Evidence map›Paper›PMID 30408342›Full record

Trial reportActa physiologica (Oxford, England)2019

Exercise training remodels human skeletal muscle mitochondrial fission and fusion machinery towards a pro-elongation phenotype.

Christopher L Axelrod, Ciarán E Fealy, Anny Mulya, John P Kirwan

Abstract readClinical Trial
In one paragraph

Trial report in Acta physiologica (Oxford, England), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 4% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.

  1. Pooled it
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  18. Mitochondrial Dysfunction in HFpEF: Potential Interventions Through Exercise.Journal of cardiovascular translational research · 2025
    Review
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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 at 2 institutions in 1 country.

Christopher L AxelrodDepartment of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.ORCID 0000-0002-1444-8557
Ciarán E FealyDepartment of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
Anny MulyaDepartment of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
John P KirwanDepartment of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.ORCID 0000-0001-7321-9917
Cleveland Clinic Lerner College of Medicine · USPennington Biomedical Research Center · US

Funding

Tracking & Evaluation CoreU54GM104940 · NIGMS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI Leigh Lamonica · 2012 to 2026
$69.1M
CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR024989 · NCRR · CASE WESTERN RESERVE UNIVERSITY · PI DAVIS, PAMELA B · 2007 to 2011
$53.7M
Clinical and Translational Science Collaborative of ClevelandUL1TR002548 · NCATS · CASE WESTERN RESERVE UNIVERSITY · PI MCCOMSEY, GRACE A · 2018 to 2022
$35.5M
Role and Regulation of Skeletal Muscle Mitochondrial Dynamics in Type 2 DiabetesR01DK108089 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI JOHN P. KIRWAN · 2015 to 2026
$4.9M
NCATS NIH HHS UL1 TR002548NCRR NIH HHS UL1 RR024989NIDDK NIH HHS R01 DK108089NIGMS NIH HHS U54 GM104940
6 · The paper itself

Abstract

aimsMitochondria exist as a morphologically plastic network driven by cellular bioenergetic demand. Induction of fusion and fission machinery allows the organelle to regulate quality control and substrate flux. Physiological stressors promote fragmentation of the mitochondrial network, a process implicated in the onset of metabolic disease, including type 2 diabetes and obesity. It is well-known that exercise training improves skeletal muscle mitochondrial volume, number, and density. However, the effect of exercise training on muscle mitochondrial dynamics remains unclear.

methodsTen sedentary adults (65.8 ± 4.6 years; 34.3 ± 2.4 kg/m

resultsExercise training led to improvements in insulin sensitivity, aerobic capacity, and fat oxidation (all P < 0.01), as well as reductions in body weight, BMI, fat mass and fasting glucose (all P < 0.001). When normalized for changes in mitochondrial content, exercise reduced skeletal muscle FIS1 and Parkin (P < 0.05), while having no significant effect on MFN1, MFN2, OPA1, and OMA1 expression. Exercise also improved the ratio of fusion to fission proteins (P < 0.05), which positively correlated with improvements in glucose disposal (r

conclusionsExercise training alters the expression of mitochondrial fusion and fission proteins, promoting a more fused, tubular network. These changes may contribute to the improvements in insulin sensitivity and substrate utilization that are observed after exercise training.

Indexed as

Mitochondrial DynamicsAgedExerciseFemaleHumansMaleMiddle AgedMitochondria, Muscleexercise traininginsulin resistancemitochondrial dynamicsobesityskeletal muscle

Identifiers

PMID30408342
PMCPMC6416060
OpenAlexW2899567634

What OpenQuestion holds

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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.