Exercise intensity influences the temporal profile of growth factors involved in neuronal plasticity following focal ischemia.
Abstract
Exercise increases brain-derived neurotrophic factor (BDNF), phosphorylated cAMP response-element binding protein (pCREB), insulin-like growth factor (IGF-I) and synapsin-I, each of which has been implicated in neuroplastic processes underlying recovery from ischemia. In this study we examined the temporal profile (0, 30, 60 and 120 min following exercise) of these proteins in the hippocampus and sensorimotor cortex following both motorized (60 min) and voluntary (12 h) running, 2 weeks after focal ischemia. Our goal was to identify the optimal training paradigms (intensity, duration and frequency) needed to integrate endurance exercise in stroke rehabilitation. Therefore we utilized telemetry to measure changes in heart rate with both exercise methods. Our findings show that although the more intense, motorized running exercise induced a rapid increase in BDNF, the elevation was more short-lived than with voluntary running. Motorized running was also associated with higher levels of synapsin-I in several brain regions but simultaneously, a more pronounced increase in the stress hormone, corticosterone. Furthermore, both forms of exercise resulted in decreased phosphorylation of CREB and downregulation of synapsin-I in hippocampus beginning 30 to 60 min after the exercise bout. This phenomenon was more robust after motorized running, the method that generated higher heart rate and serum corticosterone levels. This immediate stress response is likely specific to acute exercise and may diminish with repeated exercise exposure. The present data illustrate a complex interaction between different forms of exercise and proteins implicated in neuroplasticity. For clinical application, frequent lower intensity exercise episodes (as in voluntary running wheels), which may be safer to provide to patients with stroke, has a delayed but sustained effect on BDNF that may support brain remodeling after stroke.
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The effect of aerobic exercise on hippocampus dependent task performance in animal models depends on aspects of aerobic exercise such as duration and intensity.
“Using hippocampus dependent paradigms, AE has been reliably demonstrated to improve task performance in animal models (van Praag, 2009; Voss et al., 2013a), although this does also depend on others aspects of AE such as the duration and intensity of AE (Naylor et al., 2005; Ploughman et al., 2007; O’Callaghan et al., 2009).”
From Aerobic Exercise as a Tool to Improve Hippocampal Plasticity and Function in Humans: Practical Implications for Mental Health Treatment (2016) · cites this paper as Ploughman et al., 2007
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- Authors
- Ploughman, M., Granter-Button, S., Chernenko, G., Attwood, Z., Tucker, B. A., Mearow, K. M., & Corbett, D.
- Affiliations
- Memorial University of Newfoundland (CA)
- Corresponding author
- Corbett, Dale
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2007-05
- Volume
- 1150
- Pages
- 207-216
- ISSN
- 0006-8993 (ISSN-L)
- OpenAlex
- W2026472945
- Cited by
- 170
- References
- 58
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 3 · 2023: 6 · 2022: 9 · 2021: 7 · 2020: 8 · 2019: 12 · 2018: 12 · 2017: 13 · 2016: 10 · 2015: 10 · 2014: 22 · 2013: 8 · 2012: 10
- FWCI
- 10.38
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Rehabilitation › Stroke Rehabilitation and Recovery
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- exercise intensity, brain-derived neurotrophic factor, CREB phosphorylation, insulin-like growth factor I, synapsin I, focal cerebral ischemia, stroke rehabilitation, voluntary running, corticosterone, stress response, hippocampus, sensorimotor cortex, neuroplasticity, heart rate
- MeSH terms
- Analysis of Variance, Animals, Corticosterone, Disease Models, Animal, Heart Rate, Hippocampus, Ischemia, Male, Neuronal Plasticity, Physical Conditioning, Animal, Radioimmunoassay, Somatosensory Cortex, Time Factors, Rats, Sprague-Dawley, Intercellular Signaling Peptides and Proteins, Rats
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