Applied nutritional investigation
Effects of creatine supplementation on oxidative stress and inflammatory
markers after repeated-sprint exercise in humans
Rafael Deminice Ph.D.a,b,*, Fl? avia Troncon Rosa Ph.D.b, Gabriel Silveira Franco B.S.c,
Alceu Afonso Jordao Ph.D.b, Ellen Cristini de Freitas Ph.D.c
aDepartment of Physical Education, Faculty of Physical Education and SportdState University of Londrina, Paran? a, Brazil
bLaboratory of Nutrition and Metabolism, Faculty of Medicine of Ribeirao Preto, University of Sao Paulo, Sao Paulo, Brazil
cSchool of Physical Education and Sports of Ribeirao Preto, University of Sao Paulo, Sao Paulo, Brazil
a r t i c l e i n f o
Received 10 September 2012
Accepted 2 March 2013
a b s t r a c t
Objective: The goal of this study was to evaluate the effects of creatine (Cr) supplementation on
oxidative stress and inflammation markers after acute repeated-sprint exercise in humans.
Methods: Twenty-five players under age 20 y were randomly assigned to two groups: Cr supple-
mented and placebo. Double-blind controlled supplementation was performed using Cr (0.3 g/kg)
or placebo tablets for 7 d. Before and after 7 d of supplementation, the athletes performed two
consecutive Running-based Anaerobic Sprint Tests (RAST). RAST consisted of six 35-m sprint runs
at maximum speed with 10 sec rest between them. Blood samples were collected just prior to start
of test (pre), just after the completion (0 h), and 1 h after completion.
Results: Average, maximum, and minimum power values were greater in the Cr-supplemented
group compared with placebo (P < 0.05). There were significant increases (P < 0.05) in plasma
tumor necrosis factor alpha (TNF-a) and C-reactive protein (CRP) up to 1 h after acute sprint
exercise in the placebo-supplemented group. Malondialdehyde, lactate dehydrogenase (LDH),
catalase, and superoxide dismutase enzymes also were increased after exercise in both groups. Red
blood cell glutathione was lower after exercise in both groups. Cr supplementation reversed the
increase in TNF-a and CRP as well as LDH induced by acute exercise. Controversially, Cr supple-
mentation did not inhibit the rise in oxidative stress markers. Also, antioxidant enzyme activity
was not different between placebo and Cr-supplemented groups.
Conclusion: Cr supplementation inhibited the increase of inflammation markers TNF-a and CRP, but
not oxidative stress markers, due to acute exercise.
? 2013 Elsevier Inc. All rights reserved.
Since Harris et al  demonstrated that creatine (Cr)
supplementation increases muscle Cr and phosphorylcreatine
(PCr) content, Cr has become the most popular supplement
proposed as an ergogenic aid . This use reflects the important
role of Cr in rapid energy provision during muscle contraction
through the adenosine triphosphate (ATP)–PCr system . Cr
also has recently been shown to exert antioxidant effects .
Lawler et al  first demonstrated that Cr acts as an antioxidant
scavenger, primarily against radical species. Subsequent studies
have demonstrated the protective effects of Cr against oxidative
stress in cultured cells [6,7], DNA and RNA damage [8,9], and
in in vivo experiments with rats [10–12]. Cr also has been shown
to have anti-inflammatory activity [13,14]. Bassit et al 
demonstrated that Cr supplementation prevented the increase
in proinflammatory cytokines induced by strenuous exercise in
humans. Thus, emerging in vitro and murine experimental data
show that Cr may act as a scavenger of radical species and have
anti-inflammatory activity. However, few studies demonstrating
these properties of Cr in humans, especially against inflamma-
tion and oxidative stress induced by acute exercise, have been
published. The objective of this study was to evaluate the effects
of Cr supplementation on oxidative stress and inflammatory
markers in humans exposed to acute sprint exercise.
RD and ECF designed the research. RD, FTR, GSF, and ECF conducted the
research. RD and AAJ determined the specialized assay and analyzed data. RD
and FTR wrote the paper. All authors read and approved the final manuscript.
The authors declare that they have no conflict of interest.
* Corresponding author. Tel.: 05543 33714139; fax: 05543 33714139.
E-mail address: email@example.com (R. Deminice).
0899-9007/$ - see front matter ? 2013 Elsevier Inc. All rights reserved.
Contents lists available at ScienceDirect
journal homepage: www.nutritionjrnl.com
Nutrition 29 (2013) 1127–1132
The volunteers participating in the present study were 25 healthy and well-
trained men from a Under-20 y soccer team in the city of Ribeirao Preto, S~ ao
Paulo, Brazil. The general characteristics of the volunteers are presented in
Table 1. All volunteers belonged to the Ol? e Brasil soccer team and played in the
second division of the S~ ao Paulo State Championship, training regularly 5
d a week, about 2 h a day. They were familiar with repeated-sprint training in
their training routine. The study was approved by the Research Ethics Committee
of the Faculty of Medicine of Ribeirao Preto, University of Sao Paulo and complied
with the declaration of Helsinki. All volunteers gave written informed consent to
participate. None of the participants smoked or was taking any type of
Testing was performed weekly for 3 wk under the same conditions (day of
the week, time of day, and same place) during the presession period. In week 1,
after anthropometric data collection, the participants were familiarized with the
exercise scheme during study orientation (day 0). On the subsequent 2 test days
(days 7 and 14), subjects performed a running-sprint test. After the last running
test (day 14), venous blood sampling was performed before (pre) and 0 and 1 h
after the running test. The athletes were instructed not to exercise on the day
before the testing day.
The Running-based Anaerobic Sprint Test (RAST) was performed according to
Zagatto et al  twice with 2 min between tests in each week. RASTconsisted of
six sprints at maximum speeds with intervals of 10 sec for recovery between
races. The test was performed on a grass field using soccer shoes. Time to
complete each 35 m was recorded to determine average, maximum, and
minimum power as well as fatigue index. The order to complete the tests was
chosen randomly. Volunteers had access to water ad libitum during exercise. The
trials were completed after a warm-up of 20 min consisting of routine stretching
and low-intensity running exercises. The participants were instructed to main-
tain their training routine during the three test weeks.
Cr supplementationwas performed in a double-blind, randomizedcontrolled
manner using Cr (0.3 g/kg?1) or placebo (maltodextrin) tablets for 7 d (Ethika?
Suplementos, Ribeir~ ao Preto, S~ ao Paulo, Brazil). One week of Cr supplementation
at 0.3 g/kg?1was chosen based on previous studies showing significantly
increased plasma Cr and muscle-free and Cr phosphate [16,17]. Just after the
pre-RAST exercise protocol in week 2, the participants were divided randomly
into two groups: placebo (Pla, n ¼ 12) or Cr supplemented (Cr, n ¼ 13). A
container with Cr or placebo tablets was given to the participants with the exact
number of tablets for the 7 d of supplementation. Each container contained the
name and dosage of the supplementation for each of the participants. The coach
and researchers encouraged use of supplementation throughout the study
Anthropometric and nutritional data
Each participant was invited to come to the laboratory at the beginning
of the week scheduled for the collection of anthropometric and nutritional
data. A scale with a coupled stadiometer (Filizola?, Sao Paulo, Brazil) was used
to measure weight and height. Body fat was determined by bioelectrical
impedance (Biodynamics?BIA 310E, Seattle, USA). The participants were
instructed to follow their habitual diet throughout the week and to fill out
a food recall form for 3 non-consecutive days during the same week. The food
recall forms were analyzed using the Nutwin? software (Unifesp, Escola
Paulista de Medicina, Sao Paulo, Brazil) to determine total intake of calories,
carbohydrates, proteins, lipids, and vitamins C, E, and A. The use of food
supplements also was recorded and added to the food recall form as part of
habitual intake (Table 2).
In each case,10 mL of venous blood (5 mL in heparinized tube and 5 mL in an
EDTA vacutainer? tube) was collected. The tubes were kept in the dark and
refrigerated on ice until the end of the test and later centrifuged at 1000g for 15
min. Before centrifugation, a 50 mL aliquot of whole blood was added to 50 mL 1%
sodium fluorite in Eppendorf tubes and stored at ?20?C for lateranalysis of blood
lactate accumulation. Plasma and red blood cells (RBC) were separated and
stored in Eppendorf tubes at ?80?C for later analysis.
Plasma Cr was assayed by the Jaffe reaction using a method described by
Deminice et al . Blood lactate was assayed using a commercially available kit
from Labtest? (Lagoa Santa, Minas Gerais, Brazil).
Plasma malondyaldeide (MDA) was determined by high-performance liquid
chromatography (UV/VIS SPD-20A SHIMADZU?, Kioto, Japan) as described by
Nielsen et al. . Reduced glutathione (GSH) and oxidized glutathione (GSSG)
were determined by the method of Rahman et al  using a RBC lysate. Ferric-
reducing antioxidant power (FRAP) was assayed in plasma by the method of
Costa et al . Plasma creatine kinase (CK) and lactate dehydrogenase (LDH)
activities were determined using a commercially available kit from Labtest?
(Lagoa Santa, Minas Gerais, Brazil).
RBC catalase (CAT) and glutathione peroxidase activities were determined by
measuring the decomposition of hydrogen peroxide at 230 nm, as proposed by
Aebi and according toPaglia and Valentine , respectively. RBC superoxide
dismutase (SOD) activity was assayed using acommercially available kit from
Cayman Chemical Company? (Item #706002, Ann Arbor, MI, USA). Hemoglobin
was determined using commercially available kit from Labtest? (Laboa Santa,
Minas Gerais, Brazil).
Plasma tumor necrosis factor alpha (TNF-a) and C-reactive protein (CRP)
determined by competitive immunoassay using commercially available kits from
IMMULITE?(DPC MedLab, Los Angeles, USA) and DPC IMMULITE?1000 immu-
noassay System (DPC MedLab, Los Angeles, USA).
Whole blood hematocrit and hemoglobin were measured to correct plasma
volume shifts . The decrease in blood hemoglobin and hematocrit was
moderate but sufficient to provoke a 13.5% and 4% decrease in plasma volume
0 and 1 h after the exercise test, respectively. All the biochemical analysis was
corrected by plasma volume shifts. All the assays were determined in duplicate.
The coefficient of variation for the measurements was less than 7%.
Data are reported as mean ? SD. Linear mixed-effects model was used to
detect possible differences between groups at the same time of blood collection
and possible differences in relation to time of blood collection (pre, 0 h and 1 h
after exercise) in the same group using SAS statistical package (version 8.2) (SAS
Institute Inc. Cary, NC, USA). The level of significance was set at P < 0.05 in all
General characteristics of the volunteers after 7 d of creatine or placebo
supplementation (n ¼ 25)
Body fat (%)
17.4 ? 1.2
72.1 ? 6.5
1.79 ? 0.1
22.5 ? 1.3
14.5 ? 2.2
53.6 ? 4.7
17.1 ? 1.4
73.3 ? 8.3
1.79 ? 0.1
22.8 ? 1.8
15.6 ? 3.8
54.7 ? 5.7
BMI, body mass index
Values are reported as mean ? SD
Habitual food and supplement intake (mean ? SD)
Food and supplementation intakeReference
Total calories (kcal)
Vitamin A (mg)
Vitamin C (mg)
Vitamin E (mg)
2252.1 ? 935.1
4.1 ? 2.0
45.8 ? 14.1
1.3 ? 0.5
16.3 ? 5.8
25.0 ? 9.9
318.4 ? 234.7
138.7 ? 138.7
8.2 ? 4.9
2343.5 ? 849.3
4.5 ? 1.9
48.6 ? 11.9
1.5 ? 0.5
18.0 ? 7.6
23.7 ? 6.7
313.6 ? 212.6
158.1 ? 126.7
9.3 ? 5.4
ADA, American Dietetic Association; CHO, carbohydrate; Cr, creatinine; Pla,
placebo; VTC, vitamin C
* A range of energy expenditure values was calculated for energy recom-
mendation considering the minimum and maximum recommendations of the
ADA, 2000 for macronutrients (g/kg–1for CHO and protein and % Lip of VTC).
yPosition of the American Dietetic Association and American College of Sports
Medicine: Nutrition and Athletic Performance, 2000.
zDietary Reference Intakes (DRIs–2005) for the remaining nutrients.
R. Deminice et al. / Nutrition 29 (2013) 1127–1132
No significant difference in age, body weight or height, body
mass index, percentage of body fat, or maximal oxygen
consumption was observed between groups after 7 d of placebo
or Cr supplementation (Table 1).
Almost all (96%) volunteers reported the use of carbohydrate
supplements during their training routines. No athlete reported
the use of vitamin complex supplements. Although no significant
difference in habitual ingestion or supplementation was detec-
ted between the placebo and Cr groups, an inadequate average
intake of carbohydrates and vitamins A and E was detected
Average, maximum, and minimum power values weregreater
in the Cr-supplemented group than in the placebo group. The
fatigue index did not differ between groups (Table 3).
Blood lactate concentrations were significantly higher (P <
0.05) immediately after acute exercise than at other blood
sampling time points in both groups. Average concentrations of
blood lactate immediately after the repeated-sprint exercise in
the placebo (13.5 mmol/L) and Cr (13.7 mmol/L) groups charac-
terized the effort as intense and the exercise as predominantly
anaerobic. Cr supplementation did not alter blood lactate
concentrations after exercise (Fig. 1). As expected, the Cr-
supplemented group showed a significant increase (P < 0.05)
in plasma Cr concentration (201%) compared with the placebo
group (Fig. 1).
In both groups, we found increased plasma MDA concen-
trations (placebo 17%; Cr 18%) at 0 h and FRAP (placebo 44%;
Cr 43%) at 1 h. We also observed lower RBC GSH concentrations
(placebo 30%; Cr 21%) at 0 h after exercise in both groups.
Cr supplementation did not inhibit the increased oxidative
stress induced by repeated-sprint exercise. The concentration of
plasma LDH, a muscle damage marker, was increased only in
the placebo group (28%) at 1 h after repeated-sprint exercise
We also examined RBC antioxidant enzymes before and after
sprint exercise. Exercise significantly increased CAT (placebo
18%; Cr 24%) and SOD (placebo 14%; Cr 20%) activities 1 h after
exercise. However, Cr supplementation did not change the
activities of these enzymes compared with the placebo group
Figure 2 shows inflammatory mediator results obtained
before (0 h) and after (1 h) sprint exercise. In the placebo group,
and CRP (0 h 57%; 1 h 58%) were observed up to 1 h after acute
sprint exercise. Cr supplementation reversed these increased
levels of inflammation markers induced byacute exercise (Fig. 2).
In this study, we examined the antioxidant and anti-
inflammatory capacities of Cr in humans exposed to acute
repeated-sprint exercise using short-term Cr supplementation.
Seven days of supplementation caused a significant increase in
plasma Cr concentration that remained elevated after the exer-
cise protocol (Fig. 1). Our main findings were:
1. The repeated-sprint exercise protocol increased levels of
oxidative stress markers and antioxidant enzyme activity, as
well as levels of inflammatory mediators in plasma and RBC;
2. Cr supplementation inhibited increases in TNF-a and CRP
levels and LDH activity induced by acute exercise; and
Performance parameters determined pre- and post-7-days of placebo or creatine
supplementation (n ¼ 25)
Average power (W)
Maximum power (W)
Minimum power (W)
Fatigue index (W/s?1)
426.7 ? 51.3
453.5 ? 76.2
461.4 ? 48.1
531.2 ? 94.2*
44.1 ? 21.3
79.7 ? 43.6y
656.8 ? 98.2
673.4 ? 105.4
631.3 ? 46.8
749.8 ? 112.3*
?21.2 ? 19.8
42.9 ? 27.6y
274.1 ? 46.5
282.3 ? 60.5
314.1 ? 66.7*
396.1 ? 67.5*
61.5 ? 35.1
113.8 ? 49.5y
5.4 ? 1.2
5.7 ? 1.2
4.3 ? 0.9
4.2 ? 2.4
?10.7 ? 6.7
?12.6 ? 7.5
Cr, creatinine; Pla, placebo
Values are reported as mean ? SD
* significant difference in relation to pre.
ysignificant difference in relation to Pla (P < 0.05, Student’s t test).
Fig. 1. Blood lactate accumulation determined before (pre) and after (0 and 1 h)
a repeated-sprint test for placebo or creatine-supplemented groups (A); a, indicates
a significant difference in relation to pre; b, indicates a significant difference in
relation to 0h. (P < 0.05 by linear mixed-effects model). Plasma creatine before
(pre) and after (post) 7-d of placebo (black points) or creatine (gray points)
supplementation (B). (–) values are reported as mean; * indicates a significant
difference in relation to the experimental group at the same of blood collection (P <
0.05 by linear mixed-effects model).
R. Deminice et al. / Nutrition 29 (2013) 1127–1132
3. Cr supplementation improved sprint performance in young
soccer players, but did not reduce the oxidative stress
induced by acute sprint exercise.
Acute exercise may increase levels of lipid peroxidation
markers and impair the antioxidant defense system , as well
as elevate levels of inflammation markers . In the current
study, we demonstrated changes in oxidative stress and muscle
damage markers in response to two RASTsessions. Post-exercise
blood lactate concentrations in both groups confirmed that this
protocol successfully promoted increases in levels of oxidative
stress markers and challenged the antioxidant system.
In this study, we observed important and novel effects of
Cr supplementation on inflammatory markers. As expected,
repeated-sprint exercise provoked a proinflammatory response,
demonstrated by increased TNF-a and CRP levels; 7 d of Cr
supplementation inhibited these increases. Cr supplementation
also prevented increased LDH activity induced by repeated-sprint
exercise. Nomura et al  found that 5 mmol/L?1Cr treatment
significantly suppressed neutrophil adhesion and inhibited the
expressions of intercellular adhesion molecule 1 and E-selectin
induced by TNF-a in endothelial cells in vitro. These authors
concluded that Cr has anti-inflammatory activities against endo-
(20 g/kg?1) reduced TNF-a and prostaglandin E2 (PGE2) levels
compared with placebo after a 30-km race. They reported that
TNF-a and PGE2 are related to an inflammatoryenvironment and
increases in TNF-a, interferon-a, interleukin-1b, and PGE2 were
markedlyreduced in a Cr-supplemented (20 g/kg?1for 5 d) group
competition. More recently, Bassit et al  demonstrated that Cr
supplementation prevented increases in CK, LDH, and aldolase
activity, but not in CRP levels, in humans and rats with strenuous
suggest that Cr has anti-inflammatory properties. However, the
present study was the first to document the anti-inflammatory
properties of Cr after acute anaerobic sprint exercise.
The mechanism by which Cr inhibits inflammatory mediator
is poorly understood. Nomura et al  attributed the anti-
inflammatory capacity of Cr to the increases in intracellular
energy pools resulting from Cr supplementation. Endothelial
cells have been reported to release ATP during acute inflamma-
tion or shear stress . Thus, Cr may enhance ATP release by
increasing Cr phosphate content, resulting in anti-inflammatory
activity through the adenosine A2A receptor . Bassit et al 
speculated that Cr supplementation might reduce muscle cell
death and, consequently, the inflammatory process as a whole.
Oxidative stress markers, red blood cells antioxidant enzyme activity and muscle
damage markers determined before (pre) and after (0 and 1 h) repeated-sprint
exercise after 7-d of placebo or creatine supplementation (n ¼ 25)
Pre 0 h1 h
Oxidative stress markers
Plasma MDA (mmol/L–1)
RBC GSH (mmol/g Hb–1)
Plasma FRAP (mmol/L–1)
Antioxidant enzyme activity
RBC CAT (kU/g Hb–1)
RBC SOD (U/g Hb–1)
RBC GPx (U/g Hb–1)
Muscle damage markers
Plasma CK (U/L–1)
Plasma LDH (U/L–1)
1.33 ? 0.13
1.34 ? 0.21
1.53 ? 0.19*
1.58 ? 0.19*
1.42 ? 0.20
1.48 ? 0.16
264.9 ? 65.6
267.7 ? 45.5
163.9 ? 32.5*
175.6 ? 65.5*
187.8 ? 46.9
211.7 ? 65.8
5.43 ? 2.33
5.69 ? 2.71
4.67 ? 2.31
4.80 ? 2.34
4.45 ? 2.11
3.90 ? 1.65
887.2 ? 147.5 792.5 ? 129.1 1283.6 ? 212.7*,y
860.4 ? 161.4 807.7 ? 140.6 1241.5 ? 192.3*,y
5.71 ? 0.75
5.66 ? 0.96
6.55 ? 0.99*
6.67 ? 1.13*
6.77 ? 0.91*
7.04 ? 1.45*
472.6 ? 31.3
454.7 ? 36.3
491.2 ? 33.7
531.1 ? 58.6*
538.6 ? 42.3*
546.6 ? 55.7*
51.7 ? 2.1
54.6 ? 3.6
57.5 ? 5.3
64.3 ? 9.6
54.4 ? 6.4
61.8 ? 10.6
446.3 ? 298.4 404.4 ? 222.4
506.7 ? 352.7 541.1 ? 356.7z
427.3 ? 254.5
524.1 ? 316.4z
122.8 ? 26.5
115.4 ? 31.8
118.2 ? 24.3
156.6 ? 36.6*
122.1 ? 30.22
Cr, creatinine; FRAP, ferric-reducing ability of plasma; GPx, glutathione peroxi-
dase; GSH, glutathione; GSSG, oxidized glutathione; Hb, hemoglobin, MDA,
malondialdehyde; RBC, red blood cell; Pla, placebo; CAT, catalase; CK, creatine
kinase; LDH, lactate dehydrogenase; SOD, superoxide dismutase Values are re-
ported as mean ? SD
* a significant difference in relation to pre.
ya significant difference in relation to 0h.
za significant difference in relation to the experimental group at the same
time of blood collection (P < 0.05 by the linear mixed-effects model).
Fig. 2. Plasma TNF-a (A) and C-reactive protein (B) determined before (pre) and
after (0 and 1 h) a repeated-sprint test after 7-d of placebo (black points) or creatine
(gray points) supplementation. (–) values are reported as mean. (P < 0.05 by linear
R. Deminice et al. / Nutrition 29 (2013) 1127–1132
Additionally, several investigators have demonstrated that Cr
supplementation can increase cell hydration and membrane
stabilization , as well as prevent lipid peroxidation and
cell damage , which may be involved in the inflammation
Our results partially refuted the study hypothesis that Cr
could act as an antioxidant in humans. Since Lawler et al  first
demonstrated the direct scavenging effects of Cr on superoxide
anion, peroxynitrite, and 2,20-azino-bis(3-ethylbenzthiazoline-
6-sulfonic acid), several in vitro [5–9] and in vivo [10–12] studies
in rodents have demonstrated the antioxidant capacity of Cr.
Sestili et al  demonstrated that Cr has direct antioxidant
activity via a scavenger mechanism in cultured cells exposed to
different oxidative agents. Studies have also shown the protec-
tive effects of Cr exposure on oxidatively injured mitochondrial
DNA  and against RNA-damaging agents . More recently,
rodent models have demonstrated the antioxidant effects of Cr.
Deminice et al  demonstrated the capacity of Cr supple-
mentation (2% in the diet for 4 wk) to reduce levels of homo-
cysteine and lipid peroxidation markers in rats. Acute exercise
was shown to increase thiobarbituric acid-reactive substances
and total lipid hydroperoxides in rat plasma and muscle, and to
reduce the GSH/glutathione disulfide (GSSG) ratio in soleus
muscle; 4 wk of 2% Cr supplementation inhibited these pertur-
bations . Guimar~ aes-Ferreira et al  demonstrated that
short-term Cr supplementation (5 g/d for 6 d) reduced reactive
oxygen species (ROS) content in rat skeletal muscle despite the
absence of changes in antioxidant enzymes. These authors
concluded that their results supported evidence for the direct
role of Cr as an ROS scavenger. However, these results should be
extrapolated to humans with caution.
Few studies have examined the antioxidant effects of Cr in
humans [28,29], and conflicting findings have been reported.
Kingsley et al  showed that short-term Cr supplementation
(20 g/d for 5 d) was ineffective in attenuating the plasma
oxidative stress induced by acute cycling exercise. In contrast,
Rahini et al  found that Cr supplementation (5 g Cr mono-
hydrate, four times a day for 7 d) attenuated the changes induced
excretion and plasma MDA levels. Thus, studies in humans have
not completely reproduced the protective effects of Cr against
oxidative stress observed in vitro and in murine studies.
Deminice et al  found that the protective effects of Cr in
plasma differed from those observed in muscle, which they
explained based on the large difference in Cr retention between
these tissues (198% in plasma versus 10% in muscle). Although
the current supplementation regime has been shown to “load”
muscle cells to threshold levels [1,15], a major limitation of the
present study was the lack of Cr concentration measurement
in skeletal muscle. Also, oxidative stress markers as well as
inflammatory data from muscle should be used to clarify the
tissue-specific effects of Cr supplementation. Further studies
are necessary to elucidate the protective effects of Cr supple-
mentation on plasma and muscle in humans exposed to acute
Our results show that 7 d of Cr supplementation inhibited
increased TNF-a and CRP levels and LDH activity induced by
acute exercise. These novel findings suggest that Cr has anti-
inflammatory effects. Cr supplementation was insufficient to
prevent oxidative stress induced by acute repeated-sprint exer-
cise; this result differs from previous reports of Cr’s antioxidant
activity in in vitro and animal experiments [5,7,11]. Thus,
more studies are necessary to confirm the antioxidant and
anti-inflammatory effects of Cr supplementation in humans.
This study was supported by Brazilian grants from Coor-
denac ¸~ ao de Aperfeic ¸oamento de Pessoal de Ensino Superior –
e Tecnol? ogico – CNPq.
The authors acknowledge the Ol? e Brasil soccer team for
collaboration and Ethika Suplementos for providing creatine and
placebo tablet supplements.
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