How many years and more research is needed before a stroke protocol is put together on the levels of exercise needed to assist neuroplasticity and stroke recovery? This won't occur with our fucking lack of stroke leadership. Writeups like this are totally worthless without making translational protocols on how this can be used by survivors.
http://stroke.ahajournals.org/content/47/Suppl_1/ATP143.short

Abstract TP143: Effects of Aerobic Exercise Intensity on Novel Blood Biomarkers of Neuroplasticity After Stroke

1. Dustyn Whitesel1;
2. Pierce Boyne1;
3. Daniel Carl1;
4. Jennifer Westover1;
5. Colleen Meyrose1;
6. Johnny Wilkerson1;
7. Jane C Khoury2;
8. Myron Gerson3;
9. Kim Seroogy4;
10. Kristal Hatter5;
11. Darcy Reisman6;
12. Brett Kissela4;
13. Kari Dunning1

+ Author Affiliations

1. ¹Dept of Rehabilitation Sciences, Univ of Cincinnati, Cincinnati, OH
2. ²Div of Biostatistics and Epidemiology, Cincinnati Children's Hosp Med Cntr, Cincinnati, OH
3. ³Depts of Internal Medicine and Cardiology, Univ of Cincinnati, Cincinnati, OH
4. ⁴Dept of Neurology and Rehabilitation Medicine, Univ of Cincinnati, Cincinnati, OH
5. ⁵Clinical Translational Rsch Cntr, Cincinnati Children's Hosp Med Cntr, Cincinnati, OH
6. ⁶Dept of Physical Therapy, Univ of Delaware, Newark, DE

Abstract

Introduction: Aerobic exercise (AEX) may facilitate neurologic stroke recovery. Among healthy adults, intense AEX is known to upregulate brain-derived neurotrophic factor (BDNF), a critical facilitator of neuroplasticity, motor learning and cognition. Increased blood lactate during AEX appears to be a key mechanism underlying this effect. Intense AEX also increases blood ionized calcium (Ca++). In animal studies, some of this increased Ca++ has been shown to be transported to the brain and enhance synthesis of monoamine neurotransmitters (e.g. dopamine) that are associated with neuroplasticity and motor learning. Thus, increased blood lactate and Ca++ during AEX represent potentially important biomarkers of central neurologic benefits, but neither has been previously studied in persons with stroke.

Hypothesis: High intensity AEX will elicit significantly larger lactate and Ca++ responses than moderate intensity in chronic stroke.

Methods: Using a crossover design, eight subjects (mean ± SD age, 57 ± 8 years; years post stroke, 8.7 ± 2.7) performed one 20 minute session each of moderate and high intensity treadmill AEX in random order. Blood lactate and Ca++ were measured at baseline and multiple time points during and after AEX. Mixed effects models were used to examine changes within and between protocols using an alpha of 0.05.

Results: Blood lactate response was significantly greater for high vs moderate intensity AEX (p<<0.0001). While moderate intensity showed no significant changes with time (p=0.60), high intensity showed significant increases during and immediately after AEX (all p<0.0001). Blood Ca++ showed no significant protocol by time interaction (p=0.08) but did show a significant time effect (p<0.0001) with increases during (p<0.0001) and immediately after (p=0.01) AEX.

Conclusions: Unlike moderate intensity AEX, high intensity elicited a robust lactate response. This has promising implications for the effects of high-intensity AEX on BDNF post-stroke. Both protocols combined showed an increase in Ca++, which has promising implications for the effects of AEX on monoamine neurotransmitter synthesis after stroke.