Progress in the Study of B-Cell Immune Metabolic Regulation Mechanisms in Exercise-Induced Fatigue: A Narrative Review
- 1Naval Medical Center, Shanghai 200052, China
- 2Department of Traditional Chinese Medicine, Naval Medical University, Shanghai 200433, China
Abstract
Exercise-induced fatigue refers to the reversible decline in neuromuscular function during physical activity, whose immune–metabolic regulatory mechanisms remain incompletely understood. Recent studies have revealed that B cells can regulate hepatic glutamate metabolism via secretion of transforming growth factor-β1 (TGF-β1), thereby influencing mitochondrial function in skeletal muscle, revealing a novel immune–metabolic pathway relevant to exercise-induced fatigue. This review synthesizes current evidence on immune regulation in exercise-induced fatigue, centering on the TGF-β1-driven glutamate axis linking the liver and skeletal muscle, cross-organ signaling, and hypotheses of central fatigue. We also discuss targeted interventions along this pathway to inform future basic research and clinical management of exercise-induced fatigue.
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BibTeX
@article{yi2026progress,
title = {{Progress in the Study of B-Cell Immune Metabolic Regulation Mechanisms in Exercise-Induced Fatigue: A Narrative Review}},
author = {Li Yi and Huier Xiang and Guolin Gan and Yixuan Wang and Yi Ruan and Shangjin Song and Wei Gu and Xin Wang},
journal = {Metabolites},
year = {2026},
month = oct,
doi = {10.3390/metabo16100752},
url = {https://www.mdpi.com/2218-1989/16/10/752},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Progress in the Study of B-Cell Immune Metabolic Regulation Mechanisms in Exercise-Induced Fatigue: A Narrative Review
AU - Li Yi
AU - Huier Xiang
AU - Guolin Gan
AU - Yixuan Wang
AU - Yi Ruan
AU - Shangjin Song
AU - Wei Gu
AU - Xin Wang
PY - 2026
DA - 2026/10/01
JO - Metabolites
DO - 10.3390/metabo16100752
UR - https://www.mdpi.com/2218-1989/16/10/752
AB - Exercise-induced fatigue refers to the reversible decline in neuromuscular function during physical activity, whose immune–metabolic regulatory mechanisms remain incompletely understood. Recent studies have revealed that B cells can regulate hepatic glutamate metabolism via secretion of transforming growth factor-β1 (TGF-β1), thereby influencing mitochondrial function in skeletal muscle, revealing a novel immune–metabolic pathway relevant to exercise-induced fatigue. This review synthesizes current evidence on immune regulation in exercise-induced fatigue, centering on the TGF-β1-driven glutamate axis linking the liver and skeletal muscle, cross-organ signaling, and hypotheses of central fatigue. We also discuss targeted interventions along this pathway to inform future basic research and clinical management of exercise-induced fatigue.
SN - 2218-1989
ER -