BACKGROUND:Resveratrol is a naturally occurring polyphenolic compound in plants,recognized for its anti-inflammatory,antioxidant,and antiproliferative properties.Its role in preventing and treating various chronic diseases has been extensively documented.Recent evidence suggests that resveratrol may help delay exercise-induced fatigue,although the underlying mechanisms remain to be systematically elucidated.OBJECTIVE:To explore the possible role and mechanism of resveratrol in delaying exercise-induced fatigue,based on the mechanism of exercise-induced fatigue,in order to provide a theoretical basis for the research and application of resveratrol in the field of sports nutrition.METHODS:Chinese and English search terms were"resveratrol,exercise-induced fatigue,oxidative stress,inflammation,energy substance,muscle injury,mitochondrial quality,neurotransmitter."CNKI,WanFang Data,and PubMed were searched for relevant research literature published from January,1992 to August 2024.A total of 73 core related articles were obtained according to inclusion and exclusion criteria.RESULTS AND CONCLUSION:(1)Resveratrol is a naturally occurring polyphenolic compound commonly found in plants such as grape skins,berries,and peanuts.It exhibits multiple biological activities,including antioxidant,anti-aging,anticancer,and anti-inflammatory properties.Resveratrol shows potential for preventing and treating various chronic diseases and is also thought to delay the onset of exercise-induced fatigue.(2)Exercise-induced fatigue is a non-pathological fatigue phenomenon with a complex mechanism.It is related to peripheral mechanisms such as the depletion of energy substrates,the accumulation of metabolic by-products,inflammation,and oxidative stress,as well as central mechanisms,including protective inhibition by the central nervous system and neurotransmitter imbalances.(3)Resveratrol activates the kelch-like epichlorohydrin-associated protein 1/nuclear factor erythroid 2-related factor 2 pathway,upregulating antioxidant-related genes such as catalase and superoxide dismutase while downregulating genes such as malondialdehyde and 4-hydroxy-2-nonenal,ultimately reducing oxidative stress.Resveratrol also activates silent information regulator 1,inhibits the nuclear factor-kappaB and nucleotide-binding oligomerization domain-like receptor thermal protein domain associated protein 3 inflammasome pathways,and downregulates pro-inflammatory cytokines such as tumor necrosis factor-α,interleukin-6,and interleukin-1β,alleviating inflammation.Additionally,resveratrol increases short-chain fatty acid production by the gut microbiota,elevates the lactate/pyruvate ratio in the liver to promote gluconeogenesis,and enhances fatty acid oxidation,thereby improving energy substrate utilization.Furthermore,through silent information regulator 1/peroxisome proliferator-activated receptor-y coactivator-1α/nuclear respiratory factor 1 activation,resveratrol enhances mitochondrial biogenesis in skeletal muscle,promotes mitochondrial fusion and fission for optimal dynamics,and activates mitophagy,improving mitochondrial quality.It also diminishes plasma tryptophan levels,decreases excessive serotonin secretion in the brain,increases dopamine release,and reduces glutamate toxicity,helping regulate neurotransmitter imbalances.Moreover,resveratrol lowers plasma lactate and ammonia levels,promoting metabolic by-product clearance,thereby delaying the onset of exercise-induced fatigue.(4)While current evidence indicates that resveratrol is effective in delaying exercise-induced fatigue,the optimal dose,timing,and duration of supplementation remain uncertain.Moreover,the interactions between resveratrol and other supplements,such as caffeine and vitamins,remain underexplored.Thus,future research should focus on optimizing supplementation strategies for resveratrol.

BACKGROUND:Resveratrol is a naturally occurring polyphenolic compound in plants,recognized for its anti-inflammatory,antioxidant,and antiproliferative properties.Its role in preventing and treating various chronic diseases has been extensively documented.Recent evidence suggests that resveratrol may help delay exercise-induced fatigue,although the underlying mechanisms remain to be systematically elucidated.OBJECTIVE:To explore the possible role and mechanism of resveratrol in delaying exercise-induced fatigue,based on the mechanism of exercise-induced fatigue,in order to provide a theoretical basis for the research and application of resveratrol in the field of sports nutrition.METHODS:Chinese and English search terms were"resveratrol,exercise-induced fatigue,oxidative stress,inflammation,energy substance,muscle injury,mitochondrial quality,neurotransmitter."CNKI,WanFang Data,and PubMed were searched for relevant research literature published from January,1992 to August 2024.A total of 73 core related articles were obtained according to inclusion and exclusion criteria.RESULTS AND CONCLUSION:(1)Resveratrol is a naturally occurring polyphenolic compound commonly found in plants such as grape skins,berries,and peanuts.It exhibits multiple biological activities,including antioxidant,anti-aging,anticancer,and anti-inflammatory properties.Resveratrol shows potential for preventing and treating various chronic diseases and is also thought to delay the onset of exercise-induced fatigue.(2)Exercise-induced fatigue is a non-pathological fatigue phenomenon with a complex mechanism.It is related to peripheral mechanisms such as the depletion of energy substrates,the accumulation of metabolic by-products,inflammation,and oxidative stress,as well as central mechanisms,including protective inhibition by the central nervous system and neurotransmitter imbalances.(3)Resveratrol activates the kelch-like epichlorohydrin-associated protein 1/nuclear factor erythroid 2-related factor 2 pathway,upregulating antioxidant-related genes such as catalase and superoxide dismutase while downregulating genes such as malondialdehyde and 4-hydroxy-2-nonenal,ultimately reducing oxidative stress.Resveratrol also activates silent information regulator 1,inhibits the nuclear factor-kappaB and nucleotide-binding oligomerization domain-like receptor thermal protein domain associated protein 3 inflammasome pathways,and downregulates pro-inflammatory cytokines such as tumor necrosis factor-α,interleukin-6,and interleukin-1β,alleviating inflammation.Additionally,resveratrol increases short-chain fatty acid production by the gut microbiota,elevates the lactate/pyruvate ratio in the liver to promote gluconeogenesis,and enhances fatty acid oxidation,thereby improving energy substrate utilization.Furthermore,through silent information regulator 1/peroxisome proliferator-activated receptor-y coactivator-1α/nuclear respiratory factor 1 activation,resveratrol enhances mitochondrial biogenesis in skeletal muscle,promotes mitochondrial fusion and fission for optimal dynamics,and activates mitophagy,improving mitochondrial quality.It also diminishes plasma tryptophan levels,decreases excessive serotonin secretion in the brain,increases dopamine release,and reduces glutamate toxicity,helping regulate neurotransmitter imbalances.Moreover,resveratrol lowers plasma lactate and ammonia levels,promoting metabolic by-product clearance,thereby delaying the onset of exercise-induced fatigue.(4)While current evidence indicates that resveratrol is effective in delaying exercise-induced fatigue,the optimal dose,timing,and duration of supplementation remain uncertain.Moreover,the interactions between resveratrol and other supplements,such as caffeine and vitamins,remain underexplored.Thus,future research should focus on optimizing supplementation strategies for resveratrol.

Objective:To observe the relationship between the response to anti-vascular endothelial growth factor (VEGF) drug treatment and single nucleotide polymorphism (SNP) genotype in patients with wet age-related macular degeneration (wAMD).Methods:A retrospective clinical study. From August 2019 to September 2020, 103 eyes of 103 wAMD patients diagnosed in Tianjin Medical University Eye Hospital were included in the study. Among them, there were 59 males (57.28%, 59/103) and 44 females (42.72%, 44/103); the average age was 68.74±7.74 years. The standard logarithmic visual acuity chart was used to detect the Best Corrected Visual Acuity of the affected eye and converted to the logarithmic minimum angle of resolution (logMAR) visual acuity during statistics. Optical coherence tomography was used to detect the central retinal thickness (CRT) of the affected eye. At the same time, the patient's high-density lipoprotein cholesterol (HDL-C) was tested. All eyes were treated with intravitreal injection of anti-VEGF drugs once a month for 3 months. Before the initial treatment, peripheral venous blood from the patient were collected. Interleukin-8 ( IL-8), complement C3 gene ( C3), complement factor H ( CFH), liver lipase ( LIPC), cholesterol ester transfer protein ( CETP), ATP binding cassette subfamily a member 1 ( ABCA1), lipoprotein lipase ( LPL), fatty acid desaturation gene cluster ( FADS1) SNP. According to gene frequency, genotypes are divided into wild type and mutant type were detected. Qualitative data such as the frequency difference of the genotype distribution in the clinical phenotype and the Hardy-Weinberg equilibrium of the genotype distribution were compared with the Chi-square test or Fisher's exact test. Results:There were fewer CRT responders in IL-8 rs4073 mutant (TA+AA) patients than wild-type (TT) [odds ratio ( OR)=0.310, 95% confidence interval ( CI) 0.106-0.910, P<0.05). Among them, after the drug stratification test, the proportion of patients with IL-8 rs4073 locus TT genotype in the conbercept treatment group was less CRT non-responders ( OR=0.179, 95% CI=0.034-0.960, P=0.033). Patients with LIPC rs2043085 mutant (CT+TT) with BCVA increased ≥0.2 logMAR are more likely than wild-type (CC) ( OR=3.031, 95% CI 1.036-8.867, P<0.05); HDL-C level was significantly lower Compared with wild type (CC), the difference was statistically significant ( t=2.448, P=0.016). There was no significant difference in logMAR BCVA and CRT between IL-8 rs4073, LIPC rs2043085 mutant and wild-type patients before treatment ( IL-8 rs4073: Z=-0.198, -1.651; P=0.843, 0.099; LIPC rs2043085: Z=-0.532, -0.152; P=0.595, 0.879). C3 rs 225066, CFH rs800292, CETP rs708272, ABCA1 rs1883025, FADS1 rs174547, LPL rs12678919 have no correlation with anti-VEGF drug treatment response. Conclusions:Patients with wAMD are treated with anti-VEGF drugs. Those with IL-8 rs4073 locus A genotype may be less responsive to CRT. LIPC rs2043085 locus T genotypes may be relatively more responsive to BCVA.