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Exercise-Induced Muscle Damage, Plasma Cytokines, and Markers of Neutrophil Activation


Medicine & Science in Sports & Exercise: May 2005 - Volume 37 - Issue 5 - p 737-745
doi: 10.1249/01.MSS.0000161804.05399.3B
Basic Sciences: Original Investigations

Introduction: Unaccustomed eccentric exercise often results in muscle damage and neutrophil activation. We examined changes in plasma cytokines stress hormones, creatine kinase activity and myoglobin concentration, neutrophil surface receptor expression, degranulation, and the capacity of neutrophils to generate reactive oxygen species in response to in vitro stimulation after downhill running.

Methods: Ten well-trained male runners ran downhill on a treadmill at a gradient of −10% for 45 min at 60% V̇O2max. Blood was sampled immediately before (PRE) and after (POST), 1 h (1 h POST), and 24 h (24 h POST) after exercise.

Results: At POST, there were significant increases (P < 0.01) in neutrophil count (32%), plasma interleukin (IL)-6 concentration (460%), myoglobin (Mb) concentration (1100%), and creatine kinase (CK) activity (40%). At 1 h POST, there were further increases above preexercise values for neutrophil count (85%), plasma Mb levels (1800%), and CK activity (56%), and plasma IL-6 concentration remained above preexercise values (410%) (P < 0.01). At 24 h POST, neutrophil counts and plasma IL-6 levels had returned to baseline, whereas plasma Mb concentration (100%) and CK activity (420%) were elevated above preexercise values (P < 0.01). There were no significant changes in neutrophil receptor expression, degranulation and respiratory burst activity, and plasma IL-8 and granulocyte-colony stimulating factor concentrations at any time after exercise. Neutrophil count correlated with plasma Mb concentration at POST (r = 0.64, P < 0.05), and with plasma CK activity at POST (r = 0.83, P < 0.01) and 1 h POST (r = 0.78, P < 0.01).

Conclusion: Neutrophil activation remains unchanged after downhill running in well-trained runners, despite increases in plasma markers of muscle damage.

1School of Human Movement Studies, University of Queensland, St. Lucia, Brisbane, Queensland, AUSTRALIA; 2School of Human Sciences and Consolidated Research Institute for Advanced Science and Medical Care, Waseda University, Tokorozawa, Saitama, JAPAN; and 3School of Biomedical and Sports Science, Edith Cowan University, Joondalup, Perth, Western Australia, AUSTRALIA

Address for correspondence: Jeff Coombes, School of Human Movement Studies, University of Queensland, St. Lucia, QLD 4072 Australia; E-mail:

Submitted for publication December 2003.

Accepted for publication December 2004.

The authors would like to thank the participants of this study for their time and effort, Sports Medicine Australia for funding, and Sullivan and Nicollaides Pathology for the use of their laboratory.

©2005The American College of Sports Medicine