PMID- 16286856 OWN - NLM STAT- MEDLINE DCOM- 20060119 LR - 20190902 IS - 0195-9131 (Print) IS - 0195-9131 (Linking) VI - 37 IP - 11 DP - 2005 Nov TI - Delayed leukocytosis and cytokine response to high-force eccentric exercise. PG - 1877-83 AB - PURPOSE: Delayed leukocytosis after strenuous exercise is well documented, but the underlying mechanisms are not clear. In this study, we investigated the relationship between exercise-induced muscle damage and delayed leukocytosis, by utilizing an extreme eccentric exercise protocol. METHODS: We obtained blood samples from 11 healthy men before and after 300 maximal eccentric actions with m. quadriceps. Maximal force-generating capacity was tested before and regularly during the 7 d after exercise. Blood was analyzed for leukocytes, growth hormone (GH), cortisol, granulocyte colony-stimulating factor (G-CSF), macrophage colony-stimulating factor (M-CSF), interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1beta (MIP-1beta), creatine kinase (CK), C-reactive protein (CRP), complement activation products (C3bc and the terminal complement complex (TCC)), and chemotactic activity in plasma. RESULTS: The force-generating capacity was reduced by 47 +/- 5% (mean +/- SEM) immediately after exercise. Blood concentration of neutrophils and monocytes and the plasma concentration of G-CSF, IL-6, and MCP-1 peaked 6 h after exercise, whereas M-CSF peaked immediately after exercise. Serum concentration of GH and cortisol also peaked immediately after exercise, whereas the serum concentration of CRP and CK peaked after 2 and 4 d, respectively. At 1 h after exercise, chemotactic activity in plasma was increased; at the same time, concentration of C3bc and TCC were decreased. A positive correlation was found between the acute loss of force and the delayed leukocytosis (r = 0.66; P < 0.05), between peak G-CSF and the delayed neutrophilia (r = 0.65, P < 0.05), between acute loss of force and changes in CK (r = 0.65, P < 0.05), between acute loss of force and changes in CRP (r = 0.65, P < 0.05), and between changes in GH and monocyte blood concentrations (r = 0.68, P < 0.05). CONCLUSION: The degree of exercise-induced muscle damage seems to be reflected by the magnitude of the subsequent delayed leukocytosis. The signal between the exercised muscle and bone marrow must be investigated further, but G-CSF and GH are putative mobilizing factors. FAU - Paulsen, Goran AU - Paulsen G AD - Norwegian School of Sport Sciences, Oslo. goran.paulsen@nih.no FAU - Benestad, Haakon B AU - Benestad HB FAU - Strom-Gundersen, Inger AU - Strom-Gundersen I FAU - Morkrid, Lars AU - Morkrid L FAU - Lappegard, Knut Tore AU - Lappegard KT FAU - Raastad, Truls AU - Raastad T LA - eng PT - Journal Article PL - United States TA - Med Sci Sports Exerc JT - Medicine and science in sports and exercise JID - 8005433 RN - 0 (Cytokines) SB - IM MH - Adult MH - Bone Marrow/physiology MH - Chemotaxis MH - Cytokines/biosynthesis/blood MH - Exercise/*physiology MH - Humans MH - *Leukocytosis MH - Male MH - Monocytes MH - Muscle, Skeletal/immunology/*pathology MH - Neutrophils MH - Time Factors EDAT- 2005/11/16 09:00 MHDA- 2006/01/20 09:00 CRDT- 2005/11/16 09:00 PHST- 2005/11/16 09:00 [pubmed] PHST- 2006/01/20 09:00 [medline] PHST- 2005/11/16 09:00 [entrez] AID - 00005768-200511000-00008 [pii] AID - 10.1249/01.mss.0000177064.65927.98 [doi] PST - ppublish SO - Med Sci Sports Exerc. 2005 Nov;37(11):1877-83. doi: 10.1249/01.mss.0000177064.65927.98.