevated intraportal insulin infusions. In the group with basal glucagon levels and modest hyperinsulinemia (33 +/- 2 micro U/ml), the acute induction of hyperglycemia (mean increment of 120 mg/dl) caused marked net hepatic glucose uptake (3.7 +/- 0.5 mg . kg-1 . min-1). In contrast, similar hyperglycemia brought about in the presence of basal glucagon and basal insulin levels described net hepatic glucose output in 56%, but did not cause net hepatic glucose uptake. The length of fast was not crucial to the response because similar signals (insulin, 38 +/- 6 micro U/ml; glucose increment, 127 mg/dl) promoted identical net hepatic glucose uptake (3.8 +/- 0.6 mg . kg-1 . min-1) in dogs fasted for only 16 h. In conclusion, in the conscious dog, a) physiologic increments in plasma insulin have a marked effect on the ability of hyperglycemia to stimulate net hepatic glucose uptake, and b) it is not necessary to administer glucose orally to promote substantial net hepatic glucose uptake.

scholarly journals Effect of Exenatide on Splanchnic and Peripheral Glucose Metabolism in Type 2 Diabetic Subjects

2011 ◽  
Vol 96 (6) ◽  
pp. 1763-1770 ◽  
Author(s):  
E. Cersosimo ◽  
A. Gastaldelli ◽  
A. Cervera ◽  
E. Wajcberg ◽  
A. Sriwijilkamol ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Gastric Emptying ◽  
Glucose Uptake ◽  
Plasma Glucose ◽  
Fasting Plasma Glucose ◽  
Plasma Insulin ◽  
Hepatic Insulin Resistance ◽  
Oral Glucose ◽  
Fasting Plasma

Objective: Our objective was to examine the mechanisms via which exenatide attenuates postprandial hyperglycemia in type 2 diabetes mellitus (T2DM). Study Design: Seventeen T2DM patients (44 yr; seven females, 10 males; body mass index = 33.6 kg/m2; glycosylated hemoglobin = 7.9%) received a mixed meal followed for 6 h with double-tracer technique ([1-14C]glucose orally; [3-3H]glucose iv) before and after 2 wk of exenatide. In protocol II (n = 5), but not in protocol I (n = 12), exenatide was given in the morning of the repeat meal. Total and oral glucose appearance rates (RaT and RaO, respectively), endogenous glucose production (EGP), splanchnic glucose uptake (75 g − RaO), and hepatic insulin resistance (basal EGP × fasting plasma insulin) were determined. Results: After 2 wk of exenatide (protocol I), fasting plasma glucose decreased (from 10.2 to 7.6 mm) and mean postmeal plasma glucose decreased (from 13.2 to 11.3 mm) (P &lt; 0.05); fasting and meal-stimulated plasma insulin and glucagon did not change significantly. After exenatide, basal EGP decreased (from 13.9 to 10.8 μmol/kg · min, P &lt; 0.05), and hepatic insulin resistance declined (both P &lt; 0.05). RaO, gastric emptying (acetaminophen area under the curve), and splanchnic glucose uptake did not change. In protocol II (exenatide given before repeat meal), fasting plasma glucose decreased (from 11.1 to 8.9 mm) and mean postmeal plasma glucose decreased (from 14.2 to 10.1 mm) (P &lt; 0.05); fasting and meal-stimulated plasma insulin and glucagon did not change significantly. After exenatide, basal EGP decreased (from 13.4 to 10.7 μmol/kg · min, P = 0.05). RaT and RaO decreased markedly from 0–180 min after meal ingestion, consistent with exenatide's action to delay gastric emptying. Conclusions: Exenatide improves 1) fasting hyperglycemia by reducing basal EGP and 2) postmeal hyperglycemia by reducing the appearance of oral glucose in the systemic circulation.

Influence of somatostatin on glucagon- and epinephrine-stimulated hepatic glucose output in the dog.

1979 ◽  
Vol 236 (2) ◽  
pp. E113
Author(s):  
L Saccà ◽  
R Sherwin ◽  
P Felig
Keyword(s):  
Plasma Glucose ◽  
Glucose Production ◽  
Conscious Dogs ◽  
Insulin Deficiency ◽  
Hepatic Glucose Output ◽  
Glucose Kinetics ◽  
Insulin Levels ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
Insulin Replacement

Glucose kinetics were measured using [3-3H]glucose in conscious dogs during the infusion of: 1) glucagon alone; 2) glucagon plus somatostatin with insulin replacement; 3) epinephrine alone; and 4) epinephrine plus somatostatin with insulin and glucagon replacement. Infusion of glucagon alone resulted in a 10-15 mg/dl rise in plasma glucose and a transient 45% rise in glucose production. When somatostatin and insulin were added, a four- to fivefold greater rise in plasma glucose and glucose production was observed. Glucagon levels were comparable to those achieved with infusion of glucagon alone, whereas peripheral insulin levels increased three- to fourfold above baseline, suggesting adequate replacement of preinfusion portal insulin levels. Infusion of epinephrine alone produced a 40% rise in plasma glucose and a 100% rise in glucose production. When somatostatin, insulin, and glucagon were added to epinephrine, the rise in glucose production was reduced in 65% despite replacement of glucagon levels and presumably mild portal insulin deficiency. These findings suggest that somatostatin: 1) potentiates the stimulatory effect of physiologic hyperglucagonemia on glucose production independent of insulin availability and 2) blunts the stimulatory effect of physiologic increments of epinephrine independent of glucagon availability.

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