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Peer-reviewedCC BY 4.0Metabolites

Progress in the Study of B-Cell Immune Metabolic Regulation Mechanisms in Exercise-Induced Fatigue: A Narrative Review

  1. 1Naval Medical Center, Shanghai 200052, China
  2. 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  -