Evidence map›Paper›PMID 20837639›Full record

ArticleThe Journal of physiology2010

Increased fatigue resistance linked to Ca2+-stimulated mitochondrial biogenesis in muscle fibres of cold-acclimated mice.

Joseph D Bruton, Jan Aydin, Takashi Yamada, Irina G Shabalina, Niklas Ivarsson, Shi-Jin Zhang, Masanobu Wada, Pasi Tavi, Jan Nedergaard, Abram Katz and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

40 citing papers in PubMed, 80 citations in OpenAlex.

  1. Trial
  2. Ryanodine receptor fragmentation and sarcoplasmic reticulum Ca2+ leak after one session of high-intensity interval exercise.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Trial
  3. Article
  4. Review
  5. ERG1A KScientific reports · 2025
    Article
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  10. Review
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  13. Article
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  16. A Mechanism for Statin-Induced Susceptibility to Myopathy.JACC. Basic to translational science · 2019
    Article
  17. SR CaThe Journal of general physiology · 2019
    Article
  18. Article
  19. International journal of molecular sciences · 2018
    Article
  20. Review
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.

Joseph D BrutonDepartment of Physiology and Pharmacology, Karolinska Institutet, SE-171 77 Stockholm, Sweden.
Jan Aydin
Takashi Yamada
Irina G Shabalina
Niklas Ivarsson
Shi-Jin Zhang
Masanobu Wada
Pasi Tavi
Jan Nedergaard
Abram Katz
Håkan Westerblad
Karolinska Institutet · SEStockholm University · SEHiroshima University · JPUniversity of Eastern Finland · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mammals exposed to a cold environment initially generate heat by repetitive muscle activity (shivering). Shivering is successively replaced by the recruitment of uncoupling protein-1 (UCP1)-dependent heat production in brown adipose tissue. Interestingly, adaptations observed in skeletal muscles of cold-exposed animals are similar to those observed with endurance training. We hypothesized that increased myoplasmic free [Ca2+] ([Ca2+]i) is important for these adaptations. To test this hypothesis, experiments were performed on flexor digitorum brevis (FDB) muscles, which do not participate in the shivering response, of adult wild-type (WT) and UCP1-ablated (UCP1-KO) mice kept either at room temperature (24°C) or cold-acclimated (4°C) for 4-5 weeks. [Ca2+]i (measured with indo-1) and force were measured under control conditions and during fatigue induced by repeated tetanic stimulation in intact single fibres. The results show no differences between fibres from WT and UCP1-KO mice. However, muscle fibres from cold-acclimated mice showed significant increases in basal [Ca2+]i (∼50%), tetanic [Ca2+]i (∼40%), and sarcoplasmic reticulum (SR) Ca2+ leak (∼fourfold) as compared to fibres from room-temperature mice. Muscles of cold-acclimated mice showed increased expression of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and increased citrate synthase activity (reflecting increased mitochondrial content). Fibres of cold-acclimated mice were more fatigue resistant with higher tetanic [Ca2+]i and less force loss during fatiguing stimulation. In conclusion, cold exposure induces changes in FDB muscles similar to those observed with endurance training and we propose that increased [Ca2+]i is a key factor underlying these adaptations.

Indexed as

Cold TemperatureAdaptation, PhysiologicalAnimalsCalciumFemaleIon ChannelsMiceMice, Inbred C57BLMice, KnockoutMitochondrial ProteinsMitochondria, MuscleModels, AnimalMuscle FatigueMuscle Fibers, SkeletalPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaShiveringCalciumIon ChannelsMitochondrial ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseTrans-ActivatorsTranscription FactorsUcp1 protein, mouseUncoupling Protein 1

Identifiers

PMID20837639
PMCPMC3002456
OpenAlexW2116104160

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.