Citation

Griesbach GS, Tio DL, Vincelli J, McArthur DL, Taylor AN. J. Neurotrauma 2012; 29(7): 1426-1433.

Affiliation

UCLA School of Medicine, Neurosurgery, Los Angeles, California, United States; ggriesbach@mednet.ucla.edu.

Copyright

(Copyright © 2012, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2011.2229

PMID

22233388

PMCID

PMC3335105

Abstract

Voluntary exercise increases levels of brain derived neurotrophic factor (BDNF) after traumatic brain injury when it occurs during a delayed time window. In contrast, acute post-TBI exercise does not increase BDNF. It is well known that increases in glucocorticoids suppress levels of BDNF. Moreover recent work from our laboratory showed that there is a heightened stress response after fluid percussion injury (FPI). In order to determine if a heightened stress response is also observed with acute exercise, at post-injury days 0-4 and 7-11, corticosterone (CORT) and adrenocorticotropic hormone (ACTH) release were measured in rats running voluntarily or exposed to 2 daily 20-min periods of forced running wheel exercise. Forced, but not voluntary exercise, continuously elevated CORT. ACTH levels were initially elevated with forced exercise but decreased by postinjury day 7 in the Control but not the FPI animals. As previousy reported, voluntary exercise did not increase BDNF in the FPI group as it did in the Control animals. Forced exercise did not increase levels of BDNF in any group; it did however decrease hippocampal glucocorticoid receptors in the Control group. The results suggest that exercise regimens with strong stress responses may not be beneficial during the early post-injury period.

Language: en