BioMed Research International

BioMed Research International / 2011 / Article

Research Article | Open Access

Volume 2011 |Article ID 540458 |

C. Berzosa, I. Cebri谩n, L. Fuentes-Broto, E. G贸mez-Trull茅n, E. Piedrafita, E. Mart铆nez-Ballar铆n, L. L贸pez-Pingarr贸n, R. J. Reiter, J. J. Garc铆a, "Acute Exercise Increases Plasma Total Antioxidant Status and Antioxidant Enzyme Activities in Untrained Men", BioMed Research International, vol. 2011, Article ID 540458, 7 pages, 2011.

Acute Exercise Increases Plasma Total Antioxidant Status and Antioxidant Enzyme Activities in Untrained Men

Academic Editor: M. Firoze Khan
Received14 Oct 2010
Revised19 Dec 2010
Accepted03 Jan 2011
Published09 Mar 2011


Antioxidant defences are essential for cellular redox regulation. Since free-radical production may be enhanced by physical activity, herein, we evaluated the effect of acute exercise on total antioxidant status (TAS) and the plasma activities of catalase, glutathione reductase, glutathione peroxidase, and superoxide dismutase and its possible relation to oxidative stress resulting from exercise. Healthy untrained male subjects ( ) performed three cycloergometric tests, including maximal and submaximal episodes. Venous blood samples were collected before and immediately after each different exercise. TAS and enzyme activities were assessed by spectrophotometry. An increase of the antioxidant enzyme activities in plasma was detected after both maximal and submaximal exercise periods. Moreover, under our experimental conditions, exercise also led to an augmentation of TAS levels. These findings are consistent with the idea that acute exercise may play a beneficial role because of its ability to increase antioxidant defense mechanisms through a redox sensitive pathway.

1. Introduction

In recent decades, intensive research in the field of oxidative damage indicates that exercise exacerbates the generation of reactive oxygen (ROS) and reactive nitrogen species (RNS), some of which are free-radicals [15]. A free-radical is any specie capable of existence with one or more unpaired electron [6]. ROS/RNS refer to oxygen or nitrogen containing free-radicals and their non-free-radical derivatives.

Aerobic organisms produce free-radicals as a consequence of the oxygen metabolism, and, obviously, exercise causes an increase in oxygen utilization in mitochondria, resulting in elevated radical generation. An estimated 2% to 5% of the oxygen consumed (VO2) during normal mitochondrial metabolism in aerobic organisms may be converted to radicals and their products [7]. During exercise, the VO2 uptake is higher than at rest [8] because of the increasing energy demand in many tissues, mainly in muscle.

The role of mitochondria in free-radical production during exercise is under investigation. The increase in oxygen uptake is related to substantial rise in the production of free-radicals generated during mitochondrial respiration [9]. Several potential alternative sources of free-radicals, such as oxidase systems associated with membranes, nitric oxide production, and phagocytic processes [3], as well as an increase in lactate formation, as happens in exhaustive exercise [10], have been proposed to contribute significantly to the overproduction of free-radicals.

The elevation of metabolism by exercise results in a greater production of superoxide radicals [11], which are dismutated to hydrogen peroxide (H2O2) by superoxide dismutase (SOD). H2O2, a molecule that readily crosses cell membranes, can be detoxified to water and oxygen by other enzymes, that is, catalase (CAT) and glutathione peroxidase (GPx). But when these transformations do not take place, H2O2 is, via the Fenton reaction, converted to the hydroxyl radical, the most toxic ROS because of its high reactivity [6, 12].

Numerous studies have shown that muscle cells also release superoxide into the extracellular space [11, 13], so free-radicals readily reach the blood and act on other cells. There is a general consensus that free-radical generation during exercise occurs predominantly in skeletal and heart muscles; however, the invasive nature of obtaining biopsies from exercising humans limits their access. Therefore, some reports have claimed that the concentration of several oxidative stress markers increase immediately in the plasma after an acute exercise [14, 15].

All organisms have developed an antioxidant defence system to counter ROS/RNS production. Antioxidants are defined as any substance that, when present at low concentration compared to those of an oxidizable substrate, significantly delays or prevents the oxidation of that substrate [16]. They can be classified as enzymatic or nonenzymatic antioxidants. The first are low molecular weight proteins, which minimize oxidative damage by catalyzing chemical reactions to detoxify free-radicals in cells and tissues and can be synthesised due to the redox-activation of specific genes, primarily by affecting the binding of transcription factors to DNA. During exercise, free-radicals generated can activate different redox-sensitive transcription factors, including NF-B, which leads to an elevation in the expression of some antioxidant enzymes [17]. Nonenzymatic antioxidants are generally small molecules that directly scavenge ROS, preventing them from disfiguring lipids, proteins, or nucleic acids. Glutathione, an important intracellular antioxidant, is converted to its oxidized form (GSSG) by GPx when it is used as a scavenger; it is converted back to its reduced form by glutathione reductase (GR). Moreover, both animals and humans subjected to a long-term heavy exercise became more resistant to oxidative damage [18, 19]. Fisher et al. studied the activity of SOD, CAT, and GPX after high-intensity interval training, and they found that all of these enzymes activities were increased [20]. None of these studies have compared different types of exercise and observed changes in activities of four antioxidant enzymes and in the total antioxidant status in plasma.

Herein, we evaluated the antioxidant status after three protocols of acute exercise in untrained healthy men. Plasma samples were collected for the measurement of CAT, GR, GPx, and SOD activities and total antioxidant status (TAS) as a general marker of antioxidant defences.

2. Material and Methods

2.1. Subjects

Thirty-four healthy male volunteers, aged 19鈥29 (23.0 卤 0.41), were involved in this study. Only males were included to avoid any distortion in the hormonal response to physical exercise caused by sex differences [1]. Anthropometric characteristics of these subjects are summarized in Table 1.


Age (years)23 卤 0.41
Height (cm)177.59 卤 1.11
Weight (kg)75.25 卤 2.84
BMI (kg/m2)23.72 卤 0.69
VO2max (mL路kg鈭1路min鈭1)43.8 卤 1.58
MWC (W)239.8 卤 7.4

None of the subjects participated regularly in sport competitions, and they did not engage in any form of vigorous exercise or take medications for 24 hours before the study was performed. All subjects underwent an extensive previous medical evaluation that included a history and physical examination, electrocardiogram, and biochemical profile to discard possible pathologies. Subjects gave their informed written consent to participate in the study, designed according to the principles of the Declaration of Helsinki (1964) and approved by the Ethical Committee of Clinical Investigation of Aragon with the statement code C02/2010.

2.2. Exercise Protocols

Exercise was performed on an electronically regulated cycloergometer between 08:00 and 10:30鈥塧.m. after an overnight fast. All subjects pedaled at 60 rounds per minute. Three ergometric tests were performed on each subject in random order at intervals of at least 1 week. Firstly, the maximal oxygen consumption (VO2max) and the maximal working capacity (MWC) were determined using a continuous progressive exercise test, where the work load was increased by 10 Watts every minute [21]. The oxygen uptake was determined using a 鈥渂reath by breath鈥 gas exchange analyzer (MedGrafics CPX Express). Secondly, all subjects performed a strenuous test until exhaustion at VO2max intensity. The initial load was 100 Watts less than the MWC determined in the first test [22]. Finally, the subjects pedaled for 30 minutes at a submaximal workload chosen at 70% of the expected maximum for each individual [23].

2.3. Analytical Procedures

Peripheral venous blood samples obtained before exercise (A), and immediately after a continuous progressive exercise test (B), a strenuous test performed until exhaustion (C), and a submaximal exercise (70% of the expected maximum workload) for 30 minutes (D) were drawn by antecubital venepuncture and collected into lithium heparin-containing tubes. 10鈥塵L of blood were collected at each sampling time. Blood samples were immediately centrifuged at 1.000 脳g for 10 minutes in a Beckman Allegra 64R refrigerated centrifuge (Fullerton, USA). Plasma was stored in 250鈥L aliquots at 鈭30掳C until TAS and enzyme activities were determined.

The total antioxidant status method relies on the ability of plasma antioxidant substances to inhibit the oxidation of 2,2鈥-azino-di-[3-ethylbenzthiazioline sulphonate] (ABTS) to the radical cation ABTS.+ by metmyoglobin. This molecule formed a relative stable green substance which was measured spectrophotometrically at 600鈥塶m. Antioxidants in the sample decreased the formation of this colour proportional to their concentration [24]. The capacity of the antioxidants in the sample to prevent ABTS oxidation is compared with that of trolox, a water-soluble tocopherol analogue, and is quantified as millimolar trolox equivalents.

CAT activity was measured following the decrease in H2O2 concentration [25]. When H2O2 was added at low concentration (0.2鈥塎) to a sample with CAT, this enzyme catalyzed the transformation of this substrate to oxygen and water. To check the activity, a kinetic curve had to be measured during 30 seconds at 鈥塶m using a molar extinction coefficient 43.6鈥塩m鈭1鈥塎鈭1 [26] to know the amount of H2O2 eliminated.

Catalytic activity of GR was measured following the decrease in the absorbance at 鈥塶m for 3 minutes due to the oxidation of NADPH to NADP+, in presence of GSSG, as described by Goldberg and Spooner [27]. The molar extinction coefficient is 鈥塩m鈭1鈥塎鈭1.

To determine GPx activity, the continuous decrease in NADPH concentration was measured, while GSH levels were maintained, following the Flohe and Gunzler method [28]. This method is based on the rise of the absorbance, during 3 minutes at 鈥塶m, because of the oxidation of NADPH in presence of GSH, t-butyl hydroperoxide, GR, and the sample. The molar extinction coefficient used for the calculations is 鈥塩m鈭1鈥塎鈭1.

One CAT, GR, or GPx enzymatic unit (units) was defined as that amount of the enzyme that catalyzes the conversion of 1 micromole of substrate per minute.

SOD activity was measured as the inhibition of the rate of reduction of cytochrome c by the superoxide radical ( ), observed at 550鈥塶m. was first produced by the reaction of xanthine and oxygen catalyzed by xanthine oxidase [29]. Cytochrome c molar extinction coefficient is 鈥塩m鈭1鈥塎鈭1 [30]. The definition of one unit of SOD is the amount of protein that inhibits the rate of cytochrome c reduction by 50%.

2.3.1. Statistic Analysis

Data were analysed using repeated-measures ANOVAs. Where significant main effects were found, pairwise comparisons were conducted using Bonferroni adjustments for multiple comparisons. The level of statistical significance was .

3. Results

Total antioxidant status after all the three acute exercise protocols tested in this study: continuous progressive (1.62 卤 0.07), strenuous (1.66 卤 0.08) and submaximal exercises (1.61 卤 0.08) was elevated when compared with basal status (1.53 卤 0.07) as illustrated in Figure 1.

The strenuous protocol produced the highest increase in CAT activity (42.29 卤 2.84) although the continuous progressive (24.85 卤 2.35) and submaximal exercises (29.19 卤 3.89) also significantly elevated CAT activity relative to that at rest (18.54 卤 1.97) (Figure 2).

Both GR and GPx were elevated after submaximal exercises and even higher activity values of these enzymes were obtained after progressive and strenuous exercises (Figures 3 and 4). GR increases from a basal level of 0.021 卤 0.002 to B: 0.031 卤 0.003, C: 0.031 卤 0.003, and D: 0.026 卤 0.003. GPx level was also higher after exercises B: 1.03 卤 0.3, C: 1.02 卤 0.03, and D: 1.02 卤 0.03 from a basal level of 0.94 卤 0.02.

The SOD activity rose significantly after the strenuous exercise (0.028 卤 0.007), but it is after the nonexhaustive test (0.033 卤 0.007) when the highest increase took place versus the basal value (0.018 卤 0.004) (Figure 5).

4. Discussion

Oxidative stress is an imbalance between ROS/RNS generation and antioxidants levels in favour of the former [31]. Although there is a general consensus that free-radical overproduction due to exercise occurs mainly in the active skeletal muscles [3234], it is also well documented that exercise causes systemic oxidative damage. Based on this, Sureda et al. [35] found an augmentation of malondialdehyde, a marker of lipid peroxidation due to oxidative stress, in lymphocytes after a single bout of intense exercise. In addition, Ajmani et al. [36] noted an increase in membrane rigidity in erythrocytes after a strenuous exercise because of oxidative stress. Membrane rigidity signifies elevated lipid peroxidation.

The main finding of our work was the increase of the TAS in human blood after a single bout of exercise, either maximal or submaximal. Plasma TAS is a combination of various antioxidant defences, including enzymatic and nonenzymatic systems. As shown herein, Child et al. [37] found higher TAS levels in the plasma after an exhaustive exercise, that is, equivalent to a half marathon, and they concluded that uric acid, an important component of the antioxidant system, is responsible for one third of the TAS increase. Although uric acid may contribute to the antioxidant defences, another possible explanation for the elevation of TAS is changes in other antioxidants, for example, GSH, melatonin, or the antioxidant enzymes [38]. We also demonstrate that CAT, GPx, GR, and SOD activities were higher after exercise than at rest.

Previous reports have shown increases of GPx, GR, and CAT activities in the skeletal muscle during exercise. Ji et al. [39, 40] observed in two consecutive studies that an acute bout of exercise increased antioxidant enzymatic activities in rat muscle. In the first report, rats performed an exercise in a treadmill until exhaustion [39]. The second study was designed to compare both maximal and submaximal protocols of exercise, and, as we found, GPx, GR, and CAT activities were enhanced by exercise [40]. SOD activity also increased after a single period of exhaustive exercise and during the recovery, following a nondamaging aerobic exercise in a cycloergometer [41]. In this report, muscle samples were taken from the vastus lateralis muscle of the exercised leg in humans by biopsy.

The effect of acute exercise on the antioxidant enzyme activities appears to be systemic, involving many organs. Following a single exhaustive swimming test, Terblanche [42] reported that CAT activity was higher compared to the rest in several tissues: liver, heart, kidney, or lung in male and in female rats; thereby, these authors proposed that increasing CAT activity during acute exercise may be a defence mechanism in protecting the tissues against hydrogen peroxide generation. Also, CAT and SOD activities in rat lung tissue was increased significantly after the effort in young rats, a response that was significantly depressed in old rats. This suggests that senescence entails a decrease in the antioxidant defence system [43]. Hara et al. [44] found an elevation of GPx activity in liver and muscle after a swimming test.

The invasive nature of obtaining muscular biopsies from exercising humans limits their access; thus, a number of studies have directed their efforts to the blood. Thus, Aguil贸 et al. [45] have recently found an elevation in CAT and GR activities in the erythrocytes, while Cases et al. [46] found CAT, GPx, and SOD rises in lymphocytes after a single bicycle ride or swimming. These authors proposed that oxidative stress and the necessity of protection against oxidative damage may be responsible, at least partially, for the elevation in the activity of these enzymes induced by exercise. However, CAT and GPx activities in human neutrophils decreased after a single bout of exercise [47], perhaps because these cells released the enzymes into the plasma. Consistent with our findings, Elosua et al. [48] also reported that the activity of extracellular SOD and GPx rose from basal status after an acute bout of aerobic. Although one hour later, during recovery, the antioxidant enzyme activities fell back to basal levels. However, enzyme activities were increased again 24 hours later because a possible genetic upregulation of these enzymes [48].

Recent interest has focused on the effect of training on the antioxidant defence system. Shin et al. [49] studied the effect of 6 months aerobic endurance training on the response to the acute exercise and reported that antioxidant enzyme activities were much higher than after pretraining test. A possible explanation for the reinforcement of the antioxidant system due to training is that exercise stimulates the expression of the genes involved in the regulation of the antioxidant enzymes in a redox sensitive signal transduction pathways, mainly NF-B. It is reported the importance of the nuclear factor in the expression of SOD and inducible nitric oxide synthase (iNOS) in rat skeletal muscle [50]. Ji et al. [51] observed that exercising rats injected with allopurinol, a competitive inhibitor of xanthine oxidase, attenuated ROS production compared to untreated group, and also NF-B binding was dramatically enhanced by exercise but inhibited by allopurinol treatment. Thus, ROS produced by exercise seemed to be involved in NF-B signalling. It is also reported that physical exercise (80% VO2max for 1 hour) resulted in NF-B activation in peripheral blood cells of physically fit young men [52]. In the other hand, another study shows how an eccentric exercise for 45 minutes did not increase the expression of this transcription factor [53]. So, the influence of different exercise protocols of training in the redox status in many cells or tissues remains unclear [48, 5457].

5. Conclusions

In conclusion, the data reported herein provide evidence that a single bout of maximal and submaximal acute exercise enhances plasma TAS in healthy human subjects. This increase may be a consequence of an improvement in the plasma activities of CAT, GPx, GR, and SOD. Based on our observations and previous studies which reported that exercise causes a significant augmentation of the concentrations of several antioxidant scavengers, presumably due to its interactions with the free-radical overproduction [58, 59], it seems reasonable to propose that exercise may play a beneficial role because of its ability to increase the antioxidant defense mechanisms against oxidative stress.


This work was supported by grants from the 鈥淕obierno de Arag贸n鈥 (Aging and Oxidative Stress Physiology, Grants nos. B40 and PI036/09) and by F.I.S. from Instituto de Salud Carlos III (Grant nos. RD06/0013/1017). The authors declare that they have no conflict of interests.


  1. R. J. Bloomer and K. H. Fisher-Wellman, 鈥淏lood oxidative stress biomarkers: influence of sex, exercise training status, and dietary intake,鈥 Gender Medicine, vol. 5, no. 3, pp. 218鈥228, 2008. View at: Publisher Site | Google Scholar
  2. M. J. Jackson, 鈥淔ree radicals generated by contracting muscle: by-products of metabolism or key regulators of muscle function?鈥 Free Radical Biology and Medicine, vol. 44, no. 2, pp. 132鈥141, 2008. View at: Publisher Site | Google Scholar
  3. S. K. Powers and M. J. Jackson, 鈥淓xercise-induced oxidative stress: cellular mechanisms and impact on muscle force production,鈥 Physiological Reviews, vol. 88, no. 4, pp. 1243鈥1276, 2008. View at: Publisher Site | Google Scholar
  4. K. J. A. Davies, A. T. Quintanilha, G. A. Brooks, and L. Packer, 鈥淔ree radicals and tissue damage produced by exercise,鈥 Biochemical and Biophysical Research Communications, vol. 107, no. 4, pp. 1198鈥1205, 1982. View at: Google Scholar
  5. M. C. Gomez-Cabrera, A. Martínez, G. Santangelo, F. V. Pallardó, J. Sastre, and J. Viña, 鈥淥xidative stress in marathon runners: interest of antioxidant supplementation,鈥 The British Journal of Nutrition, vol. 96, supplement 1, pp. S31鈥揝33, 2006. View at: Google Scholar
  6. B. Halliwell, 鈥淩eactive oxygen species in living systems: source, biochemistry, and role in human disease,鈥 American Journal of Medicine, vol. 91, no. 3C, pp. 14S鈥22S, 1991. View at: Google Scholar
  7. A. Boveris, N. Oshino, and B. Chance, 鈥淭he cellular production of hydrogen peroxide,鈥 Biochemical Journal, vol. 128, no. 3, pp. 617鈥630, 1972. View at: Google Scholar
  8. R. Cazzola, S. Russo-Volpe, G. Cervato, and B. Cestaro, 鈥淏iochemical assessments of oxidative stress, erythrocyte membrane fluidity and antioxidant status in professional soccer players and sedentary controls,鈥 European Journal of Clinical Investigation, vol. 33, no. 10, pp. 924鈥930, 2003. View at: Publisher Site | Google Scholar
  9. M. J. Jackson, D. Pye, and J. Palomero, 鈥淭he production of reactive oxygen and nitrogen species by skeletal muscle,鈥 Journal of Applied Physiology, vol. 102, no. 4, pp. 1664鈥1670, 2007. View at: Publisher Site | Google Scholar
  10. M. A. Ali, F. Yasui, S. Matsugo, and T. Konishi, 鈥淭he lactate-dependent enhancement of hydroxyl radical generation by the Fenton reaction,鈥 Free Radical Research, vol. 32, no. 5, pp. 429鈥438, 2000. View at: Google Scholar
  11. F. McArdle, D. M. Pattwell, A. Vasilaki, A. McArdle, and M. J. Jackson, 鈥淚ntracellular generation of reactive oxygen species by contracting skeletal muscle cells,鈥 Free Radical Biology and Medicine, vol. 39, no. 5, pp. 651鈥657, 2005. View at: Publisher Site | Google Scholar
  12. D. M. Patwell, A. McArdle, J. E. Morgan, T. A. Patridge, and M. J. Jackson, 鈥淩elease of reactive oxygen and nitrogen species from contracting skeletal muscle cells,鈥 Free Radical Biology and Medicine, vol. 37, no. 7, pp. 1064鈥1072, 2004. View at: Publisher Site | Google Scholar
  13. M. B. Reid, T. Shoji, M. R. Moody, and M. L. Entman, 鈥淩eactive oxygen in skeletal muscle. II. Extracellular release of free radicals,鈥 Journal of Applied Physiology, vol. 73, no. 5, pp. 1805鈥1809, 1992. View at: Google Scholar
  14. T. Ashton, C. C. Rowlands, E. Jones et al., 鈥淓lectron spin resonance spectroscopic detection of oxygen-centred radicals in human serum following exhaustive exercise,鈥 European Journal of Applied Physiology and Occupational Physiology, vol. 77, no. 6, pp. 498鈥502, 1998. View at: Publisher Site | Google Scholar
  15. V. Pialoux, R. Mounier, E. Rock et al., 鈥淓ffects of acute hypoxic exposure on prooxidant/antioxidant balance in elite endurance athletes,鈥 International Journal of Sports Medicine, vol. 30, no. 2, pp. 87鈥93, 2009. View at: Publisher Site | Google Scholar
  16. B. Halliwell, R. Aeschbach, J. Löliger, and O. I. Aruoma, 鈥淭he characterization of antioxidants,鈥 Food and Chemical Toxicology, vol. 33, no. 7, pp. 601鈥617, 1995. View at: Publisher Site | Google Scholar
  17. M. C. Gomez-Cabrera, C. Borrás, F. V. Pallardo, J. Sastre, L. L. Ji, and J. Viña, 鈥淒ecreasing xanthine oxidase-mediated oxidative stress prevents useful cellular adaptations to exercise in rats,鈥 Journal of Physiology, vol. 567, no. 1, pp. 113鈥120, 2005. View at: Publisher Site | Google Scholar
  18. M. Higuchi, L. J. Cartier, M. Chen, and J. O. Holloszy, 鈥淪uperoxide dismutase and catalase in skeletal muscle: adaptive response to exercise,鈥 Journals of Gerontology, vol. 40, no. 3, pp. 281鈥286, 1985. View at: Google Scholar
  19. S. K. Powers, D. Criswell, J. Lawler et al., 鈥淚nfluence of exercise and fiber type on antioxidant enzyme activity in rat skeletal muscle,鈥 American Journal of Physiology, vol. 266, no. 2, pp. R375鈥揜380, 1994. View at: Google Scholar
  20. G. Fisher, D. D. Schwartz, J. C. Quindry et al., 鈥淟ymphocyte enzymatic antioxidant responses to oxidative stress following high-intensity interval exercise,鈥 Journal of Applied Physiology. In press. View at: Google Scholar
  21. P. Carta, G. Aru, M. T. Barbieri, and M. Mele, 鈥淏icycle ergometry exercise tests: a comparison between 3 protocols with an increasing load,鈥 Medicina del Lavoro, vol. 82, no. 1, pp. 56鈥64, 1991. View at: Google Scholar
  22. F. Caputo and B. S. Denadai, 鈥淓ffects of aerobic endurance training status and specificity on oxygen uptake kinetics during maximal exercise,鈥 European Journal of Applied Physiology, vol. 93, no. 1-2, pp. 87鈥95, 2004. View at: Publisher Site | Google Scholar
  23. R. J. Bloomer, M. J. Falvo, A. C. Fry, B. K. Schilling, W. A. Smith, and C. A. Moore, 鈥淥xidative stress response in trained men following repeated squats or sprints,鈥 Medicine and Science in Sports and Exercise, vol. 38, no. 8, pp. 1436鈥1442, 2006. View at: Publisher Site | Google Scholar
  24. N. J. Miller and G. Paganga, 鈥淎ntioxidant activity of low-density lipoprotein,鈥 Methods in Molecular Biology, vol. 108, pp. 325鈥335, 1998. View at: Google Scholar
  25. D. M. Aebi, H.E., 鈥淐atalase,鈥 in Methods of Enzymatic Analysis, H. U. Bergmeyer, J. Bergmeyer, and M. Grassl, Eds., pp. 273鈥286, Verlag Chemie, Weinheim, Germany, 1983. View at: Google Scholar
  26. C. R. Wheeler, J. A. Salzman, N. M. Elsayed, S. T. Omaye, and D. W. Korte, 鈥淎utomated assays for superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activity,鈥 Analytical Biochemistry, vol. 184, no. 2, pp. 193鈥199, 1990. View at: Google Scholar
  27. D. M. Goldberg and R. J. Spooner, 鈥淕lutathione reductase,鈥 in Methods of Enzymatic Analysis, H. U. Bergmeyer, J. Bergmeyer, and M. Grassl, Eds., pp. 258鈥266, Verlag Chemie, Weinheim, Germany, 1983. View at: Google Scholar
  28. L. Flohe and W. A. Gunzler, 鈥淎ssays of glutathione peroxidase,鈥 Methods in Enzymology, vol. 105, pp. 114鈥121, 1984. View at: Google Scholar
  29. C. C. Winterbourn, R. E. Hawkins, M. Brian, and R. W. Carrell, 鈥淭he estimation of red cell superoxide dismutase activity,鈥 Journal of Laboratory and Clinical Medicine, vol. 85, no. 2, pp. 337鈥341, 1975. View at: Google Scholar
  30. T. A. Alleyne, M. T. Wilson, G. Antonini et al., 鈥淚nvestigation of the electron-transfer properties of cytochrome c oxidase covalently cross-linked to Fe- or Zn-containing cytochrome c,鈥 Biochemical Journal, vol. 287, no. 3, pp. 951鈥956, 1992. View at: Google Scholar
  31. H. Sies and R. Mehlhorn, 鈥淢utagenicity of nitroxide-free radicals,鈥 Archives of Biochemistry and Biophysics, vol. 251, no. 1, pp. 393鈥396, 1986. View at: Google Scholar
  32. M. J. Jackson, 鈥淩eactive oxygen species and redox-regulation of skeletal muscle adaptations to exercise,鈥 Philosophical Transactions of the Royal Society B, vol. 360, no. 1464, pp. 2285鈥2291, 2005. View at: Publisher Site | Google Scholar
  33. A. McArdle, D. Pattwell, A. Vasilaki, R. D. Griffiths, and M. J. Jackson, 鈥淐ontractile activity-induced oxidative stress: cellular origin and adaptive responses,鈥 American Journal of Physiology, vol. 280, no. 3, pp. C621鈥揅627, 2001. View at: Google Scholar
  34. J. Viña, M. C. Gomez-Cabrera, A. Lloret et al., 鈥淔ree radicals in exhaustive physical exercise: mechanism of production, and protection by antioxidants,鈥 IUBMB Life, vol. 50, no. 4-5, pp. 271鈥277, 2000. View at: Publisher Site | Google Scholar
  35. A. Sureda, M. D. Ferrer, P. Tauler et al., 鈥淓ffects of exercise intensity on lymphocyte H2O2 production and antioxidant defences in soccer players,鈥 British Journal of Sports Medicine, vol. 43, no. 3, pp. 186鈥190, 2009. View at: Publisher Site | Google Scholar
  36. R. S. Ajmani, J. L. Fleg, A. A. Demehin et al., 鈥淥xidative stress and hemorheological changes induced by acute treadmill exercise,鈥 Clinical Hemorheology and Microcirculation, vol. 28, no. 1, pp. 29鈥40, 2003. View at: Google Scholar
  37. R. B. Child, D. M. Wilkinson, J. O. L. Fallowfield, and A. E. Donnelly, 鈥淓levated serum antioxidant capacity and plasma malondialdehyde concentration in response to a simulated half-marathon run,鈥 Medicine and Science in Sports and Exercise, vol. 30, no. 11, pp. 1603鈥1607, 1998. View at: Google Scholar
  38. B. P. Yu, 鈥淐ellular defenses against damage from reactive oxygen species,鈥 Physiological Reviews, vol. 74, no. 1, pp. 139鈥162, 1994. View at: Google Scholar
  39. L. L. Ji and R. Fu, 鈥淩esponses of glutathione system and antioxidant enzymes to exhaustive exercise and hydroperoxide,鈥 Journal of Applied Physiology, vol. 72, no. 2, pp. 549鈥554, 1992. View at: Google Scholar
  40. L. L. Ji, R. Fu, and E. W. Mitchell, 鈥淕lutathione and antioxidant enzymes in skeletal muscle: effects of fiber type and exercise intensity,鈥 Journal of Applied Physiology, vol. 73, no. 5, pp. 1854鈥1859, 1992. View at: Google Scholar
  41. M. Khassaf, R. B. Child, A. McArdle, D. A. Brodie, C. Esanu, and M. J. Jackson, 鈥淭ime course of responses of human skeletal muscle to oxidative stress induced by nondamaging exercise,鈥 Journal of Applied Physiology, vol. 90, no. 3, pp. 1031鈥1035, 2001. View at: Google Scholar
  42. S. E. Terblanche, 鈥淭he effects of exhaustive exercise on the activity levels of catalase in various tissues of male and female rats,鈥 Cell Biology International, vol. 23, no. 11, pp. 749鈥753, 1999. View at: Publisher Site | Google Scholar
  43. H. Hatao, S. Oh-Ishi, M. Itoh et al., 鈥淓ffects of acute exercise on lung antioxidant enzymes in young and old rats,鈥 Mechanisms of Ageing and Development, vol. 127, no. 4, pp. 384鈥390, 2006. View at: Publisher Site | Google Scholar
  44. M. Hara, M. Abe, T. Suzuki, and R. J. Reiter, 鈥淭issue changes in glutathione metabolism and lipid peroxidation induced by swimming are partially prevented by melatonin,鈥 Pharmacology and Toxicology, vol. 78, no. 5, pp. 308鈥312, 1996. View at: Google Scholar
  45. A. Aguiló, P. Tauler, E. Fuentespina, J. A. Tur, A. Córdova, and A. Pons, 鈥淎ntioxidant response to oxidative stress induced by exhaustive exercise,鈥 Physiology and Behavior, vol. 84, no. 1, pp. 1鈥7, 2005. View at: Publisher Site | Google Scholar
  46. N. Cases, A. Sureda, I. Maestre et al., 鈥淩esponse of antioxidant defences to oxidative stress induced by prolonged exercise: antioxidant enzyme gene expression in lymphocytes,鈥 European Journal of Applied Physiology, vol. 98, no. 3, pp. 263鈥269, 2006. View at: Publisher Site | Google Scholar
  47. M. D. Ferrer, P. Tauler, A. Sureda, J. A. Tur, and A. Pons, 鈥淎ntioxidant regulatory mechanisms in neutrophils and lymphocytes after intense exercise,鈥 Journal of Sports Sciences, vol. 27, no. 1, pp. 49鈥58, 2009. View at: Publisher Site | Google Scholar
  48. R. Elosua, L. Molina, M. Fito et al., 鈥淩esponse of oxidative stress biomarkers to a 16-week aerobic physical activity program, and to acute physical activity, in healthy young men and women,鈥 Atherosclerosis, vol. 167, no. 2, pp. 327鈥334, 2003. View at: Publisher Site | Google Scholar
  49. Y. A. Shin, J. H. Lee, W. Song, and T. W. Jun, 鈥淓xercise training improves the antioxidant enzyme activity with no changes of telomere length,鈥 Mechanisms of Ageing and Development, vol. 129, no. 5, pp. 254鈥260, 2008. View at: Publisher Site | Google Scholar
  50. M. C. Gomez-Cabrera, E. Domenech, and J. Viña, 鈥淢oderate exercise is an antioxidant: upregulation of antioxidant genes by training,鈥 Free Radical Biology and Medicine, vol. 44, no. 2, pp. 126鈥131, 2008. View at: Publisher Site | Google Scholar
  51. L. L. Ji, M. C. Gomez-Cabrera, and J. Vina, 鈥淩ole of nuclear factor κB and mitogen-activated protein kinase signaling in exercise-induced antioxidant enzyme adaptation,鈥 Applied Physiology, Nutrition and Metabolism, vol. 32, no. 5, pp. 930鈥935, 2007. View at: Publisher Site | Google Scholar
  52. J. Vider, D. E. Laaksonen, A. Kilk et al., 鈥淧hysical exercise induces activation of NF-κB in human peripheral blood lymphocytes,鈥 Antioxidants and Redox Signaling, vol. 3, no. 6, pp. 1131鈥1137, 2001. View at: Google Scholar
  53. T. W. Buford, M. B. Cooke, B. D. Shelmadine, G. M. Hudson, L. Redd, and D. S. Willoughby, 鈥淓ffects of eccentric treadmill exercise on inflammatory gene expression in human skeletal muscle,鈥 Applied Physiology, Nutrition and Metabolism, vol. 34, no. 4, pp. 745鈥753, 2009. View at: Publisher Site | Google Scholar
  54. L. A. da Silva, C. A. Pinho, L. G. C. Rocha, T. Tuon, P. C. L. Silveira, and R. A. Pinho, 鈥淓ffect of different models of physical exercise on oxidative stress markers in mouse liver,鈥 Applied Physiology, Nutrition and Metabolism, vol. 34, no. 1, pp. 60鈥65, 2009. View at: Publisher Site | Google Scholar
  55. R. H. Lambertucci, A. C. Levada-Pires, L. V. Rossoni, R. Curi, and T. C. Pithon-Curi, 鈥淓ffects of aerobic exercise training on antioxidant enzyme activities and mRNA levels in soleus muscle from young and aged rats,鈥 Mechanisms of Ageing and Development, vol. 128, no. 3, pp. 267鈥275, 2007. View at: Publisher Site | Google Scholar
  56. R. A. Pinho, M. E. Andrades, M. R. Oliveira et al., 鈥淚mbalance in SOD/CAT activities in rat skeletal muscles submitted to treadmill training exercise,鈥 Cell Biology International, vol. 30, no. 10, pp. 848鈥853, 2006. View at: Publisher Site | Google Scholar
  57. S. K. Powers and D. Criswell, 鈥淎daptive strategies of respiratory muscles in response to endurance exercise,鈥 Medicine and Science in Sports and Exercise, vol. 28, no. 9, pp. 1115鈥1122, 1996. View at: Google Scholar
  58. J. C. B. Ferreira, A. V. Bacurau, C. R. Bueno Jr. et al., 鈥淎erobic exercise training improves Ca handling and redox status of skeletal muscle in mice,鈥 Experimental Biology and Medicine, vol. 235, no. 4, pp. 497鈥505, 2010. View at: Publisher Site | Google Scholar
  59. E. Serrano, C. Venegas, G. Escames et al., 鈥淎ntioxidant defence and inflammatory response in professional road cyclists during a 4-day competition,鈥 Journal of Sports Sciences, vol. 28, no. 10, pp. 1047鈥1056, 2010. View at: Publisher Site | Google Scholar

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