Content uploaded by Rafael Deminice
Author content
All content in this area was uploaded by Rafael Deminice
Content may be subject to copyright.
MINERVA MEDICA
COPYRIGHT®
J SPORTS MED PHYS FITNESS 2010;50:356-62
Oxidative stress biomarkers response to high intensity interval
training and relation to performance in competitive swimmers
Aim. Aim of the study is to investigate the modulations of
oxidative stress biomarkers and some antioxidants induced by
high intensity interval training bout and its relation to swim-
ming performance.
Methods. Ten swimmers performed a set of 8 maximal swims
along 100 m by style of their specialty, with 10 minute for a
rest. The concentration of blood lactate ([Lac]) was determined
after each swim. The lactate tolerance index (LTI) was deter-
mined by the ratio between [Lac] and the respective times of exe-
cution of the 8 swims. The time to complete first 100 m swim at
maximum effort (P100) and the international point score (IPS)
reached in a specific competition were considered performance
parameters. Venous blood was collected before and after the
anaerobic training effort.
Results. Mean blood lactate concentration in the eight swims was
10.9 ± 1.2 mM. Significant increases were observed for TBARS
(pre: 4.1±0.7 ?mol/L; post: 4.9±1.1. ?mol/L), CK (pre:
206.4±170.7 U/L; post: 244.4±176.9. U/L), GSH (pre: 0.52±0.06;
post: 0.62±0.05. mM), and ascorbic acid (pre: 0.06±0.02; post:
0.11±0.03. mg/dL) after the anaerobic training bout compared
to the values obtained before it. In addition, significant corre-
lations (P < 0.05) were detected between LTI and P100 (r = -0.87)
and IPS (r = 0.64) and between variation of ascorbic acid and
P100 (r = -0.60).
Conclusions. Anaerobic training bout proposed induces oxida-
tive stress and cell muscle damage markers as well as modulates
some antioxidants of competitive swimmers. The modulation
of ascorbic acid seems to play an important role in the perfor-
mance of these athletes.
K
EY WORDS
:Anaerobic training - Oxidative stress - Performance -
Lactate - Swimming.
O
xidative stress is a condition that the cellular pro-
duction of pro-oxidants exceeds the physiological
capacity to remove this activity, which consists of the
endogenous antioxidant system and the exogenous
antioxidants acquired through the diet.1The formation
of reactive oxygen species (ROS) occurs during normal
cell metabolism, but may be increased under condi-
tions of physical stress.2While the mechanisms by
which an acute session of aerobic exercise can increase
ROS formation by increased O2 consumption are well
known,the mechanisms and consequences of a single
session of anaerobic effort are less understood. For this
reason, attempts have been made in recent studies to
understand the effects of acute anaerobic muscular
effort 3-5 of specific competitive situations,6, 7 and of
sprint exercises 8-10 on oxidative metabolism.
The main objective of interval training is to accu-
mulate a good rhythm at high intensity, which would
1Nutrition and Metabolism, Faculty of Medicine of Ribeirao Preto,
University of Sao Paulo, Brazil
2Laboratory of Exercise Physiology, Department of Physiology,
Federal University of Sao Carlos, Brazil
3Coach of the University of Ribeirao Preto swimming team.
Ribeirão Preto, SP, Brazil
Fundings.—Supported by the Brazilian agencies CAPES (Coordenação
de Aperfeiçoamento do Ensino Superior) and FAPESP (Fundação de
Amparo a Pesquisa do Estado de São Paulo). All authors declared that
there is no potential conflict of interests regarding this article.
Acknowledgments.—The authors wish to thank Fernanda Domenici
for technical assistance.
Received on April 16, 2009.
Accepted for publication on April 15, 2010.
Corresponding author: A. A. Jordao, Ph.D., Nutrition and Metabolism,
Faculty of Medicine of Ribeirao Preto /USP Av. Bandeirantes 3900 14049-
900 Ribeirão Preto/SP Brazil. E-mail: alceu@fmrp.usp.br
R. DEMINICE 1, C. SANTANA TRINDADE 2, G. CARVALHO DEGIOVANNI 1, M. RIBEIRO GARLIP 1,
G. VANNUCCHI PORTARI 1, M. TEIXEIRA 3, A. A. JORDAO 1
356 THE JOURNAL OF SPORTS MEDICINE AND PHYSICAL FITNESS September 2010
Vol. 50 - No. 3 THE JOURNAL OF SPORTS MEDICINE AND PHYSICAL FITNESS 357
OXIDATIVE STRESS AND PERFORMANCE OF COMPETITIVE SWIMMERS DEMINICE
MINERVA MEDICA
COPYRIGHT®
not be possible without constant effort.11 Maglischo12
described training of lactate tolerance through high
intensity interval efforts as a specific type of sprint
training. This type of training functions by means of an
increased buffering of lactic acid in muscle and in
blood and increased tolerance of pain caused by severe
acidosis.12 However, few studies have devoted to the
investigation of the effects of repeated efforts at the
rhythm of sprint training on the oxidative stress bio-
markers and antioxidant substances. Kingsley et al.13
reported that intermittent training bouts designed to
stimulate multiple-sprint can cause muscle damage
and pain in addition to increasing the biomarkers of cell
damage and lipid peroxidation. Bloomer 14 reported
that the lipid peroxidation, protein oxidation and
inflammation can promote the muscle cell damage
and these mechanisms can affect the structural and
contract proteins. These disorders of muscle metabo-
lism can hamper the competitive performance and
training of athletes.1Conversely, the antioxidant
defense system can play an important role by attenu-
ating the oxidative modifications or promoting a more
rapid recovery provoked by intense effort, with a con-
sequent improvement of performance. In addition,
few studies have tried to relate the modulation of oxida-
tive stress biomarkers and antioxidant substances
induced by high-intensity anaerobic training to ath-
letic performance.15
The aim of the present study was to investigate the
effects of a single section of high intensity interval
training specifically designed for lactate tolerance
training on biomarkers of oxidative stress and on some
antioxidant substances and their relationship to swim-
ming performance.
Materials and methods
Participants
The volunteers participating in the present study
were 10 well trained swimmers (8 men and 2 women)
all of them top 10 ranked brazilian swimmers in his/her
styles. The athletes aged 20.1±2 years, weighing
75.9±13.1 kg and 1.83±4.7 m in height who trained for
approximately 5200±800 meters/day, all of them
belonging to the swimming team of the University of
Ribeirão Preto, SP, Brazil. The study was approved
by the Research Ethics Committee of the Faculty of
Medicine of Ribeirão Preto, USP, and all volunteers
gave written informed consent to participate. None of
the athletes smoked or was taking any type of med-
ication. The athletes had been training regularly for
more than 5 years, 6 days a week, about 2.5 hours a day.
They participated in competitions at the national lev-
el and were familiar with the series of high-intensity
interval training within their training routine.
Anthropometric and nutritional data
Each participant was invited to come to the labora-
tory at the beginning of the week scheduled for the
collection of anthropometric and nutritional data. A
Filizolaâscale with a coupled stadiometer was used
to measure weight and height. The swimmers were
instructed to follow their habitual diet throughout the
week and to fill out a food recall form for three non-
consecutive days during the same week. The food
recall forms were analyzed using the Nutwinâsoft-
ware (Unifesp, Escola Paulista de Medicina, Brazil) in
order to determine total intake of calories, carbohy-
drates, proteins, lipids, and vitamins C, E and A. The
use of alimentary supplements was also recorded and
added to the food recall form as part of habitual intake
(Table I).
Procedures
The exercise protocol was applied in a semi-olympic
pool (25 x 12 m) with water temperature of 27±1º C.
Before the test, the swimmers performed a standard-
ized warm-up of approximately 1000 m free style.
High intensity interval bouts consisted of eight 100
m maximum swims with 10 minute intervals between
them. Each athlete trained in the style of his special-
ty (4 free style, 3 breaststroke, 2 backstroke and 1 but-
terfly style). The time needed to complete each 100 m
swim was measured with hand chronometers and
recorded. The athletes were stimulated verbally
throughout the test in order to motivate maximum
effort. None of the athletes drank or ate any type of vit-
amin and protein supplements as well as any kind of
juice during the test.
Collection and preparation of blood samples for bio-
chemical analysis
Venous blood was collected from each athlete into
vacutainerâtubes containing EDTA 10 min before and
immediately after the 8 swims maximum effort. The
DEMINICE OXIDATIVE STRESS AND PERFORMANCE OF COMPETITIVE SWIMMERS
358 THE JOURNAL OF SPORTS MEDICINE AND PHYSICAL FITNESS September 2010
MINERVA MEDICA
COPYRIGHT®
tubes were kept in the dark and refrigerated at 4 ºC
until the end of the test and later centrifuged at 3000
rpm for 10 min to separate plasma. A 500 mL aliquot
was immediately removed for the determination of
ascorbic acid and the remaining sample was stored in
Eppendorf tubes at -70ºC for later analysis.
For the determination of blood lactate ([Lac]) con-
centration, 25 ?L of blood were collected from the
earlobe into heparinized capillaries seven minutes after
each swim. The samples were stored in 1.5 mL
Eppendorf tubes containing 50 ?L 1% sodium fluoride
(NaF) and stored for later analysis.
For oxidative stress biomarkers determination, were
assayed lipid peroxidation (TBARS) and protein oxi-
dation markers (AOPP); and endogenous (GSH) and
exogenous (vitamins C and E) antioxidants as well as
muscle cell damage marker (CK). Thiobarbituric acid
reactive substances (TBARS) and total glutathione
(GSH) were determined by the method of Costa et
al18. For TBARS assay a portion of 100µL plasma was
mixed with 1 mL of a solution containing 15% (w/v)
trichloroacetic acid, 0.38% (w/v) thiobarbituric acid
and 0.25N of hydrochloric acid (HCl). The mixture
was heated at 100°C for 30 minutes and, after cen-
trifugation, the absorbance was measured at 535 nm.
The total TBARS content of the plasma samples was
determined by the difference in absorbance between
test and standard samples using a solution of MDA
as standard. For reduced GSH assay, an aliquot of
plasma (25 µL) was mixed with 1mL Tris-EDTA buffer
(0.25 mmol/L Tris base, 20mmol/L EDTA, pH 8.2)
and absorbance at 412 nm was read (A1). Next, a 25L
aliquot of DTNB stock solution (10mmol/L in absolute
methanol) was added to the solution. After 15 min-
utes at ambient temperature, the absorbance was read
again (A2).
Advanced oxidation protein products (AOPP) were
determined by the method of Witko-Sarsat et al.19
Twenty µL of plasma diluted in 200 µL PBS or chlo-
ramine-T standard solutions (0 to 100 µmol/L), were
placed in each well of a 96-well microplate and fol-
lowed by 20 µL of acetic acid. The absorbance was
read at 340 nm after the addition of 20 µL of acetic acid
against a blank containing 220 µL of PBS. AOPP con-
centrations were expressed in µmol/L of chloramine-
T equivalents.
Vitamin C (ascorbic acid) was determined as
described by Bessey.20 Vitamin E (?-tocopherol) as
described by Jordão et al.21 Plasma was deproteinized
with ethanol and then extracted with hexane. The evap-
orated organic layer was reconstituted with the mobile
phase and injected using a 4.625 cm C-18 type column
(Shimpack CLC-ODS) and a 4 mm1 cm precolumn, at
a flow of 2.0 ml/min and detection in a UV/Vis detec-
tor at 292 nm.
Creatine kinase (CK) was determined using an avail-
able commercial kit (LABTEST®; Labtest Diagnóstica,
Lagoa Santa, Minas Gerais, Brazil). Blood lactate con-
centration ([Lac]) was determined using a YSI elec-
trochemical lactimeter model 1500 Sport (YSI,Yellow
Springs, OH, USA). Lactate concentrations are report-
ed as mM.
Determination of anaerobic fitness and performance
The lactate tolerance index (LTI) was determined as
the ratio between the mean blood lactate concentration
(mM) and the time needed to complete each eight 100
m swims.11 The time needed to complete the first 100
m swim at maximum effort was adopted as the per-
formance parameter (P100). The [Lac] value detected
after this effort was considered the peak blood lactate
concentration ([Lac]peak).22 One week after the exper-
imental protocol the athletes participated in a region-
al competition as part of their preparation for the
national championship. The competitive performance
of each athlete in his specific modality was measured
using the International Point Score (IPS). This score,
as part of the FINA system (Federation Internationale
Natation Amateur), permits a comparison of the per-
formance of swimmers regardless of gender in the dif-
ferent swimming styles (free, back, breaststroke, but-
terfly, and individual medley). This scoring system is
based on the time of the eight best athletes of all times
in each swimming modality and can reach a maxi-
mum of 1000 points. The IPS system can be found at
http://www.fina.org/ swimming/FINApoints/index.php.
LTI and [Lac]peak were adopted as parameters of
anaerobic fitness and P100 and IPS as parameters of
simulated and competitive performance, respective-
ly.
Statistical analysis
Data are reported as mean ± standard deviation. The
student t-test was used to determine possible differ-
ences between pre- and post-test maximum swimming
effort variables. ANOVA followed by the Tukey post-
hoc test was used to determine possible differences
in [Lac] between the eight swimming maximum effort.
The Pearson correlation coefficient was used to deter-
mine possible associations between the variation of
Vol. 50 - No. 3 THE JOURNAL OF SPORTS MEDICINE AND PHYSICAL FITNESS 359
OXIDATIVE STRESS AND PERFORMANCE OF COMPETITIVE SWIMMERS DEMINICE
MINERVA MEDICA
COPYRIGHT®
the anaerobic fitness, performance and oxidative stress
parameters. The variation of the parameters was cal-
culated as the difference between parameters deter-
mined before and immediately after the 8 swims max-
imum effort. The level of significance was set at P
<0.05 in all analyses.
Results
Sixty percent of the athletes studied reported the
use of some type of food supplement. Sixty-seven per-
cent of these supplements were classified as energy
ones (Maltodextrin) and 39% as protein energy ones
(amino acid and high-calorie supplements). Just two
athletes reported the use vitamin complex supple-
ments. Although, there were no found significant dif-
ferences between habitual ingestion and habitual inges-
tion plus supplements. The highest inadequacies were
detected for carbohydrates, lipids and vitamin E inges-
tion (Table I).
Figure 1 illustrates the behavior of lactacidemia
during the high intensity interval training bouts. Mean
blood lactate concentration for eight swims was
10.9±1.2 mM. The high blood lactate concentrations
detected in the eight swims, which exceeded the anaer-
obic threshold (AT) of 4 mM proposed by Heck et
al.,23 demonstrated the anaerobic profile of the train-
ing bouts proposed. The blood lactate concentrations
detected in the first and second swimming laps were
significantly lower than those detected in the remain-
ing swims. Stabilization of lactacidemia was observed
from the third to the last efforts (Figure 1).
Table I illustrates the oxidative stress biomarkers
(TBARS and AOPP) and cell muscular damage mark-
er (CK) as well as antioxidants (GSH, ascorbic acid
and α-tocopherol) values detected before and after the
maximum effort swimming training bouts. The results
showed increased TBARS and CK concentration after
the test, whereas protein oxidation was not increased.
In relation to the antioxidants, high intensity interval
training significantly increased GSH and ascorbic acid
concentration. The same was not found to α-tocopherol
that was unchanged after the swimming effort test.
Table II presents the correlations between the per-
formance variables and the variation in lipid peroxi-
dation and in the parameters of the antioxidant defense
system and of anaerobic capacity. Significant corre-
lations were detected between IPS and LTI and
[Lac]peak. P100 was significantly correlated with
∆ascorbic acid, LTI and [Lac]peak.
16
14
12
10
8
6
4
2
Blood lactate (mM)
LT
63.2
|7.6
63.7
|7.1
63.9
|7.3
64.9
|6.6
65.8
|7.1
65.1
|7.5
65.2
|8.0
64.2
|7.6
Time to 100 m (s)
Figure 1.—Behavior of blood lactate during a high intensity interval trai-
ning. LT: lactate threshold (*: p < 0.05 compared to the first and second 100
meter laps, ANOVA followed by the Tukey post.hoc test).
TABLE I .—Habitual dietary intake, ingestion from supplements, number of athletes with inadequate ingestion and reference values
(mean±SD) for the athletes studied (n = 10).
Variable Habitual intake Habitual intake + supplements Inadequate ingestion Reference
Energy (kcal) 3110.3±443.8 3259.4±426.1 -
Carbohydrates (g/kg) 5.7±1.0 (54%) 5.9±0.9 (55%) 5 6-10 g/kg‡
Proteins (g/kg) 1.7±0.3 (16%) 1.8±0.3 (16%) 3 1.2-1.7 g/kg‡
Lipids (g) 106.9±24,5 (30%) 107.3±25.4 (29%) 2 20-35%‡
Vitamin C (mg) 192.8±79.4 208.8±84.1 0 75-90 mg/d†
Vitamin E (mg) 11.6±2.9 12.6±3.1 6 15 mg/d†
Vita min A (µg) 1228.6 ±601.3 1273.1±627.3 2 700 -900 µg/d†
‡ Position of the American Dietetic Association and American College of Sports Medicine for athletes, 2009;16
† Dietar y Reference Intakes (DR I).17
DEMINICE OXIDATIVE STRESS AND PERFORMANCE OF COMPETITIVE SWIMMERS
360 THE JOURNAL OF SPORTS MEDICINE AND PHYSICAL FITNESS September 2010
MINERVA MEDICA
COPYRIGHT®
Discussion
High intensity interval training permits an improve-
ment of anaerobic capacity that may make swimming
faster mainly on the basis of three mechanisms:
increased rate of energy production by anaerobic
metabolism (rate of lactate production),24 increased
buffering capacity in muscle and blood, and increased
tolerance of the pain caused by acidosis.12 When the
buffering capacity improves, swimmers can maintain
the rapid rate of lactate production for a longer period
of time, delaying the reduction of swimming velocity,
one of the possible adaptations produced by tolerance
of these exercises known as lactate tolerance.11, 12 To
train lactate tolerance in swimming, Maglischo 12 sug-
gests interval swimming efforts over distances of 75
and 200 m at maximum velocities or velocities close
to maximum, and resting intervals of more than five
minutes, since the velocities must be sufficiently intense
and long lasting in order to produce severe acidosis
while the resting intervals should permit the athlete
to rest in order to maintain high swimming velocities.
In the present study we proposed a high intensity inter-
val training of 8 bouts of 100 m swims and 10 minute
intervals. The high lactate concentrations after the
swimming and the stabilization of the lactate curve
detected during the test above the lactate threshold
line (Figure 1) confirm the predominant anaerobic
profile of the proposed training series, as previously
demonstrated by Deminice et al.11
Since the final product of anaerobic metabolism is
lactic acid, the ability of an athlete to produce energy
from this metabolism may be reflected in the rate of
production of this metabolite.12 [Lac]peak concentra-
tion has been shown to indicate the energy derived
from anaerobic glycolysis and to be related to swim-
ming performance.22, 25 However, the ability not only
to produce but also to sustain high levels of blood lac-
tate during the competitive event is associated with a
successful performance. In a recent study, Deminice et
al.11 demonstrated the significant contributions by the
ability to produce and sustain high rates of blood lac-
tate to anaerobic swimming performance. In a study on
Australian elite athletes, Pyne et al.26 concluded that the
relation between lactate tolerance and performance
reflects specific changes of high intensity training. In
the present study, the significant correlations of
[Lac]peak and LTI with P100 and IPS (Table II) con-
firm the applicability of these parameters as indica-
tors of anaerobic fitness and as determinants of swim-
ming performance, in addition to showing the pio-
neering approach of this study by presenting parame-
ters obtained in a training session that can predict spe-
cific competitive performance regarding the swim-
TABLE II .—Pearson correlation coeffi cient between performance variables (IPS and P100), variation in lipid peroxidation, advanced
products of protein oxidation and muscular injury (ΔTBARS, ΔAOPP and ΔCK), variation in the parameters of the antioxidant
defense system (ΔGSH, Δascorbic acid and Δα-tocopherol), and parameters of anaerobic capacity (LTI and [Lac]peak).
ΔTBA RS ΔAOPP ΔGSH ΔCK ΔAscorbic
acid
Δα-
tocopherol LTI [Lac]p ea k
IPS 0.10 -0.27 -0.01 0.18 -0.04 0.38 0.64* 0.89**
P100 -0.30 0.24 0.09 -0.41 -0.60* 0.01 -0.87** -0.78**
*P < 0.05; **P < 0.01.
TABLE III .—Oxidative stress biomarkers and antioxidants determined in plasma before (Pre) and after (Post) high intensity interval
training.
Pre Post % change
TBARS (µmol/L) 4.1±0.7 4.9±1.1* 16%
AOPP (µmol chloramine-T equivalents/L) 57.2±23.2 49.2±22.1 -15%
CK (U/L) 206.4±170.7 244.4±176.9* 18%
GSH (mmol/L) 0.52±0.06 0.62±0.05** 19%
Ascor bic acid (mg /dL) 0.6 ±0. 2 1.1± 0.3** 83%
α-tocoferol (µmol/L) 24.9±7.7 24.3±6.9 -2%
Vol. 50 - No. 3 THE JOURNAL OF SPORTS MEDICINE AND PHYSICAL FITNESS 361
MINERVA MEDICA
COPYRIGHT®
OXIDATIVE STRESS AND PERFORMANCE OF COMPETITIVE SWIMMERS DEMINICE
ming specialty of the athlete in real competitive situ-
ations.
Some authors have demonstrated that intermittent
multiple sprint sessions can significantly increase free
radical production and cause cell injury. Kingsley et
al.,13 in a study on amateur soccer players, detected
increased plasma hydroperoxide (HPO) and CK con-
centrations after an intermittent session of shuttle run
training at different intensities. The same was observed
by Nikolaidis et al.27 that after an intermittent training
of twelve 50 m repetitions at 75% of maximum veloc-
ity detected a significantly increased formation of plas-
ma TBARS and carbonyls, as well as modulations of the
antioxidant defense system (GSH, catalase and total
antioxidant capacity) among young swimmers. In the
present study, the interval training set proposed induced
an increased formation of TBARS and CK (Table III),
demonstrating the capacity of high intensity anaero-
bic exercise to promote lipid peroxidation and muscle
cell injury. In addition, the significant increase detect-
ed in GSH and ascorbic acid concentrations (Table III)
demonstrate the modulatory action of the antioxidant
defense system by this type of training. However,
Bloomer et al.28 did not detect an increase in the oxida-
tive stress induced by a session of six 10 s repetitions
at maximum effort on a cycle ergometer despite the
occurrence of significant muscle injury. These authors
also concluded that extenuating multiple-sprint ses-
sions cannot increase the oxidative stress of well-trained
individuals, a fact that may be attributed to the high
level training of the athletes, demonstrating that the
controversy about the modulation of oxidative metab-
olism by anaerobic exercise in athletes.
One of the main objectives of the present study was to
relate the modulations of oxidative stress biomarkers
and some antioxidants induced by high intensity train-
ing to performance. Among the numerous antioxidants
present in the diet and in food supplements, vitamin C
(ascorbic acid) and vitamin E (α-tocopherol) are those
most extensively studied. Although some investigators
have demonstrated the relation between antioxidant
modulation of and their protective role against the for-
mation of ROS induced by exercise 29-31 the evidence
about the action of these vitamins on sports performance
is still small.31 Groussard et al.32 detected a significant
relation between anaerobic sprint performance deter-
mined by the Wingate test and modulations of the con-
centration of α-tocopherol and uric acid in college stu-
dents and suggested that nutritional status may signifi-
cantly interfere in performance. In the present study,
although no modulation of α-tocopherol was detected,
a significant negative correlation was observed between
the variation of ascorbic acid and P100, as shown in
Table II. To our knowledge, this is the first study demon-
strating that modulations of ascorbic acid concentration
induced by anaerobic training can determine the spe-
cific performance of swimmers of competitive level.
These results seem to indicate that athletes who are able
to mobilize higher concentrations of ascorbic acid have
a better anaerobic performance. Peake33 reported that
high intensity exercise may promote an increase of ascor-
bic acid in the circulation minutes after the effort,
although a reduced serum concentration of this sub-
stance is detected hours and days later. These authors
also reported that these changes may be associated with
the increased oxidative damage induced by exercise.
Thus, ROS formation may play a fundamental role in the
initiation and progression of muscle fiber injury.1, 15
However, the antioxidant defense system may limit the
potential negative effects of ROS formation during train-
ing and/or competition.34 On this basis, antioxidant vit-
amins are believed to act as a scavenger of hydroxyl
radicals and to have anti-inflammatory properties.33
These properties can reduce ROS production and con-
sequently the damage to cell components related to mus-
cle function such as contractile and structural proteins 31
leading to improved performance. However, the inade-
quate ingestion of vitamins can influence the exogenous
antioxidante defense system. The high intake of vita-
min C and a high inadequacy for intake of vitamin E
(Table I) found in this study, can influence the modula-
tion of this nutrient induced by physical effort.
Despite the need for a substantial volume of high
intensity training in order to improve or maintain the
level of performance, some precautions should be tak-
en when using high intensity training during the train-
ing season. High intensity interval training is highly
stressing for an athlete both at the physical and psy-
chological level. The intensity of muscle strength
required together with the intense acidosis produced
can lead to temporary injury to muscle tissue.12 In
addition, abrupt changes in training volume or inten-
sity within the program, together with insufficient rest-
ing sessions and a deficient diet may cause metabol-
ic disorders that might progress to chronic and severe
traumas.15 For these reasons, the excessive use of lac-
tate tolerance training may lead the athlete to a state of
overtraining that will hamper his performance during
the training season.
MINERVA MEDICA
COPYRIGHT®
DEMINICE OXIDATIVE STRESS AND PERFORMANCE OF COMPETITIVE SWIMMERS
Conclusions
On the basis of the results obtained, we may con-
clude that the specific anaerobic training bouts pro-
posed induce increase in oxidative stress biomarkers
and cell muscle damage markers as well as modulate
some antioxidants of competitive swimmers. The mod-
ulation of ascorbic acid seems to play an important
role in the performance of these athletes. However,
more studies are necessary to determine the real influ-
ence of these modulations on athletes’ performance.
The LTI determined by means of high intensity inter-
val training bouts seems to be useful to predict specific
competitive swimming performance.
References
1. Bloomer RJ, Goldfarb AH. Anaerobic exercise and oxidative stress:
a review. Can J Appl Physiol 2004;29:245-63.
2. Finaud J, Lac G, Filaire E. Oxidative stress: relationship with exercise
and training. Sports Med 2006;36:327-58.
3. Souza Jr TP, Oliveira PR, Pereira B. Physical exercise and oxidative
stress: effect of intense physical exercise on the urinary chemilumi-
nescence and plasmatic malondialdehyde. Braz J Sports Med
2005;11:91-6.
4. Bloomer RJ, Goldfarb AH, Wideman L, McKenzie MJ, Consitt LA.
Effects of acute aerobic and anaerobic exercise on blood markers of
oxidative stress. J Strength Cond Res 2005,19:276-85.
5. Paschalis V, Nikolaidis MG, Fatouros IG, Giakas G, Koutedakis Y,
Karatzaferi C, et al. Uniform and prolonged changes in blood oxida-
tive stress after muscle-damaging exercise. In Vivo 2007;21:877-83.
6. Inal M, Akyüz F, Turgut A, Getsfrid WM. Effect of aerobic and anae-
robic metabolism on free radical generation swimmers. Med Sci
Sports Exerc 2001;33:564-7.
7. Finaud J, Degoutte F, Scislowski V, Rouveix M, Durand D, Filaire E.
Competition and food restriction effects on oxidative stress in judo.
Int J Sports Med 2006;27:834-41.
8. Groussard C, Rannou-Bekono F, Machefer G, Chevanne M, Vincent
S, Sergent O, et al. Changes in blood lipid peroxidation markers and
antioxidants after a single sprint anaerobic exercise. Eur J Appl Physiol
2003;89:14-20.
9. Cuevas MJ, Almar M, García-Glez JC, García-López D, De Paz JA,
Alvear-Ordenes I, et al. Changes in oxidative stress markers and NF-
kappaB activation induced by sprint exercise. Free Rad Res
2005;39:431-9.
10. Bloomer RJ, Goldfarb AH, McKenzie MJ. Oxidative stress response
to aerobic exercise: comparison of antioxidant supplements. Med Sci
Sports Exerc 2006;38:1098-105.
11. Deminice R, Gabarra L, Rizzi A, Baldissera V. High intensity inter-
val training series as indices of acidosis tolerance determination in
swimming anaerobic performance prediction. Braz J Sports Med
2007;13:185-9.
12. Maglischo EW. Swimming fastest. Human Kinetcs, 2003 Champaign,
Ill.
13. Kingsley MI, Wadsworth D, Kilduff LP, McEneny J, Benton D. Effects
of phosphatidylserine on oxidative stress following intermittent run-
ning. Med Sci Sports Exerc 2005;37:1300-6.
14. Bloomer RJ. The role of nutritional supplements in the prevention
and treatment of resistance exercise-induced skeletal muscle injury.
Sports Med 2007;37:519-32.
15. Margonis K, Fatouros IG, Jamurtas AZ, Nikolaidis MG, Douroudos
I, Chatzinikolaou A, et al. Oxidative stress biomarkers responses to phy-
sical overtraining: implications for diagnosis. Free Radic Biol Med
2007;43:901-10.
16. American College of Sports Medicine; American Dietetic Association;
Dietitians of Canada. Joint Position Statement: nutrition and athletic
performance. American College of Sports Medicine,American Dietetic
Association, and Dietitians of Canada. Med Sci Sports Exerc 2009;41:
709-31.
17. Padovani RM, Amaya-Farfan J, Colugnati FAB, Domene SMA.
Dietary reference intakes: application of tables in nutritional studies.
Braz J Nutr 2006;19:741-60.
18. Costa CM, Dos Santos RCC, Lima E. A simple automated procedu-
re for thiol measurement in human and serum samples. Braz J Pathol
Lab Med 2006;42:345-50.
19. Witko-Sarsat V, Friedlander M, Capeillère-Blandin C, Nguyen-Khoa
T, Nguyen AT, Zingraff J, Jungers P, Descamps-Latscha B. Advanced
oxidation protein products as a novel marker of oxidative stress in
uremia. Kidney Int 1996;49:1304-13.
20. Bessey OA. Ascorbic acid. Microchemical methods. In: Vitamin
Methods. New York, Academic Press. 1960. p. 303.
21. Jordão AA Jr, Chiarello PG,Arantes MR, Meirelles MS, Vannucchi
H. Effect of an acute dose of ethanol on lipid peroxidation in rats:
action of vitamin E. Food Chem Toxicol 2004;42:459-64.
22. Avlonitou E. Maximal lactate values following competitive perfor-
mance varying according to age, sex and swimming style. J Sports Med
Phys Fitness 1996;36:24-30.
23. Heck H, Mader A, Hess G, Mücke S, Müller R, Hollmann W.
Justification of the 4-mmol/l lactate threshold. Int J Sports Med
1985;6:117-30.
24. Juel C, Klarskov C, Nielsen JJ, Krustrup P, Mohr M, Bangsbo J.
Effect of high-intensity intermittent training on lactate and H+ relea-
se from human skeletal muscle. Am J Physiol Endocrinol Metab
2004;286:E245-E251.
25. Bonifazi M, Martelli G, Marugo L, Sardella F, Carli G. Blood lacta-
te accumulation in top level swimmers following competition. J Sports
Med Phys Fitness 1993;33:13-8.
26. Pyne DB, Lee H, Swanwick KM. Monitoring the lactate threshold in
world-ranked swimmers. Med Sci Sports Exerc 2001;33:291-7.
27. Nikolaidis MG, Paschalis V, Giakas G, Fatouros IG, Koutedakis
Y, Kouretas D, et al. Decreased blood oxidative stress after repea-
ted muscle-damaging exercise. Med Sci Sports Exerc 2007;39:
1080-9.
28. Bloomer RJ, Falvo MJ, Fry AC, Schilling BK, Smith WA, Moore
CA. Oxidative stress response in trained men following repeated
squats or sprints. Med Sci Sports Exerc 2006;38:1436-42.
29. Goldfarb AH, Patrick SW, Bryer S,You T. Vitamin C supplemen-
tation affects oxidative-stress blood markers in response to a 30-
minute run at 75% VO2max. Int J Sports Nutr Exerc Metab
2005;15:279-90.
30. Close GL, Ashton T, Cable T, Doran D, Holloway C, McArdle F, et
al. Ascorbic acid supplementation does not attenuate post-exercise
muscle soreness following muscle-damaging exercise but may delay
the recovery process. Br J Nutr 2006;95:976-81.
31. Bloomer RJ, Fry AC, Falvo MJ, Moore CA. Protein carbonyls are
acutely elevated following single set anaerobic exercise in resistance
trained men. The Journal of Science and Medicine in Sport
2007;10:411-7.
32. Groussard C, Machefer G, Rannou F, Faure H, Zouhal H, Sergent
O, et al. Physical fitness and plasma non-enzymatic antioxidant
status at rest and after a wingate test. Can J Appl Physiol 2003;28:79-
92.
33. Peake JM. Vitamin C: effects of exercise and requirements with trai-
ning. Int J Sports Nutr Exerc Metab 2003;13:125-51.
34. Vollaard NB, Cooper CE, Shearman JP. Exercise-induced oxidative
stress in overload training and tapering. Med Sci Sports Exerc
2006;38:1335-41.
362 THE JOURNAL OF SPORTS MEDICINE AND PHYSICAL FITNESS September 2010
