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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 2840643, 19 pages
Clinical Study

Evidence of a Redox-Dependent Regulation of Immune Responses to Exercise-Induced Inflammation

1Department of Clinical Therapeutics, Medical School, University of Athens, 11527 Athens, Greece
2School of Physical Education and Sport Sciences, University of Thessaly, Karies, 42100 Trikala, Greece
3School of Physical Education and Sport Sciences, Democritus University of Thrace, 69100 Komotini, Greece
4Department of Toxicology, Medical School, University of Athens, 11527 Athens, Greece
5Department of Clinical Biochemistry, “Aghia Sophia” Children’s Hospital, 11527 Athens, Greece
6School of Physical Education and Sport Science, University of Athens, Athens, Greece

Received 14 May 2016; Accepted 21 September 2016

Academic Editor: Victor M. Victor

Copyright © 2016 Alexandra Sakelliou et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


We used thiol-based antioxidant supplementation (n-acetylcysteine, NAC) to determine whether immune mobilisation following skeletal muscle microtrauma induced by exercise is redox-sensitive in healthy humans. According to a two-trial, double-blind, crossover, repeated measures design, 10 young men received either placebo or NAC (20 mg/kg/day) immediately after a muscle-damaging exercise protocol (300 eccentric contractions) and for eight consecutive days. Blood sampling and performance assessments were performed before exercise, after exercise, and daily throughout recovery. NAC reduced the decline of reduced glutathione in erythrocytes and the increase of plasma protein carbonyls, serum TAC and erythrocyte oxidized glutathione, and TBARS and catalase activity during recovery thereby altering postexercise redox status. The rise of muscle damage and inflammatory markers (muscle strength, creatine kinase activity, CRP, proinflammatory cytokines, and adhesion molecules) was less pronounced in NAC during the first phase of recovery. The rise of leukocyte and neutrophil count was decreased by NAC after exercise. Results on immune cell subpopulations obtained by flow cytometry indicated that NAC ingestion reduced the exercise-induced rise of total macrophages, HLA+ macrophages, and 11B+ macrophages and abolished the exercise-induced upregulation of B lymphocytes. Natural killer cells declined only in PLA immediately after exercise. These results indicate that thiol-based antioxidant supplementation blunts immune cell mobilisation in response to exercise-induced inflammation suggesting that leukocyte mobilization may be under redox-dependent regulation.