A068: Research Progress on the Mechanisms of Exercise Preconditioning in Promoting Neurological Repair After Stroke

Abstract

Stroke is a neurological disorder characterized by acute focal damage to the central nervous system due to vascular causes stands as a leading cause of disability and mortality worldwide. Two pivotal strategies to mitigate the global burden of stroke include the prevention of both initial and recurrent strokes, as well as the effective treatment of acute stroke patients to minimize fatalities and disabilities. Exercise, often regarded for its safety, cost-effectiveness, ease of implementation, and efficacy as a non-pharmacological intervention, has garnered widespread attention and is considered a crucial component in reducing stroke risk and aiding in stroke recovery. However, pre-stroke exercise preconditioning (EP) interventions have demonstrated superior preventive and mitigating effects. Consequently, understanding the neuroprotective mechanisms of exercise preconditioning in stroke is of paramount importance for the clinical translation of non-pharmacological treatments. Method: Using keywords such as “Stroke”, “exercise preconditioning” and “exercise pretraining”, we searched multiple databases such as PubMed and CNKI using the retrieval timeframe spans from the inception of the database up to the year 2024 included literature was systematically collated and analy. The predominant modality of EP employed in the reviewed studies was treadmill running, with less frequent utilization of swimming, voluntary wheel running, or a combination of various exercise types. Aerobic exercise constituted the primary form of EP, with a smaller proportion of studies utilizing high-intensity interval training. The exercise interventions were typically administered 5-7 times per week, with each session lasting no more than 30 minutes, and the total intervention period generally spanning 3-4 weeks. EP ameliorated brain injury and neurological deficits in stroke animals by restoring the structure and function of the cerebrovascular system and the blood-brain barrier, reducing neuronal cell death, inhibiting oxidative stress, and attenuating neuroinflammation. These beneficial effects were partially attributed to alterations in gut microbiota, modulation of the MAPK signaling pathway, and mitigation of excitotoxicity. EP exerts a positive impact on outcomes in animal models of stroke. However, the underlying mechanisms are complex, and the employed exercise protocols are relatively homogeneous. Future research should focus on translating these findings into clinical settings and evaluating the efficacy of diverse exercise intervention strategies to optimize therapeutic benefits