ORIGINAL RESEARCH
Time-course of Changes in Inflammatory and
Performance Responses Following a Soccer Game
Ioannis Ispirlidis, PhD,* Ioannis G. Fatouros, PhD,* Athanasios Z. Jamurtas, PhD,†
Michalis G. Nikolaidis, PhD,‡ Ioannis Michailidis, MS,* Ioannis Douroudos, MS,*
Konstantinos Margonis, PhD, Athanasios Chatzinikolaou, PhD,* Elias Kalistratos, PhD,§
Ioannis Katrabasas, MD,¶ Vassilios Alexiou, MS,** and Kiriakos Taxildaris, PhD*
Objective: To study the effects of a single soccer game on indices of
performance, muscle damage, and inflammation during a 6-day
recovery period.
Design: Participants were assigned to either an experimental group
(E, played in the game; n = 14) or a control group (C, did not
participate in the game; n = 10).
Setting: Data were collected on a soccer field and at the Physical
Education and Sports Science laboratory of the Democritus
University of Thrace before and after the soccer game.
Participants: Twenty-four elite male soccer players (age, 20.1 6 0.8
years; height, 1.78 6 0.08 m; weight, 75.2 6 6.8 kg).
Main Outcome Measurements: Muscle strength, vertical jump-
ing, speed, DOMS, muscle swelling, leukocyte count, creatine kinase
(CK), lactate dehydrogenase (LDH), C-reactive protein (CRP), corti-
sol, testosterone, cytokines IL-6 and IL-1b, thioburbituric acid-reactive
substances (TBARS), protein carbnyls (PC), and uric acid (UA).
Results: Performance deteriorated 1 to 4 days post-game. An acute-
phase inflammatory response consisted of a post-game peak of
leukocyte count, cytokines, and cortisol, a 24-hour peak of CRP,
TBARS, and DOMS, a 48-hour peak of CK, LDH, and PC, and a
72-hour peak of uric acid.
Conclusion: A single soccer game induces short-term muscle
damage and marked but transient inflammatory responses. Anaerobic
performance seems to deteriorate for as long as 72-hour post-game.
The acute phase inflammatory response in soccer appears to follow
the same pattern as in other forms of exercise. These results clearly
Submitted for publication August 21, 2007; accepted May 25, 2008.
From the *Department of Physical Education and Sport Science, Democritus
University of Thrace, Greece; †Department of Physical Education and
Sport Science, University of Thessaly, Greece; ‡Institute of Human
Performance and Rehabilitation, Centre for Research and Technology –
Thessaly (CERETETH), Trikala, Greece; §Department of Physical
Therapy, Technological Educational Institute of Thessaloniki, Greece.
{Department of Orthopedics, Asklipieion General Hospital, Voula,
Greece; and **School of Medicine, University of Athens, Athens, Greece.
The authors state that they have no financial interest in the products mentioned
within this article.
Reprints: Ioannis Ispirlidis, Democritus University of Thrace, 69100
Komotini, Greece (e-mail: iispyrli@phyed.duth.gr).
Copyright Ó 2008 by Lippincott Williams & Wilkins
Clin J Sport Med
Volume 18, Number 5, September 2008
indicate the need of sufficient recovery for elite soccer players after
a game.
Key Words: exercise, soccer, inflammation, DOMS, muscle damage
(Clin J Sport Med 2008;18:423–431)
INTRODUCTION
Multiple-sprint sports, such as soccer, are characterized
by periods of high-intensity activity (sprinting, running,
kicking, jumping, and tackling), interspersed with lower
intensity actions (jogging and walking) and/or active or
passive recovery.1 During a soccer game, elite athletes reach an
average and peak heart rate of 85 and 98% of their maximal
values, respectively,1 blood lactate values of 2 to 14 mM2,3
indicating a high anaerobic energy turnover rate, and an
average aerobic loading corresponding to about 75% of
maximal oxygen uptake (VO2max).1,4 Total distance covered
during a soccer game approximates 9 to 12 km,1,2,4,5 corre-
sponding to approximately 1350 runs, including 220 high-
intensity runs,5 with the activity pattern changing every 4 to
6 seconds during a game.1,4,5
A competitive soccer season includes weekly micro-
cycles consisting of training, taper, competition, and recovery.
Elite clubs may play additional games during a weekly
microcycle due to participation in local or international
tournaments. Collectively, the demand for playing 2 to 3 games
per week elevates the stress imposed on the players, thereby
increasing the injury risk, performance decline due to fatigue,
muscle damage, and/or inflammation.6 Players must fully
recover and be ready to compete for a full 90 minutes plus
stoppage time in the next game within 3 to 6 days.
Soccer requires the generation of large eccentric forces,
which have frequently been associated with muscle damage
that clinically presents as muscular pain developed some days
post-exercise.7 Muscle damage is mainly induced by mechan-
ical stress and disturbances of calcium homeostasis,8 and
a sensation of discomfort within the muscle may be
experienced by the athlete. The intensity of discomfort
increases within the first 24 hours after exercise, peaks
between 24 and 72 hours, subsides, and eventually disappears
5 to 7 days after exercise,9 a phenomenon that is referred to as
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Ispirlidis et al
delayed onset of muscle soreness (DOMS). Exercise-induced
muscle damage is associated with an acute-phase inflamma-
tory response characterized by phagocyte infiltration into
muscle, free radical production, and elevation of cytokines and
other inflammatory molecules.7,10
The ability of soccer players to fully recover before their
next major competition is crucial not only for their
performance but for injury prevention as well. Information
on the time course of changes in the acute-phase inflammatory
response, DOMS, pain, and performance after a single soccer
game is scarce. Therefore, the purpose of the present
investigation was to study the effects of a single soccer game
on indices of performance, muscle damage, and inflammation
during a 6-day recovery period.
METHODS
Subjects and Study Design
Twenty-four, injury-free, elite male soccer players (age,
21.1 6 1.2 years; weight, 75.2 6 6.8 kg; height, 1.78 6 0.08 m;
VO2max, 59.3 6 4.2 ml/kg/min) who volunteered to participate
in the study were assigned to either an experimental group
(n = 14) that participated in the game or a control group (n =
10) that did not participate in the game. Players were randomly
assigned to each group and were all recruited from a single
team. Groups were composed of both starters and reserves
(pilot data showed no differences between them relative to
oxidative stress and inflammation responses both at rest and
after a game). The experimental group was composed of
5 defenders, 5 middle fielders, and 4 forwards (including one
goalkeeper). Subjects abstained from any strenuous physical
activity for at least 7 days before and after the game. Subjects
were not taking any medication or dietary supplements for
6 months before the study. After being informed of the design
and potential risks, players signed a consent form. The insti-
tutional ethics committee approved the study, and procedures
were in accordance with the Helsinki declaration.
Subjects visited the laboratory twice before the game:
(a) 1 week before the game, a health history questionnaire was
completed, and body weight/height, percent body fat, VO2max
(during a treadmill test to exhaustion according to a standard-
ized protocol as previously described11), performance, and
muscle damage markers were determined; (b) on the morning
of the game-day, baseline blood samples were collected, and
a competitive soccer game was performed 2 hours later.
Players had their heart rate measured (Polar Vantage NV
monitor; Polar Electro, Kempele, Finland) in 5-second
intervals throughout the game. Blood sampling and measure-
ment of performance and muscle damage indices was repeated
immediately and 24, 48, 72, 96, 120, and 144 hours post-
game.
Anthropometric Measurements
During their first visit, body mass was measured to the
nearest 0.5 kg (Beam Balance 710, Seca, UK) with subjects
wearing their underclothes and barefooted. Standing height
was measured to the nearest 0.5 cm (Stadiometer 208, Seca,
UK). Percentage body fat was calculated from 7 skinfold
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Clin J Sport Med
Volume 18, Number 5, September 2008
measures (average of 2 measurements of each site), using
a Harpenden calliper (John Bull, UK).
Measurement of Performance Variables
Maximal strength (1RM) was measured bilaterally in
squat as previously described.12 Time for speed testing during
a 20-m sprint was recorded by infrared light-sensors with
a precision of 0.01 seconds (Newtest, Finland). Vertical jump
height (VJ) was measured in 3 maximal efforts (the best jump
was recorded) on an Ergojump contact platform (Newtest,
Oulu, Finland). Subjects started from a standing position,
allowed a preparatory counter-movement motion, and had
their hands on their waist throughout the jump. Flight times
were measured by means of a digital timer connected to the
platform and were used to calculate jump height.13 The
coefficient of variation for test-retest trials were was 2.9%,
3.5%, and 2.4% for 1RM, sprinting, and VJ, respectively.
Measurement of Muscle Damage Markers
DOMS was determined by palpation of the muscle belly
and the distal region of the relaxed vastus medialis, vastus
lateralis, and rectus femoris in a seated position. Perceived
soreness was then rated on a scale ranging from 1 (normal) to
10 (very, very sore) as previously described.9 Knee joint range
of motion (KJRM) was measured as an index of muscle edema
as previously described.12 The coefficient of variation for test-
retest trials for knee flexion/extension was 2.1%.
Blood Sampling
Blood samples were drawn from an antecubital arm vein
using a 20-gauge disposable needle equipped with a Vacutainer
tube holder (Becton Dickinson, Franklin Lakes, NJ) with the
subject in a seated position. Samples (10 mL) were collected
into a Vacutainer tube containing SST-Gel and Clot Activator.
Serum was allowed to clot at room temperature and
subsequently centrifuged (1500 3 g, 4°C, 15 minutes). The
resulting serum was placed into separate microcentrifuge
Eppendorf tubes in multiple aliquots and frozen at –70oC for
later analyses of the concentration of thiobarbituric acid-
reactive substances (TBARS), protein carbonyls (PC), cortisol,
testosterone, IL-6, IL-1b, C-reactive protein (CRP), and the
activities of lactate dehydrogenase (LDH) and creatine kinase
(CK). Blood samples thawed only once before analysis.
A small quantity of blood (200 mL) was immediately added to
400 mL of 5% TCA and centrifuged (2500 3 g, 15 minutes).
The supernatant was removed and frozen at –75oC until
analysis for lactate by an enzymatic method with reagents
purchased from Sigma Chemicals (St. Louis, MO). A blood
aliquot (1 mL) was immediately mixed with EDTA to prevent
clotting for haematology. Complete blood count and uric acid
(UA) was determined within 24 hours via matching duplicate
counts using an automated hematology analyser (Sysmex
K-1000 autoanalyzer; TOA Electronics, Japan). A small whole
blood aliquot was used for microcapillary determination of
hematocrit.
Assays
Glucose was determined by the glucose oxidase
method (Sigma-Aldrich, St. Louis, MO). CK was determined
spectrophotometrically by using a commercially available kit
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(Spinreact, Sant Esteve, Spain). LDH activity was determined to pre-game values 72 hours after the game. 1RM decreased
spectrophotometrically by means of a commercial diagnostic (P , 0.05) after the game, reached its lowest value at 48 hours
test kit (Sigma Diagnostics, St. Louis, MO). CRP and UA were post-game, and returned to pre-game levels 96 hours after the
measured with the COBAS INTEGRA 800 Clinical Chemistry game. Sprinting ability declined (P , 0.05) post-game,
System (Roche Diagnostics). Cortisol and testosterone were
analyzed by using 2 commercially available ELISA kits (DRG
Diagnostics, Germany). Serum IL-6 and IL-1b concentrations
were measured using 2 commercially available ELISA kits
(Immunokontact, UK) based on an immunoenzymatic method.
Total protein in serum was assayed using a Bradford reagent.
TBARS was assayed spectrohoptometrically at 530 nm
according to Keles et al.14 PC were assayed spectrophotomet-
rically at 375 nm according to Patsoukis et al.15 Each assay was
performed on the same day to eliminate variation in assay
conditions and within one month of the blood collection. Post-
game changes in plasma volume were computed based on
hematocrit and hemoglobin.16 Spectrophotometric assays were
performed on a Hitachi 2001 UV/VIS spectrophotometer
(Hitachi Instruments Inc) in duplicate. The inter- and intra-
assay coefficients of variation in all assays performed were 2.4
to 7.3 and 3.5 to 8.6, respectively.

Statistical Analyses
Results are reported as means 6 SE. Time differences
were evaluated with ANOVA repeated measures, and
a Bonfferoni adjustment was used for post-hoc comparisons.
The level of statistical significance was set at a = 0.05. Data
were analysed using SPSS 11.0 (SPSS, Chicago, IL).

RESULTS
Table 1 summarizes participants’ physiological responses
to a soccer game. Total playing time was 68 min (75%).
Mean heart rate during the game was 159.7 6 4.1 bpm, and
peak heart rate was 189 6 3.5 bpm. At the conclusion of the
game, glucose levels increased (4.4 6 0.1 mM versus 4.8 6
0.3 mM, P , 0.05), and lactate reached 4.51 6 0.4 mM
(P , 0.05).
Figure 1 illustrates performance changes after the game.
VJ decreased (P , 0.05) 24 hours after the game and returned

TABLE 1. Game Profile

Rest Post-game
Mean heart rate (bpm)
Control 62.6 6 4.9 64.8 6 6.2
Experimental 64.8 6 6.8 159.7 6 14.3*,‡
Peak heart rate (bpm)
Control 62.6 6 4.9 68.4 6 10.4
Experimental 64.8 6 6.8 189 6 11.2*,‡
Lactate (mM)
Control 0.92 6 0.07 1.02 6 0.1
Experimental 1.04 6 0.10 4.51 6 0.4*,‡
Glucose (mM)
Control 4.5 6 0.2 4.6 6 0.2
FIGURE 1. Performance changes after a soccer game. 1,
Experimental 4.4 6 0.1 4.8 6 0.3*,‡ Significant difference with baseline; 2, significant difference
*Significant difference with baseline; ‡significant difference between groups. between groups; VJ, vertical jumping; 1RM, one repetition
maximal. Statistical significance was accepted at a = 0.05.

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Ispirlidis et al
reached its lowest value 48 hours post-game, and returned to
pre-game levels after 120 hours.
Leukocyte count (Figure 2) increased (P , 0.05)
immediately post-game. Leukocytosis persisted for only
24 hours and normalized thereafter. CRP (Figure 2) increased
(P , 0.05) after the game, peaked at 24 hours, and normalized
thereafter.
DOMS (Figure 3) increased (P , 0.05) immediately
post-game, peaked at 48 hours, and returned to baseline levels
96 hours after the game. KJRM (Figure 3) decreased (P ,
0.05) 24 hours after the game, reached its lowest value
48 hours post-game, and returned to physiological values
96 hours after game completion. CK and LDH (Figure 4)
increased (P , 0.05) immediately post-game and peaked
48 hours after the game. However, LDH was normalized
earlier (96 hours) than CK (120 hours).
Oxidative marker responses are demonstrated in Figure
5. UA concentration increased (P , 0.05) at 24 hours, peaked
at 72 hours post-game, and normalized 120 hours after game
completion. TBARS increased (P , 0.05) immediately post-
FIGURE 2. Changes in leukocyte count and CRP levels after
a soccer game. 1, Significant difference with baseline; 2,
significant difference between groups; DOMS, delayed onset
of muscle soreness; KJRM, knee joint range of motion.
Statistical significance was accepted at a = 0.05.
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Clin J Sport Med
Volume 18, Number 5, September 2008
game, peaked 24 hours after the game, and returned to pre-
game values 72 hours post-game. In contrast, PC peaked
(P , 0.05) 48 hours post-game and returned to pre-game
levels after 120 hours.
Cortisol (Figure 6) concentration increased (P , 0.05)
immediately post-game and normalized thereafter. Free
testosterone levels (Figure 6) remained unchanged at all
times. IL-1b (Figure 7) values remained below the lower
detection limit of the kit used in almost all measurement times
with the exception (P , 0.05) of the samples measured
immediately post-game. IL-6 (Figure 7) increased (P , 0.05)
only immediately post-game and normalized thereafter.
Table 2 illustrates percent changes of performance and
inflammatory markers across time after the soccer game. There
were no differences among different playing positions
regarding inflammatory responses.
FIGURE 3. Delayed onset of muscle soreness and knee joint
range of motion changes after a soccer game. 1, Significant
difference with baseline; 2, significant difference between
groups; CK, creatine kinase; LDH, lactate dehydrogenase; CRP,
C-reactive protein. Statistical significance was accepted at
a = 0.05.
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FIGURE 4. CK and LDH changes after a soccer game. 1,

Significant difference with baseline; 2, significant difference
between groups; DOMS, delayed onset of muscle soreness;
KJRM, knee joint range of motion. Statistical significance was
accepted at a = 0.05.

DISCUSSION
Currently, there is no or limited information regarding
performance and inflammatory responses occurring within the
microcycle (6 days) that follows a soccer game. The present
investigation suggests that a competitive soccer game induces
time-dependent changes in various inflammatory markers
indicative of muscle trauma as well as acute performance
deterioration.
The players’ physiological strain during the game
approximated the values observed during elite soccer FIGURE 5. Changes in oxidative stress markers after a soccer
competition. Players reached a mean and peak heart rate that game. 1, Significant difference with baseline; 2, significant
corresponded to the 80% and 94% of their maximal heart rate difference between groups; TBARS, thiobarbituric acid-reactive
substances; CK, creatine kinase; PC, protein carbonyls.
and a blood lactate accumulation of 4.5 mM that have also Statistical significance was accepted at a = 0.05.
been reported for elite soccer competition.3,17 These observa-
tions indicate that the game was performed in a competitive
environment. immediately post-game, but no other measurements were
Performance deterioration lasted 24 to 72 hours after performed.18 According to these findings, soccer players may
the game. Interestingly, 1RM and speed decline was main- not be able to perform at maximal level intense anaerobic
tained for 72 hours while VJ decreased for only 24 hours. Only activities such as those seen during a game (sprinting or
1 study showed a significant decline in sprinting time jumping) for at least 3 days after their most recent competition.

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Ispirlidis et al
FIGURE 6. Hormonal responses to a soccer game. 1, Significant
difference with baseline; 2, significant difference between
groups. Statistical significance was accepted at a = 0.05.
The catabolic state that accompanies elevated cortisol levels
may result in decreased physical performance due to reduced
protein synthesis, losses of contractile proteins, neurotrans-
mitters, and muscular force, resulting in strength reductions.19
These adaptations cannot be counterbalanced when testoster-
one declines or remains unchanged as in the present study.
More studies are needed to determine whether a refractory
post-game period exists for soccer performance. Future studies
should employ more specific soccer performance tests. Elite
athletes cannot abstain from training for more than 24 hours
during the in-season period, performance deterioration may be
greater than the one seen in this study.
The large attenuation in strength and KJRM and the
marked elevation of DOMS, CK, and LDH levels provide
indirect evidence of muscle microtrauma after a single game.
This is the first report to provide insight of soccer game-
induced muscle damage persisting for 48 to 72 hours. Peak CK
activity, which occurred at 48 hours after the game, was 950
U/L, almost as high as after a football game or a marathon
race.20,21 The CK and LDH protein efflux from muscle may be
attributed to the increased permeability of plasma membrane
and/or intramuscular vasculature.22 Soccer’s intermittent
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Clin J Sport Med
Volume 18, Number 5, September 2008
FIGURE 7. Cytokine responses to a soccer game. IL-1b is
illustrated in a 24-hour time frame because it was undetectable
at all times except post-game. 1, Significant difference with
baseline; 2, significant difference between groups; IL-1b,
interleukin 1b; IL-6, interleukin 6. Statistical significance was
accepted at a = 0.05.
nature and subjects’ high conditioning level are probably
the reasons that these markers peaked 1 to 2 days post-game
compared to an eccentric exercise protocol in unaccustomed
subjects, which elicits a more prolonged response.23 In
accordance with previous studies, DOMS increased within
the first 24 hours post-game, peaked between 24 and 72 hours,
and disappeared 5 to 7 days post-exercise.24 However, peak
KJRM decline due to muscle swelling was observed 1 to
2 days post-game. The pressure and swelling around the
injured tissue contributes to the muscle soreness sensation and
to the decline of strength and joint’s range of motion, leading
to an alteration in the execution of technical skills due to
compensatory movements in an attempt to protect the injured
tissue.9,25
Soccer consists of high-intensity intermittent running
and jumping as well as rapid acceleration and deceleration
movements. During running’s landing phase, hamstrings are
activated eccentrically to slow hip flexion and knee extension,
decelerating the body. Eccentric activation produces higher
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TABLE 2. Percent Changes of Performance and Inflammatory Markers Across Time in the Experimental Group After the
Football Game
Post-game 1stDay 2ndDay 3rdDay 4thDay 5thDay 6thDay
Jumping -9.3%*,‡ – – – – –
Sprinting –2%* –2.5%*,‡ –1.6%* – – –
Muscle strength –8.8%* –12.7%*,‡ –7%* – – –
DOMS +610%* +730%*,‡ +560%* – – – –
Muscle swelling – +4%* +8.2%*,‡ – – – –
Leukocyte count +34%*,‡ +19.5%* – – – – –
CRP +66.3%* +150%*,‡ – – – – –
CK +154.3%* +400%* +710%*,‡ +637%* +358%* – –
LDH +62.6%* +169.6%*,‡ +163.5%*,‡ +90.5%* – – –
Lipid peroxidation +14.5%* +22.6%*,‡ +13%* – – – –
Protein oxidation +35.1%* +81.1%*,‡ +64.8%* +29.8%* +18.9%* – –
Cortisol +50.3%*,‡ – – – – – –
Testosterone – – – – – – –
Cytokines – +390%*,‡ – – – – –
*Significant changes; ‡peak changes. DOMS, delayed onset of muscle soreness; CRP, C-reactive protein; CK, creatine kinase; LDH, lactate dehydrogenase.

tension per cross-sectional area of active muscle mass
compared to concentric actions,8 resulting in significant
structural muscle damage (disruption of structural proteins
such as Z-lines, troponing, tropomyosin).9 Consequently,
muscle injury seen after a soccer game is at least partially
attributed to intermittent repetitions of intense eccentric
activation. Similar findings have been reported for other
sports that involve prolonged (ie, 90 minutes) high-intensity
shuttle running such as rugby and field hockey.26 Repeated
muscle loading may cause strains or tears accompanied by
a marked reduction in muscle performance during training and
actual game-playing, thereby increasing the risk for knee
ligament injuries due to higher joint laxity.27,28 However, other
factors such as physical contact and ball contact may also
contribute to potential perturbations of the inflammatory
system during a soccer game. A combination of repetitive
loading and limited recovery due to increased training and
games may also lead to chronic inflammation and
overtraining.6
Although not tested, one should expect soccer players to
be more resistant to exercise-induced muscle damage
compared to novice exercisers. Skeletal muscle appears to
adjust rather rapidly to repetitive periods of damaging
exercise, such that the muscle is protected against subsequent
periods of exercise-induced trauma.29 This cytoprotection is
related to changes in gene expression, enhancement of cellular
protective mechanisms, and remodelling of muscle tissue,
sometimes involving mitochondrial biogenesis.29 Further-
more, it was shown that resistance-trained men are less
susceptible to muscle damage induced by maximal eccentric
exercise than untrained subjects.30 However, elite soccer
players are more vulnerable to exercise-induced trauma due to
the increased demands of their training and game scheduling.
Acute strenuous exercise induces a systemic acute-phase
inflammatory response, with leukocyte infiltration in the
damaged tissue resulting in leukocytosis31,32 and with
neutrophils representing 50 to 60% of the total circulating
pool.23,34 Neutrophils demonstrate a transient increase imme-
diately post-exercise followed by a delayed rise several hours
later, a response that was also seen in the present study.10 The
post-exercise immunological response has been partially
attributed to increased circulating cortisol, which exerts
complex action on leukocyte subpopulations.32 Cortisol is
increased by IL-6, which is in agreement with our findings of
a simultaneous post-game rise of IL-6 and cortisol.35 Cortisol
may be implicated in immunoglobin M production and
leukocyte adhesion capacity after a soccer game.11 Although
testosterone has been correlated with leukocyte number in
muscle31 and immunological responses after a soccer game,11
it remained unaffected in the present study, leaving the post-
game catabolic state unopposed.
Cytokines are involved in the control of immune and
acute-phase response, inflammatory reactions, and tissue
repair process. Two of the initial cytokines in the cytokine
cascade are IL-1b and IL-6. Although there is limited
information regarding IL-1b response to soccer, our results
verify a previous report of IL-1b elevation immediately post-
exercise.32 IL-1b produced by muscle cells may be involved in
muscle adaptation by inducing protein degradation and muscle
atrophy.36 IL-6 stimulates neutrophil degranulation, hepato-
cyte-derived acute-phase proteins, and cortisol production.35
Although exercise-induced muscle injury has been suggested
to be the primary stimulus for the IL-6 response, it has been
shown that muscle- and adipose tissue-derived IL-6 partic-
ipates in exercise energy metabolism independently of muscle
damage.37 Muscle damage per se elicits a repair response,
including macrophage entry into the muscle, causing further
IL-6 production. This IL-6 response related to inflammation is
smaller and delayed compared to the muscle-derived IL-6
production. In the present study, IL-6 increased only
immediately post-game and at a lesser extent (4-fold)
compared to other studies.38 More research is needed to
determine the physiological significance of IL-6 rise in sports
like soccer.

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Ispirlidis et al
During inflammation, increased circulating IL-6 acts on
hepatocytes to stimulate the synthesis of acute-phase proteins
such as CRP. Cortisol and cytokines act to degrade muscle
protein, resulting in amino-acid release into the circulation and
stimulate hepatocytes to absorb these amino acids to
synthesize new acute-phase proteins.39,40 In agreement with
these observations, cortisol and IL-6 peaks in the present study
preceded CRP peak in the circulation. Soccer induced
a marked but transient CRP rise within 24 hours post-game
as previously was shown in other exercise protocols.31,41 CRP
rise has been implicated in monocyte activation and adhesion
molecules synthesis that recruit leukocytes.42
Intense exercise generates reactive oxygen species,
producing oxidative stress.43 Reactive oxygen species promote
leukocyte muscle infiltration in inflammation, demargination,
and release from endogenous stores.38,44 Superoxide produced
by neutrophils and macrophages is converted to hydrogen
peroxide, which then reacts with superoxide in the presence of
a transition metal to form toxic hydroxyl radical that oxidizes
lipids and proteins.45 TBARS, a lipid peroxidation marker,
remained elevated for 48 hours, peaking 24 hours post-game.
TBARS levels have been shown to increase for several days
after intense exercise.43 The TBARS rise in blood is probably
caused by peroxidation of low-density lipoproteins and
oxygen-mediated injury of muscle cell membranes.46 PC,
a protein oxidation biomarker, levels remained elevated for
96 hours post-exercise, peaking at 48 hours. These results
coincide with previous reports of a sustained PC rise after
damaging exercise.43 The increased PC post-exercise should
be mainly derived from oxidation of albumin and other serum
proteins.47 Oxidized protein removal from blood may be
a time-consuming process because PC levels remained
elevated for 96 hours. UA, an oxidative stress marker because
of its free-radical scavenging properties (which accounts for
nearly one third of total antioxidant capacity increase during
exercise) also remained elevated for 96 hours after the game,
peaking at 72 hours. These results clearly indicate that soccer
enhances oxidative stress responses as a part of the in-
flammatory response to exercise-induced muscle injury.
In summary, a soccer game induces marked but transient
inflammatory responses as well as anaerobic performance
decline lasting 72 hours post-game. These results clearly
indicate the need for sufficient recovery for soccer players after
a game and for better game/training scheduling. More research
is needed to determine the required time for recovery in soccer.
ACKNOWLEDGEMENTS
We thank all the subjects for their participation and
commitment to the study.
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