Exercise promotes neurological recovery by enhancing neuroplasticity and the spinal cord compensation in stroke-affected rats

Abstract Stroke stands as the main cause of mortality and disability, mainly leaving survivors with sensorimotor and cognitive impairments. Although the therapeutic benefits of exercise for neurological disorders are widely acknowledged, the underlying mechanisms have still remained elusive. The spinal cord serves as a crucial pathway for nerve conduction and a pivotal link between the brain and limbs, while its potential for compensation post-stroke should be elucidated. This study explored the influences of exercise on sensorimotor function recovery post-stroke, assessed alterations in brain and spinal cord neuroplasticity, and elucidated potential molecular mechanisms underlying spinal cord tissue compensation. It was revealed that exercise facilitated sensorimotor function recovery, elevated the expression levels of key neuroplasticity markers, mitigated neuronal damage, and increased brain-derived neurotrophic factor expression level post-stroke induced by middle cerebral artery occlusion/reperfusion (MCAO/R). Subsequent investigations unveiled significant upregulation of the expression levels of neuroplasticity markers and brain-derived neurotrophic factor (BDNF) in the spinal cord following ischemic stroke, which were further augmented after exercise. Exercise also downregulated tumor necrosis factor-α (TNF-α) expression level and upregulated interleukin-10 (IL-10) expression level in both the brain and spinal cord of rats. However, these exercise-induced effects were eliminated following spinal cord injury. The mechanism could be linked to the augmentation of neuroplasticity and the compensatory function of the spinal cord.