scholarly journals Postexercise muscle glycogen resynthesis in humans

2017 ◽  
Vol 122 (5) ◽  
pp. 1055-1067 ◽  
Author(s):  
Louise M. Burke ◽  
Luc J. C. van Loon ◽  
John A. Hawley
Keyword(s):  
Muscle Glycogen ◽  
Glycogen Synthesis ◽  
Practical Interest ◽  
Time Frame ◽  
Glycogen Storage ◽  
Future Research ◽  
Glycogen Depletion ◽  
Muscle Glycogen Synthesis ◽  
The 1960S ◽  
Dietary Strategies

Since the pioneering studies conducted in the 1960s in which glycogen status was investigated using the muscle biopsy technique, sports scientists have developed a sophisticated appreciation of the role of glycogen in cellular adaptation and exercise performance, as well as sites of storage of this important metabolic fuel. While sports nutrition guidelines have evolved during the past decade to incorporate sport-specific and periodized manipulation of carbohydrate (CHO) availability, athletes attempt to maximize muscle glycogen synthesis between important workouts or competitive events so that fuel stores closely match the demands of the prescribed exercise. Therefore, it is important to understand the factors that enhance or impair this biphasic process. In the early postexercise period (0–4 h), glycogen depletion provides a strong drive for its own resynthesis, with the provision of CHO (~1 g/kg body mass) optimizing this process. During the later phase of recovery (4–24 h), CHO intake should meet the anticipated fuel needs of the training/competition, with the type, form, and pattern of intake being less important than total intake. Dietary strategies that can enhance glycogen synthesis from suboptimal amounts of CHO or energy intake are of practical interest to many athletes; in this scenario, the coingestion of protein with CHO can assist glycogen storage. Future research should identify other factors that enhance the rate of synthesis of glycogen storage in a limited time frame, improve glycogen storage from a limited CHO intake, or increase muscle glycogen supercompensation.

Dietary Strategies to Promote Glycogen Synthesis After Exercise

2001 ◽  
Vol 26 (S1) ◽  
pp. S236-S245 ◽  
Author(s):  
John L. Ivy
Keyword(s):  
Muscle Glycogen ◽  
Tissue Repair ◽  
Glycogen Synthesis ◽  
Effective Means ◽  
Post Exercise ◽  
Muscle Glycogen Synthesis ◽  
Added Benefit ◽  
Glycogen Stores ◽  
Dietary Strategies ◽  
Carbohydrate Supplement

Muscle glycogen is an essential fuel for prolonged intense exercise, and therefore it is important that the glycogen stores be copious for competition and strenuous training regimens. While early research focused on means of increasing the muscle glycogen stores in preparation for competition and its day-to-day replenishment, recent research has focused on the most effective means of promoting its replenishment during the early hours of recovery. It has been observed that muscle glycogen synthesis is twice as rapid if carbohydrate is consumed immediately after exercise as opposed to waiting several hours, and that a rapid rate of synthesis can be maintained if carbohydrate is consumed on a regular basis. For example, supplementing at 30-min intervals at a rate of 1.2 to 1.5 g CHO kg-1 body wt h-1 appears to maximize synthesis for a period of 4- to 5-h post exercise. If a lighter carbohydrate supplement is desired, however, glycogen synthesis can be enhanced with the addition of protein and certain amino acids. Furthermore, the combination of carbohydrate and protein has the added benefit of stimulating amino acid transport, protein synthesis and muscle tissue repair. Research suggests that aerobic peiformance following recovery is related to the degree of muscle glycogen replenishment.

The second-meal phenomenon is associated with enhanced muscle glycogen storage in humans

2009 ◽  
Vol 117 (3) ◽  
pp. 119-127 ◽  
Author(s):  
Ana Jovanovic ◽  
Emily Leverton ◽  
Bhavana Solanky ◽  
Balasubramanian Ravikumar ◽  
Johanna E. M. Snaar ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Muscle Glycogen ◽  
Standardized Test ◽  
Glycogen Synthesis ◽  
Random Order ◽  
Glycogen Storage ◽  
Resonance Spectroscopy ◽  
Plasma Nefa ◽  
Muscle Glycogen Synthesis ◽  
Metabolic Basis

The rise in blood glucose after lunch is less if breakfast has been eaten. The metabolic basis of this second-meal phenomenon remains uncertain. We hypothesized that storage of ingested glucose as glycogen could be responsible during the post-meal suppression of plasma NEFAs (non-esterified fatty acids; ‘free’ fatty acids). In the present study we determined the metabolic basis of the second-meal phenomenon. Healthy subjects were studied on two separate days, with breakfast and without breakfast in a random order. We studied metabolic changes after a standardized test lunch labelled with 3 g of 13C-labelled (99%) glucose. Changes in post-prandial muscle glycogen storage were measured using 13C magnetic resonance spectroscopy. The rise in plasma glucose after lunch was significantly less if breakfast had been taken (0.9±0.3 compared with 3.2±0.3 mmol/l, with and without breakfast respectively; P<0.001), despite comparable insulin responses. Pre-lunch NEFAs were suppressed after breakfast (0.13±0.03 compared with 0.51±0.04 mmol/l) and levels correlated positively with the maximum glucose rise after lunch (r=0.62, P=0.001). The increase in muscle glycogen signal was greater 5 h after lunch on the breakfast day (103±21 compared with 48±12 units; P<0.007) and correlated negatively with plasma NEFA concentrations before lunch (r=−0.48, P<0.05). The second-meal effect is associated with priming of muscle glycogen synthesis consequent upon sustained suppression of plasma NEFA concentrations.

scholarly journals Skeletal-muscle glycogen synthesis during the starved-to-fed transition in the rat

1988 ◽  
Vol 254 (3) ◽  
pp. 855-859 ◽  
Author(s):  
M J Holness ◽  
M J L Schuster-Bruce ◽  
M C Sugden
Keyword(s):  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Glycogen Synthesis ◽  
Glucose Disposal ◽  
Glycogen Depletion ◽  
Fibre Composition ◽  
Skeletal Muscle Glycogen ◽  
Muscle Glycogen Synthesis ◽  
Muscle Fibre Composition ◽  
Glycogen Deposition

The pattern of glycogen deposition in skeletal muscles of varying fibre composition was examined in rats during the starved-to-fed transition. In all the muscles studied, glycogen concentrations steadily increased during the first 8 h after chow re-feeding, and the fed value was exceeded. Rates of glycogen deposition varied, not with muscle fibre composition, but with the extent of glycogen depletion during starvation. There was no evidence for skeletal-muscle glycogen breakdown during the period of hepatic glycogenesis, making it unlikely that recycling of carbon from muscle glycogen to lactate is quantitatively important for the provision of glycogenic precursors to the liver, but moderate glycogen loss was observed from 8 to 24 h after re-feeding, when the liver is in the lipogenic mode. The factors influencing glucose disposal by skeletal muscle after re-feeding are discussed.

Insulin promotes glycogen synthesis in the absence of GSK3 phosphorylation in skeletal muscle

2008 ◽  
Vol 294 (1) ◽  
pp. E28-E35 ◽  
Author(s):  
Michale Bouskila ◽  
Michael F. Hirshman ◽  
Jørgen Jensen ◽  
Laurie J. Goodyear ◽  
Kei Sakamoto
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Muscle Glycogen ◽  
Glycogen Content ◽  
Glycogen Synthase ◽  
Glycogen Synthesis ◽  
Wild Type ◽  
Muscle Glycogen Synthesis ◽  
Mutant Forms

Insulin promotes dephosphorylation and activation of glycogen synthase (GS) by inactivating glycogen synthase kinase (GSK) 3 through phosphorylation. Insulin also promotes glucose uptake and glucose 6-phosphate (G-6- P) production, which allosterically activates GS. The relative importance of these two regulatory mechanisms in the activation of GS in vivo is unknown. The aim of this study was to investigate if dephosphorylation of GS mediated via GSK3 is required for normal glycogen synthesis in skeletal muscle with insulin. We employed GSK3 knockin mice in which wild-type GSK3α and -β genes are replaced with mutant forms (GSK3α/βS21A/S21A/S9A/S9A), which are nonresponsive to insulin. Although insulin failed to promote dephosphorylation and activation of GS in GSK3α/βS21A/S21A/S9A/S9Amice, glycogen content in different muscles from these mice was similar compared with wild-type mice. Basal and epinephrine-stimulated activity of muscle glycogen phosphorylase was comparable between wild-type and GSK3 knockin mice. Incubation of isolated soleus muscle in Krebs buffer containing 5.5 mM glucose in the presence or absence of insulin revealed that the levels of G-6- P, the rate of [14C]glucose incorporation into glycogen, and an increase in total glycogen content were similar between wild-type and GSK3 knockin mice. Injection of glucose containing 2-deoxy-[3H]glucose and [14C]glucose also resulted in similar rates of muscle glucose uptake and glycogen synthesis in vivo between wild-type and GSK3 knockin mice. These results suggest that insulin-mediated inhibition of GSK3 is not a rate-limiting step in muscle glycogen synthesis in mice. This suggests that allosteric regulation of GS by G-6- P may play a key role in insulin-stimulated muscle glycogen synthesis in vivo.

Can photobiomodulation therapy (PBMT) control blood glucose levels and alter muscle glycogen synthesis?

2020 ◽  
Vol 207 ◽  
pp. 111877 ◽  
Author(s):  
Kenia Mendes Rodrigues Castro ◽  
Rodrigo Leal de Paiva Carvalho ◽  
Geraldo Marco Rosa Junior ◽  
Beatriz Antoniassi Tavares ◽  
Luis Henrique Simionato ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Muscle Glycogen ◽  
Glycogen Synthesis ◽  
Photobiomodulation Therapy ◽  
Control Blood Glucose ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Muscle Glycogen Synthesis
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