《生命科学》 2026, 38(10): 1778-1790
运动干预在治疗孤独症谱系障碍中的作用机制研究进展
摘 要：
孤独症谱系障碍（autism spectrum disorder，ASD）是一类以社交沟通障碍、重复刻板行为和兴趣受限为核心特征的神经发育性疾病，常伴随认知受损、胃肠道功能异常和睡眠障碍。作为非药物干预手段，运动干预被证实可改善多种神经系统疾病的症状，且对缓解ASD核心症状和共病问题亦展现积极作用，但其潜在的神经生物学机制尚未完全阐明。本综述系统梳理近年来临床与基础研究证据，重点从神经发育异常、神经炎症失衡、肠-脑轴以及睡眠障碍等方面，探讨运动干预影响ASD相关表型与脑功能网络的可能机制，为进一步优化ASD的治疗策略提供理论依据。
通讯作者：曾燕 , Email:zengyan68@wust.edu.cn 陈雨珊 , Email:yschen@wust.edu.cn
Abstract:
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by core symptoms including social communication deficits, repetitive stereotyped behaviors, and restricted interests. It is frequently accompanied by comorbidities such as cognitive impairment, gastrointestinal dysfunction, and sleep disturbances. As a non-pharmacological intervention, exercise-based therapy has been demonstrated to alleviate symptoms across various neuropsychiatric disorders and appears promising for mitigating both core ASD symptoms and related comorbidities. However, the neurobiological mechanisms supporting these effects remain incompletely elucidated, which limits the development of systematic and precision-guided exercise prescription for ASD. To address this gap, this review systematically synthesizes recent clinical and preclinical evidence, focusing on key pathophysiological domains, including abnormal neurodevelopment, neuroinflammation imbalance, gut-brain axis dysfunction, and sleep disturbances. We discuss how exercise interventions may reshape ASD-related behavioral phenotypes and brain network functions through convergent, multi-system mechanisms. At the neurodevelopmental level, exercise intervention is associated with region-specific structural adaptations, remodeling of synaptic plasticity, and partial normalization of γ -aminobutyric acid (GABA) system function. From a neuroimmune perspective, exercise intervention contributes to restoring the dynamic balance between pro-inflammatory and anti-inflammatory phenotypes of brain-resident microglia, while modulating the composition of gut microbiota and enhancing the production of short-chain fatty acids, thereby influencing peripheral-central immune crosstalk and reducing neuroinflammatory responses in ASD. In terms of sleep regulation, exercise intervention may support circadian stability by enhancing endogenous melatonin secretion and attenuating hyperarousal-related activity within the locus coeruleus-norepinephrine (LC-NE) system, thus helping to stabilize sleep-wake cycles and improve sleep quality. By systematically integrating evidence across these multidimensional mechanisms, this review constructs a cross-system, integrative neuroscientific framework. This review aims to deepen the mechanistic understanding of how exercise intervention confers therapeutic benefits in ASD. We further propose that future research should focus on defining the safety window and dose-response relationships of exercise to inform the development of truly personalized intervention regimens. This approach is intended to provide sustained momentum for advancing precision medicine and translational research in ASD.
Communication Author：ZENG Yan , Email:zengyan68@wust.edu.cn CHEN Yu-Shan , Email:yschen@wust.edu.cn
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