Katsuhiko Suzuki

TL;DR: Examination of possible changes of not only plasma but also urine concentrations of a broad spectrum of cytokines following maximal exercise, including the time course of recovery concluded that cytokines that are considered to induce systemic bioactivity following exercise are not only anti-inflammatory cytokines but also colony-stimulating factors and chemokines, which were secreted in an earlier phase of exercise without the kinetic involvement of traditional pro inflammatory cytokines.

TL;DR: In this paper, the inflammatory response to exercise-induced muscle damage is characterized by leukocyte infiltration and production of pro-inflammatory cytokines within damaged muscle tissue, systemic release of leukocytes and cytokines, in addition, alterations in leucocyte receptor expression and functional activity.

TL;DR: Chronic exercise might contribute to inhibit inflammation in adipose tissue via down regulation of TLR4, which induces pro-inflammatory cytokine production after fatty acid recognition, besides inhibiting M1 macrophage infiltration into adipOSE tissue.

TL;DR: The results indicate that stress-induced systemic release of bioactive substances may determine neutrophil mobilization and functional status, which then may affect local tissue damage of susceptible organs.

TL;DR: Although many cytokines recruiting and priming neutrophils and monocytes were secreted and functional after exhaustive exercise, overwhelming antioxidant and antiinflammatory defenses were induced, preventing exercise-induced oxidative stress.