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

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.

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Effect of carbohydrate ingestion on glycogen resynthesis in human liver and skeletal muscle, measured by 13C MRS

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.2000.278.1.e65 ◽

2000 ◽

Vol 278 (1) ◽

pp. E65-E75 ◽

Cited By ~ 65

Author(s):

Anna Casey ◽

Rob Mann ◽

Katie Banister ◽

John Fox ◽

Peter G. Morris ◽

...

Keyword(s):

Exercise Capacity ◽

Muscle Glycogen ◽

Glycogen Content ◽

Liver Glycogen ◽

Placebo Control ◽

Resonance Spectroscopy ◽

Carbohydrate Ingestion ◽

Glycogen Resynthesis ◽

Liver Glycogen Content ◽

Significant Difference

This study investigated the effect of carbohydrate (CHO) ingestion on postexercise glycogen resynthesis, measured simultaneously in liver and muscle ( n = 6) by 13C magnetic resonance spectroscopy, and subsequent exercise capacity ( n = 10). Subjects cycled at 70% maximal oxygen uptake for 83 ± 8 min on six separate occasions. At the end of exercise, subjects ingested 1 g/kg body mass (BM) glucose, sucrose, or placebo (control). Resynthesis of glycogen over a 4-h period after treatment ingestion was measured on the first three occasions, and subsequent exercise capacity was measured on occasions four through six. No glycogen was resynthesized during the control trial. Liver glycogen resynthesis was evident after glucose (13 ± 8 g) and sucrose (25 ± 5 g) ingestion, both of which were different from control ( P < 0.01). No significant differences in muscle glycogen resynthesis were found among trials. A relationship between the CHO load (g) and change in liver glycogen content (g) was evident after 30, 90, 150, and 210 min of recovery ( r = 0.59–0.79, P< 0.05). Furthermore, a modest relationship existed between change in liver glycogen content (g) and subsequent exercise capacity ( r= 0.53, P < 0.05). However, no significant difference in mean exercise time was found (control: 35 ± 5, glucose: 40 ± 5, and sucrose: 46 ± 6 min). Therefore, 1 g/kg BM glucose or sucrose is sufficient to initiate postexercise liver glycogen resynthesis, which contributes to subsequent exercise capacity, but not muscle glycogen resynthesis.

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Contribution of net hepatic glycogenolysis to glucose production during the early postprandial period

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1996.270.1.e186 ◽

1996 ◽

Vol 270 (1) ◽

pp. E186-E191 ◽

Cited By ~ 23

Author(s):

K. F. Petersen ◽

T. Price ◽

G. W. Cline ◽

D. L. Rothman ◽

G. I. Shulman

Keyword(s):

Magnetic Resonance ◽

Glycogen Content ◽

Hepatic Glucose Production ◽

Liver Volume ◽

Glucose Production ◽

Liver Glycogen ◽

Whole Body ◽

Hepatic Glycogen ◽

Resonance Spectroscopy ◽

13C Nuclear Magnetic Resonance

Relative contributions of net hepatic glycogenolysis and gluconeogenesis to glucose production during the first 12 h of a fast were studied in 13 healthy volunteers by noninvasively measuring hepatic glycogen content using 13C nuclear magnetic resonance spectroscopy. Rates of net hepatic glycogenolysis were calculated by multiplying the change in liver glycogen content with liver volume determined by magnetic resonance imaging. Rates of gluconeogenesis were calculated as the difference between rates of glucose production determined with an infusion of [6,6-2H]-glucose and net hepatic glycogenolysis. At 6 P.M. a liquid mixed meal (1,000 kcal; 60% as glucose) was given, to which [2-2H]glucose was added to trace glucose absorption. Hepatic glycogen content was measured between 11 P.M. and 1 A.M. and between 3 and 6 A.M. At 11 P.M. the concentration was 470 mM and it decreased linearly during the night. The mean liver volume was 1.47 +/- 0.06 liters. Net hepatic glycogenolysis (5.8 +/- 0.8 mumol.kg body wt-1.min-1) accounted for, on average, 45 +/- 6% and gluconeogenesis for 55 +/- 6% of the rate of whole body glucose production (12.6 +/- 0.6 mumol.kg body wt-1.min-1). In conclusion, this study shows that, even early in the phase of the postabsorptive period when liver glycogen stores are maximal, gluconeogenesis contributes approximately 50% to hepatic glucose production.

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The Role of Hormones in the Regulation of Glycogen Metabolism in the Clawed Toad Xenopus Laevis (Daudin)

Journal of Obesity and Diabetes ◽

10.33805/2638-812x.112 ◽

2019 ◽

pp. 17-24

Author(s):

Daphna Atar-Zwillenberg ◽

Michael Atar ◽

Gianni Morson ◽

Udo Spornitz

Keyword(s):

Blood Glucose ◽

Xenopus Laevis ◽

Muscle Glycogen ◽

Hormonal Regulation ◽

Glycogen Content ◽

Glycogen Metabolism ◽

Liver Glycogen ◽

Hepatic Glycogen ◽

Lipid Levels ◽

Liver Glycogen Content

The hormonal regulation of amphibian glycogen metabolism was studied in Xenopus laevis as a typical member of the anurans (tailless amphibians).The main focus of this study was given to the effects of various hormones on the glycogen/glucose balance in adult toads. We determined biochemically the liver and muscle glycogen contents as well as the blood glucose and lipid levels for a number of hormones and also diabetes inducing substances. Additionally, we examined ultrastructure changes in hepatocytes induced by the various treatments, and also investigated the activity of carbohydrate-relevant enzymes by histochemistry. With one exception, the liver glycogen content of Xenopus remained basically unchanged by the treatments or was even slightly enhanced. Only human chorionic gonadotropin, through which the vitellogenic response is triggered, prompts a significant decrease of liver glycogen in females. Under the same conditions the male liver glycogen content remained stable. Muscle glycogen contents were not affected by any of the treatments. Blood glucose and lipid levels on the other hand were elevated considerably in both sexes after application of either epinephrine or cortisol. The ultrastructural examination revealed a proliferation of Rough Endoplasmic Reticulum (RER) in hepatocytes from epinephrine treated toads of both sexes as well as from HCG treated females. By histochemistry, we detected an elevated glucose-6-phosphatase activity in the hepatocytes from toads treated with either epinephrine or cortisol. These treatments also led to enhanced glycogen phosphorylase activity in males, and to a slightly elevated glyceraldehyde-3-phosphate dehydrogenase activity in females. Our results show that the hepatic glycogen is extremely stable in adult Xenopus. Only vitellogenesis causes a marked utilization of glycogen. Since the blood glucose levels are elevated in epinephrine or cortisol treated toads without the liver glycogen being affected, we conclude that either protein and/or lipid metabolism are involved in carbohydrate metabolism in Xenopus laevis.

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Ingestion of glucose or sucrose prevents liver but not muscle glycogen depletion during prolonged endurance-type exercise in trained cyclists

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00376.2015 ◽

2015 ◽

Vol 309 (12) ◽

pp. E1032-E1039 ◽

Cited By ~ 38

Author(s):

Javier T. Gonzalez ◽

Cas J. Fuchs ◽

Fiona E. Smith ◽

Pete E. Thelwall ◽

Roy Taylor ◽

...

Keyword(s):

Muscle Glycogen ◽

Liver Glycogen ◽

Whole Body ◽

Peak Power Output ◽

Resonance Spectroscopy ◽

Glycogen Depletion ◽

Carbohydrate Utilization ◽

Glucose Ingestion ◽

Before And After ◽

Effect Of Glucose

The purpose of this study was to define the effect of glucose ingestion compared with sucrose ingestion on liver and muscle glycogen depletion during prolonged endurance-type exercise. Fourteen cyclists completed two 3-h bouts of cycling at 50% of peak power output while ingesting either glucose or sucrose at a rate of 1.7 g/min (102 g/h). Four cyclists performed an additional third test for reference in which only water was consumed. We employed 13C magnetic resonance spectroscopy to determine liver and muscle glycogen concentrations before and after exercise. Expired breath was sampled during exercise to estimate whole body substrate use. After glucose and sucrose ingestion, liver glycogen levels did not show a significant decline after exercise (from 325 ± 168 to 345 ± 205 and 321 ± 177 to 348 ± 170 mmol/l, respectively; P > 0.05), with no differences between treatments. Muscle glycogen concentrations declined (from 101 ± 49 to 60 ± 34 and 114 ± 48 to 67 ± 34 mmol/l, respectively; P < 0.05), with no differences between treatments. Whole body carbohydrate utilization was greater with sucrose (2.03 ± 0.43 g/min) vs. glucose (1.66 ± 0.36 g/min; P < 0.05) ingestion. Both liver (from 454 ± 33 to 283 ± 82 mmol/l; P < 0.05) and muscle (from 111 ± 46 to 67 ± 31 mmol/l; P < 0.01) glycogen concentrations declined during exercise when only water was ingested. Both glucose and sucrose ingestion prevent liver glycogen depletion during prolonged endurance-type exercise. Sucrose ingestion does not preserve liver glycogen concentrations more than glucose ingestion. However, sucrose ingestion does increase whole body carbohydrate utilization compared with glucose ingestion. This trial was registered at https://www.clinicaltrials.gov as NCT02110836.

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Liver and muscle glycogen repletion using 13C magnetic resonance spectroscopy following ingestion of maltodextrin, galactose, protein and amino acids

British Journal Of Nutrition ◽

10.1017/s0007114512005818 ◽

2013 ◽

Vol 110 (5) ◽

pp. 848-855 ◽

Cited By ~ 5

Author(s):

Eva Detko ◽

John P. O'Hara ◽

Peter E. Thelwall ◽

Fiona E. Smith ◽

Djordje G. Jakovljevic ◽

...

Keyword(s):

Amino Acids ◽

Magnetic Resonance ◽

Magnetic Resonance Spectroscopy ◽

Body Mass ◽

Muscle Glycogen ◽

Liver Glycogen ◽

Resonance Spectroscopy ◽

Post Exercise ◽

Glycogen Repletion ◽

Postprandial Insulin

The present study evaluated whether the inclusion of protein (PRO) and amino acids (AA) within a maltodextrin (MD) and galactose (GAL) recovery drink enhanced post-exercise liver and muscle glycogen repletion. A total of seven trained male cyclists completed two trials, separated by 7 d. Each trial involved 2 h of standardised intermittent cycling, followed by 4 h recovery. During recovery, one of two isoenergetic formulations, MD–GAL (0·9 g MD/kg body mass (BM) per h and 0·3 g GAL/kg BM per h) or MD–GAL-PRO+AA (0·5 g MD/kg BM per h, 0·3 g GAL/kg BM per h, 0·4 g whey PRO hydrolysate plus l-leucine and l-phenylalanine/kg BM per h) was ingested at every 30 min. Liver and muscle glycogen were measured after depletion exercise and at the end of recovery using 1H-13C-magnetic resonance spectroscopy. Despite higher postprandial insulin concentations for MD–GAL-PRO+AA compared with MD–GAL (61·3 (se 6·2) v. 29·6 (se 3·0) mU/l, (425·8 (se 43·1) v. 205·6 (se 20·8) pmol/l) P= 0·03), there were no significant differences in post-recovery liver (195·3 (se 2·6) v. 213·8 (se 18·0) mmol/l) or muscle glycogen concentrations (49·7 (se 4·0) v. 51·1 (se 7·9) mmol/l). The rate of muscle glycogen repletion was significantly higher for MD–GAL compared with MD–GAL-PRO+AA (5·8 (se 0·7) v. 3·7 (se 0·6) mmol/l per h, P= 0·04), while there were no significant differences in the rate of liver glycogen repletion (15·0 (se 2·5) v. 13·0 (se 2·7) mmol/l per h). PRO and AA within a MD–GAL recovery drink, compared with an isoenergetic mix of MD–GAL, did not enhance but matched liver and muscle glycogen recovery. This suggests that the increased postprandial insulinaemia only compensated for the lower MD content in the MD–GAL-PRO+AA treatment.

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Food deprivation alters liver glycogen metabolism and endocrine responses to hemorrhage

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1990.259.5.e692 ◽

1990 ◽

Vol 259 (5) ◽

pp. E692-E698 ◽

Cited By ~ 3

Author(s):

O. Ljungqvist ◽

P. O. Boija ◽

H. Esahili ◽

M. Larsson ◽

J. Ware

Keyword(s):

Blood Glucose ◽

Food Deprivation ◽

Glycogen Content ◽

Glycogen Metabolism ◽

Liver Glycogen ◽

Nutritional State ◽

Adrenergic Blockade ◽

Insulin Levels ◽

Liver Glycogen Content ◽

Glycogen Repletion

Liver glycogen content, blood glucose, insulin, glucagon, and epinephrine were determined during 1 h hemorrhagic hypotension at 60 mmHg and 23 h thereafter in fed and two groups of 24-h food-deprived rats receiving either no infusion or 30% glucose intravenously during hemorrhage. Liver glycogen content was reduced by greater than 90% after 24-h food deprivation. Fed and food-deprived rats given glucose developed similar and substantial elevations of blood glucose during hemorrhage, whereas changes in blood glucose were modest in food-deprived rats given no infusion. In fed rats, liver glycogen was reduced by 60% during the 1-h bleed, but within 2 h after hemorrhage repletion of liver glycogen content commenced. By 6 h, approximately 75% of the glycogen lost during hemorrhage had been restored, and 23 h after hemorrhage liver glycogen content was six times greater compared with nonbled controls. Although glycogen levels increased after hemorrhage in food-deprived animals, the increase was negligible compared with that found in fed rats. Infusion of glucose during hemorrhage or adrenergic blockade after hemorrhage did not alter glycogen repletion in food-deprived rats. Posthemorrhage fed animals had high levels of insulin, glucagon, and epinephrine during hemorrhage, whereas insulin levels remained low in food-deprived rats despite exogenously induced hyperglycemia. It is concluded that rapid and substantial glycogen repletion can occur even immediately poststress. The conditions seem to be related to the nutritional state at the time of the insult.

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The effect of fasting on the glycogen metabolism in heat-acclimated rats

Archives of Biological Sciences ◽

10.2298/abs0801049m ◽

2008 ◽

Vol 60 (1) ◽

pp. 49-58 ◽

Cited By ~ 1

Author(s):

Biljana Miova ◽

Suzana Dinevska-Kjovkarevska ◽

S. Mitev ◽

Mirsada Dervisevic

Keyword(s):

Phosphatase Activity ◽

Muscle Glycogen ◽

Glycogen Phosphorylase ◽

Room Temperature ◽

Glycogen Content ◽

Muscle Metabolism ◽

Glycogen Metabolism ◽

Liver Glycogen ◽

Short Term ◽

Liver Glycogen Content

We investigated the influence of successive fasting for 24,48,72, and 96 h on some key enzymes and substrates of liver, kidney, and muscle in control and heat-acclimated (30days at 35 ? 1?C)rats. Short-term fasting (for 24 and 48 h)resulted in decrease of liver glycogen content, blood glucose level, and concentration of glucose-6-phosphate, as well as increase of glucose-6-phosphatase activity, regardless of the previous temperature of acclimation. During a period of prolonged fasting (for 72 and 96 h),there was a rebound of liver glycogen content only in animals kept at room temperature. Fasting induced increase of renal glycogen content in animals kept at room temperature and increase of renal glucose-6-phosphatase activity in both experimental groups. As for muscle metabolism, endogenous nutrition resulted in decrease of muscle glycogen content in heat-acclimated animals. Activity of muscle glycogen phosphorylase (a+b)was decreased in the control and increased in heat-acclimated animals. The obtained results indicate that the examined carbohydrate-related parameters show time-dependent changes during 4 days of fasting. Twenty-four- and 48-h fasting intensifies glycogenolytic processes, while 72- and 96-h fasting intensifies gluconeogenic processes, doing so to a lesser extent in heat-acclimated animals. The changes caused by the fasting were modified by acclimation to moderate heat, primarily in the liver and to a lesser extent in the kidney and muscle.

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Hypothalamic HSP10 Impacts Mitochondrial Dynamics, Insulin Signaling, and Liver Glycogen Content

Diabetes ◽

10.2337/db18-1801-p ◽

2018 ◽

Vol 67 (Supplement 1) ◽

pp. 1801-P

Author(s):

KRISTINA WARDELMANN ◽

JOSÉ PEDRO CASTRO ◽

MICHAELA RATH ◽

JÜRGEN WEIß ◽

ANNETTE SCHUERMANN ◽

...

Keyword(s):

Insulin Signaling ◽

Glycogen Content ◽

Mitochondrial Dynamics ◽

Liver Glycogen ◽

Liver Glycogen Content

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BIOCHEMICAL STUDIES ON SOCKEYE SALMON DURING SPAWNING MIGRATION: XII. LIVER GLYCOGEN

Canadian Journal of Biochemistry and Physiology ◽

10.1139/y60-067 ◽

1960 ◽

Vol 38 (1) ◽

pp. 553-558 ◽

Cited By ~ 4

Author(s):

Violet M. Chang ◽

D. R. Idler

Keyword(s):

Sex Differences ◽

Sockeye Salmon ◽

Glycogen Content ◽

Steroid Hormone ◽

Liver Glycogen ◽

Spawning Migration ◽

Energy Expenditures ◽

Liver Glycogen Content ◽

Biochemical Studies ◽

River Migration

Liver glycogen levels were determined for a pure stock of sockeye salmon (Oncorhynchus nerka) taken at three locations during spawning migration. The liver glycogen content of the male was found to be consistently greater than that of the female throughout the entire river migration. In both sexes liver glycogen decreased during the earlier phase of migration, but increased during the later stage so that the levels at the spawning grounds were approximately twice those at the mouth of the river. The changes which occur are discussed in relation to sex differences, energy expenditures, and plasma steroid hormone levels.

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Liver glycogen-induced enhancements in hypoglycemic counterregulation require neuroglucopenia.

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00501.2020 ◽

2021 ◽

Author(s):

Shana O Warner ◽

Abby M Wadian ◽

Marta S. Smith ◽

Ben Farmer ◽

Yufei Dai ◽

...

Keyword(s):

Glycogen Content ◽

Hormone Secretion ◽

Control Period ◽

Liver Glycogen ◽

Saline Infusion ◽

Glucose Levels ◽

Liver Glycogen Content ◽

Patients With Diabetes ◽

Arterial Plasma ◽

The Brain

Iatrogenic hypoglycemia is a prominent barrier to achieving optimal glycemic control in patients with diabetes, in part due to dampened counterregulatory hormone responses. It has been demonstrated that elevated liver glycogen content can enhance these hormonal responses through signaling to the brain via afferent nerves, but the role that hypoglycemia in the brain plays in this liver glycogen effect remains unclear. During the first 4hrs of each study, the liver glycogen content of dogs was increased by using an intraportal infusion of fructose to stimulate hepatic glucose uptake (HG; n=13), or glycogen was maintained near fasting levels with a saline infusion (NG; n=6). After a 2hr control period, during which the fructose/saline infusion was discontinued, insulin was infused intravenously for an additional 2hrs to bring about systemic hypoglycemia in all animals, whereas brain euglycemia was maintained in a subset of the HG group by infusing glucose bilaterally into the carotid and vertebral arteries (HG-HeadEu; n=7). Liver glycogen content was markedly elevated in the two HG groups (43±4, 73±3 and 75±7 mg/g in NG, HG and HG-HeadEu, respectively). During the hypoglycemic period, arterial plasma glucose levels were indistinguishable between groups (53±2, 52±1 and 51±1 mg/dL, respectively), but jugular vein glucose levels were kept euglycemic (88±5 mg/dL) only in the HG-HeadEu group. Glucagon and epinephrine responses to hypoglycemia were higher in HG compared to NG, whereas despite the increase in liver glycogen, neither increased above basal in HG-HeadEu. These data demonstrate that the enhanced counterregulatory hormone secretion that accompanies increased liver glycogen content requires hypoglycemia in the brain.

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