Physical activity is known to have beneficial health effects. Despite this, many studies have reported that physical exercise induces oxidative stress damage in different tissues by increasing the generation of reactive oxygen species (ROS) and influences the antioxidant defense system (ADS) in different ways (20,25,29). Free oxygen radicals rapidly react with polyunsaturated fatty acids in the cell membranes, proteins, and other cellular components. As a protective mechanism, the body has developed an ADS against free-radical damage (5) and generally in the rest condition, the ADS is effective at controlling circulating free radicals and limiting cellular damage (7). Although, it has been demonstrated that acute aerobic exercise induces oxidative stress (19,21), regular aerobic exercise decreases malondialdehyde (MDA) and thiobarbituric acid reactive substances concentration (11) and increases antioxidant enzyme activities (superoxide dismutase [SOD], glutathione peroxidase, catalase [CAT]) in both men and women (9,17).
Resistance exercise training (RET), also known as strength or weight training, has become one of the most popular forms of exercise for enhancing an individual's physical fitness (12). The main target of RET is to gain strength or muscle size (muscular hypertrophy) and many different training models (e.g., isokinetic, variable resistance, isometric) and systems (e.g., combinations of sets, repetitions and resistance) are used for this purpose (12). There are limited data that examined the lipid peroxidation response after acute RET (7,14,22,30), and the findings of these studies demonstrated that lipid peroxidation either increased (14,22) or did not differ after RET (7,30). Recent evidence indicates that chronic RET may provide a protective effect similar to aerobic exercises. Interestingly, it has been demonstrated that 6 months of resistance training also reduced serum lipid peroxidation after an acute bout of aerobic exercise (33).
Despite the lower oxygen demands, generation of free radicals during resistance exercise is possible through other mechanisms: (a) xanthine oxidase pathway, (b) respiratory burst of neutrophils, (c) catecholamine autooxidation, (d) local muscle ischemia, and (e) conversion of the weak superoxide to the strong hydroxyl radical by lactic acid (5,16,32). A limited number of studies on this topic and their conflicting results encourage us to design this study. In general, resistance trained men were used as subjects, and mostly circuit training or acute resistance exercise (2,22,30) was used as an exercise form. The effects of different forms of RET on different populations are not well known. To increase the knowledge in this field, this study purposed to determine whether acute dynamic RET induces oxidative stress, and if so, to determine whether RET performed regularly for 6 weeks decreases oxidative stress levels at rest condition in previously untrained men. In addition, we aimed to investigate how the RET intensity influences the magnitude of the training-induced oxidative stress response. Based on previous findings, we hypothesized that acute RET would increase oxidative stress markers; however, regular training for 6 weeks would decrease oxidative stress and increase defense system in previously untrained men.
Experimental Approach to the Problem
An experimental research design was used to determine the acute and chronic effects of RET performed at different intensities on indices of oxidative stress, as determined by serum MDA concentration and reduced glutathione (GSH) level. Sixteen young male subjects, who did not have resistance exercise or weight training experience in the past, were randomly divided into 2 groups: (a) the hypertrophy-intensity group (n = 9) performed 3 sets of 12 repetitions at an intensity corresponding to 70% of 1 repetition maximum (1RM), with a 90-second rest period between sets and (b) the strength-intensity group (n = 7) performed 3 sets of 6 repetitions at an intensity corresponding to 85% of 1RM, with a 180-second rest period between sets. Therefore, training volume was not equated between groups. Resistance exercise training protocol involved upper and lower body exercises (chest press, leg extension, lat pull down, leg curl, shoulder press, and biceps curl), and resistance training was performed 3 times a week on nonconsecutive days for 6 weeks under staff supervision. Blood samples were obtained just before (pre-RET) and immediately after the RET (post-RET) on the first day of the first week, on the last day of the fourth and sixth weeks of RET program for biochemical analyses. The dependent variables, MDA and GSH levels, were compared within groups to determine acute and chronic effects and between groups to determine effects of training intensity. The independent variable was resistance training intensity.
Sixteen healthy young male subjects (20-28 years) who did not have resistance exercise or weight training experience in the past, volunteered to participate in this study. Thirteen of the subjects were physical education students, and 3 of them were primary school education students. These volunteers were recreationally physically active, that is, running, boxing, folk dancing, or playing football once or twice a week but were not engaged in resistance or weight lifting training. Subjects were informed of the experimental risks and signed an informed consent document before the investigation. The investigation was approved by an institutional review board for use of human subjects. Inclusion criteria for the study were as follows: (a) Subjects did not have resistance exercise or weight training experience in the past to observe chronic adaptation to RET; (b) they were nontobacco users; (c) were nonalcohol users; and (d) were apparently healthy. Exclusion criteria for the study were as follows: (a) current use of any medicine or any antioxidant supplementation such as vitamin and (b) having any musculoskeletal disorders. Subjects were randomly divided into 2 groups: the hypertrophy-intensity group (n = 9) and the strength-intensity group (n = 7). Subjects' descriptive data are presented in Table 1.
All subjects were familiarized to the RET protocol that involved the upper and lower body exercises. The familiarization period took 1 week; before the experimental RET protocol (22,30) (Figure 1). During this period, weight training machines used to perform chest press, leg extension, lat pull-down, leg curl, shoulder press, and biceps curl were introduced to the subjects in the given order, and they were informed about the correct technique of exercises (the posture of the body), the correct velocity of movement (moderate velocity) and breathing. Eccentric and concentric phases of the movements were performed at the same velocity. In the last familiarization session, subjects' 1RM strength (pre-RET 1RM) for each exercise was determined according to the Brzycki formula “predicted 1RM = weight lifted/[1.0278 − (0.0278 × the number of repetitions performed)]” (3). In addition, after 6 weeks of training, after 72 hours after last RET, 1RM strength (post-RET 1RM) was assessed again to verify the effectiveness of exercise protocol (Figure 1).
Resistance Exercise Training
Target training load for each subject for each exercise was determined according to their experimental training group. The hypertrophy-intensity group (n = 9) performed 3 sets of 12 repetitions at an intensity corresponding to 70% of 1RM, with a 90-second rest period between sets, and the strength-intensity group (n = 7) performed 3 sets of 6 repetitions at an intensity corresponding to 85% of 1RM, with a 180-second rest period between sets. All subjects performed RET 3 times a week on nonconsecutive days for 6 weeks under staff supervision. The warm-up procedure consisted of 5-7 minute riding a stationary bicycle and 5-7 minute light stretching exercises in regard to the muscles involved in the main experiment. All experimental sessions were performed at the same time of the day (08.00-11.00 am), and the temperature was measured 18-20°C during all training sessions.
Blood Collection and Biochemical Analyses
With the subjects in an upright, seated position, blood samples were obtained before RET (pre-RET) and after RET (post-RET) on the first day of the first week, on the last day of the fourth and sixth weeks of the RET program (Figure 1). Pre-RET blood samples were taken after 10 minutes of rest in the seated position, before the warm-up, and after collecting the pre-RET blood samples, the subjects rested for 20 minutes and then started the RET program. Post-RET blood samples were taken immediately after RET within 30 seconds. All blood samples were drawn while the subject was in a seated position.
Whole blood samples were allowed to clot at room temperature and were centrifuged at 3,500 rpm (4°C) for 20 minutes; the resultant serum was then harvested. Serum samples were stored at −80°C until subsequent analyses. Lipid peroxidation was assayed as the MDA levels reacting with thiobarbituric acid, according to the method of Ohkawa (24). Briefly, 0.5 mL serum and standard sample were mixed with 1.5 mL thiobarbituric acid, 1.5 mL glacial acetic acid, and 0.2 mL sodium dodecyl sulfate. All tests tubes were then capped, sealed tight, and placed in a preheated water bath at 95°C for 60 minutes. After heating, samples were removed from the water bath and immediately placed in an ice water bath (0°C) until analyses and was extracted with 4.0 mL n-butanol. After centrifugation at 4,000 rpm for 10 minutes, the supernatant was removed and was measured spectrophotometrically (UV-1601, Shimadzu UV-visible spectrophotometer) at 532 nm. A standard curve was generated simultaneously using 1,1,3,3 tetramethoxypropane, which was converted into MDA during the procedure. The results were expressed as nmol of MDA equivalents. The intraassay coefficients of variation for MDA were 5%, and all blood samples were studied on the same day.
Glutathione levels were determined by measuring the rate of formation of reduced 5,5'-dithio-bis (2-nitrobenzoic acid) (DTNB) according to the method of Ellman (8). Briefly, 0.2 mL blood and 1.8 mL distilled water was mixed and then 3 mL precipitating solution was added. The mixture was allowed to stand for 5 minutes at room temperature and then filtered through coarse-grade filter paper. Then, 0.4 mL filtrate, 1.6 mL disodium-hydrogen phosphate (Na2HPO4) solution and 0.2 mL DTNB solutions were mixed. The absorbance of the reduced chromogen, DTNB was measured at 412 nm, and it was directly proportional to the GSH concentration. The results were expressed as mg·dL−1 of RBC. The intra-assay coefficients of variation for GSH were 3%.
All values were presented as mean ± SD. Before parametric analyses were done, the normality of distribution of the data was assessed with kolmogorov-smirnov test. Statistical analyses of within group data for the acute effects (pre-RET and post-RET values) was achieved through the use of a paired sample t-tests, furthermore for the chronic effects (pre-RET measurements of the first, fourth, and sixth weeks), statistical analyses was achieved through the use of a 2-way analysis of variance with repeated measures. In the event of a significant F-ratio, post hoc comparisons using the Bonferroni method were applied to determine pairwise differences. Independent sample t-tests were performed to determine possible group differences for the pre-RET MDA and GSH levels and for the following variables: age, height, weight, body mass index, and pre-RET 1RM strength and post-RET 1RM strength. All statistical analyses were performed using the 16.0 version of SPSS (statistical package for social sciences, SPSS Inc.) for Windows, and p ≤ 0.05 was accepted as statistically significant. A sample size of 9 and 7 subjects (for hypertrophy- and strength-intensity groups) provided >41% and >82% statistical power, respectively, at an α level of 0.05 (2-tailed).
The hypertrophy-intensity and the strength-intensity groups' subjects did not differ as to age, height, weight, and body mass index (p > 0.05). These data are presented in Table 1. At the beginning of the study, there was no significant difference in pre-RET 1RM strength, and at the end of the study, there was no significant difference in post-RET 1RM strength for each exercise (chest press, leg extension, lat pull down, leg curl, shoulder press, and biceps curl) between groups (p > 0.05). Furthermore, there was no significant difference in serum MDA concentration and GSH level (p > 0.05) between groups at the beginning of the study. After 6 weeks of RET, post-RET 1RM strength significantly increased for all applied exercise types (chest press, leg extension, lat pull down, leg curl, shoulder press, and biceps curl) in both hypertrophy-intensity and strength-intensity groups (p < 0.05).
Malondialdehyde, a product of lipid peroxidation, was used as an indirect marker for oxidative stress. The results indicated that MDA significantly decreased immediately after RET in the hypertrophy-intensity group on the last day of the fourth and sixth weeks (p < 0.05) and in the strength-intensity group at all measured time points (p < 0.05) (Figure 2). Mean MDA values decreased from 1.16 ± 0.36 to 0.91 ± 0.24 nmol·mL−1 on the last day of the fourth week (p < 0.01; 41%), and from 0.99 ± 0.26 to 0.74 ± 0.18 nmol·mL−1 on the last day of the sixth week (p < 0.05; 62.8%) in the hypertrophy-intensity group. Mean MDA values decreased from 1.52 ± 0.35 to 0.92 ± 0.20 nmol·mL−1 on the first day of the first week (p ≤ 0.01; 97.2%), from 1.22 ± 0.25 to 0.79 ± 0.20 nmol·mL−1 on the last day of the fourth week (p < 0.01; 94.4%), and from 0.90 ± 0.27 to 0.58 ± 0.10 nmol·mL−1 on the last day of the sixth week (p < 0.05; 82.4%) in the strength-intensity group.
After 6 weeks of training, it was observed that MDA concentration measured in rest (pre-RET measurements) significantly decreased in both hypertrophy- and strength-intensity groups (p < 0.01; power > 95%) (Figure 2). Mean MDA values decreased from 1.64 ± 0.29 to 0.99 ± 0.26 nmol·mL−1 in the hypertrophy-intensity group, and from 1.52 ± 0.35 to 0.90 ± 0.27 nmol·mL−1 in the strength-intensity group after 6 weeks of training. In addition, there were no significant intensity group × time interaction for MDA concentration (p > 0.05).
The results indicated that there was no significant alteration between pre-RET and post-RET GSH levels at all measured time points in both groups (p > 0.05) (Figure 3). After 6 weeks of training, it was observed that GSH level measured in rest (pre-RET measurements) significantly increased in both groups (p < 0.05; 100%) (Figure 3). Mean GSH values increased from 67.5 ± 11.8 to 84.2 ± 19.5 mg·dL−1 RBC in the hypertrophy-intensity group, and from 69.7 ± 5.60 to 88.9 ± 25.6 mg·dL−1 RBC in the strength-intensity group. Furthermore, there were no significant intensity group × time interaction for GSH level (p > 0.05).
The acute and chronic effects of RET performed at intensities corresponding to hypertrophy and strength training intensity, on MDA and GSH levels were investigated. The results of this study showed that MDA concentration significantly decreased immediately after RET in the strength-intensity group at all measured time points; furthermore, after 6-weeks' training, MDA concentration measured in rest significantly decreased in both groups. These decrements occurred independently of training intensity. On the other hand, GSH levels did not alter after RET, but after 6-weeks' training, GSH level measured in rest increased independently of training intensity in both groups.
Malondialdehyde is used as a quantitative marker for free-radical interaction with cell membranes and is the most widely used index of lipid peroxidation. Prior investigations that examined the effects of RET on lipid peroxidation reported conflicting results (2,7,22,30). It has been shown that, MDA significantly increased from preexercise level at 6 and 24 hours postexercise in healthy young men after circuit RET, performed at an intensity corresponding to 10 RM (22). Furthermore, Hoffman et al. (14) reported a significant increment in MDA that occurs independently of exercise intensity (60 and 90% of 1RM) after a bout of resistance exercise. On the other hand, Ramel et al. (30) reported that, MDA slightly increased in both resistance trained and untrained men after circuit RET, performed at 75% of 1RM, but these increments were not significant. In concordance with this finding, Dixon et al. (7) demonstrated that moderate intensity whole-body circuit RET (8 exercises performed 3 sets with 10 repetitions) had no effect on serum MDA concentration in the resistance trained and untrained men. In contrast to previous studies that reported significant elevation (14,22) or no significant alteration in MDA postexercise (7,30), we observed significant decrement in MDA concentration in the hypertrophy-intensity and strength-intensity groups. In agreement with findings of the present study, Groussard et al. (13) demonstrated that plasma MDA concentration decreased immediately after Wingate anaerobic power test and continuing decreases at 10, 20, and 40 minutes of postexercise recovery. Furthermore, Bloomer et al. (2) reported a 10% decrease in MDA after intermittent dumbbell squatting performed at an intensity corresponding to 70% of 1RM, but this decrement was not significant.
Such a decrease may be explained by removal of MDA from the plasma during the immediate postexercise period, which is likely because of increased catabolism, excretion, or redistribution throughout the body (18). It should be noted that RET includes recovery periods between exercises and sets. Short recovery time (30-90 seconds) is suggested for low intensity with high training volume, and long recovery time (2-5 minutes) is suggested for high intensity with low training volume (1). The results of our study showed that MDA concentration decreased by 21-24% in the hypertrophy-intensity group and by 35-39% in the strength-intensity group. Longer recovery time in strength-intensity group may explain the bigger decrement of MDA. In addition, it has been reported that training status influences the production of ROS during intense exercise (26). Many studies have demonstrated that the antioxidant enzyme activities (SOD) are higher in physically active people (rugby players, footballers) (4,10,23). Besides this, it should be noted that, the subjects in our study were not engaged in any regular resistance training but were physically active people, and this physical activity background may be an explanation for the decrement of MDA. Also, the lack of measurements of maximum oxygen consumption (o2max) in our study unfortunately disables us to comment more on that.
The results of the present study demonstrated that hypertrophy- and strength-intensity whole-body RET performed regularly for 6 weeks, decreased MDA concentration in rest conditions in previously untrained healthy young men. In concordance with the present study findings, Vincent et al. (33) demonstrated that RET performed for 6 months resulted in an attenuated MDA and hydroperoxide response after an acute aerobic exercise as compared with pretraining status in older adults. Furthermore, it has been demonstrated that conjugated dienes, a quantitative marker for free-radical interaction with cell membranes, significantly increased only in untrained men after circuit RET, and it has been suggested that regular RET partly prevents lipid peroxidation during exercise (30). These results confirming our results that RET have protective effects against lipid oxidative stress. Furthermore, it should be noticed that the pre-RET values for fourth and sixth weeks have been done about 48 hours after the previous RET session. Several acute metabolic changes from exercise have been found to persist for at least 72 hours postexercise. The short time line since the previous RET session makes it difficult to differentiate acute from chronic changes.
Researchers have routinely studied GSH status as a marker of oxidative stress within biological systems, because this seems to be one of the most reliable indices of exercise-induced oxidant production (31). Inal et al. (15) noted a decrease in blood GSH after a 100-m swim sprint, leading them to suggest an increased oxidative stress imposed on the GSH system. Most recently, Cuevas et al. (6) reported a significant decrease in blood reduced GSH level immediately after and at 15, 60, and 120 minutes after a single Wingate anaerobic power test. Furthermore, Groussard et al. (13) found a slight but nonsignificant decrease in erythrocyte GSH levels after a short-term supramaximal anaerobic exercise. The findings of the present study show that whole-body RET did not have any significant acute effect on GSH level in both groups.
However, if RET has been performed regularly for a long time, it has been reported that antioxidant enzyme activities increased (27,28). Parise et al. (27) demonstrated that CuZn-SOD and CAT enzyme activities significantly increased in vastus lateralis of the trained leg, 48 hours after the final exercise bout, in healthy elderly participants. They performed a progressive RET program with only 1 leg for 12 weeks (27). In addition, Peters et al. (28) reported that after 6 weeks of isometric exercise training, oxidative stress markers were significantly decreased and whole blood GSH/oxidized GSH ratio increased (+61%) in hypertensive adults. In concordance with the mentioned studies above, the results of the current study show that GSH values measured in rest significantly increased in both groups that occur independently of training intensity. The training volume and the training intensity, or the interaction of these 2 variables (low intensity-high training volume or high intensity-low training volume) may have an affirmative effect on rise of GSH values.
In conclusion, the results of the current study indicated that serum MDA decreased after 6 weeks of RET performed at intensity corresponding to hypertrophy (70% of 1RM) and strength (85% of 1RM) training intensity, and this decrement occurred independently of training intensity (or training volume). Furthermore, although the GSH values were not altered immediately after RET; GSH values of rest conditions (pre-RET) significantly increased in both groups after 6 weeks of training. These increments also seemed to be independent of training intensity. Further investigations are necessary to make sure what kinds of RET programs are more effective and even if they can be suggested for health. Also, different combination of intensity and training volume should be studied to make sure which of them is more important on ADS and oxidative stress mechanism. Finally, it should be noticed that, in the current study, we have analyzed only 2 oxidative stress biomarkers. This limitation makes it difficult to reach a final conclusion. It is possible that, different implementation of RET may affect different oxidative stress biomarkers in different way.
Many people (coaches and athletes) may be considering the implementation of antioxidant supplements as a method to prevent potential free radical-mediated muscle damage postexercise. These preliminary findings indicate that whole-body RET, without any antioxidant supplementation, performed regularly 3 times a week for 6 weeks have protective effects against oxidative stress similar to aerobic exercises in previously untrained young men. Furthermore, these positive effects seem to be independent of the training intensity. Additional research appears to be warranted to further examine the effect of gender, training status, and age and to examine how training frequency and duration can impact such changes.
This study was supported by Pamukkale University research fund (2006-SBE-001) and is a part of the MS thesis of Hayriye Çakir (Atabek), presented to the Health Sciences Institute, Pamukkale University, Denizli, Turkey. This study was presented as a poster at 15th International Congress of Balkan Clinical Laboratory Federation on 04th-07th September, 2007, Antalya/Turkey and printed in the abstract book. We are thankful to Piray Atsak, Meltem Demirkol, and Hüseyin Gökçe for their valuable help.
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