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Indexed/Abstracted in: Chemical Abstracts, CINAHL, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,111
Online ISSN 1827-1928
Packer N., Hoffman-Goetz L.
School of Public Health and Health Systems, University of Waterloo, Waterloo, Ontario, Canada
AIM: Regular exercise may protect against cognitive decline by preventing central inflammation. The effect of an acute exercise bout on central cytokine and apoptotic protein expression is not known. The brain may be protected from transient oxidative stress such as that induced by acute-exercise. The purpose of this exploratory study was to determine the effect of a single bout of intense exercise on hippocampal expression of inflammatory mediators (TNF-α) and apoptotic proteins (caspase-3, caspase-7), and to evaluate any potential age-related differences.
METHODS: Using a C57BL/6 mouse model (N.=98), we evaluated the effect of an acute exercise bout (90 minutes of treadmill running: 10 min warm-up, 30 min at 22m.min-1, 30 min at 25m.min-1, and 30 min at 28m.min-1, 2° slope) on hippocampal inflammation in young (3-4 months), middle-aged (13-14 months) and older (16-17 months) C57BL/6 mice.
RESULTS: Our results show post-exercise increases in hippocampal TNF-α and caspase-3/7 in each age group (main effect of acute exercise, P<0.05). Older mice displayed higher TNF-α (main effect of age, P<0.05) expression compared with younger animals at baseline. Young mice demonstrated greater increases in caspase-7 following acute exercise, compared to older mice (interaction effect for caspase-7, P<0.05).
CONCLUSION: Given the relationship between aging, inflammation and neurodegenerative disease, and the protective effects of exercise, we cautiously propose that acute-exercise induced inflammation may be a normal physiologic response that elicits a favorable (anti-inflammatory) hippocampal environment.