Evidence map›Paper›PMID 30093357›Full record

ArticleMolecular metabolism2018

Exercise-induced molecular mechanisms promoting glycogen supercompensation in human skeletal muscle.

Janne R Hingst, Lea Bruhn, Mads B Hansen, Marie F Rosschou, Jesper B Birk, Joachim Fentz, Marc Foretz, Benoit Viollet, Kei Sakamoto, Nils J Færgeman and 7 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
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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

17 authors at 5 institutions in 5 countries.

Janne R HingstSection of Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, DK-2100, Copenhagen, Denmark.
Lea BruhnSection of Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, DK-2100, Copenhagen, Denmark.
Mads B HansenSection of Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, DK-2100, Copenhagen, Denmark.
Marie F RosschouSection of Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, DK-2100, Copenhagen, Denmark.
Jesper B BirkSection of Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, DK-2100, Copenhagen, Denmark.
Joachim FentzSection of Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, DK-2100, Copenhagen, Denmark.
Marc ForetzINSERM, U1016, Institut Cochin, 75014, Paris, France; CNRS, UMR8104, 75014, Paris, France; Université Paris Descartes, Sorbonne Paris Cité, 75014, Paris, France.
Benoit ViolletINSERM, U1016, Institut Cochin, 75014, Paris, France; CNRS, UMR8104, 75014, Paris, France; Université Paris Descartes, Sorbonne Paris Cité, 75014, Paris, France.
Kei SakamotoMRC Protein Phosphorylation and Ubiquitylation Unit, College of Life Sciences, University of Dundee, Dundee, DD1 5EH, Scotland, United Kingdom.
Nils J FærgemanDepartment of Biochemistry and Molecular Biology and VILLUM Center for Bioanalytical Sciences, University of Southern Denmark, Campusvej 55, DK-5230, Odense, Denmark.
Jesper F HavelundDepartment of Biochemistry and Molecular Biology and VILLUM Center for Bioanalytical Sciences, University of Southern Denmark, Campusvej 55, DK-5230, Odense, Denmark.
Benjamin L ParkerCharles Perkins Centre, School of Life and Environmental Sciences, University of Sydney, Sydney, NSW, 2006, Australia.
David E JamesCharles Perkins Centre, School of Life and Environmental Sciences, University of Sydney, Sydney, NSW, 2006, Australia; School of Medicine, University of Sydney, Sydney, NSW, 2006, Australia.
Bente KiensSection of Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, DK-2100, Copenhagen, Denmark.
Erik A RichterSection of Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, DK-2100, Copenhagen, Denmark.
Jørgen JensenSection of Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, DK-2100, Copenhagen, Denmark; Department of Physical Performance, Norwegian School of Sports Sciences, Oslo, Norway.
Jørgen F P WojtaszewskiSection of Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, DK-2100, Copenhagen, Denmark. Electronic address: jwojtaszewski@nexs.ku.dk.
University of Copenhagen · DKDélégation Paris 5 · FRThe University of Sydney · AUUniversity of Southern Denmark · DKUniversity of Dundee · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveA single bout of exercise followed by intake of carbohydrates leads to glycogen supercompensation in prior exercised muscle. Our objective was to illuminate molecular mechanisms underlying this phenomenon in skeletal muscle of man.

methodsWe studied the temporal regulation of glycogen supercompensation in human skeletal muscle during a 5 day recovery period following a single bout of exercise. Nine healthy men depleted (day 1), normalized (day 2) and supercompensated (day 5) muscle glycogen in one leg while the contralateral leg served as a resting control. Euglycemic hyperinsulinemic clamps in combination with leg balance technique allowed for investigating insulin-stimulated leg glucose uptake under these 3 experimental conditions. Cellular signaling in muscle biopsies was investigated by global proteomic analyses and immunoblotting. We strengthened the validity of proposed molecular effectors by follow-up studies in muscle of transgenic mice.

resultsSustained activation of glycogen synthase (GS) and AMPK in combination with elevated expression of proteins determining glucose uptake capacity were evident in the prior exercised muscle. We hypothesize that these alterations offset the otherwise tight feedback inhibition of glycogen synthesis and glucose uptake by glycogen. In line with key roles of AMPK and GS seen in the human experiments we observed abrogated ability for glycogen supercompensation in muscle with inducible AMPK deletion and in muscle carrying a G6P-insensitive form of GS in muscle.

conclusionOur study demonstrates that both AMPK and GS are key regulators of glycogen supercompensation following a single bout of glycogen-depleting exercise in skeletal muscle of both man and mouse.

Indexed as

AdultAnimalsCarbohydrate MetabolismCarbohydratesDietary CarbohydratesExerciseGlucoseGlycogenGlycogen SynthaseHumansInsulinMaleMiceMice, TransgenicMuscle, SkeletalPhosphorylationCarbohydratesDietary CarbohydratesGlucoseGlycogenGlycogen SynthaseInsulinAMP-activated protein kinase (AMPK)ExerciseGlucose uptakeGlycogen synthase (GS)Insulin actionTBC1 domain family member 4 (TBC1D4)

Identifiers

PMID30093357
PMCPMC6158101
OpenAlexW2882971477

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.