Evidence map›Paper›PMID 26447205›Full record

ArticleAmerican journal of physiology. Cell physiology2016

Slow recovery of the impaired fatigue resistance in postunloading mouse soleus muscle corresponding to decreased mitochondrial function and a compensatory increase in type I slow fibers.

Han-Zhong Feng, Xuequn Chen, Moh H Malek, J-P Jin

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Mitochondrial Biogenesis in Skeletal Muscle.Advances in experimental medicine and biology · 2025
    Review
  5. Article
  6. Mitochondrial Bioenergetics and Turnover during Chronic Muscle Disuse.International journal of molecular sciences · 2021
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Evidence-based complementary and alternative medicine : eCAM · 2019
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

4 authors.

Han-Zhong FengDepartment of Physiology, Wayne State University, Detroit, Michigan;
Xuequn ChenDepartment of Physiology, Wayne State University, Detroit, Michigan;
Moh H MalekDepartment of Health Care Sciences, Wayne State University, Detroit, Michigan.
J-P JinDepartment of Physiology, Wayne State University, Detroit, Michigan; jjin@med.wayne.edu.

Funding

Role of Troponin T Isoforms in Nemaline MyopathyR01AR048816 · NIAMS · WAYNE STATE UNIVERSITY · PI JIN, JIAN-PING · 2003 to 2014
$3.2M
Proteolytic Regulation of Troponin T & Cardiac FunctionR01HL098945 · NHLBI · WAYNE STATE UNIVERSITY · PI JIN, JIAN-PING · 2010 to 2014
$2.0M
Proinsulin ER export and beta cell ER homeostasis in health and diabetesR56DK102039 · NIDDK · WAYNE STATE UNIVERSITY · PI CHEN, XUEQUN · 2015 to 2015
$153k
NHLBI NIH HHS HL098945NIAMS NIH HHS AR048816NIDDK NIH HHS R56 DK102039
6 · The paper itself

Abstract

Unloading or disuse rapidly results in skeletal muscle atrophy, switching to fast-type fibers, and decreased resistance to fatigue. The recovery process is of major importance in rehabilitation for various clinical conditions. Here we studied mouse soleus muscle during 60 days of reloading after 4 wk of hindlimb suspension. Unloading produced significant atrophy of soleus muscle with decreased contractile force and fatigue resistance, accompanied by switches of myosin isoforms from IIa to IIx and IIb and fast troponin T to more low-molecular-weight splice forms. The total mass, fiber size, and contractile force of soleus muscle recovered to control levels after 15 days of reloading. However, the fatigue resistance showed a trend of worsening during this period with significant infiltration of inflammatory cells at days 3 and 7, indicating reloading injuries that were accompanied by active regeneration with upregulations of filamin-C, αB-crystallin, and desmin. The fatigue resistance partially recovered after 30-60 days of reloading. The expression of peroxisome proliferator-activated receptor γ coactivator 1α and mitofusin-2 showed changes parallel to that of fatigue resistance after unloading and during reloading, suggesting a causal role of decreased mitochondrial function. Slow fiber contents in the soleus muscle were increased after 30-60 days of reloading to become significantly higher than the normal level, indicating a secondary adaption to compensate for the slow recovery of fatigue resistance.

Indexed as

Mitochondria, MuscleMuscle ContractionMuscle FatigueMuscle Fibers, Slow-TwitchRegenerationAnimalsDisease Models, AnimalGene Expression RegulationHindlimb SuspensionMaleMice, Inbred C57BLMuscle ProteinsMuscle, SkeletalMuscular AtrophyRecovery of FunctionTime FactorsMuscle Proteinsin situ fatigue resistanceperoxisome proliferator-activated receptor γ coactivator 1αreloading injury and adaptationskeletal muscle unloadingtype I slow fiber

Identifiers

PMID26447205
PMCPMC4698445

What OpenQuestion holds

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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.