Forced treadmill exercise prevents oxidative stress and memory deficits following chronic cerebral hypoperfusion in the rat

Abstract

Physical activity impacts functional recovery following stroke in humans, however its effects in experimental animals submitted to chronic cerebral hypoperfusion have not been investigated. The aim of this study was to evaluate the therapeutic potential of exercise, as assessed by cognitive activity in the Morris water maze and the brain oxidative status, through measurement of macromolecules damage, TBARS levels and total cellular thiols, as well as antioxidant enzymes in hippocampus, striatum and cerebral cortex. Adult male Wistar rats were submitted to the modified permanent bilateral occlusion of the common carotid arteries (2VO) method, with right common carotid artery being first occluded, and tested 3 months after the ischemic event. The effects of three different exercise protocols were examined: pre-ischemia, post-ischemia and pre+post-ischemia. Physical exercise consisted of sessions of 20-min, 3 times per week during 12 weeks (moderate intensity). Rats were submitted to cognitive assessment, in both reference and working spatial memory and after the last testing session were sacrificed to have oxidative stress parameters determined. Hypoperfusion caused a significant cognitive deficit in both spatial water maze tasks and this effect was reversed in rats receiving exercise protocol post and pre+post the ischemic event. Moreover, forced regular treadmill exercise regulated oxidative damage and antioxidant enzyme activity in the hippocampus. These results suggest that physical exercise protects against cognitive and biochemical impairments caused by chronic cerebral hypoperfusion.

Effect of forced exercise and exercise withdrawal on memory, serum and hippocampal corticosterone levels in rats

“…It seems that in addition to the CORT levels, multiple systems extensively interact with the memory function during the exercise, such as the changes in the neurotransmitter release, oxidative stress and neurotrophic factors (Meeusen and De Meirleir 1995;Ke et al 2011;Cechetti et al 2012), the increase in neuronal activity (Stummer et al 1994;Carro et al 2001), the promotion of angiogenesis (Swain et al 2003;Foster et al 2011) and the stimulation of the neurogenesis (Van Praag et al 1999a).…”

Effects of different delayed exercise regimens on cognitive performance in fimbria-fornix transected rats

“…It may be argued that exposure to forced exercise is a stressful event, however, as previously noted (see Greenwood et al 2013), stress per definition does not have to hinder the positive effects of exercise and may, under certain circumstances, even promote posttraumatic cognitive recovery (Gram et al 2015, Malá et al 2008. Several studies report a positive impact of post-injury exercise on spatial acquisition paradigms (Cechetti et al 2012, Griesbach et al 2004b, Kim et al 2010, Piao et al 2013, Shen et al 2013, Shih et al 2013, Sim et al 2004. There are also studies reporting detrimental or no effects of exercise on spatial acquisition measures (Clark et al 2008, Griesbach et al 2004a, Hicks et al 1998, Luo et al 2007, Piao et al 2013, Song et al 2012.…”

New Four-herb Formula Ameliorates Memory Impairments via Neuroprotective Effects on Hippocampal Cells

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