Deans' stroke musings: Vigorous treadmill exercise improves reactivity of cerebral arterioles and reduces brain injury following transient focal ischemia

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, April 23, 2014

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

+ Author Affiliations

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.