PDF(Pubmed)
Abstract：
Physical activity (PA) in the form of aerobic exercise (AE) preserves and improves neurocognitive function across the lifespan. However, a mechanistic understanding of the pathways by which aerobic exercise impacts brain health is still lacking, particularly with respect to stress-related pathways. One mechanistic hypothesis is that AE improves neurocognitive health in part by modifying circulating levels of stress-related hormones and signaling factors associated with the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system (ANS), as commonly measured by the biomarkers cortisol (CORT) and salivary α-amylase (sAA). Thus, this hypothesis predicts that changes in stress biomarkers, such as CORT and sAA, are possible explanatory pathways mediating the positive effects of AE on neurocognitive health. In the present review article, we provide a summary of available studies examining the possibility that exercise-induced changes to stress biomarkers could partly account for exercise-related improvements in neurocognitive health. Our review indicates that despite the intuitive appeal of this hypothesis, there is insufficient evidence available to conclude that chronic and habitual AE affects neurocognitive health by altering stress biomarker pathways. The cross-sectional nature of the majority of reviewed studies highlights the need for well-controlled studies to adequately test this hypothesis.
摘要：
有氧运动（AE）形式的身体活动（PA）可在整个生命周期中保留并改善神经认知功能。然而,对有氧运动影响大脑健康的途径的机械理解仍然缺乏，特别是与压力相关的途径。一个机制假设是，AE部分通过改变与下丘脑-垂体-肾上腺（HPA）轴和自主神经系统（ANS）相关的应激相关激素和信号因子的循环水平来改善神经认知健康。通常由生物标志物皮质醇(CORT)和唾液α-淀粉酶(sAA)测量。因此，这个假设预测压力生物标志物的变化，如CORT和SAA，是可能的解释途径介导AE对神经认知健康的积极影响。在本评论文章中，我们总结了现有研究,这些研究检验了运动诱导的应激生物标志物变化可能部分解释了运动相关神经认知健康改善的可能性.我们的审查表明，尽管这一假设具有直观的吸引力，没有足够的证据可以得出结论,慢性和习惯性AE通过改变应激生物标志物通路影响神经认知健康.大多数综述研究的横截面性质突出了需要良好的对照研究来充分检验这一假设。
