Evidence map›Paper›PMID 28490439›Full record

ArticleEndocrine connections2017

Skeletal muscle metabolism during prolonged exercise in Pompe disease.

Nicolai Preisler, Pascal Laforêt, Karen Lindhardt Madsen, Edith Husu, Christoffer Rasmus Vissing, Gitte Hedermann, Henrik Galbo, Christopher Lindberg, John Vissing

Open access · goldAbstract read
In one paragraph

Article in Endocrine connections, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Trial
  2. Review
  3. Molecular genetics and metabolism · 2019
    Article
  4. Pompe disease: what are we missing?Annals of translational medicine · 2019
    Review
  5. Article
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

9 authors at 4 institutions in 3 countries.

Nicolai PreislerCopenhagen Neuromuscular CenterDepartment of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark npreisler@hotmail.com.
Pascal LaforêtCentre de Référence de Pathologie Neuromusculaire Paris-EstInstitut de Myologie, GH Pitié-Salpêtrière, Assistance Publique-Hôpitaux de Paris, Paris, France.
Karen Lindhardt MadsenCopenhagen Neuromuscular CenterDepartment of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Edith HusuCopenhagen Neuromuscular CenterDepartment of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Christoffer Rasmus VissingCopenhagen Neuromuscular CenterDepartment of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Gitte HedermannCopenhagen Neuromuscular CenterDepartment of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Henrik GalboDepartment of Inflammation ResearchRigshospitalet, Copenhagen, Denmark.
Christopher LindbergDepartment of NeurologySahlgrenska University Hospital, Gothenburg, Sweden.
John VissingCopenhagen Neuromuscular CenterDepartment of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Rigshospitalet · DKUniversity of Copenhagen · DKAssistance Publique – Hôpitaux de Paris · FRSahlgrenska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivePompe disease (glycogenosis type II) is caused by lysosomal alpha-glucosidase deficiency, which leads to a block in intra-lysosomal glycogen breakdown. In spite of enzyme replacement therapy, Pompe disease continues to be a progressive metabolic myopathy. Considering the health benefits of exercise, it is important in Pompe disease to acquire more information about muscle substrate use during exercise.

methodsSeven adults with Pompe disease were matched to a healthy control group (1:1). We determined (1) peak oxidative capacity (VO

resultsIn the patients, VO

conclusionReflecting muscle weakness and wasting, Pompe disease is associated with markedly reduced maximal exercise capacity. However, glycogenolysis is not impaired in exercise. Unlike in other metabolic myopathies, skeletal muscle substrate use during exercise is normal in Pompe disease rendering exercise less complicated for e.g. medical or recreational purposes.

Indexed as

exerciseglycogenglycogenosisPompe diseaseskeletal muscle metabolism

Identifiers

PMID28490439
PMCPMC8450668
OpenAlexW2612435638

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.