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Forced, not voluntary, exercise effectively induces neuroprotection in stroke
Katherine Hayes1, Shane Sprague, Miao Guo
1Department of Neurosurgery, The University of Texas Health Science Center at San Antonio, Mail Code 7843, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA.
Acta Neuropathologica
|January 23, 2008
Summary
Treadmill exercise, but not voluntary running, reduced stroke damage in rats. This neuroprotection was linked to stress hormones and increased heat shock proteins, suggesting stressful exercise is key.
Area of Science:
- Neuroscience
- Exercise Physiology
- Stroke Research
Background:
- Previous studies suggest exercise offers neuroprotection, but the role of exercise-induced stress remains unclear.
- Investigating whether forced exercise, voluntary exercise, or stress alone impacts stroke outcomes is crucial for understanding neuroprotective mechanisms.
Purpose of the Study:
- To compare the neuroprotective effects of forced treadmill exercise, voluntary wheel running, and stress-only conditions on stroke-induced brain damage.
- To elucidate the role of stress hormones and heat shock proteins in exercise-mediated neuroprotection.
Main Methods:
- Adult male rats were assigned to control, treadmill exercise, voluntary running, restraint stress, or electric shock groups for 3 weeks.
- Corticosterone levels were measured via ELISA; stroke was induced via middle cerebral artery occlusion.
- Infarct volume was quantified, and gene expression of heat shock proteins (Hsp) 27 and 70 was analyzed using real-time PCR.
Main Results:
- Treadmill exercise and stress groups showed elevated corticosterone levels; voluntary exercise did not.
- Treadmill exercise significantly reduced infarct volume (P < 0.01), an effect not seen in voluntary exercise.
- Stress (electric shock) increased infarct volume (P < 0.01), while treadmill exercise increased Hsp 27 and 70 mRNA expression compared to voluntary exercise (P < 0.01).
Conclusions:
- Exercise regimens involving a stressful component, like treadmill running, confer greater neuroprotection against stroke than voluntary exercise or stress alone.
- Up-regulation of stress-induced heat shock proteins (Hsp 27 and 70) likely mediates the observed exercise-induced neuroprotection.
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