Preconditioning by high-intensity interval training and moderate continuous training differentially affect hippocampal neurotrophic and inflammatory gene expression under acute noise stress in rats.

Authors

Mohammadamin Safari, Elaheh Farahbakht, Alireza Sharifabadi, Parvin Barzideh, Maryam Koushkie Jahromi

Published in

The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry. Pages 1-17. Aug 02, 2026. Epub Aug 02, 2026.

Abstract

This study compared high-intensity interval training (HIIT) versus moderate continuous training (MCT) as preconditioning on hippocampal BDNF, TrkB, and TNF-α gene expression in rats exposed to acute noise stress.
Forty-two male Wistar rats were randomised into seven groups (n = 6): control, time-control, stress, HIIT, MCT, HIIT+stress, and MCT+stress. Exercise groups underwent 8-week treadmill training (5 sessions/week). HIIT (6x2-min intervals, 85-90% Vmax) or MCT (22-min continuous, 65-70% Vmax). Stress groups received a single 4-hour noise exposure. Hippocampal mRNA was quantified via real-time PCR.
Both HIIT and MCT significantly upregulated BDNF versus time-control, with HIIT eliciting greater increases. MCT significantly elevated TrkB versus time-control. Noise stress reduced BDNF and TrkB while increasing TNF-α. Both exercise protocols attenuated these alterations. Under stress, HIIT+stress exhibited significantly higher TrkB than MCT+stress. MCT elevated TNF-α versus time-control, but stress-induced increases were similarly mitigated in both preconditioned groups. Correlation analysis revealed strong positive correlations between BDNF and TrkB and moderate correlations between BDNF and TNF-α, and TrkB and TNF-α.
HIIT and MCT differentially modulate hippocampal gene expression. While MCT effectively upregulates basal TrkB, HIIT provides superior protection against stress-induced TrkB suppression, highlighting intensity-specific neuroprotective adaptations and integrated pathway regulation among BDNF, TrkB, and TNF-α.

PMID:
42542948
Bibliographic data and abstract were imported from PubMed on 02 Aug 2026.

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