Frontiers in nutrition · 2026
The herbal pair of Smilax glabra Roxb. and Ficus hirta Vahl. improves exercise performance by regulating mitochondrial function via the adiponection receptors-mediated AMPK signaling pathway.
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Bao Ya-Nan, Wang Wen-Hao, Yang Hai-Xia, Qian Lei, Sui Xue, Wang Meng, Su Bo-Wei, Chen Fang-Yuan, Cui Xiao-Hui, Lao Jia-Yi, Wen Rui-Kang, Ji Hong-Yu, Hu Wen-Juan, Wen Lin, Ren Hui-Wen, Luan Zhi-Lin
Аннотация
INTRODUCTION: Exercise fatigue can significantly impair physical function, while herbal medicines exhibit broad application prospects in anti-fatigue research. The herbal pair of Smilax glabra Roxb. and Ficus hirta Vahl. (FSP) is well-known for its hepatoprotective, dampness-eliminating, and detoxifying effects. However, its mechanism of action in improving exercise performance remains unclear.
METHODS: The impact of FSP on exercise performance was assessed through motor behavioral tests and monitoring of energy metabolism in both resting and exercise states. The anti-fatigue effects were evaluated by measuring fatigue-related biochemical markers in serum and urine using biochemical assay kits. Transcriptome sequencing of liver tissues from the animal model was conducted, and differentially expressed genes as well as significantly enriched pathways were identified via GO and KEGG enrichment analyses. Subsequently, a multi-parameter evaluation system was established, and in conjunction with molecular docking technology, two potential key active components in FSP were screened. Finally, their mechanisms of action were further verified using animal and cell-based experiments.
RESULTS: This study confirmed that FSP intervention significantly improved exercise performance in mice, accelerated lactate clearance, enhanced energy metabolism, and increased hepatic and muscular glycogen reserves, while alleviating oxidative stress and reducing systemic inflammation levels. Mechanistic investigations demonstrated that FSP activated the expression of adiponectin receptors (AdipoR1 and AdipoR2) in mouse liver, promoting the overexpression of downstream phosphorylated AMPK (p-AMPK) and PGC-1α, thereby regulating mitochondrial function and lipid metabolism. Furthermore, the study identified taxifolin and apigenin as the potential primary active components in FSP responsible for modulating the AdipoRs-AMPK pathway, with evidence of a synergistic effect between these two compounds.
CONCLUSIONS: FSP regulates mitochondrial function through the AdipoRs-AMPK signaling pathway to exert anti-fatigue effects and enhance exercise performance.
METHODS: The impact of FSP on exercise performance was assessed through motor behavioral tests and monitoring of energy metabolism in both resting and exercise states. The anti-fatigue effects were evaluated by measuring fatigue-related biochemical markers in serum and urine using biochemical assay kits. Transcriptome sequencing of liver tissues from the animal model was conducted, and differentially expressed genes as well as significantly enriched pathways were identified via GO and KEGG enrichment analyses. Subsequently, a multi-parameter evaluation system was established, and in conjunction with molecular docking technology, two potential key active components in FSP were screened. Finally, their mechanisms of action were further verified using animal and cell-based experiments.
RESULTS: This study confirmed that FSP intervention significantly improved exercise performance in mice, accelerated lactate clearance, enhanced energy metabolism, and increased hepatic and muscular glycogen reserves, while alleviating oxidative stress and reducing systemic inflammation levels. Mechanistic investigations demonstrated that FSP activated the expression of adiponectin receptors (AdipoR1 and AdipoR2) in mouse liver, promoting the overexpression of downstream phosphorylated AMPK (p-AMPK) and PGC-1α, thereby regulating mitochondrial function and lipid metabolism. Furthermore, the study identified taxifolin and apigenin as the potential primary active components in FSP responsible for modulating the AdipoRs-AMPK pathway, with evidence of a synergistic effect between these two compounds.
CONCLUSIONS: FSP regulates mitochondrial function through the AdipoRs-AMPK signaling pathway to exert anti-fatigue effects and enhance exercise performance.