Exercise rehabilitation immediately following ischemic stroke exacerbates inflammatory injury.

OBJECTIVES

The rehabilitative benefits of physical exercise after stroke appear to be contingent upon exercise initiation timing. The present study assessed the hypothesis that very early post-stroke exercise would amplify cellular stress and increases expression of pro-inflammatory mediators, while exercise initiated later would limit the inflammation associated with cerebral ischemia/reperfusion injury.

METHODS

Adult rats were subjected to middle cerebral artery occlusion and subsequently assigned to one of seven groups: one sham injury control group, three stroke groups subjected to exercise initiated after 6, 24 hours, or 3 days of reperfusion, and three stroke groups not subjected to exercise. Expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule (VCAM-1), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) were examined 3 and 24 hours after completion of exercise regimens (and at corresponding time points in non-exercise controls). Heat shock protein-70 (Hsp70) and hypoxia inducible factor-1α (HIF-1α) expression levels were also compared between exercise and non-exercise groups.

RESULTS

Early post-stroke exercise was associated with increased expression of pro-inflammatory mediators (ICAM-1, VCAM-1, TNF-α, and IL-1β) and increased expression of cell stress markers (Hsp70 and HIF-1α). Exercise initiated after 3 days of reperfusion was associated with decreased expression of these molecules.

CONCLUSION

Post-stroke exercise, if too early, may result in elevated levels of cell stress and increased expression of pro-inflammatory cytokines, which may amplify the tissue damage associated with cerebral ischemia/reperfusion injury. The results shed light on the manner in which exercise initiation timing may affect post-stroke rehabilitation.