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Conducting Maximal and Submaximal Endurance Exercise Testing to Measure Physiological and Biological Responses to Acute Exercise in Humans
Published on: October 17, 2018
Delayed leukocytosis and cytokine response to high-force eccentric exercise
Gøran Paulsen1, Haakon B Benestad, Inger Strøm-Gundersen
1Norwegian School of Sport Sciences, Oslo. goran.paulsen@nih.no
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.
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