In rats with mild traumatic brain injury, delayed voluntary exercise increased hippocampal BDNF levels, whereas forced exercise markedly stimulated the corticotrophic axis without increasing BDNF.
Does delayed voluntary or forced exercise improve stress responses, autonomic function, and BDNF levels in rats following mild traumatic brain injury?
Delayed voluntary exercise after mild TBI increases hippocampal BDNF and coincides with normalized stress and autonomic responses, whereas forced exercise acts as a stressor without neurotrophic benefits.
We have recently shown that there is a heightened stress response after a mild traumatic brain injury (TBI) during the first 2 post-injury weeks. This corresponds to the same post-injury period when exercise does not increase brain-derived neurotrophic factor (BDNF) and autonomic dysfunction becomes evident with exercise. Here we determined stress and autonomic responses to voluntary and forced exercise at a post-injury time window when exercise has been found to elicit beneficial effects. Rats underwent a mild fluid percussion injury and were exercised at post-injury days 28–32 and 35–39. Cardiac and temperature autonomic function were evaluated. Hippocampal tissue was obtained immediately after exercise for analysis of BDNF. In contrast to the sub-acute period, corticosterone and adrenocorticotropic hormone responses to exercise were normalized in the TBI group. Irrespective of injury, forced exercise markedly stimulated the corticotrophic axis and did not increase BDNF. BDNF levels were increased with voluntary exercise in all animals. Rats exposed to forced exercise had lower activity levels during periods of non-exercise. This effect was more pronounced in the TBI rats. Cardiac and temperature autonomic responses to delayed exercise also recuperated. Rats with TBI that underwent forced exercise, however, had higher core body temperatures during experimental manipulations, thus suggesting that exposure to a potent stressor facilitates responsiveness to environmental stimulations.
Griesbach et al. (2013) studied Traumatic Brain Injury (n=57). Voluntary and forced exercise vs. Sedentary condition and sham injury was evaluated on Corticosterone, ACTH, and BDNF responses to exercise. In rats with mild traumatic brain injury, delayed voluntary exercise increased hippocampal BDNF levels, whereas forced exercise markedly stimulated the corticotrophic axis without increasing BDNF.
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