Acute Exercise Modulates BDNF and pro-BDNF Protein Content in Immune Cells.

2012 
BRUNELLI, A., I. DIMAURO, P. SGRO ` , G. P. EMERENZIANI, F. MAGI, C. BALDARI, L. GUIDETTI, L. DI LUIGI, P. PARISI, AND D. CAPOROSSI. Acute Exercise Modulates BDNF and pro-BDNF Protein Content in Immune Cells. Med. Sci. Sports Exerc., Vol. 44, No. 10, pp. 1871–1880, 2012. Purpose: Although several studies have shown that immune cells stimulated by in vitro stress are capable to produce neurotrophins, there is still no evidence whether physiological stress, such as exercise, can modulate the in vivo levels of brain-derived neurotrophic factor (BDNF) in peripheral blood mononuclear cells (PBMCs). Methods: This work investigated whether acute exercise modulates the expression of BDNF, pro-BDNF, and p75 NTR in the PBMCs of 10 healthy young men who performed a cycling incremental test to exhaustion (MAX) or exercised at individual anaerobic threshold (IAT). The PBMC expression of stress response proteins and the level of circulating BDNF, vascular endothelial growth growth factor, platelet-derived growth factor subunit B, basic fibroblast growth factor pro-inflammatory, and anti-inflammatory cytokines were analyzed as well. Results: A major finding is that both sessions of acute exercise regulated the content of BDNF isoforms within PBMCs in a manner related to the physiological stress exerted. Although the pro-BDNF increased after both MAX and IAT protocols, BDNF showed a kinetics dependent on exercise type: MAX induced a 54% protein increase immediately after exercise, followed by a significant drop 60 min after its conclusion (38% lower than the baseline). Differently, in the IAT, BDNF increased significantly up to 75% from the baseline throughout the recovery phase. All physiological parameters, as well as the p75 NTR receptor and the stress-inducible proteins, were also differently regulated by the two exercise conditions. Conclusions: These data supported the hypothesis that PBMCs might produce and secrete BDNF isoforms, as well as modulate the proteins p75 NTR , Bcl-xL, hsp90, hsp27, and >B-crystallin, as part of the physiological stress response induced by acute
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