Antioxidant in Response to Anaerobic or Aerobic Exercise Alone or

ADVANCES IN LIFE SCIENCES AND HEALTH
Volume 1, Number 1, August 2014
ADVANCES IN LIFE SCIENCES AND HEALTH
Antioxidant in Response to Anaerobic or
Aerobic Exercise Alone or in Combination
in Male Judokas
Kais Elabed1 *, Liwa Masmoudi2 , Abdessalem Koubaa1 and Ahmad Hakim1
1
Laboratory of Pharmacology, Faculty of Medicine, Sfax 3029, Tunisia.
Department of Biology, ISSEP Sfax, Tunsia.
*Corresponding author: [email protected]
2
Abstract:
The purpose of this study was to compare oxidative modifications during recovery following
anaerobic or aerobic exercise alone or in combination. Ten judokas were studied during the
anaerobic, aerobic, and combined exercise. Judokas performed in random order a standard
Wingate test, a low-intensity aerobic exercise at an intensity equal to 60% of maximal aerobic
power (MAP) for a duration of 30 minutes, and a combined exercise consisting of both the
anaerobic and aerobic exercise tests. Blood samples taken before, and immediately, 5, 10,
and 20 minutes postexercise were analyzed for total antioxidant status (TAS), malondiladehyde
(MDA), glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione reductase (GR),
and a-tocopherols. The main results of this study were anaerobic and combined exercise had
no significant effect (P<0.05) on TAS, while aerobic exercise induced an increase in TAS at
5, 10, and 20 minutes of recovery, lipid peroxidation indicated by the levels of MDA showed a
significant increase (P<0.05) after aerobic anaerobic and combined exercise, with a significant
difference (P<0.05) between the anaerobic and aerobic exercise at 10, and 20 minutes of
recovery and between the aerobic and combined exercise at 5, 10, and 20 minutes of recovery
(P<0.05), aerobic and combined exercise induced an increase in GPx, SOD and GR (P<0.05),
and a-tocopherol concentrations were lower after the three tests (P<0.05) and no significant
difference was observed between the three types of exercises (P>0.05). Results suggest
different responses within the antioxiant system dependent on the intensity and duration of
exercise.
Keywords:
Antioxidant; Exercise; Oxidative Stress
1. INTRODUCTION
Oxidative stress is a situation where an imbalance exists between prooxidants and antioxidants, in such
a manner that the production of prooxidants overwhelms antioxidant defense, often leading to oxidation
of lipids, DNA and other molecules which can alter cell function [1]. To defend themselves against the
harmful effects of free radicals, the body has anti-radical Indeed, since the early work of Davies et al.
24
Antioxidant in Response to Anaerobic or Aerobic Exercise Alone or in Combination in Male Judokas
[2] showing that exercise increases the generation of free radicals in the body, numerous studies have
demonstrated that acute exercise induces oxidative stress [1]; and disturbances in intracellular homeostasis
occur with an imbalance between prooxidants and antioxidants. The chain of electron transport within
mitochondria, the phenomenon of ischemia-reperfusion injury, and local inflammation have all been
identified as major sources of production of free radicals during exercise [3].
It is well described that regular exercise training allows for adaptations to the antioxidant defense
system which allow for an attenuation in acute exercise-induced oxidative stress [4]. However, what is
less well described is the type of acute exercise that actually results in the greatest increase in oxidative
stress. Indeed, studies on the effects of anaerobic, aerobic and combined exercise on oxidative stress and
antioxidant status are rare. Fisher [5] provide a review of investigations comparing the effects of aerobic
and anaerobic exercise on oxidative stress markers [6–8].
In their studies Bloomer et al. [6] showed that the aerobic exercise induces a greater increase in protein
carbonyl than anaerobic exercise. Furthermore, Inal et al. [7] and Marzatico et al. [8] demonstrated that
both acute aerobic and anaerobic exercise increase the activities of antioxidant defense enzymes. Studies
on the effects of combined exercise on antioxidant defense and oxidative stress are extremely rare, and
to our knowledge, no studies exist comparing combined aerobic-anaerobic exercise with one form of
exercise in isolation. Therefore, it was our aim to compare the effects of anaerobic or aerobic exercise
alone or in combination on markers of antioxidant activity and oxidative stress.
2. METHODS
Ten regional level judokas (mean age, 18.1 ± 1.7 years; mean body weight, 77.2 ± metricconverterProductID11.7 kg11.7 kg; mean height, 176.4 ± metricconverterProductID4.6 cm4.6 cm) were studied
during the anaerobic exercise, and ten regional level judokas (mean age, 19.1 ± 1.4 years; mean body
weight, 73.8 ± 1.4 kg; mean height, 176.1 ± 4.8 cm) were studied during the aerobic, and combined
exercise.
Judokas performed in random order a standard Wingate test on a cycle ergometer (Monark type 894E),
used as the anaerobic exercise test. As the aerobic exercise test, a low-intensity aerobic exercise bout on a
cycle ergometer was performed at an intensity equal to 60% of maximal aerobic power for a duration of
30 minutes. The combined exercise consisted of both anaerobic and aerobic exercise, with the Wingate
test performed first.
For Standard Wingate test the participants were instructed to pedal as fast as possible for 30 seconds.
Then low-intensity aerobic exercise consisted of pedaling on a cycle ergometer at an intensity equal
to 60% of maximal aerobic power for a duration of 30 minutes, and the combined exercise protocol
consisted of both anaerobic and aerobic exercise. Specifically, the participants performed a warm up for 5
minutes followed by the performance of a standard Wingate test. At the conclusion of the Wingate test,
participants recovered for 3 minutes, and then performed a low-intensity aerobic exercise bout on a cycle
ergometer at an intensity equal to 60% of maximal aerobic power for a duration of 30 minutes.
Blood samples were taken via Vacutainerrfrom an antecubital vein. All markers were analyzed
using commercially available assay kits procured from Randox Laboratories (Randox Laboratories Ltd,
placecountry-regionUK). SOD, GR, GPx, and TAS were measured using standard colorimetric assays.
a-tocopherols was extracted with hexane from human plasma and then measured via high performance
liquid chromatography (HPLC).
25
ADVANCES IN LIFE SCIENCES AND HEALTH
For specimen preparation, first 100 µl of internal standard and 100 µl of plasma were mixed during
5seconds. The second step consisted of adding 200 µl of Ethanol and mixed during 30 seconds. 500 µl
of Hexane was supplemented and mixed during 1 minute, and 450 µl of the upper layer were removed
after centrifugation (4000 rpm to 4 C) for 8 min. 500 µl of Hexane were added in the sediment tubes
and 450 µl of the upper layer were removed after centrifugation (4000 rpm to 4 C) for 8 min and finally
evaporated to dryness under a stream of nitrogen at room temperature. Solids were taken by 250 µl of
methanol and finally centrifuged under the same conditions after shaking 30 seconds, and then analyzed
using the HPLC method.
Malondiadehyde (MDA), a measure of lipid peroxidation, was analyzed using a commercially available
Malondiadehyde HPLC procedure (Randox Laboratories Ltd, placecountry-regionUK). MDA concentrations were measured by the following formula: sample = (Peak height sample ⇥ concentration of the
calibrator)/ Peak height calibrator.
Data were analyzed using the software Statistica (CityplaceStatSoft, country-regionFrance). Because
of the large inter-individual variations in the measured data, we calculated the ratios of post-exercise to
pre-exercise values. Values are reported as mean±SE (standard error of the mean). Two-way ANOVA
was used to detect significant differences between the three types of exercise. Comparisons between
pre-exercise and post-exercise within one type of exercise were performed by one way ANOVA with
the LSD test. To compare between the three exercises at each post exercise recovery time, the t-test for
independent samples was performed. Statistical significance was set at p < 0.05.
3. RESULTS
Figure 1 shows the changes in TAS (Figure 1(a)) and MDA (Figure 1(b)) levels following aerobic
anaerobic and combined exercise. No significant differences between the three types of exercise were
detected. After aerobic exercise, TAS level increased significantly (p<0.05) at 5 minutes of recovery (P5:
1.012 ± 0.01 mmol·l 1 ).
Concerning the concentration of TAS, the ANOVA shows a non-significant effect of exercise [F(2.18) =
1.27 ; p > 0.05]. Secondly it shows a significant effect of recovery [F(4.36) = 3.47 ; p < 0.05]. Finally it
shows a non-significant interaction of exercise vs recovery [F(8.72) = 0.44 ; p > 0.05].
Concerning the concentration of MDA, the ANOVA shows a non-significant effect of exercise [F(2.18) =
3.03 ; p > 0.05], a significant effect of recovery [F(4.36) = 24.66 ; p < 0.001] and a significant interaction
of exercise vs recovery [F(8.72) = 3.51 ; p < 0.01].
Figure 1(b) shows the effects of exercise on MDA levels. Immediately after aerobic anaerobic and
combined exercise, MDA levels increased significantly (P<0.05). But after the aerobic exercise, MDA
levels increased above the pre-exercise level (P<0.05). We found a significant difference (P<0.05)
between anaerobic and aerobic exercise in terms of the change in MDA levels at P10 and P20, and a
significant difference (P<0.05) between combined and aerobic exercise in MDA levels at 5, 10, and
20 minutes of recovery. The aerobic group had a higher MDA level (P<0.05) than the anaerobic and
combined group.
The levels of GPx, SOD, and GR following the three types of exercise are shown in Figure 2(A, B, C).
The ANOVA shows respectively, a significant interaction ”exercise x recovery” for the three parameters
[F(8.72) = 5.79 ; p < 0.001], [F(8.72) = 3.16 ; p < 0.01] , and [FF(8.72) = 2.99 ; p < 0.01].
26
Antioxidant in Response to Anaerobic or Aerobic Exercise Alone or in Combination in Male Judokas
Figure 1. Plasma TAS (A) and MDA (B) levels before (Rest), immediately after (P0), and 5 (P5) and 10 (P10) and 20
(P20) minutes after aerobic, anaerobic, and combined exercise. Data are expressed as ratios to pre-exercise
levels and are shown as means±SE. The average level of TAS in samples before anaerobic exercise was
1.797±0.037 mmol·l-1 and that in samples before aerobic exercise was 1.799±0.037 mmol·l-1 and that
in samples before combined exercise was 1.803±0.022 mmol·l-1. And the average level of MDA in
samples before anaerobic exercise was 1.64±0.27 µmol.l-1 and that in samples before aerobic exercise
was 1.49±0.13 µmol.l-1 and that in samples before combined exercise was 1.74±0.08 µmol.l-1.
After aerobic exercise, a significant increase (P<0.05) in GPx level was apparent at P5, while for the
combined exercise it increased at P0. In contrast, a significant increase was detected in samples taken after
anaerobic exercise at P0 and P5. The GPx levels were returned to baseline values at P10. A significant
difference was noted between aerobic and anaerobic exercise at P0, P10, and P20, and between aerobic
and combined exercise at P0. A significant difference also appeared between anaerobic and combined
exercise at P10 and P20. The anaerobic group had a higher GPx level than the aerobic group at P0,
and combined exercise increased the levels of GPx more than aerobic exercise at P0. Concerning the
comparison between anaerobic exercise and combined exercise, we note that combined exercise resulted
in a greater GPx than anaerobic exercise at P10. For concentrations of SOD and GR, statistical analysis
shows that aerobic exercise and combined exercise have SOD and GR concentrations significantly higher
than those for anaerobic exercise at P20. We also note that the concentrations of these two parameters
returning to basal values at P20 after anaerobic exercise and remain elevated after aerobic exercise and
combined exercise after 20 minutes of recovery.
After combined exercise, a significant decrease was noted (p <0.05) in concentrations of a-tocopherol
at P20 (Figure 3), while this decline appeared at P0 for anaerobic exercise and at P5 for aerobic exercise.
27
ADVANCES IN LIFE SCIENCES AND HEALTH
Figure 2. Plasma GPx (A) SOD (B) and GR (C) levels before (Rest), immediately after (P0), and 5 (P5) and 10
(P10) and 20 (P20) minutes after aerobic, anaerobic, and combined exercise. Data are expressed as ratios
to pre-exercise levels and are shown as means±SE. The average levels of GPx, SOD and GR in samples
before anaerobic exercise were respectively 36.5±7 U/g Hg, 1354.1±239.2 U/g Hg, 9±2.1 U/g Hg; and
that in samples before aerobic exercise was 35.2±4.9 U/g Hg, 1313.08±115.9 U/g Hg, 9.8±1.3 U/g Hg,
and that in samples before combined exercise were respectively 38.4±6.5 U/g Hg, 1338±161.7 U/g Hg,
10.5±2.2 U/g Hg.
28
Antioxidant in Response to Anaerobic or Aerobic Exercise Alone or in Combination in Male Judokas
Figure 3. Title: a-tocopherol levels before (Rest), immediately after (P0), and 5 (P5) and 10 (P10) and 20 (P20)
minutes after aerobic, anaerobic, and combined exercise. Data are expressed as ratios to pre-exercise
levels and are shown as means±SE. The average levels of a-tocopherol in samples before anaerobic
exercise was 7.5±0.5 µmol.l-1 and that in samples before aerobic exercise was 8.8±0.9 µmol.l-1 and
that in samples before combined exercise was 7±1 µmol.l-1.
No significant difference was found between the types of exercise in terms of a-tocopherol levels.
4. DISCUSSION
The purpose of this study was to compare oxidative modifications during recovery following anaerobic
or aerobic exercise alone or in combination.
Results indicate that TAS concentration was not significantly elevated at any time point post exercise
following either anaerobic or combined exercise, while aerobic exercise induced an increase in this
parameter at 5, 10, and 20 minutes of recovery. Some authors [9] have reported that aerobic exercise
causes an increase in TAS. Furthermore, an increase in uric acid (a primary contributor of TAS) after
endurance exercise has been noted [10, 11].
Concerning the combined exercise, our results are in disagreement with Ascensao et al. [12] who
demonstrated that a football match causes an increase in TAS concentrations. As others have noted, they
attributed the increase in TAS to an increase in uric acid. It seems necessary therefore, to include a measure
of uric acid in future investigations. Our results showed a significant increase in MDA immediately
post both aerobic anaerobic and combined exercise with a significant difference between the anaerobic
and aerobic exercise and between aerobic and combined exercise. In a similar way, Baker et al. [13]
noted an increase in both lipid hydroperoxides and MDA immediately post a single sprint exercise. This
increase of lipid peroxidation can be explained by an increased production of free radicals during and/or
following exercise in the judokas. In contrast to our results, but in agreement with those of Groussard et
al. [14], Bloomer et al. [15] demonstrated a decrease in MDA concentrations after the anaerobic exercise.
The authors suggested that this decrease may be due to a removal of MDA from the plasma during the
immediate post exercise period. In addition, Surmen-Gur et al. [16] found no change in MDA after 20
maximal contractions.
29
ADVANCES IN LIFE SCIENCES AND HEALTH
This may be explained by the fact that the exercise used was not intense enough to cause a significant
increase in free radicals. These findings suggest that the volume and intensity of exercises may play an
important role in the overall oxidative stress response to sprint exercise, as also suggested by Bloomer
et al. [15]. Aerobic exercise studies [17] are in agreement with our results. In contrast, other authors
[18, 19] have reported no changes in indices of MDA following aerobic exercise. This discrepancy of
results may arise from the diversity of assays used to evaluate products of lipid peroxidation in circulation,
but also in reference to trained participants, a lack of identification regarding their specific training status
could confound the results.
Our data show that the combined exercise causes a significant increase in MDA levels. These results
are in agreement with the work of Thompson et al. [20] and Ascensao et al. [12], but are in disagreement
with the findings of Svensson et al. [21] and Bloomer et al. [22]. This discrepancy probably results from
the specificity of training loads applied and physiological characteristics of participants studied. It is likely
that the increase in MDA after the combined exercise is attributed to the combination of radicals produced
during both the Wingate test and submaximal aerobic exercise. Our results showed at the end of the three
exercises an increase in the level of GPx, SOD and GR. Increasing concentrations of antioxidant enzymes
may occur in response to an increased production of free radicals, in an attempt to counteract the radical
production and minimize oxidative damage. Statistical analysis showed a difference between anaerobic
exercise and the two other exercises (i.e., the concentrations of these parameters returned to baseline after
20 minutes of recovery after the Wingate test and remained elevated after the other two tests).
These results are in agreement both with those of Childs et al. [23] following strength eccentric exercise,
and those of Inal et al. [7] following 100m swim, with reports of increased activity of SOD and GPx.
However, these results are in disagreement with those of Groussard et al. [14], in which a Wingate test
caused a decrease in SOD without modification of GPx. According to the authors, the decrease of SOD
would be evidence of sudden increase in the production of H2 O2 . Regarding aerobic exercise, our results
are in agreement with several studies in the literature [7, 24] who showed that aerobic exercise, whether
running or swimming, increases the activity of antioxidant enzymes (SOD, GPx, GR). Ji (1993) explains
these findings by the fact that the response mechanism of antioxidants may take place after 5 minutes of
effort in response to an increase in free radicals. However, this response is proportional to the intensity of
exercise and not specifically to the production of free radicals [25]. Contrary to these findings, Miyazaki
et al. [26] found no change in CAT, GPx or SOD in athletes, results that may be explained by the training
status of the athletes involved in this investigation.
Regarding combined exercise, our results are agreement with the work of Marzatico et al. [8], which
demonstrated that SOD and GPx are increased immediately after intermittent exercise (6 * 150m sprints).
The increase on the level of the enzymatic antioxidant may be explained by the increase of the oxygen
consumption, acidosis, catecholamines and xanthine oxidase activity.
To our knowledge, no study has examined the effect of a combined exercise on GR activity. The relative
paucity of data related to the effect of exercise of mixed intensity on GR activity merits attention and
further study. Regarding a-tocopherol concentrations, a decrease was noted after the three tests and no
significant difference was observed between the three types of exercises. Anaerobic exercise causes a
decrease of a-tocopherol concentrations, which is in accordance with the work of Groussard et al. [27].
However our results concerning aerobic exercise are in disagreement with other studies [10, 28]. The
same applies for combined exercise, with our results in discordance with the work of Kingsley et al.
[29] and Ferrer et al. [30]. The absence of differences in the effects of the three exercises studied on
a-tocopherol concentrations might be explained by possible changes in the diet of participants studied
during the entire experimental period. Our failure to control dietary intake is a limitation of this work and
30
Antioxidant in Response to Anaerobic or Aerobic Exercise Alone or in Combination in Male Judokas
we suggest that future studies include the careful monitoring of dietary intake in order to detect changes
in the vitamin status.
5. CONCLUSION
The results of this study were showed that the three exercises studied alter the antioxidant status as
reflected by an increase in the antioxidant defense system with different kinetics for the two types of
exercise.
6. ACKNOWLEDGEMENTS
The authors express thanks to the individuals who provided helpful comments and editing assistance
with the manuscript, in addition to those who assisted with the exercise experiments.
The results of the present study do not constitute endorsement of the product by the authors or the
NSCA.
References
[1] R. J. Bloomer, “Effect of exercise on oxidative stress biomarkers,” Advances in clinical chemistry,
vol. 46, pp. 1–50, 2008.
[2] K. Davies, A. Sevanian, S. Muakkassah-Kelly, and P. Hochstein, “Uric acid-iron ion complexes. A
new aspect of the antioxidant functions of uric acid,” Biochem. J, vol. 235, pp. 747–754, 1986.
[3] R. J. Bloomer and A. H. Goldfarb, “Anaerobic exercise and oxidative stress: a review,” Canadian
journal of applied physiology, vol. 29, no. 3, pp. 245–263, 2004.
[4] L. L. Ji, “Antioxidants and oxidative stress in exercise,” Experimental Biology and medicine, vol. 222,
no. 3, pp. 283–292, 1999.
[5] K. Fisher-Wellman and R. J. Bloomer, “Acute exercise and oxidative stress: a 30 year history,”
Dynamic Medicine, vol. 8, no. 1, p. 1, 2009.
[6] R. J. BLOOMER, A. H. GOLDFARB, L. WIDEMAN, M. J. MCKENZIE, and L. A. CONSITT,
“Effects of acute aerobic and anaerobic exercise on blood markers of oxidative stress,” The Journal
of Strength & Conditioning Research, vol. 19, no. 2, pp. 276–285, 2005.
[7] M. Inal, F. Akyüz, A. Turgut, and W. M. Getsfrid, “Effect of aerobic and anaerobic metabolism
on free radical generation swimmers,” Medicine and science in sports and exercise, vol. 33, no. 4,
pp. 564–567, 2001.
[8] F. Marzatico, O. Pansarasa, L. Bertorelli, L. Somenzini, and G. Della Valle, “Blood free radical
antioxidant enzymes and lipid peroxides following long-distance and lactacidemic performances
in highly trained aerobic and sprint athletes.,” The Journal of sports medicine and physical fitness,
vol. 37, no. 4, pp. 235–239, 1997.
[9] A. Kyparos, I. S. Vrabas, M. G. Nikolaidis, C. S. Riganas, and D. Kouretas, “Increased oxidative
stress blood markers in well-trained rowers following two thousand-meter rowing ergometer race,”
The Journal of Strength & Conditioning Research, vol. 23, no. 5, pp. 1418–1426, 2009.
[10] M.-L. Liu, R. Bergholm, S. Mäkimattila, S. Lahdenperä, M. Valkonen, H. Hilden, H. Yki-Järvinen,
31
ADVANCES IN LIFE SCIENCES AND HEALTH
[11]
[12]
[13]
[14]
[15]
[16]
[17]
[18]
[19]
[20]
[21]
[22]
[23]
[24]
[25]
32
and M.-R. Taskinen, “A marathon run increases the susceptibility of LDL to oxidation in vitro and
modifies plasma antioxidants,” American Journal of Physiology-Endocrinology and Metabolism,
vol. 276, no. 6, pp. E1083–E1091, 1999.
G. Schippinger, F. Fankhauser, P. Abuja, B. Winklhofer-Roob, K. Nadlinger, G. Halwachs-Baumann,
and W. Wonisch, “Competitive and seasonal oxidative stress in elite alpine ski racers,” Scandinavian
journal of medicine & science in sports, vol. 19, no. 2, pp. 206–212, 2009.
A. Ascensão, A. Rebelo, E. Oliveira, F. Marques, L. Pereira, and J. Magalhães, “Biochemical impact
of a soccer matchanalysis of oxidative stress and muscle damage markers throughout recovery,”
Clinical biochemistry, vol. 41, no. 10, pp. 841–851, 2008.
J. S. Baker, D. M. Bailey, D. Hullin, I. Young, and B. Davies, “Metabolic implications of resistive
force selection for oxidative stress and markers of muscle damage during 30 s of high-intensity
exercise,” European journal of applied physiology, vol. 92, no. 3, pp. 321–327, 2004.
C. Groussard, F. Rannou-Bekono, G. Machefer, M. Chevanne, S. Vincent, O. Sergent, J. Cillard, and
A. Gratas-Delamarche, “Changes in blood lipid peroxidation markers and antioxidants after a single
sprint anaerobic exercise,” European journal of applied physiology, vol. 89, no. 1, pp. 14–20, 2003.
R. J. Bloomer, A. C. Fry, M. J. Falvo, and C. A. Moore, “Protein carbonyls are acutely elevated
following single set anaerobic exercise in resistance trained men,” Journal of Science and Medicine
in Sport, vol. 10, no. 6, pp. 411–417, 2007.
E. Sürmen-Gür, E. Öztürk, H. Gür, Z. Pündük, and P. Tuncel, “Effect of vitamin E supplementation
on post-exercise plasma lipid peroxidation and blood antioxidant status in smokers: with special
reference to haemoconcentration effect,” European journal of applied physiology and occupational
physiology, vol. 79, no. 6, pp. 472–478, 1999.
R. B. Child, D. M. Wilkinson, J. Fallowfield, and A. E. Donnelly, “Elevated serum antioxidant
capacity and plasma malondialdehyde concentration in response to a simulated half-marathon run,”
Medicine and science in sports and exercise, vol. 30, no. 11, pp. 1603–1607, 1998.
I. Margaritis, F. Tessier, M. Richard, P. Marconnet, et al., “No evidence of oxidative stress after a
triathlon race in highly trained competitors,” International journal of sports medicine, vol. 18, no. 3,
pp. 186–190, 1997.
A. Niess, A. Hartmann, M. Grünert-Fuchs, B. Poch, and G. Speit, “DNA damage after exhaustive
treadmill running in trained and untrained men,” International journal of sports medicine, vol. 17,
no. 06, pp. 397–403, 1996.
D. Thompson, C. Williams, P. Garcia-Roves, S. McGregor, F. McArdle, and M. Jackson, “Postexercise vitamin C supplementation and recovery from demanding exercise,” European journal of
applied physiology, vol. 89, no. 3-4, pp. 393–400, 2003.
M. Svensson, C. Malm, M. Tonkonogi, B. Ekblom, B. Sjoedin, and K. Sahlin, “Effect of Q10
supplementation on tissue Q10 levels and adenine nucleotide catabolism during high-intensity
exercise,” International journal of sport nutrition, vol. 9, pp. 166–180, 1999.
R. J. Bloomer, M. J. Falvo, A. C. Fry, B. K. Schilling, W. A. Smith, and C. A. Moore, “Oxidative
stress response in trained men following repeated squats or sprints,” Medicine and science in sports
and exercise, vol. 38, no. 8, pp. 1436–1442, 2006.
A. Childs, C. Jacobs, T. Kaminski, B. Halliwell, and C. Leeuwenburgh, “Supplementation with
vitamin C and N-acetyl-cysteine increases oxidative stress in humans after an acute muscle injury
induced by eccentric exercise,” Free Radical Biology and Medicine, vol. 31, no. 6, pp. 745–753,
2001.
L. L. Ji, “Antioxidant enzyme response to exercise and aging,” Medicine and science in sports and
exercise, vol. 25, no. 2, pp. 225–231, 1993.
D. Criswell, S. Powers, S. Dodd, J. Lawler, W. Edwards, K. Renshler, S. Grinton, et al., “High
Antioxidant in Response to Anaerobic or Aerobic Exercise Alone or in Combination in Male Judokas
intensity training-induced changes in skeletal muscle antioxidant enzyme activity.,” Medicine and
science in sports and exercise, vol. 25, no. 10, pp. 1135–1140, 1993.
[26] H. Miyazaki, S. Oh-ishi, T. Ookawara, T. Kizaki, K. Toshinai, S. Ha, S. Haga, L. L. Ji, and H. Ohno,
“Strenuous endurance training in humans reduces oxidative stress following exhausting exercise,”
European journal of applied physiology, vol. 84, no. 1-2, pp. 1–6, 2001.
[27] C. Groussard, “Stress oxydatif et exercice anaérobie,” Science & sports, vol. 21, no. 2, pp. 62–67,
2006.
[28] A. Mastaloudis, S. W. Leonard, and M. G. Traber, “Oxidative stress in athletes during extreme
endurance exercise,” Free Radical Biology and Medicine, vol. 31, no. 7, pp. 911–922, 2001.
[29] M. I. Kingsley, D. Wadsworth, L. P. Kilduff, J. McEneny, and D. Benton, “Effects of phosphatidylserine on oxidative stress following intermittent running,” Medicine and science in sports and exercise,
vol. 37, no. 8, pp. 1300–1306, 2005.
[30] M. D. Ferrer, P. Tauler, A. Sureda, P. Pujol, F. Drobnic, J. A. Tur, and A. Pons, “A soccer match’s ability to enhance lymphocyte capability to produce ROS and induce oxidative damage,” International
Journal of Sport Nutrition & Exercise Metabolism, vol. 19, no. 3, 2009.
33
About This Journal
ALSH is an open access journal published by Scientific Online Publishing. This journal focus on the
following scopes (but not limited to):
Agricultural Sciences
Life sciences
Clinical Sciences
Nursing Sciences
Biotechnology
Medical Technology
Molecular biology
Welcome to submit your original manuscripts to us. For more information, please visit our website:
http://www.scipublish.com/journals/ALSH/
You can click the bellows to follow us:
Facebook:
Twitter:
https://www.facebook.com/scipublish
https://twitter.com/scionlinepub
LinkedIn: https://www.linkedin.com/company/scientific-online-publishing-usa
Google+:
https://google.com/+ScipublishSOP
SOP welcomes authors to contribute their research outcomes under the following rules:
Although glad to publish all original and new research achievements, SOP can’t bear any misbehavior:
plagiarism, forgery or manipulation of experimental data.
As an international publisher, SOP highly values different cultures and adopts cautious attitude towards
religion, politics, race, war and ethics.
SOP helps to propagate scientific results but shares no responsibility of any legal risks or harmful
effects caused by article along with the authors.
SOP maintains the strictest peer review, but holds a neutral attitude for all the published articles.
SOP is an open platform, waiting for senior experts serving on the editorial boards to advance the
progress of research together.