Vigorous treadmill exercise improves reactivity of cerebral arterioles and reduces brain injury following transient focal ischemia - In rats

So pretreatment with vigorous exercise reduces brain injury. The week prior to my stroke I was working my butt off carrying a 60 lb canoe and 50-70 lb. packs over portages including one at 1.5 miles.
http://www.fasebj.org/content/28/1_Supplement/1070.2.short

1. Denise Arrick1,
2. Shu Yang1,
3. Chun Li1,
4. Hong Sun1 and
5. William Mayhan1

+ Author Affiliations

1. ¹Cellular Biology and Anatomy LSU Health Sciences Center Shreveport LA United States

Abstract

Exercise training (ExT) has been shown to play a significant role in the prevention of cardiovascular-related diseases. Our goal was to examine whether vigorous exercise training (ExT) could influence nitric oxide synthase (NOS)-dependent dilation of cerebral arterioles and transient focal ischemia-induced brain injury in rats. Sprague-Dawley rats were divided into sedentary (SED) or exercised trained (ExT) groups. Treadmill exercise was carried out 5 days/week for a period of 6-8 weeks. In the first series of studies, a craniotomy was made over the parietal cortex and we measured responses of pial arterioles to eNOS-dependent (ADP), nNOS-dependent (NMDA) and NOS-independent (nitroglycerin) agonists. In a second series of studies, we measured infarct volume in SED and ExT rats following right middle cerebral artery occlusion (MCAO) for 2 hours followed by 24 hours of reperfusion. In a third series of studies, we measured eNOS, nNOS, SOD1 and SOD2 protein levels in cerebral vessels and brain tissue of SED and ExT rats. We found that eNOS- and nNOS-dependent, but not NOS-independent vasodilation, was increased in ExT compared to SED rats. In addition, we found that ExT significantly reduced total, cortical and subcortical infarct volumes following ischemia/reperfusion when compared to sedentary rats. Surprisingly, we found that eNOS and nNOS protein levels were similar in ExT and SED rats, but SOD1 and SOD2 protein levels were increased by ExT. We suggest that ExT improves NOS-dependent vascular function and reduces infarct volume by mechanisms that appear to be related to alterations in oxidative stress. We suggest that ExT may be a viable preventative therapeutic approach to lessen ischemia-induced brain injury.