Evidence map›Paper›PMID 14634202›Full record

ArticleThe Journal of physiology2004

Effects of acute and chronic endurance exercise on mitochondrial uncoupling in human skeletal muscle.

Maria Fernström, Michail Tonkonogi, Kent Sahlin

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 144 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
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  9. A Review of the Role of Endo/Sarcoplasmic Reticulum-Mitochondria CaInternational journal of environmental research and public health · 2021
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  10. Factors determining training-induced changes in V̇OJournal of applied physiology (Bethesda, Md. : 1985) · 2021
    Article
  11. βCells · 2021
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  18. Article
  19. Potential Causes of Elevated REE after High-Intensity Exercise.Medicine and science in sports and exercise · 2017
    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

3 authors at 2 institutions in 2 countries.

Maria FernströmInstitute of Sports Science and Clinical Biomechanics, University of Southern Denmark, Campusvej 55, 5230 Odense, Denmark. ksahlin@health.sdu.dk
Michail Tonkonogi
Kent Sahlin
University of Southern Denmark · DKKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial proteins such as uncoupling protein 3 (UCP3) and adenine nucleotide translocase (ANT) may mediate back-leakage of protons and serve as uncouplers of oxidative phosphorylation. We hypothesized that UCP3 and ANT increase after prolonged exercise and/or endurance training, resulting in increased uncoupled respiration (UCR). Subjects were investigated with muscle biopsies before and after acute exercise (75 min of cycling at 70% of .VO2peak) or 6 weeks endurance training. Mitochondria were isolated and respiration measured in the absence (UCR or state 4) and presence of ADP (coupled respiration or state 3). Protein expression of UCP3 and ANT was measured with Western blotting. After endurance training, .VO2peak, citrate synthase activity (CS), state 3 respiration and ANT increased by 24, 47, 40 and 95%, respectively (all P < 0.05), whereas UCP3 remained unchanged. When expressed per unit of CS (a marker of mitochondrial volume) UCP3 and UCR decreased by 54% and 18%(P < 0.05). CS increased by 43% after acute exercise and remained elevated after 3 h of recovery (P < 0.05), whereas the other muscle parameters remained unchanged. An intriguing finding was that acute exercise reversibly enhanced the capacity of mitochondria to accumulate Ca2+(P < 0.05) before opening of permeability transition pores. In conclusion, UCP3 protein and UCR decrease after endurance training when related to mitochondrial volume. These changes may prevent excessive basal thermogenesis. Acute exercise enhances mitochondrial resistance to Ca2+ overload but does not influence UCR or protein expression of UCP3 and ANT. The increased Ca2+ resistance may prevent mitochondrial degradation and the mechanism needs to be further explored.

Indexed as

Physical Education and TrainingPhysical EnduranceAdenosine DiphosphateAdultBlotting, WesternCalciumCarrier ProteinsCitrate (si)-SynthaseExerciseFemaleHumansIon ChannelsMaleMitochondrial ADP, ATP TranslocasesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreAdenosine DiphosphateCalciumCarrier ProteinsCitrate (si)-SynthaseIon ChannelsMitochondrial ADP, ATP TranslocasesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMitochondrial ProteinsUCP3 protein, humanUncoupling Protein 3

Identifiers

PMID14634202
PMCPMC1664806
OpenAlexW2105580366

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.