Evidence map›Paper›PMID 16491397›Full record

ArticlePflugers Archiv : European journal of physiology2006

Increased resistance to fatigue in creatine kinase deficient muscle is not due to improved contractile economy.

Frank ter Veld, Klaas Nicolay, Jeroen A L Jeneson

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Article in Pflugers Archiv : European journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

3 authors.

Frank ter VeldDepartment of Experimental In Vivo NMR, Image Sciences Institute, University Medical Center Utrecht, Utrecht, The Netherlands. frank.terveld@ddz.uni-duesseldorf.de
Klaas Nicolay
Jeroen A L Jeneson

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There has been speculation on the origin of the increased endurance of skeletal muscles in creatine kinase (CK)-deficient mice. Important factors that have been raised include the documented increased mitochondrial capacity and alterations in myosin heavy chain (MyHC) isoform composition in CK-deficient muscle. More recently, the absence of inorganic phosphate release from phosphocreatine hydrolysis in exercising CK-deficient muscle has been postulated to contribute to the lower fatigueability in skeletal muscle. In this study, we tested the hypothesis that the reported shift in MyHC composition to slower isoforms in CK-deficient muscle leads to a decrease in oxygen cost of twitch performance. To that aim, extensor digitorum longus (EDL) and soleus (SOL) muscles were isolated from wild-type (WT) and knock-out mice deficient in the cytoplasmic muscle-type and sarcomeric mitochondrial isoenzymes of CK, and oxygen consumption per twitch time-tension-integral (TTI) was measured. The results show that the adaptive response to loss of CK function does not involve any major change to contractile economy of skeletal muscle.

Indexed as

AnimalsBiomechanical PhenomenaCreatine KinaseGuanidinesIn Vitro TechniquesMiceMice, Inbred C57BLMuscle ContractionMuscle FatigueMuscle Fibers, Fast-TwitchMuscle Fibers, Slow-TwitchMuscle, SkeletalMyosin Heavy ChainsOxygen ConsumptionPropionatesProtein IsoformsCreatine KinaseGuanidinesguanidinopropionic acidMyosin Heavy ChainsPropionatesProtein Isoforms

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Registered trials

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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.