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<p>Ischemic stroke is a leading cause of disability worldwide, disrupting motor function through damage to neurons and neuronal tracts. Aerobic exercise is a cornerstone of neurorehabilitation, with its efficacy closely tied to the activation of specific neuroplastic pathways, particularly those driving motor recovery. This narrative review examines the roles of brain-derived neurotrophic factor (BDNF), phosphoinositide 3-kinase (PI3K), and protein kinase B (Akt) signaling in promoting nerve regeneration and repair post-ischemic stroke, with a focus on how exercise intensity modulates these pathways. For this narrative review, an electronic literature search was performed using PubMed, Medline, Embase, Cochrane databases, and Google Scholar until 30 December 2025. For the PubMed search, the following MeSH terms combined with Boolean operators were used: “Brain-Derived Neurotrophic Factor” OR “BDNF” AND “phosphoinositide 3-Kinases” OR “PI3K” AND “protein kinase B” OR “Akt” AND “Aerobic Exercise” OR “Aerobic Exercise Intensity” AND “Stroke” OR “Ischemic Stroke” AND “Neuroplasticity” OR “Neurorehabilitation” OR “Motor Function” (the MeSH term for motor recovery). These keyword searches were limited to the article title and abstract. Relevant articles, written in English with sufficient information on BDNF/PI3K/AKT signaling, exercise intensity, and stroke neurorehabilitation, published before January 2014, were included. We synthesize evidence to identify the optimal exercise intensity for enhancing neuroplasticity and motor recovery, drawing comparisons with other neurological conditions such as neurodegenerative and cardiovascular diseases. While the BDNF/PI3K/Akt axis represents a conserved exercise-induced mechanism across pathologies, the unique environment of the ischemic penumbra and the heightened sensitivity of the post-stroke brain may necessitate tailored exercise intensity protocols to maximize neuroplastic benefits and mitigate risks. This review seeks to bridge molecular mechanisms with clinical application, providing a rationale for prescribing focused, intensity-driven aerobic exercise programs to advance neurorehabilitation strategies for ischemic stroke survivors.</p>

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The effect of different intensities of aerobic exercise on neurorepair based on BDNF, PI3K, and Akt signaling pathways after ischemic stroke: a narrative review

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月28日

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  • Areej Fatima,
  • Huiyi Jiang,
  • Jifang Qiu

摘要

Ischemic stroke is a leading cause of disability worldwide, disrupting motor function through damage to neurons and neuronal tracts. Aerobic exercise is a cornerstone of neurorehabilitation, with its efficacy closely tied to the activation of specific neuroplastic pathways, particularly those driving motor recovery. This narrative review examines the roles of brain-derived neurotrophic factor (BDNF), phosphoinositide 3-kinase (PI3K), and protein kinase B (Akt) signaling in promoting nerve regeneration and repair post-ischemic stroke, with a focus on how exercise intensity modulates these pathways. For this narrative review, an electronic literature search was performed using PubMed, Medline, Embase, Cochrane databases, and Google Scholar until 30 December 2025. For the PubMed search, the following MeSH terms combined with Boolean operators were used: “Brain-Derived Neurotrophic Factor” OR “BDNF” AND “phosphoinositide 3-Kinases” OR “PI3K” AND “protein kinase B” OR “Akt” AND “Aerobic Exercise” OR “Aerobic Exercise Intensity” AND “Stroke” OR “Ischemic Stroke” AND “Neuroplasticity” OR “Neurorehabilitation” OR “Motor Function” (the MeSH term for motor recovery). These keyword searches were limited to the article title and abstract. Relevant articles, written in English with sufficient information on BDNF/PI3K/AKT signaling, exercise intensity, and stroke neurorehabilitation, published before January 2014, were included. We synthesize evidence to identify the optimal exercise intensity for enhancing neuroplasticity and motor recovery, drawing comparisons with other neurological conditions such as neurodegenerative and cardiovascular diseases. While the BDNF/PI3K/Akt axis represents a conserved exercise-induced mechanism across pathologies, the unique environment of the ischemic penumbra and the heightened sensitivity of the post-stroke brain may necessitate tailored exercise intensity protocols to maximize neuroplastic benefits and mitigate risks. This review seeks to bridge molecular mechanisms with clinical application, providing a rationale for prescribing focused, intensity-driven aerobic exercise programs to advance neurorehabilitation strategies for ischemic stroke survivors.