This study aimed to explore the effects of exercise on sensorimotor recovery after stroke, neuroplasticity changes in the brain and spinal cord, and spinal cord compensation mechanisms. A rat model of ischemic stroke was induced using the middle cerebral artery occlusion/reperfusion method. A T10 spinal cord injury (SCI) model was induced using a modified Allen procedure. The animals were randomly assigned into: Sham group (S), stroke group (M), stroke+SCI group (MS), stroke+exercise+SCI group (MSI), and stroke+SCI group (MI). Neurological function was assessed poststroke using the modified Neurological Severity Score (mNSS) and Garcia scores. Infarct volumes were evaluated using triphenyl tetrazolium chloride staining, and neuronal damage was assessed using Nissl staining. Tumor necrosis factor-α (TNF-α), interleukin (IL)-10, and IL-1β levels were measured using ELISA. Neuroplasticity markers GAP43, PSD-95, synapsin I, and brain-derived neurotrophic factor (BDNF) levels were analyzed using WB, IHC, and ELISA. Exercise improved neurological function in stroke rats, as evidenced by the enhanced mNSS and Garcia scores in the MS group compared to the M group. Exercise also alleviated neuronal damage, with the MS group showing higher neuron counts and more intact Nissl bodies than the M group. Exercise in the MS group downregulated inflammation (TNF-α down, IL-10 up) compared to the M group. Furthermore, exercise upregulated neuroplasticity markers and BDNF in both the brain and spinal cord. The beneficial effects of exercise on neurological recovery were diminished in the presence of SCI, as evidenced by the impaired recovery in the MSI group. Exercise enhances stroke recovery by improving neuroplasticity, reducing inflammation, and highlighting the spinal cord's role in compensation. These findings suggest spinal cord-targeted therapies may improve rehabilitation outcomes.
Li et al. (Mon,) studied this question.