Activation of brain lactate receptor GPR81 aggravates exercise-induced central fatigue
Abstract
Exercise-induced fatigue is a complex physiological phenomenon and is greatly influenced by central mechanisms in brain. As one of the most abundant circulating carbon metabolites, l-lactate in brain has been considered to be an important supplementary fuel during exercise; however, whether it plays a signaling role in fatigue remains largely obscure. In this study, our results initially revealed that brain l-lactate levels were increased after an exhaustive swimming session in several brain regions including motor cortex, hippocampus, and cerebellum. Then, we examined the specific role of brain lactate receptor, also known as hydroxycarboxylic acid receptor 1 (GPR81), in exercise-induced fatigue. We found that intracerebroventricular injection of either d-lactate (an enantiomer that could mediate activation of GPR81 as l-lactate) or a potent GPR81 agonist 3-chloro-5-hydroxybenzoic acid (CHBA), significantly decreased the swimming time to fatigue. After being subjected to the same weight-loaded swimming for 30 min, no obvious changes of blood lactate levels, gastrocnemius pAMPK/AMPK ratio, and glycogen contents were observed between intracerebroventricular CHBA-injected mice and vehicle-treated ones, which suggested a comparable degree of peripheral fatigue. Meanwhile, there were higher extracellular γ-aminobutyric acid (GABA) levels and lower extracellular glutamate levels and glutamate/GABA ratio in motor cortex of the intracerebroventricular CHBA-injected mice than that of vehicle-treated ones, indicating a greater extent of central fatigue in CHBA-injected mice than that in vehicle animals. Collectively, our results suggested that an increased level of brain l-lactate acts as a signaling molecule via activating GPR81, which in turn exacerbates central fatigue during exercise.
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In the brain, GPR81 is located primarily at excitatory synapses that inhibits neuronal excitability via cAMP when bound to lactate, suggesting lactate could exacerbate central fatigue by GPR81 during acute exercise.
“In the brain, GPR81 is located primarily at excitatory synapses that inhibits neuronal excitability via cAMP when bound to lactate, which suggested lactate could exacerbate central fatigue by GPR81 during acute exercise [56].”
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- Authors
- Li, J., Xia, Y., Xu, H., Xiong, R., Zhao, Y., Li, P., Yang, T., Huang, Q., & Shan, F.
- Affiliations
- Army Medical University (CN)
- Corresponding author
- Shan, Fabo
- Venue
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Publisher
- American Physiological Society
- Published
- 2022-11-01
- Volume
- 323
- Issue
- 5
- Pages
- R822-R831
- ISSN
- 0363-6119 (ISSN-L)
- 1522-1490
- OpenAlex
- W4300690633
- Cited by
- 29
- References
- 56
- Citations by year
- 2026: 8 · 2025: 9 · 2024: 6 · 2023: 6
- FWCI
- 1.53
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (NO. 32071167)
- Topics
- Physical Sciences › Engineering › Biomedical Engineering › Muscle activation and electromyography studies
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Sports Performance and Training
- Keywords
- exercise fatigue, central fatigue, brain lactate, GPR81, intracerebroventricular administration, motor cortex, glutamate/GABA ratio, GABA, glutamate, exhaustive swimming, AMPK, glycogen
- MeSH terms
- Animals, Benzoates, Brain, Carrier Proteins, Fatigue, gamma-Aminobutyric Acid, Glutamates, Lactic Acid, Receptors, G-Protein-Coupled, Mice, Hydroxybenzoates
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