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Excessive vigorous exercise impairs cognitive function through a muscle-derived mitochondrial pretender.

Yan Huang1, Biao Hu1, Ya Liu1

  • 1Department of Endocrinology, Endocrinology Research Center, Xiangya Hospital of Central South University, Changsha 410008, Hunan, China.

Cell Metabolism
|December 4, 2025
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Summary
This summary is machine-generated.

Excessive exercise causes cognitive decline by releasing muscle-derived vesicles that impair brain mitochondria. Blocking these vesicles improves cognitive function and synaptic health.

Keywords:
MDVscognitive declineexcessive vigorous exercise

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Area of Science:

  • Neuroscience
  • Exercise Physiology
  • Cell Biology

Background:

  • Excessive exercise can negatively impact cognitive function, with the precise biological mechanisms not fully understood.
  • Lactate accumulation during intense physical activity is a known metabolic byproduct.
  • Mitochondria play a critical role in cellular energy production and neuronal function.

Purpose of the Study:

  • To elucidate the mechanism by which excessive exercise impairs cognitive function.
  • To identify the specific cellular components involved in exercise-induced cognitive deficits.
  • To investigate potential therapeutic targets for mitigating cognitive impairment from over-exercise.

Main Methods:

  • Investigated the role of muscle-derived mitochondria-derived vesicles (MDVs) in response to excessive exercise in a mouse model.
  • Characterized the specific subtype of MDVs (otMDVs) involved, analyzing their molecular markers (mtDNA, PAF) and migratory behavior.
  • Utilized molecular assays to examine the impact of otMDVs on hippocampal neuron mitochondrial transport and synaptic function.
  • Employed a PAF-neutralizing antibody to block otMDV activity and assessed cognitive and synaptic outcomes.
  • Correlated circulating otMDV levels with cognitive function in human studies.

Main Results:

  • Excessive exercise induced lactate accumulation, prompting muscle secretion of otMDVs with high mtDNA and PAF.
  • otMDVs were found to enter hippocampal neurons, displace endogenous mitochondria, and trigger synaptic energy deficits.
  • Released mtDNA from otMDVs activated the cGAS-STING pathway, inhibiting kinesin family member 5 and blocking mitochondrial transport.
  • PAF on otMDVs, along with syntaphilin, blocked synaptic mitochondrial anchoring sites, further impairing energy supply.
  • Blocking otMDV migration with a PAF-neutralizing antibody reversed synapse loss and cognitive impairment.
  • Elevated circulating otMDV levels in humans correlated with cognitive impairment.

Conclusions:

  • A specific subpopulation of muscle-derived MDVs (otMDVs) mediates cognitive decline following excessive exercise.
  • otMDVs disrupt hippocampal mitochondrial function by displacement and impaired transport, leading to synaptic energy crisis.
  • Targeting otMDVs, particularly their migration via PAF, offers a potential therapeutic strategy for exercise-induced cognitive dysfunction.