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These researchers examined a potential mechanism for the protective effects of exercise against stroke. They hypothesized that exercise would increase levels of endothelial nitric oxide synthase (eNOS) in vascular endothelial cells. The product of eNOS, nitric oxide (NO), is a potent vasodilator. The authors reasoned that baseline increases in vasodilation would be protective in experimental stroke in mice.
Indeed, mice that were placed in voluntary or forced running cages for 21 days subsequently had smaller strokes after transient occlusion of the middle cerebral artery than did nonexercised mice. Exercise significantly increased eNOS messenger RNA and protein levels in cerebral vessels and increased basal cerebral blood flow and vessel-wa…