Evidence map›Paper›PMID 23114964›Full record

ArticleAmerican journal of physiology. Cell physiology2013

Combined in vivo and in silico investigations of activation of glycolysis in contracting skeletal muscle.

J P J Schmitz, W Groenendaal, B Wessels, R W Wiseman, P A J Hilbers, K Nicolay, J J Prompers, J A L Jeneson, N A W van Riel

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

  1. The return of metabolism: biochemistry and physiology of glycolysis.Biological reviews of the Cambridge Philosophical Society · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. NMR in biomedicine · 2020
    Article
  6. Review
  7. Impact of age on exercise-induced ATP supply during supramaximal plantar flexion in humans.American journal of physiology. Regulatory, integrative and comparative physiology · 2015
    Article
  8. Article
  9. Review
  10. Review
  11. 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 3 institutions in 2 countries.

J P J SchmitzComputational Biology, Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands. J.P.J.Schmitz@tue.nl
W Groenendaal
B Wessels
R W Wiseman
P A J Hilbers
K Nicolay
J J Prompers
J A L Jeneson
N A W van Riel
Eindhoven University of Technology · NLMichigan State University · USUniversity Medical Center Groningen · NL

Funding

Integrated Modeling of Cardiac Metabolism and TransportR01HL072011 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BEARD, DANIEL A · 2004 to 2016
$4.0M
Mechanisms of Metabolic Dysfunction in Type 2 DiabetesR01DK095210 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BEARD, DANIEL A, WISEMAN, ROBERT W · 2012 to 2016
$2.7M
Multi-scale systems analysis of blood pressure control and hypertensionR01HL139813 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BEARD, DANIEL A · 2018 to 2021
$2.0M
NHLBI NIH HHS HL-072011NIDDK NIH HHS DK-095210NIDDK NIH HHS R01 DK095210
6 · The paper itself

Abstract

The hypothesis was tested that the variation of in vivo glycolytic flux with contraction frequency in skeletal muscle can be qualitatively and quantitatively explained by calcium-calmodulin activation of phosphofructokinase (PFK-1). Ischemic rat tibialis anterior muscle was electrically stimulated at frequencies between 0 and 80 Hz to covary the ATP turnover rate and calcium concentration in the tissue. Estimates of in vivo glycolytic rates and cellular free energetic states were derived from dynamic changes in intramuscular pH and phosphocreatine content, respectively, determined by phosphorus magnetic resonance spectroscopy ((31)P-MRS). Computational modeling was applied to relate these empirical observations to understanding of the biochemistry of muscle glycolysis. Hereto, the kinetic model of PFK activity in a previously reported mathematical model of the glycolytic pathway (Vinnakota KC, Rusk J, Palmer L, Shankland E, Kushmerick MJ. J Physiol 588: 1961-1983, 2010) was adapted to contain a calcium-calmodulin binding sensitivity. The two main results were introduction of regulation of PFK-1 activity by binding of a calcium-calmodulin complex in combination with activation by increased concentrations of AMP and ADP was essential to qualitatively and quantitatively explain the experimental observations. Secondly, the model predicted that shutdown of glycolytic ATP production flux in muscle postexercise may lag behind deactivation of PFK-1 (timescales: 5-10 s vs. 100-200 ms, respectively) as a result of accumulation of glycolytic intermediates downstream of PFK during contractions.

Indexed as

Adenosine TriphosphateAnimalsCalciumCalmodulinComputer SimulationGlycolysisHydrogen-Ion ConcentrationIschemiaMagnetic Resonance SpectroscopyMaleModels, BiologicalMuscle ContractionMuscle, SkeletalPhosphocreatinePhosphofructokinase-1, Muscle TypePhysical Conditioning, AnimalAdenosine TriphosphateCalciumCalmodulinPhosphocreatinePhosphofructokinase-1, Muscle Type

Identifiers

PMID23114964
PMCPMC3546809
OpenAlexW2127436339

What OpenQuestion holds

Textmetadata
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.