Exploratory study of β-endorphin, immune profiles, and skeletal muscle endoplasmic reticulum stress following an overtraining-like forced swimming regimen in rats.

Authors

Ferbian Milas Siswanto, Periskila Abigail, Amanda Putri Elvandari, Alex Pangkahila

Published in

Physiology international. Sep 15, 2026. Epub Sep 15, 2026.

Abstract

Physical exercise triggers wide range of physiological responses, including immunological and neuroendocrine alterations. Although moderate exercise is beneficial, overtraining may cause various detrimental effects.
To assess the effects of overtraining-like forced exercise on beta-endorphin levels, immune modulation, and endoplasmic reticulum (ER) stress in rats.
Twenty-one male Wistar rats were randomly divided into three groups: negative control (NC) group (without any training program), moderate exercise (ME) group (30 min of swimming, 3 times a week for 4 weeks) and overtraining-like forced exercise (OT) group (60 min of swimming, 7 times a week for 4 weeks). Plasma levels of β-endorphin, corticosterone, and cytokines (IL-6, TNF-α, IL-10), as well as skeletal muscle ER stress markers (GRP78 and CHOP), were measured using ELISA. Total and differential leukocyte counts were analyzed with an automated hematology analyzer.
The extensive training protocol in the OT group increased plasma beta-endorphin levels (P < 0.05), depleted leukocyte counts and differentials (P < 0.05) and altered cytokines profile (P < 0.05). The GRP78/CHOP ratio revealed a significant depletion in the OT group compared to the NC (P < 0.05), indicating ER stress activation.
Elevated beta-endorphin reflects a neuroendocrine stress response that may become maladaptive over time. The observed immune dysregulation and increased ER stress suggest that overtraining-like forced exercise imposes a physiological burden potentially leading to tissue dysfunction and inflammation.
Prolonged overtraining-like forced exercise, if not properly regulated, may lead to maladaptive stress responses and adverse health outcomes.

PMID:
42742976
Bibliographic data and abstract were imported from PubMed on 16 Sep 2026.

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