Original articleVariable effects of exercise intensity on reduced glutathione, thiobarbituric acid reactive substance levels, and glucose concentration
Introduction
In recent years it has been suggested that free oxygen radicals (FORs) induced by acute exercise were involved in damage to muscles and other tissues. Despite little availability of direct evidence for FORs production during exercise, there is an abundance of literature providing indirect support that oxidative stress occurred during exercise 1., 2., 3., 4., 5.. Cells continuously produce FORs as part of the metabolic processes. Among the earliest biochemical reactions found were hydrolysis of fatty acids from membrane phospholipids, production of biologically active eicosanoids, and peroxidation of lipids with formation of FORs. These latter reactions were the main agents responsible for cellular damage (4). Superoxide, ferryl, and hydroxyl anions were common reactive compounds that caused lipid peroxidation 4., 5.. Under normal conditions, superoxide (O2−) anions were generated during mitochondrial electron transport. There was a balance between antioxidants and oxidants produced by aerobic cellular systems. These free radicals were neutralized by an elaborate antioxidant defense system consisting of enzymes such as catalane, superoxide dismutase, and glutathione peroxidase, and numerous nonenzymatic antioxidants including vitamins A, E, and C, glutathione, ubiquinone, and flavonoids. Exercise can produce an imbalance between FORs and antioxidants, which was referred to as oxidative stress 2., 3..
Physical exercise could induce peroxidation of lipids in cellular membranes and increased level of thiobarbituric acid reactive substance (TBARS) in plasma observed in post-exercise sample is a consequence of leakage of peroxides from tissues, especially from muscle into plasma. Oxidative modification of plasma constituents was an expression of oxidative damage that occurred in tissues (6). Physical activity increased generation of FORs in several ways; for instance, oxidative phosphorylation increased in response to exercise and there was concomitant increase in FORs (3). Finally, regular physical exercise caused up to a 10-fold increase in oxygen consumption and 10- to 20-fold increase in metabolism of cells, in turn increasing formation of FORs (7). FORs promoted peroxidation of lipids and were able to attack polyunsaturated fatty acids in cell membrane, leading to a chain of chemical reactions called lipid peroxidation. Peroxidation products were observed in blood after extreme exercise (8). Most commonly measured were by-products of lipid peroxidation, but changes in status of antioxidant compounds such as glutathione, protein, DNA oxidation products, and antioxidant enzyme activities have also been used. Aldehydes, especially malonildialdehyde, which was an end-product of lipid peroxidation, were frequently used as markers of oxidative stress in response to exercise. They were all indirect measures of FORs activity 4., 5., 9., 10., 11.. The present study examined indices of lipid peroxidation and TBARS in plasma of subjects under different exercise conditions. Although TBA test was a very nonspecific technique, it was able to offer empirical insight into the complex process of lipid peroxidation, but it remained a simple and inexpensive technique 2., 12..
Training reduces production of lipid peroxide products and prevents oxidative damage in tissues by inducing the antioxidant system in athletes (13). One endogenous antioxidant, reduced glutathione (GSH), played a central role in coordinating synergism between different lipid- and aqueous-phase antioxidants. During normal function of antioxidant defense system, GSH was used by glutathione peroxidase (GSH-Px), a peroxidase used to detoxify hydrogen peroxide. It was a substrate for GSH-Px reducing hydrogen peroxide. Additionally, glutathione reductase was necessary to convert hydrogen peroxide into GSH, which would also contribute to detoxification of hydrogen peroxide. Primary scavenger for exercise generated by oxygen radicals was mitochondrial superoxide dismutase 13., 14., 15., 16., 17., 18., 19.. We documented 1) the manner in which endogenous GSH may affect exhaustive exercise-induced changes in tissue GSH status, lipid peroxides, and endurance and 2) the relative role of endogenous GSH in circumvention of exercise-induced oxidative stress (20). Physical exercise may cause oxidation of GSH in tissues such as blood, skeletal muscle, and liver 15., 18., 19., 20., 21..
Metabolism produced energy in the body. Immediate source of energy for biological work was adenosine triphosphate (ATP). Amount of ATP stored in muscles was limited. Therefore, muscle ATP needed to be replenished during exercise aerobically and anaerobically. This anaerobic energy process broke down muscle glycogen stores (or blood glucose) and produced only a limited amount of ATP. During longer-term aerobic exercise, it became necessary to consume oxygen, utilize additional muscle glycogen and blood glucose, and use lipids (fat) to sustain energy output 22., 23., 24., 25.. Fatty acids in circulation increased during exercise due to mobilization from lipid stores. At the same time, glycogen stores decreased. Because of continuous exercise, blood glucose concentrations could remain either normal or increase (24).
It is well known that there was a close relationship between oxidant stress and exercise, although it has not yet been investigated whether exercise-induced oxidant stress caused post-exercise alteration. The aim of this study was to determine the effect of different types of exercise on oxidative stress markers and the effect of gender on this exercise-mediated oxidative stress.
Section snippets
Subjects
Sixty students from the School of Physical Training and Higher Sport Education in Elazig, Turkey, between the ages of 19 and 22 years (mean 20.4 ± 1.2 years) and who were involved in sports as amateurs for at least 6 years were included in the study. All subjects (n = 60, 10 females and 10 males in each of three groups) initially signed voluntary and informed consent to participate in the experiment, which was approved in advance by the respective institutional Ethics Review Committees (July 23,
Results
Table 1 shows physical characteristics of subjects. Male and female subgroups were identified in all three groups. All participants in the three groups were found similar in terms of average age, height, BMI, and remaining characteristics (comparing for male/male, female/female, p >0.05).
Average levels of TBARS, GSH, and glucose measured in all three groups before and after exercise are shown in Table 2.
According to these findings, in Aer group average GSH levels were slightly higher (p <0.05)
Discussion
In the present study, plasma TBARS levels mildly increased after different types of exercise and subsequently returned to pre-exercise levels at 48 h post-exercise; however, they increased in TBARS levels, these findings not statistically meaningful in males and females. Several studies consistently showed that physical exercise may induce oxidative stress in both humans and experimental animals 28., 29., 30..
Several studies reported that single bouts of exercise increased TBARS blood levels 7.
References (44)
- et al.
Exercise, oxidative damage and effects of antioxidant manipulation
J Nutr
(1992) - et al.
Free radicals and tissue damage produced by exercise
Biochim Biophys Res Commun
(1982) Secondary products of lipid peroxidation
Chem Phys Lipids
(1987)- et al.
Oxidative stress, exercise, and antioxidant supplementation
Toxicology
(2003) Redox signaling and the emerging potential of thiol antioxidants
Biochem Pharmacol
(1998)Nutritional biochemistry of cellular glutathione
J Nutr Biochem
(1997)Lipid peroxides and human diseases
Chem Phys Lipids
(1987)Oxidative stress during exercise: implication of antioxidant nutrients
Free Radic Biol Med
(1995)- et al.
Vitamin E prevents exercise-induced DNA damage
Mutat Res
(1995) - et al.
Stress hormonal factors, fatigue, and antioxidant responses to prolonged speed driving
Pharmacol Biochem Behav
(1998 Jul)
Mitochondria in exercise-induced oxidative stress
Biol Signals Recept
Generation of reactive oxygen species after exhaustive aerobic and isometric exercise
Med Sci Sports Exerc
Free radicals in skin and muscle: damaging agents or signals for adaptation?
Proc Nutr Soc
Lipid peroxidation: its mechanism, measurement, and significance
Am J Clin Nutr
Physiological antioxidants
Serum creatine kinase and lactate dehydrogenase changes following an eighty kilometer race. Relationship to lipid peroxidation
EU J Appl Physiol Occup Physiol
Microsomal lipid peroxidation
Methods Enzymol
Free radicals and other reactive oxygen metabolites: clinical relevance and the therapeutic efficacy of antioxidant therapy
Surgery
Malondialdehyde and thiobarbituric acid reactivity as diagnostic indices of lipid peroxidation and peroxidative tissue injury
Free Radic Biol Med
Increased blood antioxidant systems of runners in response to training load
Clin Sci
Antioxidant intervention in Down's syndrome
Smart Drug News
Plasma glutathion and glutathione disulfide in the rat regulation and response to oxidative stress
J Pharmacol Exp Ther
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