<p>Vascular cognitive impairment (VCI) is a neurological disorder in which chronic cerebral hypoperfusion is one of the common causes, often leading to cognitive and motor dysfunction. Moderate-intensity exercise is a non-pharmacological intervention that promotes long-term, sustainable, and low-risk brain health restoration. However, the multidimensional functional effects and underlying mechanisms of such training remain insufficiently understood. This study aimed to explore how moderate-intensity training relates to improvements in cognitive and gait functions in VCI, with a focus on neurovascular unit (NVU)-related processes and the potential involvement of vasculogenic Sema3G signaling within the hippocampus. Male Sprague–Dawley rats underwent bilateral common carotid artery occlusion (BCAO) surgery to induce VCI, followed by four weeks of moderate-intensity treadmill training in the exercise group. Moderate-intensity training effectively improved memory performance and gait stability in VCI rats. Exercise also corresponded with increased hippocampal Sema3G expression and higher levels of its related intercellular signaling components (Nrp2/PlexinA4). At the neuronal level, exercise was associated with enhanced synaptic marker expression and elevated hippocampal neuronal firing. In terms of immune modulation, exercise shifted microglial phenotypes toward an anti-inflammatory profile, suggesting a more supportive environment for neurovascular repair. Collectively, these findings indicate that moderate-intensity training may influence multiple NVU components, and that the Sema3G/Nrp2/PlexinA4 signaling axis could be one pathway contributing to the observed cognitive and motor benefits in VCI rats. Moderate-intensity exercise may therefore represent a promising approach for mitigating cognitive and motor decline associated with cerebral hypoperfusion.</p>