Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Sunday, October 2, 2016

Hippocampal and Cerebral Blood Flow after Exercise Cessation in Master Athletes

In order to keep your cerebral blood flow up you will need to keep on a continuous exercise program. Your doctor should have the details on the specific exercise you need to do, how long and when to start post-stroke to get the correct amount of cerebral blood flow for your best recovery. Sorry, had to pick myself off the floor from laughing so hard at that last sentence.
http://journal.frontiersin.org/article/10.3389/fnagi.2016.00184/full
Alfonso J. Alfini, Lauren R. Weiss, Brooks P. Leitner, Theresa J. Smith, James M. Hagberg and J. Carson Smith*
  • Department of Kinesiology, University of Maryland, College Park, MD, USA
While endurance exercise training improves cerebrovascular health and has neurotrophic effects within the hippocampus, the effects of stopping this exercise on the brain remain unclear. Our aim was to measure the effects of 10 days of detraining on resting cerebral blood flow (rCBF) in gray matter and the hippocampus in healthy and physically fit older adults. We hypothesized that rCBF would decrease in the hippocampus after a 10-day cessation of exercise training. Twelve master athletes, defined as older adults (age ≥ 50 years) with long-term endurance training histories (≥15 years), were recruited from local running clubs. After screening, eligible participants were asked to cease all training and vigorous physical activity for 10 consecutive days. Before and immediately after the exercise cessation period, rCBF was measured with perfusion-weighted MRI. A voxel-wise analysis was used in gray matter, and the hippocampus was selected a priori as a structurally defined region of interest (ROI), to detect rCBF changes over time. Resting CBF significantly decreased in eight gray matter brain regions. These regions included: (L) inferior temporal gyrus, fusiform gyrus, inferior parietal lobule, (R) cerebellar tonsil, lingual gyrus, precuneus, and bilateral cerebellum (FWE p < 0.05). Additionally, rCBF within the left and right hippocampus significantly decreased after 10 days of no exercise training. These findings suggest that the cerebrovascular system, including the regulation of resting hippocampal blood flow, is responsive to short-term decreases in exercise training among master athletes. Cessation of exercise training among physically fit individuals may provide a novel method to assess the effects of acute exercise and exercise training on brain function in older adults.

Introduction

Endurance exercise training (exercise) produces physiological adaptations that enhance aerobic fitness and cardiovascular health (Brooks et al., 1996). Consistent exercise effectively augments the maximal rate of oxygen consumption (VV O2max) centrally, by increasing cardiac output, and/or peripherally by widening the arterial-venous oxygen (A-VV O2) difference (Seals et al., 1981). VV O2max is the gold-standard index of cardiorespiratory fitness and is highly correlated with both morbidity and mortality (Hoekstra et al., 2008; Sawada et al., 2012), with greater fitness status associated with a reduced risk of chronic disease and a longer lifespan. In addition to enhancing the function of the cardiovascular system, exercise has been shown to increase bone density, improve muscle quality, and protect against metabolic dysfunction (Brooks et al., 1996). Conversely, when the exercise stimulus is removed many of these systemic adaptations rapidly dissipate (Mujika and Padilla, 2000a, 2001a,b), thereby increasing the potential for adverse health effects. For example, 20 days of bed rest immobilization resulted in a substantial 28% decrease in VV O2max (Saltin et al., 1968); a prolonged detraining period reduced muscle fiber capillarization and oxidative enzyme activity (Klausen et al., 1981); and a 10-day period of physical inactivity was related to the development of impaired glucose tolerance and insulin resistance (Rogers et al., 1990).
A growing body of empirical evidence supports the notion that exercise also robustly affects the human brain. Multimodal neuroimaging studies, including both structural and functional MRI, have helped elucidate the brain's complex neurobiological response to exercise. These exercise-induced effects include cytoarchitectonic modifications (Erickson et al., 2009; Smith et al., 2014; ten Brinke et al., 2015); altered patterns of neural activity (Smith et al., 2013); and improved performance across the cognitive domains (Tomporowski, 2003; Kramer et al., 2005; Davranche and McMorris, 2009; Chapman et al., 2013). The hippocampus, a subcortical brain structure well known for its role in learning and memory, has shown neurotrophic effects as the result of exercise training in humans and animal models (van Praag et al., 1999; Pereira et al., 2007; Erickson et al., 2009). Exercise interventions in humans have been shown to affect hippocampal-dependent cognition and to increase hippocampal blood perfusion (Pereira et al., 2007) and volume (Erickson et al., 2009). While the effects of detraining have been reported in peripheral physiological systems, the effects of detraining on brain function, and on cortical and hippocampal blood flow, have not been reported.
A key unanswered question, and the primary aim of this study, was to determine how short-term exercise cessation impacts cerebrovascular function in healthy highly physically active and physically fit older adults. To accomplish this goal we measured the resting cerebral blood flow (rCBF) of master athletes both before and immediately after 10 days of exercise cessation. To quantify rCBF we employed pseudo-continuous arterial spin labeling (pCASL), a perfusion-weighted MRI technique. Our hypotheses were twofold. We predicted (1) that 10 days of physical inactivity would alter rCBF in areas known to be susceptible to age-related decline (Greicius et al., 2004; Buckner et al., 2005), and (2) that detraining would decrease hippocampal blood flow, which we chose as an a priori region of interest (ROI).

Results

The Master Athlete Profile

The master athletes who volunteered for this study are a unique population and should not be considered equivalent to older adults who engage in regular moderate to vigorous intensity leisure-time physical activity. Our participants had a mean continuous endurance training history of ~29 years, and on average were running 59 km per week and training 5 days per week just prior to the baseline testing. They also regularly participated in regional and national endurance competition. Moreover, as a group these master athletes had a V O2max above the 90th percentile for their age and sex.

Gray Matter rCBF

Results of the gray matter voxel-wise analysis demonstrated that the 10-day exercise cessation period significantly reduced absolute rCBF in eight brain regions (Figure 1). Of note are the Pre > Post comparisons, shown in blue on the Δ rCBF maps in Figure 1, revealing significantly decreased rCBF in each ROI (total volume = 5,640 mm3) that remained after correction for multiple comparisons using the False Discovery Rate (see Table 2). These regions included: (L) inferior temporal gyrus, fusiform gyrus, inferior parietal lobule, (R) cerebellar tonsil, lingual gyrus, precuneus, and (L/R) cerebellum. No statistically significant change in whole brain absolute CBF in gray matter was detected [mean (±SD) baseline = 69.4 (±10.4 ml/100g/min), post-cessation = 67.2 (±12.6 ml/100g/min)].

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