---
title: "Interval Training Intensity Modulates Brain Mitophagy, Metabolic Signaling, and Neuroinflammation"
id: "pubmed-42667305"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42667305"
content_type: "clinical_feed_article"
specialty: "Pharmacology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42667305/"
doi: "10.1007/s11011-026-01944-3"
published_at: "2026-08-29T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Interval Training Intensity Modulates Brain Mitophagy, Metabolic Signaling, and Neuroinflammation
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42667305
- **Specialty:** [Pharmacology](https://medichelpline.com/clinical-feed/pharmacology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42667305/)
- **DOI:** [10.1007/s11011-026-01944-3](https://doi.org/10.1007%2Fs11011-026-01944-3)
- **Published At:** 2026-08-29T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- This animal study used fifty male rats (n = 10 per group) to examine how interval training intensity affects brain **mitophagy**, metabolic signaling, oxidative stress, and neuroinflammation in a model of **type 2 diabetes**. - Groups were: healthy control (HC), diabetic control (DC), diabetic + low-intensity interval training (LIIT), diabetic + moderate-intensity interval training (MIIT), and diabetic + high-intensity interval training (HIIT). - Post-intervention analyses were performed on hippocampal and cortical tissues for metabolic signaling markers (AMPK, ULK1, mTOR), mitophagy-related proteins (PINK1, Parkin, LC3-II/I, p62), oxidative and antioxidant indices (MDA, SOD, CAT, TAC), pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), and lipid peroxidation marker 4-HNE. - Statistical significance was set at p < 0.05 for all comparisons reported in the source. - MIIT and HIIT activated **AMPK-ULK1** signaling and suppressed **mTOR** in both hippocampus and cortex, with a stronger effect in the hippocampus, leading to enhanced mitophagy markers (increased PINK1, Parkin, LC3-II/I; reduced p62) relative to diabetic controls. - Improvements in redox balance (lower MDA and 4-HNE; increased SOD, CAT, TAC) accompanied the signaling and mitophagy changes, indicating reduced lipid peroxidation and oxidative stress with higher-intensity interval training. - Pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) were attenuated following interval training, with greater reductions at moderate and high intensities. - Overall, effects followed an intensity-dependent pattern: LIIT < MIIT < HIIT. The authors conclude moderate- and high-intensity interval protocols may confer greater neuroprotective adaptations than low intensity, but note the need for confirmation in broader experimental contexts. - Keywords reported: Brain metabolism; Exercise intensity; Interval training; **Mitophagy**; Neuroinflammation; **Type 2 diabetes**.
## Clinical Analysis & Structured Key Points
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Mahdihayati@phd.tabrizu.ac.ir.") Affiliations Expand ### Affiliations * 1 Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Tabriz, Tabriz, Iran. * 2 Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Tabriz, Tabriz, Iran. Mahdihayati@phd.tabrizu.ac.ir. * PMID: **42667305** * DOI: [ 10.1007/s11011-026-01944-3 ](https://doi.org/10.1007/s11011-026-01944-3) Item in Clipboard # Intensity-dependent effects of interval training on brain mitophagy, metabolic signaling pathways, and neuroinflammation in a rat model of type 2 diabetes Babak Esmealy et al. Metab Brain Dis. 2026. Show details Display options Display options Format Abstract PubMed PMID Metab Brain Dis Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Metab+Brain+Dis%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Metab+Brain+Dis%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667305/) . 2026 Aug 29;41(1):196. doi: 10.1007/s11011-026-01944-3. ### Authors [Babak Esmealy](https://pubmed.ncbi.nlm.nih.gov/?term=Esmealy+B&cauthor_id=42667305)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42667305/#short-view-affiliation-1 "Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Tabriz, Tabriz, Iran."), [Kosar Zeinizadeh](https://pubmed.ncbi.nlm.nih.gov/?term=Zeinizadeh+K&cauthor_id=42667305)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42667305/#short-view-affiliation-1 "Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Tabriz, Tabriz, Iran."), [Elaheh Piralaiy](https://pubmed.ncbi.nlm.nih.gov/?term=Piralaiy+E&cauthor_id=42667305)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42667305/#short-view-affiliation-1 "Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Tabriz, Tabriz, Iran."), [Farnaz Derakhti](https://pubmed.ncbi.nlm.nih.gov/?term=Derakhti+F&cauthor_id=42667305)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42667305/#short-view-affiliation-1 "Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Tabriz, Tabriz, Iran."), [Mahdi Hayati](https://pubmed.ncbi.nlm.nih.gov/?term=Hayati+M&cauthor_id=42667305)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42667305/#short-view-affiliation-2 "Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Tabriz, Tabriz, Iran. Mahdihayati@phd.tabrizu.ac.ir.") ### Affiliations * 1 Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Tabriz, Tabriz, Iran. * 2 Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Tabriz, Tabriz, Iran. Mahdihayati@phd.tabrizu.ac.ir. * PMID: **42667305** * DOI: [ 10.1007/s11011-026-01944-3 ](https://doi.org/10.1007/s11011-026-01944-3) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID ## Abstract Type 2 diabetes mellitus impairs brain metabolic and mitochondrial homeostasis, yet the intensity-dependent neuroprotective effects of exercise remain poorly defined. This study examined the intensity‑dependent effects of interval training on brain mitophagy, metabolic signaling, oxidative stress, and neuroinflammation in a type 2 diabetes model. Fifty male rats were assigned to five groups (n = 10 each): healthy control (HC), diabetic control (DC), diabetic + low-intensity interval training (LIIT), diabetic + moderate-intensity interval training (MIIT), and diabetic + high-intensity interval training (HIIT). Following the intervention, hippocampal and cortical tissues were analyzed for metabolic signaling markers (AMPK, ULK1, mTOR), mitophagy-related proteins (PINK1, Parkin, LC3-II/I, p62), oxidative and antioxidant indices (MDA, SOD, CAT, TAC), pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), and lipid peroxidation (4-HNE). Statistical significance was set at p < 0.05. MIIT and HIIT activated AMPK-ULK1 signaling and suppressed mTOR in the hippocampus and cortex, leading to enhanced mitophagy, particularly in the hippocampus. These adaptations were accompanied by improved redox balance, reduced lipid peroxidation, and attenuated neuroinflammation, with effects increasing in an intensity-dependent manner (LIIT < MIIT < HIIT). Interval training may support neuroprotective adaptations in type 2 diabetes, with moderate- and high-intensity protocols potentially offering greater benefits than low intensity. Still, these effects require confirmation in broader experimental contexts. **Keywords:** Brain metabolism; Exercise intensity; Interval training; Mitophagy; Neuroinflammation; Type 2 diabetes. © 2026. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declarations. Consent to participate and publish: Not applicable. Competing interest: The authors declare that they have no competing financial or non-financial interests, directly or indirectly related to the work submitted for publication. ## References 1. 1. Butterfield DA, Halliwell B (2019) Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease. 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Egan DF, Shackelford DB, Mihaylova MM, Gelino S, Kohnz RA, Mair W, Taylor R (2011) Phosphorylation of ULK1 (hATG1) by AMP-activated protein kinase connects energy sensing to mitophagy. Science 331(6016):456–461 - [DOI](https://doi.org/10.1126/science.1196371) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/21205641/) 5. 1. Flynn MG, McFarlin BK, Markofski MM (2007) State of the art reviews: The anti-inflammatory actions of exercise training. Am J Lifestyle Med 1(3):220–235 - [DOI](https://doi.org/10.1177/1559827607300283) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/25431545/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/4243532/) Show all 34 references ## MeSH terms * Animals Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Animals%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Animals) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667305/) * Brain* / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Brain%2Fmetabolism%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Brain) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667305/) * Diabetes Mellitus, Experimental* / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Diabetes+Mellitus%2C+Experimental%2Fmetabolism%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH 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