Exercise-induced muscle damage is associated with an acute-phase inflammatory response characterized by phagocyte infiltration into muscle and free radical production. Although soccer includes intense eccentric muscle actions that cause muscle damage, the oxidative stress responses after a soccer game are currently unknown. The present investigation attempted to determine the responses of circulating levels of oxidative stress and antioxidant status markers during recovery from a soccer game. Twenty soccer players (experimental group) were assigned to 2 different teams that competed against each other (2 × 45 minutes). Ten other players served as controls (rested). Creatine kinase (CK) activity, uric acid, leukocyte count, malondialdehyde (MDA), protein carbnyls (PC), reduced (GSH) and oxidized glutathione (GSSG), antioxidant capacity (TAC), catalase, glutathione peroxidase activity (GPX), delayed-onset of muscle soreness (DOMS), and anaerobic performance (speed, vertical jump performance) were measured before and following (immediately post, 24 hours, 48 hours, 72 hours) the game. Performance deteriorated (2-17%, p < 0.05) throughout recovery. Leukocytosis developed (p < 0.05) immediately following the game and at 24 hours. Both CK and DOMS (3-8-fold, p < 0.05) increased from baseline and remained elevated (p < 0.05) through 48 hours. Thiobarbituric acid reactive substances (TBARS), PC, uric acid, GPX, and TAC increased (13-67%, p < 0.05) throughout recovery, whereas catalase was elevated (38%, p < 0.05) only immediately after the game. GSH/GSSG declined (17-75%, p < 0.05) throughout recovery. Our results suggest that oxidative stress is markedly upregulated by a soccer game, probably as a part of the exercise-induced inflammatory response, and is accompanied by a marked deterioration of anaerobic performance for as long as 72 hours.

SummaryThe central aim of this review is to address the highly multidisciplinary topic of redox biology as related to exercise using an integrative and comparative approach rather than focusing on blood, skeletal muscle or humans. An attempt is also made to redefine ʻoxidative stressʼ as well as to introduce the term ʻalterations in redox homeostasisʼ to describe changes in redox homeostasis indicating oxidative stress, reductive stress or both. The literature analysis shows that the effects of non-muscledamaging exercise and muscle-damaging exercise on redox homeostasis are completely different. Non-muscle-damaging exercise induces alterations in redox homeostasis that last a few hours post exercise, whereas muscle-damaging exercise causes alterations in redox homeostasis that may persist for and/or appear several days post exercise. Both exhaustive maximal exercise lasting only 30s and isometric exercise lasting 1-3min (the latter activating in addition a small muscle mass) induce systemic oxidative stress. With the necessary modifications, exercise is capable of inducing redox homeostasis alterations in all fluids, cells, tissues and organs studied so far, irrespective of strains and species. More importantly, ʻexercise-induced oxidative stressʼ is not an ʻoddityʼ associated with a particular type of exercise, tissue or species. Rather, oxidative stress constitutes a ubiquitous fundamental biological response to the alteration of redox homeostasis imposed by exercise. The hormesis concept could provide an interpretative framework to reconcile differences that emerge among studies in the field of exercise redox biology. Integrative and comparative approaches can help determine the interactions of key redox responses at multiple levels of biological organization.Key words: antioxidant, biomarker, eccentric, free radical, training. THE JOURNAL OF EXPERIMENTAL BIOLOGY 1616The ʻgoodʼ (antioxidants), the ʻbadʼ (reactive species) and the ʻuglyʼ (oxidative stress) 1 The distinction drawn in the section heading is schematically used to parody the popular manichaeistic view that antioxidants are considered 'useful' entities, reactive species are considered 'harmful' entities and oxidative stress is considered a 'negative' state. Certainly, the reality is much more complicated and antioxidants, reactive species and oxidative stress can serve both useful and detrimental roles, which are dependent on the biological context (within an organism), which in turn are greatly dependent on the environmental context (outside an organism). AntioxidantsAdmittedly, to define the term 'antioxidant' is a difficult task. In this paper, antioxidant is defined as any mechanism, structure and/or substance that delays, prevents or removes oxidative modifications to a target molecule (Halliwell and Gutteridge, 2007;Pamplona and Costantini, 2011). Antioxidants can be complex molecules such as the superoxide dismutases and peroxiredoxins, or simpler ones such as uric acid and glutathione (Gutteridge and Halliwell, 2010). They can be broa...

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Aim: The aim of this study was to reveal the role of reactive oxygen and nitrogen species (RONS) in exercise adaptations under physiological in vivo conditions and without the interference from other exogenous redox agents (e.g. a pro-oxidant or antioxidant). Methods: We invented a novel methodological set-up that exploited the large redox interindividual variability in exercise responses. More specifically, we used exercise-induced oxidative stress as the 'classifier' measure (i.e. low, moderate and high) and investigated the physiological and redox adaptations after a 6-week endurance training protocol. Results: We demonstrated that the group with the low exercise-induced oxidative stress exhibited the lowest improvements in a battery of classic adaptations to endurance training (VO 2 max, time trial and Wingate test) as well as in a set of redox biomarkers (oxidative stress biomarkers and antioxidants), compared to the high and moderate oxidative stress groups. Conclusion: The findings of this study substantiate, for the first time in a human in vivo physiological context, and in the absence of any exogenous redox manipulation, the vital role of RONS produced during exercise in adaptations. The stratification approach, based on a redox phenotype, implemented in this study could be a useful experimental strategy to reveal the role of RONS and antioxidants in other biological manifestations as well.

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Without effective countermeasures, the musculoskeletal system is altered by the microgravity environment of long-duration spaceflight, resulting in atrophy of bone and muscle tissue, as well as in deficits in the function of cartilage, tendons, and vertebral disks. While inflight countermeasures implemented on the International Space Station have evidenced reduction of bone and muscle loss on low-Earth orbit missions of several months in length, important knowledge gaps must be addressed in order to develop effective strategies for managing human musculoskeletal health on exploration class missions well beyond Earth orbit. Analog environments, such as bed rest and/or isolation environments, may be employed in conjunction with large sample sizes to understand sex differences in countermeasure effectiveness, as well as interaction of exercise with pharmacologic, nutritional, immune system, sleep and psychological countermeasures. Studies of musculoskeletal biomechanics, involving both human subject and computer simulation studies, are essential to developing strategies to avoid bone fractures or other injuries to connective tissue during exercise and extravehicular activities. Animal models may be employed to understand effects of the space environment that cannot be modeled using human analog studies. These include studies of radiation effects on bone and muscle, unraveling the effects of genetics on bone and muscle loss, and characterizing the process of fracture healing in the mechanically unloaded and immuno-compromised spaceflight environment. In addition to setting the stage for evidence-based management of musculoskeletal health in long-duration space missions, the body of knowledge acquired in the process of addressing this array of scientific problems will lend insight into the understanding of terrestrial health conditions such as age-related osteoporosis and sarcopenia.

This study investigated the effect of an acute swimming protocol on selected blood redox status indices in trained children. Eleven boys and 11 girls (aged 9-11 y) swam 12 bouts of 50 m at a pace corresponding to 70%-75% of the participant's 50 m maximum velocity, with each bout separated by 1 min rest periods. At rest, no differences in any redox status marker between boys and girls were observed. As compared with the pre-exercise values, significant increases in thiobarbituric acid-reactive substances (TBARS), protein carbonyls, catalase activity, total antioxidant capacity (TAC), and oxidized glutathione (GSSG) concentration, as well as significant decreases in reduced glutathione (GSH) concentration and GSH:GSSG, were found post-exercise in both boys and girls. The magnitude of the exercise-induced alterations in the blood redox status based on the calculated effect sizes could be considered large for all parameters in both sexes (median effect size in absolute values was equal to 1.38). The main finding of the present study is that an acute swimming bout at 70%-75% maximum velocity resulted in blood oxidative stress in a similar manner in both trained young boys and girls.

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