Evidence map›Paper›PMID 22232606›Full record

ArticleFrontiers in physiology2011

The role of skeletal muscle glycogen breakdown for regulation of insulin sensitivity by exercise.

Jørgen Jensen, Per Inge Rustad, Anders Jensen Kolnes, Yu-Chiang Lai

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
184citing papers in PubMed, 10 pooled it
4.2field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

184 citing papers in PubMed, 10 syntheses or guidelines pooled it, 396 citations in OpenAlex.

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  11. Trial
  12. Metabolic and Mechanical Effects of Laddermill Graded Exercise Testing.Journal of strength and conditioning research · 2018
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  20. Metabolic Health and Fitness Do Not Differ Substantially Between Overweight Adults With and Without α-Actinin-3 Deficiency.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article

124 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 3 countries.

Jørgen JensenDepartment of Physical Performance, Norwegian School of Sport Sciences Oslo, Norway.
Per Inge Rustad
Anders Jensen Kolnes
Yu-Chiang Lai
Norwegian School of Sport Sciences · NOCharles University · CZUCLouvain · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycogen is the storage form of carbohydrates in mammals. In humans the majority of glycogen is stored in skeletal muscles (∼500 g) and the liver (∼100 g). Food is supplied in larger meals, but the blood glucose concentration has to be kept within narrow limits to survive and stay healthy. Therefore, the body has to cope with periods of excess carbohydrates and periods without supplementation. Healthy persons remove blood glucose rapidly when glucose is in excess, but insulin-stimulated glucose disposal is reduced in insulin resistant and type 2 diabetic subjects. During a hyperinsulinemic euglycemic clamp, 70-90% of glucose disposal will be stored as muscle glycogen in healthy subjects. The glycogen stores in skeletal muscles are limited because an efficient feedback-mediated inhibition of glycogen synthase prevents accumulation. De novo lipid synthesis can contribute to glucose disposal when glycogen stores are filled. Exercise physiologists normally consider glycogen's main function as energy substrate. Glycogen is the main energy substrate during exercise intensity above 70% of maximal oxygen uptake ([Formula: see text]) and fatigue develops when the glycogen stores are depleted in the active muscles. After exercise, the rate of glycogen synthesis is increased to replete glycogen stores, and blood glucose is the substrate. Indeed insulin-stimulated glucose uptake and glycogen synthesis is elevated after exercise, which, from an evolutional point of view, will favor glycogen repletion and preparation for new "fight or flight" events. In the modern society, the reduced glycogen stores in skeletal muscles after exercise allows carbohydrates to be stored as muscle glycogen and prevents that glucose is channeled to de novo lipid synthesis, which over time will causes ectopic fat accumulation and insulin resistance. The reduction of skeletal muscle glycogen after exercise allows a healthy storage of carbohydrates after meals and prevents development of type 2 diabetes.

Indexed as

de novo lipogenesisexerciseglycogen phosphorylaseglycogen synthaseinsulin resistancetype 2 diabetes

Identifiers

PMID22232606
PMCPMC3248697
OpenAlexW2171588919

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.