Splanchnic glucose and muscle glycogen metabolism after glucose feeding during postexercise recovery.

1978 ◽  
Vol 235 (3) ◽  
pp. E255 ◽  
Author(s):  
S Maehlum ◽  
P Felig ◽  
J Wahren
Keyword(s):  
Muscle Glycogen ◽  
Work Load ◽  
Hepatic Glycogen ◽  
Oral Glucose ◽  
Glycogen Concentration ◽  
Glucose Feeding ◽  
Glucose Ingestion ◽  
In Series ◽  
Postexercise Recovery ◽  
Glucose Output

Glucose (100 g) was ingested 15 min after bicycle exercise until exhaustion at a work load corresponding to 70% of maximal uptake (series 1), 14--15 h after an identical exercise period, no food being taken in the interval (series 2), and by nonexercised control subjects. Splanchnic glucose output in the exercised groups rose to values 50--300% greater than in controls, amounting to (over 135 min) 59 +/- 5 g in series 1 and 58 +/- 6 in series 2 compared to 28 +/- 6 in controls. The glycogen concentration of quadriceps muscle in series 1 was 65 +/- 2 mmol glycosyl U/kg wet wt before exercise, 16 +/- 13 at the end of work, and 32 +/- 4 at 135 min after glucose ingestion. In series 2, muscle glycogen concentration was 20 +/- 3 immediately after exercise and rose to 44 +/- 5 over the ensuing 14--15 h in spite of continued fasting. It rose to 56 +/- 3 at 135 min after glucose loading. Repletion of leg muscle glycogen after glucose feeding could account for 50--66% of total splanchnic glucose release. It is concluded that during postexercise recovery, a greater proportion of an oral glucose load escapes hepatic retention, allowing repletion of muscle glycogen to take precedence over hepatic glycogen repletion.

Effect of prior exercise on glucose metabolism in trained men

2001 ◽  
Vol 281 (4) ◽  
pp. E766-E771 ◽  
Author(s):  
Adam J. Rose ◽  
Kirsten Howlett ◽  
Douglas S. King ◽  
Mark Hargreaves
Keyword(s):  
Tolerance Test ◽  
Whole Body ◽  
Oral Glucose ◽  
Glucose Response ◽  
Prior Exercise ◽  
Glucose Ingestion ◽  
Main Effect ◽  
Glucose Output ◽  
Insulin Responses ◽  
G Tolerance

Several studies have demonstrated that oral glucose tolerance is impaired in the immediate postexercise period. A double-tracer technique was used to examine glucose kinetics during a 2-h oral glucose (75 g) tolerance test (OGTT) 30 min after exercise (Ex, 55 min at 71 ± 2% of peak O2 uptake) and 24 h after exercise (Rest) in endurance-trained men. The area under the plasma glucose curve was 71% greater in Ex than in Rest ( P = 0.01). The higher glucose response occurred even though whole body rate of glucose disappearance was 24% higher after exercise ( P = 0.04, main effect). Whole body rate of glucose appearance was 25% higher after exercise ( P = 0.03, main effect). There were no differences in total (2 h) endogenous glucose appearance (Ra e) or the magnitude of suppression of Ra e, although Ra e was higher from 15 to 30 min during the OGTT in Ex. However, the cumulative appearance of oral glucose was 30% higher in Ex ( P = 0.03, main effect). There were no differences in glucose clearance rate or plasma insulin responses between the two conditions. These results suggest that adaptations in splanchnic tissues by prior exercise facilitate greater glucose output from the splanchnic region after glucose ingestion, resulting in a greater glycemic response and, consequently, a greater rate of whole body glucose uptake.

Reduction in Muscle Glycogen and Protein Utilization with Glucose Feeding during Exercise

2005 ◽  
Vol 15 (4) ◽  
pp. 350-365 ◽  
Author(s):  
Dennis van Hamont ◽  
Christopher R. Harvey ◽  
Denis Massicotte ◽  
Russell Frew ◽  
François Peronnet ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Indirect Calorimetry ◽  
Muscle Glycogen ◽  
Protein Oxidation ◽  
Glucose Oxidation ◽  
Protein Utilization ◽  
Warm Up ◽  
Glucose Feeding ◽  
Endogenous Protein ◽  
Glucose Ingestion

Effects of feeding glucose on substrate metabolism during cycling were studied. Trained (60.0 ± 1.9 mL · kg−1 · min−1) males (N = 5) completed two 75 min, 80% VO2max trials: 125 g 13C-glucose (CHO); 13C-glucose tracer, 10 g (C). During warm-up (30 min 30% VO2max) 2 ⋅ 2 g 13C-glucose was given as bicarbonate pool primer. Breath samples and blood glucose were analyzed for 13C/ 12C with IRMS. Protein oxidation was estimated from urine and sweat urea. Indirect calorimetry (protein corrected) and 13C/ 12C enrichment in expired CO2 and blood glucose allowed exogenous (Gexo), endogenous (Gendo), muscle (Gmuscle), and liver glucose oxidation calculations. During exercise (75 min) in CHO versus C (respectively): protein oxidation was lower (6.8 ± 2.7, 18.8 ± 5.9 g; P = 0.01); Gendo was reduced (71.2 ± 3.8, 80.7 ± 5.7%; P = 0.01); Gmuscle was reduced (55.3 ± 6.1, 65.9 ± 6.0%; P = 0.01) compensated by increased Gexo (58.3 ± 2.1, 3.87 ± 0.85 g; P = 0.000002). Glucose ingestion during exercise can spare endogenous protein and carbohydrate, in fed cyclists, without gly-cogen depletion.

scholarly journals Effects of glucose ingestion at different frequencies on glycogen recovery in mice during the early hours post exercise

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Yutaka Matsunaga ◽  
Kenya Takahashi ◽  
Yumiko Takahashi ◽  
Hideo Hatta
Keyword(s):  
Muscle Glycogen ◽  
Blood Glucose Concentration ◽  
Liver Glycogen ◽  
Glycogen Storage ◽  
Carbohydrate Intake ◽  
Treadmill Running ◽  
Plasma Insulin Concentration ◽  
Post Exercise ◽  
Glycogen Concentration ◽  
Glucose Ingestion

Abstract Background When a high-carbohydrate diet is ingested, whether as small frequent snacks or as large meals, there is no difference between the two with respect to post-exercise glycogen storage for a period of 24 h. However, the effect of carbohydrate intake frequency on glycogen recovery a few hours after exercise is not clear. Athletes need to recover glycogen quickly after physical exercise as they sometimes exercise multiple times a day. The aim of this study was to determine the effect of carbohydrate intake at different frequencies on glycogen recovery during the first few hours after exercise. Methods After 120 min of fasting, 6-week-old male ICR mice were subjected to treadmill running exercise (20 m/min for 60 min) to decrease the levels of muscle and liver glycogen. Mice were then given glucose as a bolus (1.2 mg/g of body weight [BW], immediately after exercise) or as a pulse (1.2 mg/g of BW, every 15 min × 4 times). Following this, the blood, tissue, and exhaled gas samples were collected. Results In the bolus group, blood glucose concentration was significantly lower and plasma insulin concentration was significantly higher than those in the pulse group (p < 0.05). The plantaris muscle glycogen concentration in the bolus group was 25.3% higher than that in the pulse group at 60 min after glucose ingestion (p < 0.05). Liver glycogen concentration in the pulse group was significantly higher than that in the bolus group at 120 min after glucose ingestion (p < 0.05). Conclusions The present study showed that ingesting a large amount of glucose immediately after exercise increased insulin secretion and enhanced muscle glycogen recovery, whereas frequent and small amounts of glucose intake was shown to enhance liver glycogen recovery.

scholarly journals Sucrose ingestion after exhaustive exercise accelerates liver, but not muscle glycogen repletion compared with glucose ingestion in trained athletes

2016 ◽  
Vol 120 (11) ◽  
pp. 1328-1334 ◽  
Author(s):  
Cas J. Fuchs ◽  
Javier T. Gonzalez ◽  
Milou Beelen ◽  
Naomi M. Cermak ◽  
Fiona E. Smith ◽  
...  
Keyword(s):  
Muscle Glycogen ◽  
Glycogen Content ◽  
Liver Volume ◽  
Liver Glycogen ◽  
Resonance Spectroscopy ◽  
Time Treatment ◽  
Liver Glycogen Content ◽  
Glucose Ingestion ◽  
Postexercise Recovery ◽  
Glycogen Repletion

The purpose of this study was to assess the effects of sucrose vs. glucose ingestion on postexercise liver and muscle glycogen repletion. Fifteen well-trained male cyclists completed two test days. Each test day started with glycogen-depleting exercise, followed by 5 h of recovery, during which subjects ingested 1.5 g·kg−1·h−1 sucrose or glucose. Blood was sampled frequently and 13C magnetic resonance spectroscopy and imaging were employed 0, 120, and 300 min postexercise to determine liver and muscle glycogen concentrations and liver volume. Results were as follows: Postexercise muscle glycogen concentrations increased significantly from 85 ± 27 (SD) vs. 86 ± 35 mmol/l to 140 ± 23 vs. 136 ± 26 mmol/l following sucrose and glucose ingestion, respectively (no differences between treatments: P = 0.673). Postexercise liver glycogen concentrations increased significantly from 183 ± 47 vs. 167 ± 65 mmol/l to 280 ± 72 vs. 234 ± 81 mmol/l following sucrose and glucose ingestion, respectively (time × treatment, P = 0.051). Liver volume increased significantly over the 300-min period after sucrose ingestion only (time × treatment, P = 0.001). As a result, total liver glycogen content increased during postexercise recovery to a greater extent in the sucrose treatment (from 53.6 ± 16.2 to 86.8 ± 29.0 g) compared with the glucose treatment (49.3 ± 25.5 to 65.7 ± 27.1 g; time × treatment, P < 0.001), equating to a 3.4 g/h (95% confidence interval: 1.6-5.1 g/h) greater repletion rate with sucrose vs. glucose ingestion. In conclusion, sucrose ingestion (1.5 g·kg−1·h−1) further accelerates postexercise liver, but not muscle glycogen repletion compared with glucose ingestion in trained athletes.

Low muscle glycogen concentration does not suppress the anabolic response to resistance exercise

2012 ◽  
Vol 113 (2) ◽  
pp. 206-214 ◽  
Author(s):  
Donny M. Camera ◽  
Daniel W. D. West ◽  
Nicholas A. Burd ◽  
Stuart M. Phillips ◽  
Andrew P. Garnham ◽  
...  
Keyword(s):  
Resistance Exercise ◽  
Muscle Glycogen ◽  
Vastus Lateralis ◽  
Recovery Period ◽  
Peak Oxygen Uptake ◽  
Constant Infusion ◽  
Glycogen Depletion ◽  
Glycogen Concentration ◽  
Postexercise Recovery ◽  
Muscle Glycogen Concentration

We determined the effect of muscle glycogen concentration and postexercise nutrition on anabolic signaling and rates of myofibrillar protein synthesis after resistance exercise (REX). Sixteen young, healthy men matched for age, body mass, peak oxygen uptake (V̇o2peak) and strength (one repetition maximum; 1RM) were randomly assigned to either a nutrient or placebo group. After 48 h diet and exercise control, subjects undertook a glycogen-depletion protocol consisting of one-leg cycling to fatigue (LOW), whereas the other leg rested (NORM). The next morning following an overnight fast, a primed, constant infusion of l-[ ring-13C6] phenylalanine was commenced and subjects completed 8 sets of 5 unilateral leg press repetitions at 80% 1RM. Immediately after REX and 2 h later, subjects consumed a 500 ml bolus of a protein/CHO (20 g whey + 40 g maltodextrin) or placebo beverage. Muscle biopsies from the vastus lateralis of both legs were taken at rest and 1 and 4 h after REX. Muscle glycogen concentration was higher in the NORM than LOW at all time points in both nutrient and placebo groups ( P < 0.05). Postexercise Akt-p70S6K-rpS6 phosphorylation increased in both groups with no differences between legs ( P < 0.05). mTORSer2448 phosphorylation in placebo increased 1 h after exercise in NORM ( P < 0.05), whereas mTOR increased ∼4-fold in LOW ( P < 0.01) and ∼11 fold in NORM with nutrient ( P < 0.01; different between legs P < 0.05). Post-exercise rates of MPS were not different between NORM and LOW in nutrient (0.070 ± 0.022 vs. 0.068 ± 0.018 %/h) or placebo (0.045 ± 0.021 vs. 0.049 ± 0.017 %/h). We conclude that commencing high-intensity REX with low muscle glycogen availability does not compromise the anabolic signal and subsequent rates of MPS, at least during the early (4 h) postexercise recovery period.

Mechanisms of starvation diabetes: a study with double tracer and indirect calorimetry

1990 ◽  
Vol 259 (6) ◽  
pp. E770-E777 ◽  
Author(s):  
F. Fery ◽  
N. P. d'Attellis ◽  
E. O. Balasse
Keyword(s):  
Glucose Metabolism ◽  
Glucose Intolerance ◽  
Indirect Calorimetry ◽  
Normal Subjects ◽  
Systemic Circulation ◽  
Oral Glucose ◽  
Glucose Ingestion ◽  
Before And After ◽  
Total Glucose ◽  
Glucose Output

To analyze the mechanisms of fasting-induced glucose intolerance, glucose metabolism was studied before and after the ingestion of 75 g glucose in 24 normal subjects fasted for either 14 h (n = 12) or 4 days (n = 12). The techniques included intravenous infusion of [6-3H]glucose and oral administration of [1-14C]glucose combined with indirect calorimetry. Compared with the controls, the starved subjects exhibited the following differences in glucose metabolism during the 5 h after glucose ingestion. 1) Mean incremental levels were fourfold higher for glucose and 40% higher for insulin. 2) Absorption of oral glucose was delayed and prolonged, but total amount reaching systemic circulation in 5 h was identical in the two groups (approximately 63 g). 3) Suppression of hepatic glucose output was reduced (-12 +/- 1 vs. -22 +/- 2 g). 4) Consequently, the increment in peripheral appearance of total glucose (exogenous plus endogenous) was augmented (+ 52 +/- 2 vs. +41 +/- 2 g). 5) Mean glucose clearance increased significantly less (+28 +/- 7 vs. +96 +/- 10 ml/min). 6) Oxidation of oral glucose was reduced (9 +/- 2 vs. 36 +/- 3 g), and nonoxidative disposal (presumably storage) was enhanced (56 +/- 2 vs. 36 +/- 3 g) in the presence of an elevated fat oxidation (35 +/- 2 vs. 22 +/- 4 g). Thus the alterations in glucose homeostasis responsible for the starvation-induced glucose intolerance are located both at the splanchnic (hepatic) and peripheral levels.

Early glycogenolysis and late glycogenesis in human liver after intravenous administration of galactose

1996 ◽  
Vol 270 (1) ◽  
pp. G14-G19 ◽  
Author(s):  
R. Fried ◽  
N. Beckmann ◽  
U. Keller ◽  
R. Ninnis ◽  
G. Stalder ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Competitive Inhibition ◽  
Glycogen Synthesis ◽  
Liver Volume ◽  
Hepatic Glycogen ◽  
Resonance Spectroscopy ◽  
Hepatic Glucose Output ◽  
Glycogen Concentration ◽  
Hepatic Glucose ◽  
Glucose Output

Galactose is incorporated by a different metabolic pathway than glucose. Its contribution to glycogen synthesis has not been studied in humans. We administered galactose (0.5 g/kg iv) to overnight-fasted normal human volunteers and examined its effects on hepatic glycogen synthesis and hepatic glucose output (HGO). Hepatic glycogenesis was assessed noninvasively, determining glycogen concentration by 13C magnetic resonance spectroscopy (MRS) and liver volume by magnetic resonance imaging. HGO was determined by [6,6-2H2]glucose and gluconeogenesis calculated by adding the amount of hepatic glycogenesis to the HGO. After galactose administration, liver glycogen concentration (baseline 254 +/- 11 mmol/l) decreased in the first 45 min to 207 +/- 15 mmol/l (P < 0.05) and increased thereafter to 313 +/- 7 mmol/l (P < 0.01). Net hepatic glycogenesis was 101 +/- 12 mmol over 150 min. HGO (baseline 14.3 +/- 1.9 mumol.kg-1.min-1) increased threefold in the first 15 min and then returned to baseline. The average rate of gluconeogenesis was 12.3 mumol.kg-1.min-1. Intravenous galactose leads to an increase in hepatic glycogen and hepatic glucose output in normal humans. Competitive inhibition of UDP-glucose pyrophosphorylase by UDP-galactose could explain the apparent glycogenolysis observed early after galactose administration. 13C MRS in combination with a stable isotope tracer is a noninvasive and safe method to study hepatic carbohydrate metabolism in humans.

Metabolic effects of oral glucose in the liver of fasted rats

1984 ◽  
Vol 246 (1) ◽  
pp. E89-E94 ◽  
Author(s):  
C. B. Niewoehner ◽  
D. P. Gilboe ◽  
F. Q. Nuttall
Keyword(s):  
Plasma Glucose ◽  
Glycogen Synthase ◽  
Lactate Production ◽  
Glucose Absorption ◽  
Metabolic Effects ◽  
Hepatic Glycogen ◽  
Oral Glucose ◽  
Glucose Ingestion ◽  
Total Glucose ◽  
Fasted Rats

Twenty-four-hour-fasted rats were given glucose (4 g/kg) by gavage. Glucose absorption and portal and peripheral plasma glucose, lactate, and insulin concentrations, as well as liver glucose, UDPglucose, glucose-6-P, lactate, ATP, and inorganic phosphate (Pi), and % glycogen synthase I and % phosphorylase a were measured at 10, 20, 30, 40, 60, and 120 min after the glucose was given. Liver and muscle glycogen also were measured. Ninety-one percent of the glucose load had disappeared from the gut in 2 h. Despite increased plasma glucose and insulin levels the liver continued to produce glucose. Lactate produced in the periphery was the major substrate for gluconeogenesis, and lactate utilization could account for the hepatic glycogen synthesized. Glucose ingestion did not affect lactate production by the splanchnic bed. In the liver glucose-6-P was transiently increased; UDP glucose decreased after glucose administration. ATP and Pi were unchanged. Glycogen synthase was activated by 20 min without a significant change in phosphorylase a. Hepatic glycogen increased linearly after 20 min. Total glucose storage as glycogen was similar in liver (20%) and muscle (19%). We could account for 41% of the glucose absorbed as glycogen, unmetabolized glucose, or glucose metabolites. Most of the remainder probably was oxidized.

NEONATAL ISLET CELL TRANSPLANTATION IN THE DIABETIC RAT: EFFECT ON HEPATIC ENZYME ACTIVITY AND GLUCOSE HOMEOSTASIS

1977 ◽  
Vol 74 (2) ◽  
pp. 231-241 ◽  
Author(s):  
YVONNE MANGNALL ◽  
ANNE SMYTHE ◽  
D. N. SLATER ◽  
GILLIAN R. MILNER ◽  
R. D. G. MILNER ◽  
...  
Keyword(s):  
Diabetic Animal ◽  
Pancreatic Tissue ◽  
Diabetic Rats ◽  
Neonatal Rat ◽  
Diabetic Rat ◽  
Immunoreactive Insulin ◽  
Hepatic Glycogen ◽  
Islet Cell Transplantation ◽  
Glycogen Concentration ◽  
Serum Immunoreactive Insulin

Intraperitoneal transplantation of collagenase-digested, isogeneic, neonatal rat pancreatic tissue successfully reversed streptozotocin-induced diabetes in 77% of recipients. The low serum immunoreactive insulin, hyperglycaemia, glycosuria and weight loss, characteristic of the diabetic animal, were corrected and the reduced activities of hepatic glucokinase and pyruvate kinase, and the low glycogen concentration of the liver of diabetic rats were restored to normal. Forty-three per cent of the successfully transplanted rats became normoglycaemic within 1 month of transplantation whereas 57% took from 1 to 6 months to achieve normoglycaemia and displayed a mild glucose intolerance when subjected to a glucose load. The rats which had not become normoglycaemic 6 months after transplantation showed some amelioration of the diabetic state, as shown by increased serum immunoreactive insulin and hepatic glycogen concentration and a slow weight gain compared with diabetic controls.

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