RESUMO
BACKGROUND: The aim of this study is to make sure whether polymorphism Ala54Thr of gene Fatty Acid-Binding Protein 2 (FABP2) is associated with stroke risk in Hunan Han population of China. MATERIAL AND METHODS: A total of 206 cerebral infarction (CI), 185 cerebral hemorrhage (CH) and 172 controls were enrolled in our study. Ala54Thr was applied by polymerasechain reaction (PCR) and restriction fragment length polymorphism (RFLP). RESULTS: No significant difference in Ala54Thr genotypic distribution of FABP2 was observed between stroke group (CI subgroup, CH subgroup included) and controls group. In stroke group, plasma TG level of who carried Ala54Thr, Thr54Thr of FABP2 is significantly higher than who carring Ala54Ala. In controls group, blood lipid is not significantly different among 3 genotypes of Ala54Thr. There is no significant difference in blood pressure and fasting blood sugar between strokes and controls. CONCLUSIONS: Our study shows that Ala54Thr of FABP2 may be not associated with stroke risk but associated with plasma TG level of stroke patients for Hunan Han population of China.
Assuntos
Etnicidade/genética , Proteínas de Ligação a Ácido Graxo/genética , Estudos de Associação Genética , Predisposição Genética para Doença , Polimorfismo de Nucleotídeo Único/genética , Acidente Vascular Cerebral/genética , Substituição de Aminoácidos , Estudos de Casos e Controles , China , Demografia , Feminino , Frequência do Gene/genética , Humanos , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Fatores de RiscoRESUMO
Fatigue, commonly experienced in daily life, is a feeling of extreme tiredness, shortage or lack of energy, exhaustion, and difficulty in performing voluntary tasks. Central fatigue, defined as a progressive failure to voluntarily activate the muscle, is typically linked to moderate- or light-intensity exercise. However, in some instances, high-intensity exercise can also trigger the onset of central fatigue. Exercise-induced central fatigue often precedes the decline in physical performance in well-trained athletes. This leads to a reduction in nerve impulses, decreased neuronal excitability, and an imbalance in brain homeostasis, all of which can adversely impact an athlete's performance and the longevity of their sports career. Therefore, implementing strategies to delay the onset of exercise-induced central fatigue is vital for enhancing athletic performance and safeguarding athletes from the debilitating effects of fatigue. In this review, we discuss the structural basis, measurement methods, and biomarkers of exercise-induced central fatigue. Furthermore, we propose non-pharmacological interventions to mitigate its effects, which can potentially foster improvements in athletes' performances in a healthful and sustainable manner.