Evidence map›Paper›PMID 20595537›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2010

Grip force, EDL contractile properties, and voluntary wheel running after postdevelopmental myostatin depletion in mice.

Kirkwood E Personius, Aditi Jayaram, David Krull, Roger Brown, Tianshun Xu, Bajin Han, Kerri Burgess, Christopher Storey, Bharati Shah, Rabi Tawil and 1 more

Abstract read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Adenosine AFrontiers in pharmacology · 2024
    Article
  6. Article
  7. Article
  8. Voluntary wheel running: patterns and physiological effects in mice.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Blockade of ActRIIB signaling triggers muscle fatigability and metabolic myopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2014
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Effect of postdevelopmental myostatin depletion on myofibrillar protein metabolism.American journal of physiology. Endocrinology and metabolism · 2011
    Article
  20. 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

11 authors at 4 institutions in 3 countries.

Kirkwood E PersoniusDepartment of Rehabilitation Science, University at Buffalo, Buffalo, NY, USA.
Aditi Jayaram
David Krull
Roger Brown
Tianshun Xu
Bajin Han
Kerri Burgess
Christopher Storey
Bharati Shah
Rabi Tawil
Stephen Welle
GlaxoSmithKline (India) · INImmunovaccine (Canada) · CAUniversity at Buffalo, State University of New York · USUniversity of Rochester · US

Funding

Muscle protein synthesis and gene expression in myostatin-deficient miceR01AR054366 · NIAMS · UNIVERSITY OF ROCHESTER · PI WELLE, STEPHEN L · 2007 to 2010
$1.1M
NIAMS NIH HHS AR-054366
6 · The paper itself

Abstract

There is no consensus about whether making muscles abnormally large by reducing myostatin activity affects force-generating capacity or the ability to perform activities requiring muscular endurance. We therefore examined grip force, contractile properties of extensor digitorum longus (EDL) muscles, and voluntary wheel running in mice in which myostatin was depleted after normal muscle development. Cre recombinase activity was induced to knock out exon 3 of the myostatin gene in 4-mo-old mice in which this exon was flanked by loxP sequences (Mstn[f/f]). Control mice with normal myostatin genes (Mstn[w/w]) received the same Cre-activating treatment. Myostatin depletion increased the mass of all muscles that were examined (gastrocnemius, quadriceps, tibialis anterior, EDL, soleus, triceps) by approximately 20-40%. Grip force, measured multiple times 2-22 wk after myostatin knockout, was not consistently greater in the myostatin-deficient mice. EDL contractile properties were determined 7-13 mo after myostatin knockout. Twitch force tended to be greater in myostatin-deficient muscles (+24%; P=0.09), whereas tetanic force was not consistently elevated (mean +11%; P=0.36), even though EDL mass was greater than normal in all myostatin-deficient mice (mean +36%; P<0.001). The force deficit induced by eccentric contractions was approximately twofold greater in myostatin-deficient than in normal EDL muscles (31% vs. 16% after five eccentric contractions; P=0.02). Myostatin-deficient mice ran 19% less distance (P<0.01) than control mice during the 12 wk following myostatin depletion, primarily because of fewer running bouts per night rather than diminished running speed or bout duration. Reduced specific tension (ratio of force to mass) and reduced running have been observed after muscle hypertrophy was induced by other means, suggesting that they are characteristics generally associated with abnormally large muscles rather than unique effects of myostatin deficiency.

Indexed as

Motor ActivityMuscle ContractionMuscle StrengthPhysical ExertionAnimalsBehavior, AnimalHypertrophyIntegrasesMaleMiceMice, Inbred C57BLMice, KnockoutMuscle, SkeletalMyostatinOrgan SizeCre recombinaseIntegrasesMstn protein, mouseMyostatin

Identifiers

PMID20595537
PMCPMC2944632
OpenAlexW2139996704

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.