Bosn l Basic Med Sci 201+, 1+ (2).

36-62
Abstract
lxercise trainin mav increase production ot tree radicals and reactive oxven species in dierent vavs. Te trainin tvpe and intensitv mav
inuence tree radicals production, vhich leads to dierences in oxidative stress status betveen athletes, but the results ot the previous studies
are incosistent. Te aim ot our studv vas to estimate oxidative stress status in elite athletes enaed in dierent sport disciplines. Te studv
included , male hihlv skilled protessional competitors vith international experience (. Olvmpic plavers). +. vrestlers, +| soccer plavers and
+ basketball plavers in vhom ve determined the levels ot advanced oxidation protein products (AOPP) and malondialdehvde (MDA), as
markers ot oxidative stress and the total antioxidative capacitv (lmAnOX) usin commerciallv available assav kits. Te mean AOPP concen-
tration vas not sinicantlv dierent betveen soccer plavers, vrestler and basketball plavers (6o.o-..o vs. 68.,-o.8 and 8o.;.-.,.+ moll
respectivelv). Mean lmAnOX concentration vas not dierent betveen soccer plavers (||.8-,.6 moll), vrestlers (|..,-6.. moll)
and basketball plavers (|;.,,-+. moll). Mean MDA concentration vas sinicantlv hiher in basketball plavers (+,+..+-66;.; nml)
compared to soccer plavers (+o6o.+-,+.o nml, po.oo). ln spite ot this tact, oxidative stress markers levels vere increased compared to
reterral values provided bv the manutacturer. Tvpe ot sports (soccer, vrestler or basketball) have no impact on the levels ot oxidative stress
markers. llite sports enaement is a potent stimulus ot oxidative stress that leads to the lare recruitment ot antioxidative detense. Oxidative
stress status monitorin tolloved bv appropriate use ot antioxidants is recommended as a part ot trainin reime.
.o+| Association ot Basic Medical Sciences ot lB8H. All rihts reserved
llY WOkDS. oxidative stress, elite athletes, dierent sport disciplines
Oxidative stress status in elite athletes
enaed in dierent sport disciplines
Almira Hadovi - Duvo
1
, Amina Valevac
1
, Orhan lepara
1
, Samra Pani
2
,
Adnan Hadimuratovi
3
, Amel Meki
+
1
Department of Physiology, Faculty of Medicine, University of Sarajevo, ekalua 90, 71000 Sarajevo, Bosnia and Herzegovina.
2
Institute
for Physical Medicine and Rehabilitation Dr Miroslav Zotovi, Slatinska 11, 78 000 Banja Luka, Bosnia and Herzegovina.
3
Clinic of pediatric
surgery, Clinical center University of Sarajevo, Bolnika 25, 71000 Sarajevo, Bosnia and Herzegovina.
4
Faculty of Sport and Physical
Education, University of Sarajevo, Patriotske lige 41, 71000 Sarajevo, Bosnia and Herzegovina.
INTRODUCTION
Te cells in our bodv continuouslv produce tree radicals and
reactive oxven species (kOS) as part ot metabolic processes.
lree radicals are molecules or part ot molecules vhich have
one or more unpaired electrons in external electronic shell.
Main characteristics ot these molecules are verv short lite
span and extremelv hih reactivitv. lnurious eects ot tree
radicals are induced bv necessitv to establish electronic stabil-
itv and theretore thev react vith next stable molecule, takin
its electron and creatin nev tree radical. Tat vav this mole-
cules also becomes unstable and turther interteres vith other
molecules trom its surroundin vhich leads to impairments
ot cellular components. lree radicals are created durin the
process ot oxidative phosphorvlation in mitochondria +.
Oxidative stress occurs as a result ot kOS activitv and
reduced protective mechanisms that lead to impaire-
ments in cells and tissues tunctions. lt causes second-
arv damae throuh late cell death and intlammation
.. Various studies have shovn that oxidative stress rep-
resents pathoenetic toundation ot manv diseases .
kOS are normallv neutralized bv complex svstem ot antioxi-
dant detence |. Te svstem ot antioxidant detence can be
divided into tvo roups. enzvmes includin superoxid dis-
mutase (SOD), catalase (CAT), lutathione preoxidase (GPX),
and non-enzvmes includin vitamins C and l, retinol, biliru-
bin, uric acid, redox lutathione, thiols, coenzvme Q+o, stress
proteins, albumins, as vell as transport proteins and storae
proteins tor le
.-
i Cu
.-
vhich disable potentiallv harmtul met-
al ions and their involvement in production ot tree radicals ,.
Nevertheless, lov levels ot kOS appear to be neces-
* Corresponding author: Almira Hadovi- Duvo,
Department of Physiology, Faculty of Medicine, University of
Sarajevo, ekalua 90, 71000 Sarajevo, Bosnia and Herzegovina
Phone: +387 33 203 670
Fax: +387 33 651 014
e-mail: almhad@yahoo.com
Submitted: 27 September 2013 / Accepted: 21 February 2014
Bosn l Basic Med Sci 201+, 1+ (2). 3-62
AlMlkA HADOVl DUVO lT Al.. OXlDATlVl STklSS STATUS lN lllTl ATHllTlS lNGAGlD lN DllllklNT SPOkT DlSClPllNlS
sarv tor important phvsioloical tunctions such as
cell sinalin, immune response, and apoptosis 6.
Manv studies have shovn that exercise induces oxidative
stress and causes adaptations in antioxidant detences ;, 8.
Trainin can have positive or neative eects on oxidative
stress dependin on trainin load, trainin speciticitv and
the basal level ot trainin. Data suest that reular lon
term trainin can induce antioxidant response to the oxida-
tive stress. Te results ot a studv vhich investiated the rela-
tionship betveen oxidative stress and exercise overtrainin
overreachin support the possibilitv that the beneticial et-
tect ot phvsical exercise on oxidative stress miht be associ-
ated vith increased antioxidant detences ,. lt is also vell
knovn that active and non active skeletal muscles produce
reactive oxven and nitroen species althouh it is not quite
clear vhere oxidants oriinate durin phvsical activitv +o.
Te deree ot oxidative damae, as vell as the time course
tor elevation in oxidative stress markers has varied across
studies, and appears to be dependent, amon all, on the
tvpe, intensitv, volume and duration ot exercise ++.
This leads to ditterences in oxidative status betveen
athletes in ditterent sport disciplines, but the results
ot the previous studies are inconsistent. Theretore the
aim ot our studv vas to estimate oxidative stress status
in elite athletes enaed in ditterent sports disciplines.
MATERIALS AND METHODS
Subjects
The studv vas pertormed on , voun (...+ - |.| vears
old) male elite plavers. All the athletes vere hihlv skilled
protessional competitors vith international experience
(tvo Olvmpic plavers) in three sport disciplines. +. vres-
tlers, +| soccer plavers and + basketball plavers. All par-
ticipants undervent routine health checks and ave vrit-
ten intormed consent to participate in the studv. All
participants completed a questionnaire assessin their dailv
and veeklv trainin vorkload, duration ot protessional
sports involvement. Anv participant vith suspect patho-
loical tindins durin phvsical examination, recent his-
torv ot disease or inuries, intake ot medications that miht
have had intluence on oxidative markers vere excluded.
All studv procedures vere in accordance vith the Helsinki
declaration. The studv vas approved bv the lthical com-
mittee ot the lacultv ot Medicine, Universitv ot Saraevo.
Procedures
Tvo davs prior to takin part in the studv all participants re-
trained trom strenuous phvsical trainin. One month prior to
blood samplin, the athletes vere instructed to abstain trom
anv vitamin or antioxidant dietarv supplementation. All par-
ticipants vere nonsmokers. Betore the beinnin ot the studv,
athletes passed standard sports-medicine examination that
included a health questionnaire, electrocardioraphic exami-
nation, blood pressure and anthropometrical measurement.
BMl tor each subect vas calculated (veiht in kilorams
divided bv heiht in meters squared). Heiht vas measured
vith stadiometer and veiht vas measured vith Toledo
selt-zeroin electronic diital scale (Mettler-Toledo, lnc.,
Worthinton, OH.). Trained persons measured blood pres-
sure usin a mercurv sphvmomanometer (MD+oXX, MlDl,
Shanhai, China) on the riht arm atter at least a ,-min rest.
Biochemical analysis
Blood samples vere taken trom athletes in order to
determine the redox state. As the markers ot oxida-
tive stress ve used advanced oxidation protein prod-
ucts (AOPP) and mal ondi al dechvde (MDA) and
lmAnOx as marker ot total antioxidative capacitv.
Blood samples vere taken trom an antecubital vein into
Vacutainer test lDTA tube and stored immediatelv.
AOPP Assay
Determination ot AOPP vas based on spectroscopic
analvsis ot moditied proteins usin AOPP assav kit (lm-
munodianostic AG). Standards, controls and samples
assaved tor AOPP vere placed in each vell ot a ,6-vell
microtiter plate. Te absorbance at |o nm vas measured
at microplate reader (Stattax .+oo, USA). Concentra-
tion ot AOPP is expressed in hloramine units (moll).
MDA Assay
level ot malondialdehvde in plasma vas determined bv us-
in lllSA assav kit tor MDA (Uscn lite Science lnc.). Tis
assav emplovs the competitive enzvme immunoassav tech-
nique. A monoclonal antibodv specic tor MDA has been
pre-coated onto a microplate. A competitive inhibition
reaction is launched betveen biotin labeled MDA and un-
labeled MDA (standards and samples) vith the pre-coated
antibodv specic tor MDA. Atter incubation the unbound
conuate is vashed ott. Avidin conuated to Horserad-
ish Peroxidase (HkP) is added to each microplate vell and
incubated. Te amount ot bound HkP conuate is reverse
proportional concentration ot MDA in the sample. At-
ter addition ot the substrate solution, the intensitv ot color
developed vas reverse proportional to the concentration
ot MDA in sample. The absorbance vas read at |,o nm.
ImAnOx (Total antioxidative capacity-TAC)
Te determination ot the total antioxidative capacitv is per-
tormed bv photometric test svstem lmAnOX (lmmuno-
dianostic AG, Bensheim). Te antioxidants in the sample
Bosn l Basic Med Sci 201+, 1+ (2). 38-62
AlMlkA HADOVl DUVO lT Al.. OXlDATlVl STklSS STATUS lN lllTl ATHllTlS lNGAGlD lN DllllklNT SPOkT DlSClPllNlS
reacted vith the dened amount ot exoenouslv provided
hvdroen peroxide (H.O.) and eliminated a certain amount.
Te residual H.O. is determined photometricallv bv an en-
zvmatic reaction. Te absorbance vas measured at |,o nm.
Statistical analysis
Values are expressed as mean-SlM or median and inter-
quartile rane dependin on data distribution. Normal
distribution ot continuous variables vas tested usin Sha-
piro-Wilk test. Dierences in mean betveen roups vere
tested usin ANOVA tolloved bv post hoc Tuckev test
and dierences in median betveen the roups vere tested
bv use ot lruskal-Wallis test tolloved bv Mann-Whitnevs
test. Associations betveen continuous variables vere test-
ed vith Spearmans rank or Pearson correlation analvsis.
RESULTS
Baseline characteristics ot the male elite athletes are
iven in Table +. There vas no siniticant ditterence in
ae and trainin habits betveen soccer plavers, vres-
tlers or basketball plavers. Hovever, mean veiht vas
tound to be siniticantlv hiher in basketball compared
to soccer plavers, vhile mean BMl vas siniticantlv
hiher in vrestlers compared to soccer plavers (Table +.).
The mean AOPP concentration in soccer plavers vas
6o.o-..o moll, in vrestlers 68.,-o.8 moll and
8o.;.-.,.+ moll in basketball plavers, but the dit-
terence vas not siniticant (po.|.|, NS)(liure +).
Te mean lmAnOX concentration vas ||.8-,.6 moll in
soccer plavers, |..,-6.. moll in vrestlers and |;.,,-+.
FIGURE 1. AOPP concentration in male elite athletes.
Concentration of AOPP is expressed in chloramine units (mol/l).
FIGURE 2. ImAnOx concentration in male elite athletes.
FIGURE 3. MDA concentration in male elite athletes.
* soccer players vs. wrestlers
**wrestlers vs. basketball players
*** soccer players vs. basketball players
Soccer
plavers
Wrestlers
Basketball
plavers
P value
Ae (v) 22.1-+.+ 21.-6.0 20.2-2.3 NS
Weiht (k) +.9-9.+ 83.9-16.6 93.0-11.3 p0.00+
BMl (km2) 22.6-1.8 26.3-+.+ 23.6-1.3 p0.02+
Duration ot trainin (v) 13.2-+.1 12.3-3.6 10.3-3.1 NS
Trainin trequencv
(nrveek)
6.2-0.8 6.0-1.0 9.8-0.8 NS
TABLE 1. Baseline characteristics of male elite athletes.
* soccer players vs. wrestlers
** soccer players vs. basketball players
AOPP lmAnOx MDA
Ae (v) r-0.19 r0.33 r-0.0
Weiht (k) r-0.2 r0.11 r-0.1
BMl (km
2
) r-0.33 r0.18 r-0.1
Duration ot trainin (v) r-0.13 r0.12 r-0.1
TABLE 2. Correlation coef cients between age, antropometric
parameters, duration of training and oxidant/antioxidant markers
in soccer players
Bosn l Basic Med Sci 201+, 1+ (2). 39-62
AlMlkA HADOVl DUVO lT Al.. OXlDATlVl STklSS STATUS lN lllTl ATHllTlS lNGAGlD lN DllllklNT SPOkT DlSClPllNlS
moll in basketball plavers (po.+, NS)(liure .).
Mean MDA concentration vas sinicantlv hiher in bas-
ketball plavers (+,+..+-66;.; nml) compared to soccer
plavers (+o6o.+-,+.o nml)(po.oo). There vas no si-
nicant dierence in MDA concentration betveen vrestlers
(+,+..+-666.+ nml), soccer or basketball plavers (liure ).
Tere vas no sinicant correlation ot AOPP, lmanOx, MDA
vith ae and anthropometric characteristic in soccer plav-
ers, vrestlers and basketball plavers (Table ., Table , Table
|). Duration ot trainin vas sinicantlv positivelv associated
vith MDA levers in basketball plavers (ro.,8, po.o,) (Table
|, liure |). There vas no siniticant correlation betveen
AOPP, lmAnOx and MDA levels in soccer plavers, vrestlers
or basketball plavers (Table ,). Tere vas no sinicant dit-
terences in AOPP, lmAnOx and MDA concentration in male
athlete plavers vith or vithout supplement (Table 6) and in
male elite athletes vithout supplement in dierent sport dis-
ciplines (Table ;).
DISCUSSION
While kOS are constantlv produced in small quantities vith-
in bioloical svstems, their presence increases vhen exposed
to both environmental and phvsical stressors +.. lxercise
is one such stressor. Simplv stated, anv situation in vhich
the consumption ot oxven is increased, as durin phvsi-
cal exercise, could result in an acute state ot oxidative stress.
ln our studv ve evaluated oxidative stress status in elite ath-
letes enaed in dierent sports disciplines includin soccer,
basketball and vrestlin. We used AOPP (advanced oxida-
tion protein products) and MDA (secondarv product ot lipid
peroxidation) as markers ot oxidative stress and lmAnOx
as marker ot total antioxidative capacitv (TAC) vhich is
dened as the sum ot antioxidant activities ot the nonspe-
cic pool ot antioxidants, consistin ot antioxidant enzvmes
(GPX, catalase, superoxide dismutase), metal chelators, and
nonspecic antioxidants (GSH, ascorbic acid, albumin, uric
acid, tocopheroles, carotenoids, coenzvme-Q, bilirubin, and
amino acids (cvstein, methionine, tvrosine) +. The re-
sults ot our studv shov that mean oxidative stress markers
levels, both AOPP and MDA and total antioxidant capac-
itv in elite athletes included in the studv vere increased
compared to reterral values provided bv the manutacturer
suestin that phvsical activitv leads to increased kOS tol-
FIGURE 4. Relationship between duration of training and MDA
concentration in basketball players.
AOPP lmAnOx MDA
Ae (v) r0.+9 r-0.1 r-0.33
Weiht (k) r0.3+ r-0.0+ r-0.33
BMl (km
2
) r0.28 r-0.19 r-0.32
Duration ot trainin (v) r0.33 r0.0 r-0.3
TABLE 3. Correlation coef cients between age, antropometric
parameters, duration of training and oxidant/antioxidant markers
in wrestlers
AOPP lmAnOx MDA
Ae (v) r-0.19 r-0.1 r-0.03
Weiht (k) r-0.2 r-0.3 r-0.+
BMl (km
2
) r-0.33 r-0.03 r-0.1
Duration ot trainin (v) r-0.13 r0.+ r0.38
TABLE 4. Correlation coef cients between age, antropometric
parameters, duration of training and oxidant/antioxidant markers
in basketball players
*p<0.05
Soccer
plavers
Wrestlers
Basketball
plavers
AOPP
lmAnOx r0.13 r0.33 r-0.12
MDA r0.0+ r0.18 r-0.12
TABLE 5. Correlation coef cients between AOPP, ImAnOx and
MDA in male elite athletes.
AOPP lmAnox MDA P value
Without supplement +.6-29.1 3+8.0-29.3 13.9-693.2 NS
With supplement 33.-23.+ 333.9-36.9 1292.2-391.1 NS
TABLE 6. AOPP, ImAnOx and MDA concentration in male athlete
players with and without supplement
Soccer plavers Wrestlers Basketball plavers
AOPP
lmAnOx r0.38 r0.09 r-0.22
MDA r0.12 r0.39 r-0.03
TABLE 7. Correlation coef cients between AOPP, ImAnOx and
MDA in male elite athletes without supplement
Bosn l Basic Med Sci 201+, 1+ (2). 60-62
AlMlkA HADOVl DUVO lT Al.. OXlDATlVl STklSS STATUS lN lllTl ATHllTlS lNGAGlD lN DllllklNT SPOkT DlSClPllNlS
loved bv increased antioxidant capacitv in order to counter
tiht oxidative stress. lvidence tor increased reactive oxv-
en and nitroen species (kONS) production durin and
tollovin exercise is provided bv numerous investiations
notin an increase in various oxidative stress biomarkers
tollovin both acute aerobic and anaerobic exercise +|.
ln healthv males a period ot intensitied trainin elic-
ited a biphasic TAC response, a siniticant increase atter
lov- and hih-volume trainin, and a decline atter verv-
hih-volume trainin +,. The increase in TAC suests
that the bodvs antioxidant detense svstem is activated
durin exercise. Mobilization ot antioxidant tissue stores
mav help to maintain the antioxidant status it needed +.
The results in other researches +6, +; vhere oxidative
stress vas assessed in elite soccer lavers shoved increased
levels ot oxidative stress but also an improved plasma anti-
oxidant status toether vith more tluid ervthrocvte mem-
brane status, so thev concluded that elevation in plasma
activities ot antioxidant enzvmes and the hiher levels ot
tree radical scaveners ot lov molecular mass mav com-
pensate the oxidative stress caused bv phvsical activitv.
Primarv kONS eneration in response to acute exercise can
occur via several pathvavs. These include mitochondrial
respiration (electron leakae trom electron transport chain
and subsequent production ot the superoxide radical), pros-
tanoid metabolism, the autooxidation ot catecholoamines,
and oxidase enzvmatic activitv (NAD(P)H oxidase, xanthine
oxidase) +8. Te initial increase in kONS durin exercise,
as vell as tollovin cessation ot the vork bout can lead to
additional secondarv eneration ot prooxidants via phao-
cvtic respiratorv burst, a loss ot calcium homeostasis and
or the destruction ot iron-containin proteins. Moreover,
vhile the pathvavs listed above represent potential sources
ot kONS durin exercise, specic kONS eneration likelv
depends on the mode (aerobic, anaerobic), intensitv, and du-
ration ot exercise, as varvin tvpes ot exercise dier in their
respective enerv requirements, levels ot oxven consump-
tion, and mechanical stresses imposed on the tissues +8.
Both acute aerobic and anaerobic exercise has the poten-
tial to result in increased tree radical production, vhich
mav or mav not result in acute oxidative stress +|. ln or-
der tor oxidative stress to occur, the kOS produced dur-
in exercise must exceed the antioxidant detense svstem
present, therebv resultin in oxidative damae to specitic
biomolecules. Ditterent exercise protocols mav induce
varvin levels ot kONS production, as oxidative damae
has been shovn to be both intensitv and duration depen-
dent +,, .o. Durin lov-intensitv and duration protocols,
antioxidant detenses appear sutticient to meet the kONS
production, but as intensitv andor duration ot exercise in-
creases, these detenses are no loner adequate, potentiallv
resultin in oxidative damae to surroundin tissues .+.
Neubauer et al. .. shoved in their studv that in vell trained
men, competetors in triatlon, increased levels ot analvzed
biomarkers ot oxidative stress return to basal levels ve davs
atter competetion and that there is also connection betveen
trainin state, markers ot oxidative stress and activitv ot an-
tioxidant enzvmes. Theretore, alternatives ot antioxidant
svstem detense in this trained population prevent appear-
ance ot lon-term oxidative stress atter intense exertion.
Te results ot studies vhich determined oxidative stress bio-
markers and antioxidant status in dierent sport disciplines
shoved mostlv increased levels ot oxidative stress mark-
ers but also more ettective antioxidant protection. Hov-
ever, there are onlv tev studies vhich compared the levels
ot oxidative stress markers amon various sport disciplines.
Our results shoved no sinicant dierences in the levels
ot oxidative stress status markers amon various elite sports
athletes. Te dierence in the mean concentrations ot AOPP
and lmAnOx betveen plavers ot dierent sport disciplines
vas not sinicant. Mean MDA concentration vas sini-
cantlv hiher in basketball plavers comparin to soccer plav-
ers vhile there vas no sinicant dierence in MDA con-
centration betveen vrestlers, soccer or basketball plavers .
Tese results are consistent vith the results ot Cubrilo et al.
. vho assessed oxidative stress and nitrite dvnamics un-
der maximal load in elite athletes in relation to sport tvpe
(aerobic, anaerobic and aerobicanaerobic) measurin con-
centration ot lactates, nitric oxide and thiobarbituric reactive
substances (TBAkS) as index ot lipid peroxidation. Teir re-
sults shoved lon term dierent trainin strateies establish
dierent basal nitrites and lipid peroxidation levels in athletes
vhich can be explained vith dierent mechanisms ot kOS
induction bv aerobic and anaerobic exercise. Nevertheless
thev tound no statisticallv sinicant dierence in oxidative
stress parameters reardless ot sport tvpe althouh averae
concentrations (tests instructions proposed values) indicated
hih level ot oxidative stress accompanied vith increased
antioxidative response in all roups. Tis can be explained
vith the tact that aero-anaerobic tvpe ot phvsical activitv in-
cludes more mechanisms tor production ot oxidative stress.
The results ot a studv bv Stankovic et al. .| suested
that increased production ot kONS, as vell as oxidative
stress occurs in top-qualitv sportsmen under maximal
phvsical exertion is independent ot eneretic require-
ment ot sport tvpe (aerobic, anaerobic, aero-anaerobic).
Te ndins ot Shi et al. ., vho in their studv investiat-
ed the dierences in oxidative stress caused bv aerobic and
anaerobic exercise due to ditterent mechanisms suest
that similar vorkloads ot anaerobic and aerobic exercise
induce kOS ditterentlv. aerobic exercise seems to initiallv
enerate more kOS, vhereas anaerobic exercise mav in-
Bosn l Basic Med Sci 201+, 1+ (2). 61-62
AlMlkA HADOVl DUVO lT Al.. OXlDATlVl STklSS STATUS lN lllTl ATHllTlS lNGAGlD lN DllllklNT SPOkT DlSClPllNlS
duce proloned kOS eneration. Althouh more oxven
vas consumed durin aerobic exercise, the enerated kOS
did not induce siniticant oxidative damae, so thev con-
cluded that oxven consumption per se mav not be the ma-
or cause ot exercise-induced oxidative damae. Te results
ot another studv shoved that aerobic trainin increased
GPx activitv in ervthrocvtes vith a subsequent decrease in
plasma TBAkS (thiobarbituric reactive supstances) levels
but anaerobic trainin had no ettect on this process .6.
Dierent impact on oxidative stress durin acute and pro-
loned trainin vas also shovn bv some studies. Pesic et al.
.; evaluated oxidative status in elite karate plavers durin
trainin session and their results shoved that proloned
prorammed phvsical exercise doesnt emphasize occur-
rence ot oxidative stress unlike acute maximal phvsical ex-
ertion. Stankovic et al. .| monitored chanes ot particular
biomarkers ot oxidative stress durin tae-bo trainin and
pilates trainin, vhere statisticallv siniticant increase ot
total antioxidant status vas determined atter tae-bo train-
in, as vell as catalase activitv in plasma atter pilates train-
in. The authors suested that sport athletes durin lon-
er period ot exercise develop more ettective antioxidant
detence, respectivelv natural antioxidant detences ot the
bodv respond adequatelv to complex trainin proram.
When interpretin our results and the results trom our studv,
it is important to consider other tactors vhich impact the
deree ot antioxidant detences, includin ae, trainin status,
and dietarv intake +|. lt oxidative stress does occur, detec-
tion depends to a lare deree on the tissue sampled, the
timin ot a iven sample, as vell as the sensitivitv and spec-
icitv ot the biomarker chosen .8. ln our studv ve chose
tvo oxidative stress markers to analvse AOPP and MDA
and tound no dierence in the averae levels betveen dit-
terent sport tvpes. Oxidative stress has also been assessed
bv vav ot a varietv ot other miscellaneous markers. Assess-
ment ot lipid peroxidation, vith MDA and TBAkS are the
most commonlv used assavs. the maoritv ot authors have
noted an increase in TBAkS tollovin a varietv ot exercise
protocols, vhereas null tindins appear much more com-
mon vhen measurin MDA or isoprostanes speciticallv
suestin that TBAkS lack ot specicitv ot the assav vhich
miht explain possible discrepancies ot the results +|.
lrom vork over the past three decades, it is clear that exer-
cise ot su cient volume, intensitv, and duration can lead to
an increase in kONS production, vhich mav lead to the oxi-
dation ot several bioloical molecules (lipids, proteins, nucleic
acids). Whether or not this condition is indicative ot a harm-
tul stimulus hovever, remains a topic ot debate .,. Tat
is, due to the potential role ot kONS in impairin exercise
pertormance via alterin contractile tunction andor accel-
eratin muscle damaetatiue (secondarv to the oxidation
ot contractile andor mitochondrial enzvmes), coupled vith
their association vith human disease .8, exercise-induced
kONS have commonlv been vieved as a detriment to phvsi-
oloical tunction. Hence, methods to reduce radical produc-
tion and subsequent oxidative damae durin and tollovin
phvsical exercise have been a prioritv ot much research activ-
itv. While excessive prooxidant production, arisin trom anv
torm ot extreme aerobic or anaerobic exercise (i.e., marathon,
aerobicanaerobic overtrainin) mav have the potential to
result in sinicant cellular disruption, there presentlv exist
no cause and eect data to indicate that such an increase
in kONS resultin trom acute exercise actuallv causes ill-
health and disease +|. To the contrarv, and in accordance
vith the principle ot hormesis, a lov rade oxidative stress
appears necessarv tor various phvsioloical adaptations o.
Such a repeated exposure ot the svstem to increased kONS
production trom chronic exercise trainin leads to an up-
reulation in the bodvs antioxidant detense svstem and
associated shitt in redox balance in tavor ot a more reduc-
in environment, thus providin adaptive protection trom
kONS durin subsequent trainin sessions, as vell as vhen
exposed to non-exercise related conditions +|, .8. Taken
toether, exercise-induced oxidative stress mav operate in
a similar tashion to all other principles ot exercise science.
Tat is, in order tor an adaptation to occur (e.., increased
antioxidant detence, hvpertrophv, strenth), the phvsioloi-
cal stimulus applied (in this case kONS production) must
exceed a certain minimal threshold, ettectivelv overload-
in the svstem. lt overload is achieved, the phvsioloical
capacitv ot the bodv vill expand or adapt, ultimatelv lead-
in to improvements in health andor human pertormance.
CONCLUSION
Tvpe ot sports (soccer, vrestler or basketball) have no impact
on the levels ot oxidative status markers. llite sports enae-
ment is a potent stimulus ot oxidative stress that leads to the
lare recruitment ot antioxidative detense implicatin that
oxidative stress status should be monitored. Consumption
ot antioxidants is recommended as a part ot trainin reime.
DECLARATION OF INTEREST
The authors declare no contlict ot interest tor this studv.
ACKNOWLEDGMENTS
This studv vas tinanced bv lederal Ministrv ot ldu-
cation and Science, proect titled lmpact ot train-
in tvpe on oxidative status in elithe sport (Aree-
ment betveen Universitv ot Saraevo and lederal
Bosn l Basic Med Sci 201+, 1+ (2). 62-62
AlMlkA HADOVl DUVO lT Al.. OXlDATlVl STklSS STATUS lN lllTl ATHllTlS lNGAGlD lN DllllklNT SPOkT DlSClPllNlS
Ministrv ot lducation and Science No o+o+-,-,-;+.).
The part ot the results vere presented at +8th An-
uual Conress ot the luropean Collee ot Sport Sci-
ence, vhich vas held in Barcelona .6th-.,th lune, .o+.
REFERENCES
+ Martinovi l, Dopsa V, lotur-Stevulevi l, Dopsa M, Vuovi
A, Stetanovi A. et al. Oxidative stress biomarker monitorin in
elite vomen vollevball athletes durin 6-veek trainin period. l
Strenth Cond kes .o++, .,(,). +6o+6;.
. Sahiner UM, Sackesen C, lrzurum S, Birben l. Oxidative stress
and antioxidant detence. World Allerv Oran l. .o+., ,(+).,-+,.
Greabu M, Battino M, Mohora M, Totan A, Spinu T, Totan C. et
al. Could constitute saliva the rst line ot detence aainst oxidative
stress: kom l lntern Med. .oo;, |,(.)..o,-.+.
| Urso Ml, Clarkson PM. Oxidative stress, exercise, and antioxidant
supplementation. Toxicolov. .oo, +8,(+-.).|+-,|.
, Martinovi l, Dopsa V, Dopsa Ml, lotur-Stevulevi l, Vuovi A,
Stetanovi A. et al. lon-term eects ot oxidative stress in vollev-
ball plavers. lnt l Sports Med .oo,, o(+.), 8,+8,6.
6 Vollaard NB, Shearman lP, Cooper Cl. lxercise-induced oxida-
tive stress. mvths, realities and phvsioloical relevance. Sports Med.
.oo,, ,. +o|,-+o6..
; Tauler P, Sureda A, Cases N, Auilo A, kodriuez-Marrovo lA, Vil-
la G, Tur lA, Pons A. lncreased lvmphocvte antioxidant detences
in response to exhaustive exercise do not preventoxidative damae.
l Nutr Biochem. .oo6, +;(+o). 66,-6;+.
8 Cases N, Sureda A, Maestre l, Tauler P, Auilo A, Cordova A,
koche l, Tur lA, Pons A.kesponse ot antioxidant detences to oxi-
dative stress induced bv proloned exercise.antioxidant enzvme
ene expression in lvmphocvtes. lur l Appl Phvsiol. .oo6, ,8().
.6-.6,.
, Palazzetti S, kichard Ml, lavier A, Mararitis l. Overloaded train-
in increases exercise-induced oxidative stress and damae. Can l
Appl Phvsiol. .oo, .8(|). ,88-6o|.
+o Povers Sl, lackson Ml. lxercise-induced oxidative stress. cellular
mechanisms and impact on muscle torce production. Phvsiol kev.
.oo8, 88(|).+.|-+.;6.
++ Bloomer kl, Goldtarb AH. Anaerobic exercise and oxidative stress.
a reviev. Can l Appl Phvsiol .oo|, .,(). .|,-.6.
+. Sone H, Akanuma H, lukuda T. Oxvenomics in environmental
stress. kedox kep. .o+o,+,().,8-++|.
+ Goldtarb AH, Patrick SW, Brver S, You T. Vitamin C supple-
mentation aects oxidative-stress blood markers in response to
a o-minute run at ;, VO.max. lnt l Sport Nutr lxerc Metab.
.oo,,+,..;,.,o.
+| lisher-Wellman l, Bloomer kl. Acute exercise and oxidative
stress. a o vear historv. Dvn Med. .oo,, +,8.+
+, Droe W. lree radicals in the phvsioloical control ot cell tunction.
Phvsiol kev. .oo.,8..|;,,.
+6 Brites lD, lvelson PA, Christiansen MG, Nicol Ml, Basilico Ml,
Wikinski kW. et al. Soccer plavers under reular trainin shov oxi-
dative stress but an improved plasma antioxidant status. Clin Sci
(lond). +,,,, ,6(|). 8+-8,.
+; Groussard C, Macheter G, kannou l, laure H, Zouhal H, Serent
O. et al. Phvsical tness and essments ot oxidative stress, ervthro-
cvte membrane uiditv plasma non-enzvmatic antioxidant status
at rest and atter a Winate test. Can l Appl Phvsiol .oo,.8 (+). ;,-
,..
+8 lackson Ml. lxercise and oxven radical production bv muscle. ln.
Sen Cl, Packer l, Hanninen O, editors. Handbook ot oxidants and
antioxidants in exercise. Amsterdam. llsevier Science, .ooo. pp.
,;68
+, Goto C, Nishioka l, Umemura T, litsuiki D, Sakautchi A,
lavamura M, Chavama l, Yoshizumi M, Hiashi Y. Acute
moderate-intensitv exercise induces vasodilation throuh an in-
crease in nitric oxide bioavailiabilitv in humans. Am l Hvpertens.
.oo;,.o.8.,8o
.o Bloomer kl, Davis PG, Consitt lA, Wideman l. Plasma protein
carbonvl response to increasin exercise duration in aerobicallv
trained men and vomen. lnt l Sports Med. .oo;,.8..+.,.
.+ lnez Wl, lenkins DG, Coombes lS. Oxidative stress in halt and tull
lronman triathletes. Med Sci Sports lxerc. .oo;,,..8.88.
.. Neubauer O, loni D, lern N, Nics l, Waner lH. No indications
ot persistent oxidative stress in response to an ironman triathlon.
Med Sci Sports lxerc. .oo8, |o(+.)..++,-.8.
. Cubrilo D, Dordevi D, Zivkovic V, Duric D, Blaoevic D et al.
Oxidative stress and nitrite dvnamics under maximal load in elite
athletes. relation on sport tvpe. Molecular and Cellular Biochemis-
trv. .o++, ,,(+-.), .;.;,.
.| Stankovi M, kadovanovi D. Oxidative stress and phvsical activitv.
Sportloia. .o+., 8(+). +-++.
., Shi M, Wan X, Yamanaka T, Oita l, Nakatani l, Takeuchi T. lt-
tects ot anaerobic exercise and aerobic exercise on biomarkers ot
oxidative stress. lnviron Health Prev Med. .oo;, +.(,)..o.-8.
.6 Turav l, lavatekin BM, Gonenc S, Ysleen , Selamolu S. Aero-
bic and anaerobic trainin eects on the antioxidant enzvmes ot
the blood. Acta Phvsioloica Hunarica. .ooo, .6;-.;|.
.; Pesic S, lakovlevic V, Cubrilo D, Zivkovic V, lora V et al. Oxida-
tive status evaluation in elite karate athletes durin trainin process.
Chin l Phvsiol. .o+., ,,(+).8-+,.
.8 Dalle-Donne l, kossi k, Colombo k, Giustarini D, Milzani A. Bio-
markers ot oxidative damae in human disease. Clin Chem. .oo6,
,.. 6o+6..
., Niess AM, Simon P. kesponse and adaptation ot skeletal muscle to
exercise the role ot reactive oxven species. lront Biosci. .oo;,+..
|8.6|88.
o Belakovic G, Nikolova D, Gluud ll, Simonetti kG, Gluud C. Mor-
talitv in randomized trials ot antioxidant supplements tor primarv
and secondarv prevention. svstematic reviev and meta-analvsis.
lAMA. .oo;,.,;.8|.8,;.