De Las Heras Bernat, Rodrigues Lynden, Cristini Jacopo, Yu Eric, Gan-Or Ziv, Arbour Nathalie, Thiel Alexander, Tang Ada, Fung Joyce, Eng Janice J, Roig Marc
Memory and Motor Rehabilitation Laboratory (MEMORY-LAB), Jewish Rehabilitation Hospital, Laval, QC, Canada.
School of Physical and Occupational Therapy, McGill University, Montreal, QC, Canada.
Neurorehabil Neural Repair. 2025 Aug;39(8):653-665. doi: 10.1177/15459683251342150. Epub 2025 Jun 3.
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.
背景
中风后，在恢复的早期亚急性期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方面的核心作用，它已被视为人类中风恢复的潜在生物标志物，上调BDNF的干预措施具有治疗潜力。心血管运动（CE）已被推荐用于中风康复，部分原因是其具有诱导神经适应的潜力，包括上调BDNF。
目的
研究心血管运动（CE）对处于恢复早期亚急性期个体的BDNF的影响。
方法
76名首次发生缺血性中风后3个月内的参与者被随机分配至接受8周的CE加标准护理或仅接受标准护理。为了测量血清BDNF水平对运动的慢性和急性反应，在基线、第4周和第8周进行分级运动试验前及试验后立即采集血样。还探讨了BDNF Val66Met多态性在调节BDNF反应中的潜在作用。采用意向性分析方法对数据进行分析。
结果
尽管心肺适能在临床上有显著提高，但CE并未引起血清BDNF的显著慢性或急性变化。此外，对CE的反应与心肺适能和临床结局的变化无关，也不受Val66Met的调节。
结论
这些发现表明，在中风恢复的亚急性期，CE上调循环BDNF的能力有限。
亚急性中风的运动与基因型：https://clinicaltrials.gov/study/NCT05076747 。
