Delayed leukocytosis and cytokine response to high-force eccentric exercise.

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.