Abstract TP143: Effects of Aerobic Exercise Intensity on Novel Blood Biomarkers of Neuroplasticity After Stroke
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.
Author Disclosures: D. Whitesel: None. P. Boyne: None. D. Carl: None. J. Westover: None. C. Meyrose: None. J. Wilkerson: None. J.C. Khoury: None. M. Gerson: None. K. Seroogy: None. K. Hatter: None. D. Reisman: None. B. Kissela: None. K. Dunning: None.
- © 2016 by American Heart Association, Inc.