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

2015 ◽  
Vol 309 (12) ◽  
pp. E1032-E1039 ◽  
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.

Mechanism of muscle glycogen autoregulation in humans

2000 ◽  
Vol 278 (4) ◽  
pp. E663-E668 ◽  
Author(s):  
Didier Laurent ◽  
Ripudaman S. Hundal ◽  
Alan Dresner ◽  
Thomas B. Price ◽  
Suzanne M. Vogel ◽  
...  
Keyword(s):  
Muscle Glycogen ◽  
Feedback Inhibition ◽  
Glycogen Synthase ◽  
Glycogen Synthesis ◽  
Plasma Free Fatty Acid ◽  
Whole Body ◽  
Resonance Spectroscopy ◽  
Twofold Increase ◽  
Oxidation Rates ◽  
Before And After

To examine the mechanism by which muscle glycogen limits its own synthesis, muscle glycogen and glucose 6-phosphate (G-6- P) concentrations were measured in seven healthy volunteers during a euglycemic (∼5.5 mM)-hyperinsulinemic (∼450 pM) clamp using 13C/31P nuclear magnetic resonance spectroscopy before and after a muscle glycogen loading protocol. Rates of glycogen synthase ( V syn) and phosphorylase ( V phos) flux were estimated during a [1-13C]glucose (pulse)-unlabeled glucose (chase) infusion. The muscle glycogen loading protocol resulted in a 65% increase in muscle glycogen content that was associated with a twofold increase in fasting plasma lactate concentrations ( P < 0.05 vs. basal) and an ∼30% decrease in plasma free fatty acid concentrations ( P < 0.001 vs. basal). Muscle glycogen loading resulted in an ∼30% decrease in the insulin-stimulated rate of net muscle glycogen synthesis ( P < 0.05 vs. basal), which was associated with a twofold increase in intramuscular G-6- P concentration ( P < 0.05 vs. basal). Muscle glycogen loading also resulted in an ∼30% increase in whole body glucose oxidation rates ( P < 0.05 vs. basal), whereas there was no effect on insulin-stimulated rates of whole body glucose uptake (∼10.5 mg ⋅ kg body wt−1 ⋅ min−1 for both clamps) or glycogen turnover ( V syn/ V phos was ∼23% for both clamps). In conclusion, these data are consistent with the hypothesis that glycogen limits its own synthesis through feedback inhibition of glycogen synthase activity, as reflected by an accumulation of intramuscular G-6- P, which is then shunted into aerobic and anaerobic glycolysis.

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.

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

1996 ◽  
Vol 270 (1) ◽  
pp. E186-E191 ◽  
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.

Glycogen resynthesis in leg muscles of rats during exercise

1984 ◽  
Vol 247 (5) ◽  
pp. R880-R883 ◽  
Author(s):  
S. H. Constable ◽  
J. C. Young ◽  
M. Higuchi ◽  
J. O. Holloszy
Keyword(s):  
Muscle Glycogen ◽  
Prolonged Exercise ◽  
Liver Glycogen ◽  
Treadmill Running ◽  
Moderate Intensity ◽  
Glycogen Depletion ◽  
Moderate Intensity Exercise ◽  
Glycogen Resynthesis ◽  
Leg Muscles ◽  
Insulin In Plasma

This study was undertaken to determine whether glycogen resynthesis can occur in glycogen-depleted muscles in response to glucose feeding during prolonged exercise. Rats were exercised for 40 min with a treadmill running program designed to deplete muscle glycogen. One group was studied immediately after the glycogen-depletion exercise. A second group was given 1 g glucose by stomach tube and exercised for an additional 90 min at a running speed of 22 m/min on a treadmill set at an 8 degree incline; they were given additional 1-g glucose feedings after 30 and 60 min of running. The initial 40-min run resulted in liver glycogen depletion, large decreases in plasma glucose and insulin concentrations, and a marked lowering of muscle glycogen. The glucose feedings resulted in greater than twofold increases in the concentrations of glucose and insulin in plasma, and of glycogen in leg muscles, during the 90 min of running. No repletion of liver glycogen occurred. These results provide evidence that glycogen resynthesis can occur in glycogen-depleted muscle despite continued moderate intensity exercise if sufficient glucose is made available.

The Effect Of Glucose Ingestion On Muscle Glycogen Oxidation During Exercise In Males And Females

2005 ◽  
Vol 37 (Supplement) ◽  
pp. S306
Author(s):  
Gareth A. Wallis ◽  
Ruth Dawson ◽  
Juul Achten ◽  
Asker E. Jeukendrup
Keyword(s):  
Muscle Glycogen ◽  
Glucose Ingestion ◽  
Males And Females ◽  
Effect Of Glucose

scholarly journals Inhibition of lipolysis in Type 2 diabetes normalizes glucose disposal without change in muscle glycogen synthesis rates

2011 ◽  
Vol 121 (4) ◽  
pp. 169-177 ◽  
Author(s):  
Ee L. Lim ◽  
Kieren G. Hollingsworth ◽  
Fiona E. Smith ◽  
Peter E. Thelwall ◽  
Roy Taylor
Keyword(s):  
Muscle Glycogen ◽  
Glycogen Synthesis ◽  
Diabetic Group ◽  
Whole Body ◽  
Glucose Disposal ◽  
Resonance Spectroscopy ◽  
Turnover Rates ◽  
Atp Turnover ◽  
Glucose Storage

Suppression of lipolysis by acipimox is known to improve insulin-stimulated glucose disposal, and this is an important phenomenon. The mechanism has been assumed to be an enhancement of glucose storage as glycogen, but no direct measurement has tested this concept or its possible relationship to the reported impairment in insulin-stimulated muscle ATP production. Isoglycaemic–hyperinsulinaemic clamps with [13C]glucose infusion were performed on Type 2 diabetic subjects and matched controls with measurement of glycogen synthesis by 13C MRS (magnetic resonance spectroscopy) of muscle. 31P saturation transfer MRS was used to quantify muscle ATP turnover rates. Glucose disposal rates were restored to near normal in diabetic subjects after acipimox (6.2±0.8 compared with 4.8±0.6 mg·kgffm−1·min−1; P<0.01; control 6.6±0.5 mg·kgffm−1·min−1; where ffm, is fat-free mass). The increment in muscle glycogen concentration was 2-fold higher in controls compared with the diabetic group, and acipimox administration to the diabetic group did not increase this (2.0±0.8 compared with 1.9±1.1 mmol/l; P<0.05; control, 4.0±0.8 mmol/l). ATP turnover rates did not increase during insulin stimulation in any group, but a modest decrease in the diabetes group was prevented by lowering plasma NEFAs (non-esterified fatty acids; 8.4±0.7 compared with 7.1±0.5 μmol·g−1·min−1; P<0.05; controls 8.6±0.8 μmol·g−1·min−1). Suppression of lipolysis increases whole-body glucose uptake with no increase in the rate of glucose storage as glycogen but with increase in whole-body glucose oxidation rate. ATP turnover rate in muscle exhibits no relationship to the acute metabolic effect of insulin.

Diurnal variation in skeletal muscle and liver glycogen in humans with normal health and Type 2 diabetes

2015 ◽  
Vol 128 (10) ◽  
pp. 707-713 ◽  
Author(s):  
Mavin Macauley ◽  
Fiona E Smith ◽  
Peter E Thelwall ◽  
Kieren G Hollingsworth ◽  
Roy Taylor
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Liver Glycogen ◽  
Glycogen Storage ◽  
Resonance Spectroscopy ◽  
Model Assessment ◽  
Glycogen Concentration

In health, food carbohydrate is stored as glycogen in muscle and liver, preventing a deleterious rise in osmotically active plasma glucose after eating. Glycogen concentrations increase sequentially after each meal to peak in the evening, and fall to fasting levels thereafter. Skeletal muscle accounts for the larger part of this diurnal buffering capacity with liver also contributing. The effectiveness of this diurnal mechanism has not been previously studied in Type 2 diabetes. We have quantified the changes in muscle and liver glycogen concentration with 13C magnetic resonance spectroscopy at 3.0 T before and after three meals consumed at 4 h intervals. We studied 40 (25 males; 15 females) well-controlled Type 2 diabetes subjects on metformin only (HbA1c (glycated haemoglobin) 6.4±0.07% or 47±0.8 mmol/mol) and 14 (8 males; 6 females) glucose-tolerant controls matched for age, weight and body mass index (BMI). Muscle glycogen concentration increased by 17% after day-long eating in the control group (68.1±4.8 to 79.7±4.2 mmol/l; P=0.006), and this change inversely correlated with homoeostatic model assessment of insulin resistance [HOMA-IR] (r=−0.56; P=0.02). There was no change in muscle glycogen in the Type 2 diabetes group after day-long eating (68.3±2.6 to 67.1±2.0 mmol/mol; P=0.62). Liver glycogen rose similarly in normal control (325.9±25.0 to 388.1±30.3 mmol/l; P=0.005) and Type 2 diabetes groups (296.1±16.0 to 350.5±6.7 mmol/l; P<0.0001). In early Type 2 diabetes, the major physiological mechanism for skeletal muscle postprandial glycogen storage is completely inactive. This is directly related to insulin resistance, although liver glycogen storage is normal.

Influence of fasting on carbohydrate and fat metabolism during rest and exercise in men

1988 ◽  
Vol 64 (5) ◽  
pp. 1923-1929 ◽  
Author(s):  
J. J. Knapik ◽  
C. N. Meredith ◽  
B. H. Jones ◽  
L. Suek ◽  
V. R. Young ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Muscle Glycogen ◽  
Ketone Bodies ◽  
Carbohydrate Oxidation ◽  
Metabolic Effects ◽  
Whole Body ◽  
Time To Exhaustion ◽  
Carbohydrate Utilization ◽  
Insulin Levels ◽  
Glucose Flux

Metabolic effects of an overnight fast (postabsorptive state, PA) or a 3.5-day fast (fasted state, F) were compared in eight healthy young men at rest and during exercise to exhaustion at 45% maximum O2 uptake. Glucose rate of appearance (Ra) and disappearance (Rd) were calculated from plasma glucose enrichment during a primed, continuous infusion of [6,6–2H]glucose. Serum substrates and insulin levels were measured and glycogen content of the vastus lateralis was determined in biopsies taken before and after exercise. At rest, whole-body glucose flux (determined by the deuterated tracer) and carbohydrate oxidation (determined from respiratory exchange ratio) were lower in F than PA, but muscle glycogen levels were similar. During exercise, glucose flux, whole-body carbohydrate oxidation, and the rate of muscle glycogen utilization were significantly lower during the fast. In the PA state, glucose Ra and Rd increased together throughout exercise. However, in the F state Ra exceeded Rd during the 1st h of exercise, causing an increase in plasma glucose to levels similar to those of the PA state. The increase in glucose flux was markedly less throughout F exercise. Lower carbohydrate utilization in the F state was accompanied by higher circulating fatty acids and ketone bodies, lower plasma insulin levels, and the maintenance of physical performance reflected by similar time to exhaustion.

scholarly journals NMR of glycogen in exercise

1999 ◽  
Vol 58 (4) ◽  
pp. 851-859 ◽  
Author(s):  
Thomas B. Price ◽  
Douglas L. Rothman ◽  
Robert G. Shulman
Keyword(s):  
Time Resolution ◽  
Muscle Glycogen ◽  
Time Course ◽  
Glycogen Synthesis ◽  
Liver Glycogen ◽  
Invasive Technique ◽  
Human Populations ◽  
Glycogen Depletion ◽  
Non Invasive ◽  
C Nmr

Natural-abundance 13CNMR spectroscopy is a non-invasive technique that enables in vivo assessments of muscle and/or liver glycogen concentrations. Over the last several years, 13C NMR has been developed and used to obtain information about human glycogen metabolism with diet and exercise. Since NMR is non-invasive, more data points are available over a specified time course, dramatically improving the time resolution. This improved time resolution has enabled the documentation of subtleties of muscle glycogen re-synthesis following severe glycogen depletion that were not previously observed. Muscle and liver glycogen concentrations have been tracked in several different human populations under conditions that include: (1) muscle glycogen recovery from intense localized exercise with normal insulin and with insulin suppressed; (2) muscle glycogen recovery in an insulin-resistant population; (3) muscle glycogen depletion during prolonged low-intensity exercise; (4) effect of a mixed meal on postprandial muscle and liver glycogen synthesis. The present review focuses on basic 13C NMR and gives results from selected studies.

scholarly journals Muscle Glycogenolysis and Resynthesis in Response to a Half Ironman Triathlon: A Case Study

2006 ◽  
Vol 1 (4) ◽  
pp. 408-413 ◽  
Author(s):  
Trevor L. Gillum ◽  
Charles L. Dumke ◽  
Brent C. Ruby
Keyword(s):  
Body Weight ◽  
Energy Expenditure ◽  
Muscle Glycogen ◽  
Vastus Lateralis ◽  
High Rate ◽  
Whole Body ◽  
Glycogen Depletion ◽  
Glycogen Resynthesis ◽  
Wet Weight ◽  
Ironman Triathlon

Purpose:To describe the degrees of muscle-glycogen depletion and resynthesis in response to a half Ironman triathlon.Methods:One male subject (38 years of age) completed the Grand Columbian half Ironman triathlon (1.9-km swim, 90-km bike, 21.1-km run, Coulee City, Wash). Three muscle biopsies were obtained from his right vastus lateralis (prerace, immediately postrace, and 4 hours postrace). Prerace and postrace body weight were recorded, in addition to macronutrient consumption before, during, and after the race. Energy expenditure and whole-body substrate oxidation were estimated from linear regression established from laboratory trials (watts and run pace relative to VO2 and VCO2).Results:Body weight decreased 3.8 kg from prerace to postrace. Estimated CHO energy expenditure was 10,003 kJ for the bike segment and 5759 kJ for the run segment of the race. The athlete consumed 308 g of exogenous CHO (liquid and gel; 1.21 g CHO/min) during the race. Muscle glycogen decreased from 227.1 prerace to 38.6 mmol · kg wet weight−1 · h−1 postrace. During the 4 hours postrace, the athlete consumed a mixed diet (471 g CHO, 15 g fat, 64 g protein), which included liquid CHO sources and a meal. The calculated rate of muscle-glycogen resynthesis was 4.1 mmol · kg wet weight−1 · h−1.Conclusion:Completing a half Ironman triathlon depends on a high rate of muscle glycogenolysis, which demonstrates the importance of exogenous carbohydrate intake during the race. In addition, rates of muscle-glycogen resynthesis might be dampened by the eccentric damage resulting from the run portion of the race.

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