Systems modelling of mitochondrial dynamics in different exercise regimes.

Ali Khalilimeybodi, Lingxia Qiao, Allen Leung, Andrew D McCulloch, Simon Schenk, Padmini Rangamani

Abstract read

In one paragraph

Article in The Journal of physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

6 authors.

Ali KhalilimeybodiDepartment of Mechanical and Aerospace Engineering, University of California, San Diego, CA, USA.

Lingxia QiaoDepartment of Pharmacology, University of California San Diego, La Jolla, CA, USA.

Allen LeungDepartment of Chemical and Nanoengineering, University of California, San Diego, CA, USA.

Andrew D McCullochShu Chien - Gene Lay Department of Bioengineering, University of California, San Diego, CA, USA.ORCID https://orcid.org/0000-0002-1708-5675

Simon SchenkDepartment of Orthopedic Surgery, University of California San Diego, San Diego, CA, USA.

Padmini RangamaniDepartment of Mechanical and Aerospace Engineering, University of California, San Diego, CA, USA.ORCID https://orcid.org/0000-0001-5953-4347

Funding

Wu Tsai Human Performance Alliance

6 · The paper itself

Abstract

Exercise stimulates skeletal muscle signalling and mitochondrial metabolism. Emerging evidence shows that mitochondrial dynamics (i.e. fission and fusion) could be regulated by exercise. Yet, key gaps remain in identifying (i) the signals that drive fission vs. fusion; (ii) how energy status and reactive oxygen species (ROS) shift control between dynamin-related protein 1 (DRP1) and mitofusin (MFN)/optic atrophy 1 (OPA1); and (iii) which intensity-duration combinations yield similar cytosolic signals but different mitochondrial remodelling. Therefore, we developed an integrative computational framework connecting exercise regimens to mitochondria fission-fusion machinery by linking blood-myofibre energetics in cytosol and mitochondria to signalling pathways. The influence of sprint, resistance and endurance exercise regimens on mitochondrial fission and fusion has been simulated. Classified qualitative validation of the signalling network model achieved 80% accuracy. The model predicts regimen-specific dynamics starting with an acute DRP1-driven fission during exercise followed by MFN1/2-OPA1-mediated re-fusion as energy stress declines, consistent with a cyclical triage-then-rebuild paradigm. Changes are most pronounced and sustained with endurance, sharp but brief with sprint, and minimal with resistance. Global sensitivity analysis identified AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor gamma coactivator-1α→MFN1/2 as dominant fusion drivers, ROS and AMPK→mitochondrial fission factor/DRP1 as primary fission switches, and Ca

Indexed as

ExerciseMitochondrial DynamicsModels, BiologicalAnimalsDynaminsGTP PhosphohydrolasesHumansMuscle, SkeletalReactive Oxygen SpeciesSignal TransductionDynaminsGTP PhosphohydrolasesReactive Oxygen Speciesexercise regimemetabolic signallingmitochondrial fissionmitochondrial fusionROS‐mediated signalling

Identifiers

PMID42385159

DOI10.1113/JP290424

PMCPMC13423126

What Socratic 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 Socratic graph.