探讨心血管运动对早期亚急性脑卒中脑源性神经营养因子的急慢性影响。

IF 3.7
Bernat De Las Heras, Lynden Rodrigues, Jacopo Cristini, Eric Yu, Ziv Gan-Or, Nathalie Arbour, Alexander Thiel, Ada Tang, Joyce Fung, Janice J Eng, Marc Roig
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引用次数: 0

摘要

中风后,在恢复的早期亚急性阶段会出现促进生长的反应,导致神经可塑性增强,在此期间大脑可能对治疗干预更敏感。鉴于脑源性神经营养因子(BDNF)在动物模型中调节神经可塑性过程和脑修复中的核心作用,BDNF已被定位为人类中风恢复的潜在生物标志物,干预上调BDNF具有治疗潜力。心血管运动(CE)已被推荐用于中风康复,部分原因是其诱导神经适应的潜力,包括BDNF的上调。目的探讨CE对亚急性康复早期个体BDNF的影响。方法76例首次缺血性卒中患者在3个月内随机分为8周CE加标准治疗组或单独标准治疗组。为了测量运动对血清BDNF水平的慢性和急性反应,在基线、4周和8周进行分级运动测试之前和之后立即收集血液样本。我们还探讨了BDNF Val66Met多态性在调节BDNF反应中的潜在作用。采用意向治疗法分析数据。结果尽管在临床上具有重要意义的心肺功能增强,CE并没有引起血清BDNF的显著慢性或急性变化。此外,对CE的反应与心肺功能和临床结果的变化无关,也不受Val66Met的调节。这些发现表明,CE在卒中亚急性期恢复时上调循环BDNF的能力有限。试验注册:亚急性卒中的运动和基因型:https://clinicaltrials.gov/study/NCT05076747。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Investigating the Acute and Chronic Effects of Cardiovascular Exercise on Brain-Derived Neurotrophic Factor in Early Subacute Stroke.

BackgroundFollowing stroke, a growth-promoting response resulting in heightened neuroplasticity occurs during the early subacute stages of recovery, a period during which the brain may be more responsive to therapeutical interventions. Given its central role in regulating neuroplastic processes and brain repair in animal models, brain-derived neurotrophic factor (BDNF) has been targeted as a potential biomarker for stroke recovery in humans, with interventions upregulating BDNF holding therapeutical potential. Cardiovascular exercise (CE) has been recommended for stroke rehabilitation, partly due to its potential to induce neural adaptations, including upregulation of BDNF.ObjectivesTo examine the effects of CE on BDNF in individuals at early subacute stages of recovery.MethodsSeventy-six participants within 3 months of first-ever ischemic stroke were randomly assigned to 8 weeks of either CE plus standard care or standard care alone. To measure the chronic and acute responses to exercise in serum BDNF levels, blood samples were collected before and immediately after a graded exercise test conducted at baseline, 4, and 8 weeks. The potential role of the BDNF Val66Met polymorphism in modulating the BDNF response was also explored. Data were analyzed following an intention-to-treat approach.ResultsDespite clinically important increases in cardiorespiratory fitness, CE did not induce significant chronic or acute changes in serum BDNF. Furthermore, the response to CE was not associated with changes in cardiorespiratory fitness and clinical outcomes or was modulated by Val66Met.ConclusionsThese findings indicate that CE has a limited capacity to upregulate circulating BDNF in subacute stages of stroke recovery.Trial Registration:Exercise and Genotype in Sub-acute Stroke: https://clinicaltrials.gov/study/NCT05076747.

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