Abstract
Introduction: Although physical exercise has been demonstrated to augment recovery of the post-stroke brain, how exercise patten optimizes neurological outcomes post-stroke remains to be determined. Forced exercise containing a stressful component is reported to be better than voluntary exercise on functional recovery. The present study attempted to explore a suitable exercise patten for better functional recovery and stronger neuroplasticity. Methods: Sprague-Dawley adult rats were subjected to 2 h middle cerebral artery occlusion followed by reperfusion. Treadmill exercise (15m/min) was initiated 24 hours after reperfusion for up to 21 days. Rats were assigned to a control group entailing post-stroke rest or three exercise groups: 1) exercise 5 min and rest 5 min for 6 cycles (E5), exercise 10 min and rest 10 min for 3 cycles (E10), and exercise for 30 min without rest for 1 cycle (E30). Infarct volume was determined by TTC after 48 h. Motor and cognitive functions were tracked. Western blotting was used to assess the proteins expression for neuroplasticity, including GAP-43, PSD-95, synapsin I, and BDNF. Levels of corticosterone were measured using ELISA. Changes in gene expression of stress-induced heat shock proteins (Hsp) 27 and 70 were compared using real-time PCR. Results: E30 but not E5 and E10 exercise models reduced brain infarct. All the exercise protocols significantly induced neuroplasticity and functional outcomes in ischemic rats, with E30 being most effective on the neuroplasticity and neurorehabilitation. A significant increase in corticosterone level in E30 were observed, indicating physical stress endurance may actually lead to a decrease in the resultant damage to the brain after an ischemic attack. mRNA expression of Hsp 27 and 70 were increased in E30, suggesting increasing response to physical stress in terms of the protection against cerebral ischemia. Conclusion: These findings contribute to the growing body of literature regarding the positive effects of long-term treadmill exercise on neuroplasticity and functional outcome. Additionally, the results suggested that physical stress played a role in the biochemical processes underlying exercise-induced post-stroke neuroplasticity.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.