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Influence of tart cherry juice on indices of recovery following marathon running


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This investigation determined the efficacy of a tart cherry juice in aiding recovery and reducing muscle damage, inflammation and oxidative stress. Twenty recreational Marathon runners assigned to either consumed cherry juice or placebo for 5 days before, the day of and for 48 h following a Marathon run. Markers of muscle damage (creatine kinase, lactate dehydrogenase, muscle soreness and isometric strength), inflammation [interleukin-6 (IL-6), C-reactive protein (CRP) and uric acid], total antioxidant status (TAS) and oxidative stress [thiobarbituric acid reactive species (TBARS) and protein carbonyls] were examined before and following the race. Isometric strength recovered significantly faster (P=0.024) in the cherry juice group. No other damage indices were significantly different. Inflammation was reduced in the cherry juice group (IL-6, P<0.001; CRP, P<0.01; uric acid, P<0.05). TAS was ~10% greater in the cherry juice than the placebo group for all post-supplementation measures (P<0.05). Protein carbonyls was not different; however, TBARS was lower in the cherry juice than the placebo at 48 h (P<0.05). The cherry juice appears to provide a viable means to aid recovery following strenuous exercise by increasing total antioxidative capacity, reducing inflammation, lipid peroxidation and so aiding in the recovery of muscle function.
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Influence of tart cherry juice on indices of recovery following
marathon running
G. Howatson
, M. P. McHugh
, J. A. Hill
, J. Brouner
, A. P. Jewell
, K. A. van Someren
, R. E. Shave
S. A. Howatson
School of Psychology and Sport Sciences, Northumbria University, Newcastle upon Tyne, UK,
Nicholas Institute of Sports
Medicine and Athletic Trauma, Lenox Hill Hospital, New York, USA,
St. Mary’s University College, Twickenham, UK,
School of
Life Sciences, Kingston University, Kingston-upon-Thames, UK,
Faculty of Health and Social Sciences, St. George’s Medical
School, London, UK,
English Institute of Sport, Marlow, UK,
Centre for Sports Medicine and Human Performance, Brunel
University, Uxbridge, UK
Corresponding author: Glyn Howatson, School of Psychology and Sport Sciences, Northumbria University, Northumberland
Building, Newcastle upon Tyne NE1 8ST, UK. Tel: 100 44 0 191 227 3571, Fax: 00 44 0 191 227 4515, E-mail:
Accepted for publication 25 June 2009
This investigation determined the efficacy of a tart cherry
juice in aiding recovery and reducing muscle damage,
inflammation and oxidative stress. Twenty recreational
Marathon runners assigned to either consumed cherry juice
or placebo for 5 days before, the day of and for 48 h
following a Marathon run. Markers of muscle damage
(creatine kinase, lactate dehydrogenase, muscle soreness
and isometric strength), inflammation [interleukin-6 (IL-6),
C-reactive protein (CRP) and uric acid], total antioxidant
status (TAS) and oxidative stress [thiobarbituric acid re-
active species (TBARS) and protein carbonyls] were exam-
ined before and following the race. Isometric strength
recovered significantly faster (P50.024) in the cherry juice
group. No other damage indices were significantly different.
Inflammation was reduced in the cherry juice group (IL-6,
Po0.001; CRP, Po0.01; uric acid, Po0.05). TAS was
10% greater in the cherry juice than the placebo group
for all post-supplementation measures (Po0.05). Protein
carbonyls was not different; however, TBARS was lower in
the cherry juice than the placebo at 48 h (Po0.05). The
cherry juice appears to provide a viable means to aid
recovery following strenuous exercise by increasing total
antioxidative capacity, reducing inflammation, lipid perox-
idation and so aiding in the recovery of muscle function.
Muscle damage, inflammation and oxidative stress
typically occur in response to long-distance running
races such as half-Marathons (Duthie et al., 1990),
Marathons (Weight et al., 1991; Ostrowski et al.,
1999; Starkie et al., 2001; Kratz et al., 2002; Suzuki
et al., 2003; Smith et al., 2004) and ultraendurance
running events (Kim et al., 2007) and have subse-
quently proven to be useful models in which to study
the stress response to prolonged endurance exercise.
Numerous studies have examined the effect of dietary
supplements that contain antioxidants on markers of
muscle damage, inflammation and oxidative stress in
response to running. Because the goal of antioxidant
supplementation is to boost the body’s defenses
against oxidative stress it is not surprising that several
investigations using supplementation have shown
reductions in markers of oxidative stress in response
to running (Itoh et al., 2000; Mastaloudis et al., 2004;
Bloomer et al., 2006; Machefer et al., 2007). Despite
these positive effects, some studies have shown no
effect of antioxidant supplementation on markers of
running-induced oxidative stress (Rokitzki et al.,
1994; Kaikkonen et al., 1998; Dawson et al., 2002).
In addition, most investigations have shown that
antioxidant supplementation has no effect on the
indices of muscle damage following running (Kaikko-
nen et al., 1998; Dawson et al., 2002; Kingsley et al.,
2005; Mastaloudis et al., 2006; Machefer et al., 2007),
although a few studies have shown reductions in
markers of muscle damage (Rokitzki et al., 1994; Itoh
et al., 2000). Furthermore, several studies have shown
that antioxidant supplementation does not decrease
markers of inflammation after prolonged running
(Castell et al., 1997; Kaikkonen et al., 1998; Peters
et al., 2001b; Mastaloudis et al., 2004; Machefer et al.,
2007). However, some aspects of immune response to
prolonged running may be enhanced by glutamine
supplementation (Castell & Newsholme, 1997).
The efficacy of a nutritional intervention to lessen
exercise-induced muscle damage, inflammation and
oxidative stress might be improved by providing a
food or supplement that contains phytochemicals
with both antioxidant and anti-inflammatory proper-
ties. For example, cherries are known to be high in
numerous different phytochemicals with both anti-
oxidant and cyclooxygenase inhibitory properties
Scand J Med Sci Sports 2009 &2009 John Wiley & Sons A/S
doi: 10.1111/j.1600-0838.2009.01005.x
(Wang et al., 1999; Seeram et al., 2001). Evidence of
anti-inflammatory effects from consuming cherries
has been demonstrated in studies involving healthy
human subjects (Jacob et al., 2003; Kelley et al.,
2006). Additionally, animal investigations have also
demonstrated pain inhibition (Tall et al., 2004) and
anticarcinogenic (Kang et al., 2003) effects with the
consumption of cherries. Only one previous piece of
research has used a cherry intervention with an
exercise model in hominids; Connolly et al. (2006)
supplemented subjects with a tart cherry juice before
and following high-intensity eccentric muscle con-
tractions and found a reduction in some markers of
muscle damage when compared with a placebo.
Despite the investigators not recording measures of
inflammation or oxidative stress, they speculated that
the differences were due to the anti-inflammatory and
antioxidant properties of the cherry juice (Connolly
et al., 2006); consequently it would be of benefit for
future investigations to examine measures of inflam-
mation and oxidative stress in order to provide an
insight into the potential mechanisms of cherry juice
supplementation (Howatson & van Someren, 2008).
This growing body of literature (Wang et al., 1999;
Seeram et al., 2001; Jacob et al., 2003; Kang et al.,
2003; Tall et al., 2004; Connolly et al., 2006; Kelley
et al., 2006) indicates that cherries may have potent
antioxidant and anti-inflammatory effects, which
make the expectation tenable that supplementation
with cherries, may have beneficial effects following
strenuous endurance activity. Therefore, the purpose
of this study was to examine the effect of a tart cherry
juice blend taken before and following running a
Marathon on markers of muscle damage, inflamma-
tion and oxidative stress. It was hypothesized that
consumption of cherry juice on the days before and
following the Marathon would reduce the subse-
quent markers of muscle damage, inflammation
and oxidative stress.
Materials and methods
Before the start of the investigation all procedures were
approved by the institutional ethics committee in accordance
with the Declaration of Helsinki. Twenty volunteers, male
(n513) and female (n57), participated in this investigation.
Eighteen of the participants were accepted for, and completed
the 2008 London Marathon, the environmental conditions on
the day of the race were: barometric pressure, 758 mmHg;
temperature, 7 1C; wind speed, 4 km/h; relative humidity,
56%; there were also intermittent showers throughout the
day. Fourteen days later the remaining two volunteers com-
pleted the Marathon distance on similar terrain and similar
environmental conditions: barometric pressure, 751 mmHg;
temperature, 10 1C; wind speed 12 km/h; relative humidity,
50%; there were also intermittent showers throughout the day.
All participants completed a health screening questionnaire
and a written informed consent. In addition, the participant
characteristics, predicted Marathon time, Marathon history
and training mileage leading up to the race were recorded and
are presented in Table 1. We also asked participants to
complete a food diary, refrain from taking nutritional supple-
ments and strenuous exercise (other than completing training
runs before the Marathon) for the duration of the study.
Experimental overview
Volunteers were equally assigned to either a placebo or cherry
juice group based upon predicted finish time in a pseudo-
randomized fashion. We also attempted to balance the num-
ber of male and female subjects in each group to account for
possible sex differences in the response to Marathon running.
Of the two participants who completed a Marathon distance
over similar terrain to the London Marathon, one was
randomly assigned to the cherry juice group and the other
was assigned to the placebo group. Markers of muscle damage
(with the exception of muscle soreness and isometric force,
which were not measured pre-supplementation), antioxidative
status, oxidative stress and inflammation were taken on five
occasions; 6 days before the Marathon, the day before the
Marathon, immediately after, and at 24 and 48 h after the
Marathon. Following the initial visit to the laboratory subjects
were allocated to treatment groups and were instructed to take
the supplement every day before, the day of the Marathon and
for the 48 h following the Marathon. This equated to 5 days
supplementation before the Marathon and 8 days of supple-
mentation in total.
Treatment groups
The placebo group was instructed to take two servings of a
fruit flavoured concentrate that was mixed with approximately
8 oz of water and was intended to have similar visual
properties but without the phytonutrient content found in
the cherry juice blend. The cherry juice group took two 8 oz
bottles of a commercially available tart cherry juice blend. The
cherry juice blend was a mixture of freshly prepared tart
cherry juice with commercially available apple juice in a
proprietary ratio (Cherrypharm Inc., Geneva, New York,
USA). Frozen tart cultivar Montmorency cherries (Prunus
cerasus) were used to prepare the cherry juice following
standard industrial processing procedures. The blended juice
was pasteurized by heating it to 85 1C, hot packed into 8 oz
bottles with a 3-min hold time to achieve commercial sterility,
and then forced cooled in a water bath. One 8 oz bottle of the
juice (containing the equivalent of 50–60 cherries) provided at
least 600 mg phenolic compounds, expressed as gallic acid
equivalents, 32 g carbohydrate and at least 40 mg anthocya-
nins, calculated as cyanidin-3-glucoside equivalents by the pH
differential (Connolly et al., 2006). The remaining 560 mg of
compounds is comprised of other flavonoids compounds, such
as the flavonols quercetin, kaempferol and isoramnetin and
their glucosides, flavanols such as catechin, epicatechin and
procyanidins and their glucosides and phenolic acids such as
neochlorogenic acid, 3-coumaroylquinic acid, chlorogenic
acid and ellagic acid. The oxygen radical absorbance capacity
(ORAC) of a sample bottle was 55 mmol/L Trolox equiva-
lents, which compares favorably with reported ORAC values
ranging from 9.1 to 31.7 mmol/L Trolox equivalents for other
commercially available juices, such as grape juice, black cherry
juice, pomegranate juice, blueberry juice, acai juice and
cranberry juice (Seeram et al., 2008).
Participants were instructed to take one bottle or serving in
the morning and one in the afternoon for the duration of the
supplementation period. In addition, participants were asked
Howatson et al.
to keep the supplement in cool dark storage, preferably
refrigerated, until it was consumed to attenuate the possibility
of degradation of the active compounds by light and heat.
Blood sampling and handling
Approximately 8.5 mL of blood was taken from a branch of
the basilic vein at the ante-cubital fossa and collected into
serum separation tubes. The blood was spun in a refrigerated
(4 1C) centrifuge at 3500 gfor 20 min; serum supernatant was
aspirated, protected from the light and immediately frozen
at 80 1C for later analysis.
Dependent variables
Indices of muscle damage were serum creatine kinase (CK)
and lactate dehydrogenase (LDH), muscle soreness (DOMS)
and maximum voluntary isometric contraction (MVIC). In-
flammation markers were C-reactive protein (CRP), interleu-
kin-6 (IL-6) and uric acid. Markers of antioxidative status and
stress were total antioxidant status (TAS), thiobarbituric acid
reactive species (TBARS) and protein carbonyls (PC) –
TBARS and PC are measures of lipid and protein peroxida-
tion, respectively. All blood measures were run in duplicate.
Muscle damage indices
Serum CK concentration was determined using an automated
analyzer (c8000, Abbott Architect, Abbot Park, Illinois, USA).
The normal range for CK using this assay in males and females is
reported as 29–200 IU/L. Serum LDH was analyzed using a dry
slide chemistry analyzer (Ektachem DT60 II and DTSC II
Module, Ortho-clinical Diagnostics, Amersham, UK). The coeffi-
cient of variation (CV) of intra-sample reliability was o3% for
both CK and LDH. DOMS was determined using a 200 mm
visual analogue scale with ‘‘no soreness’’ indicated at one end
and ‘‘unbearably painful’’ at the other. The subject stood with
the hands on hips and feet approximately shoulder width
apart. The participant was then asked to squat down to 901
(internal joint angle), rise to the start position and then
indicate on the visual analogue scale the soreness felt in the
lower limbs. MVIC of the non-dominant knee extensors was
determined using a strain gauge (MIE Medical Research Ltd.,
Leeds, UK). Participants were seated on a platform and the
non-dominant ankle was attached to the strain gauge at an
internal joint angle of 801(verified by a goniometer). Partici-
pants were given three submaximal trials at approximately
50%, 70% and 90% of their perceived maximum, followed by
two maximal trials, each separated by 1 min. Each contraction
lasted for approximately 3 s and all participants were given
standardized verbal encouragement throughout. If there was
o5% variance between the two MVICs the highest output
recorded on the strain gauge was used for data analysis. On
some occasions (13% of all trials) a third trial was necessary in
order to attain two trials within the 5% tolerance.
Inflammation indices
Serum IL-6 concentration was determined in duplicate using a
quantitative sandwich enzyme immunoassay ELISA techni-
que (Quantikine, R&D Systems Europe Ltd., Abingdon, UK).
Normal reference ranges for this assay are reported at o3 pg/
mL. The serum intra- and inter-assay precision, determined
by CV was o5%. Serum CRP concentration was determined
using an automated analyzer (c8000, Abbott Architect). The
normal reference values for this assay are reported at
o0.8 mg/L with an intra-assay CV of 3.7%. Uric acid was
determined using a dry slide chemistry analyzer (Ektachem
DT60 II and DTSC II Module, Ortho-clinical Diagnostics),
the intra-assay CV was 4.2%.
Antioxidative status and oxidative stress
TAS was assessed using a colorimetric assay kit (Randox
Laboratories Ltd., Antrim, UK) that was run on an auto-
mated analyzer (c8000, Abbott Architect); intra-assay relia-
bility was reported as a CV of o3%. TBARS and PC were
measured using commercially available kits (Cayman Chemi-
cal, Ann Arbor, Michigan, USA); the intra-assay CV was
5.5% and 4.7%, respectively.
Statistical analyses
Based on the available literature on prolonged endurance
exercise, estimates were made of the expected change, and
the inter-subject variation in change for each marker of muscle
damage, inflammation and oxidative stress in response to
running a Marathon. Assuming that the placebo group would
have the expected responses, estimates were made on how
much lower that response would need to be in the cherry juice
group with a sample of 10 per group at an alevel of 0.05 and a
blevel of 0.2 (80% power). Estimated effect sizes are reported
as percentage with a maximum possible effect of 100% (i.e., no
response in the cherry juice group). For markers of muscle
damage the estimated effect sizes (percent lower response in
cherry juice vs placebo) were 23% for MVIC (Suzuki et al.,
2006), 45% for DOMS (Suzuki et al., 2006), 90% for CK
activity (Duthie et al., 1990; Rokitzki et al., 1994; Starkie
et al., 2001; Kratz et al., 2002; Suzuki et al., 2003; Smith et al.,
2004) and 56% for LDH activity (Rokitzki et al., 1994; Smith
et al., 2004; Kim et al., 2007). For markers of inflammation the
estimated effect sizes were 85% for CRP (Weight et al., 1991;
Fallon, 2001), 63% for IL-6 (Ostrowski et al., 1999; Starkie
et al., 2001; Suzuki et al., 2003; Kim et al., 2007) and 27% for
uric acid (Duthie et al., 1990; Rokitzki et al., 1994; Kratz et al.,
2002). For markers of oxidative stress the estimated effect sizes
were 69% for TBARS (Duthie et al., 1990; Machefer et al.,
2007) and 35% for PC (Bloomer et al., 2006).
All data analyses were conducted using SPSS for windows,
v. 15 and are reported as mean SD. Descriptive group
characteristics were examined for differences using an inde-
pendent samples Student’s t-test. For the purposes of data
analysis MVIC and TAS were expressed as a percentage
change from baseline to account for inter-individual variation.
All dependent variables were analyzed using a treatment
(cherry juice vs placebo) by time (pre-supplement, pre-race,
immediately post-race, 24 and 48 h post-race) mixed model
analysis of variance (ANOVA). DOMS and MVIC were not
recorded pre-supplementation so the time factor in the AN-
OVA had one less level. Maulchy’s Test of Sphericity was used
to check homogeneity of variance for all ANOVA analyses;
where necessary any violations of the assumption were cor-
rected using the Greenhouse–Geisser adjustment. Significant
interaction effects were followed up using LSD post hoc
analysis. A significance level of P0.05 was established
before analyses.
There were no significant differences in previous
Marathon history, weekly mileage, longest single
training run and predicted finish time (Table 1),
and hence the groups were generally well matched.
Cherry juice supplementation and Marathon running
This was the first Marathon for three participants in
the cherry juice group and for two subjects in the
placebo group. The mean ‘‘actual finish time’’ was
significantly slower than the ‘‘predicted finish time’’
(t52.477, P50.023); although not significant the
difference between the ‘‘predicted finish time’’ and
‘‘actual finish time’’ was greater in the placebo group
(19 min) than the cherry juice group (7 min). Post-
race body mass was significantly lower than body
mass the day before the race (Po0.001) with similar
declines in the cherry juice group and placebo group
(1.2 1.3 vs 1.7 1.5 kg, respectively).
All dependent variables showed a significant time
effect (P0.009) and demonstrated a power of
0.74. The decrement in MVIC, expressed as a
percentage of baseline (Fig. 1.), was similar between
groups post-race (24.3% in cherry juice vs 26.9% in
placebo) but a significant group effect indicated the
recovery of strength over the following 48 h was more
rapid in the cherry juice group (F
Po0.024). For illustrative purposes the absolute
changes in MVIC are presented in Table 2. Despite
the accelerated recovery in strength no other indices
of muscle damage were different between groups
(Table 2).
Serum IL-6 (Fig. 2.) showed a significant group
effect (F
58.659, P50.009) and group by time
interaction (F
58.401, Po0.001) and was ele-
vated immediately post-race, with a smaller elevation
in the cherry juice group vs placebo (41.8 vs 82.1 pg/
mL; Po0.001). IL-6 values had returned to baseline
by 24 h post-race. Serum CRP concentrations (group
512.920, P50.002; group by time – F
510.938, Po0.001, Fig. 3.) were increased at 24 and
48 h post-Marathon with significantly smaller eleva-
tions in the cherry juice group vs placebo (P0.025).
Serum uric acid (group – F
57.944, Po0.011;
group by time – F
52.801, Po0.032, Fig. 4.) was
MVIC (% change)
Cherry Juice
Pre-race Post-race 24h 48h
Fig. 1. Maximum voluntary isometric contraction (MVIC)
for the cherry juice and placebo groups before and following
the Marathon.
Significantly greater recovery of force in the
cherry juice group (Po0.05); values are mean SD (n510
per group).
Table 1. Descriptive data of the volunteer Marathon runners in the cherry juice and placebo groups
Group Sex
Predicted time
Actual time
Highest weekly
Longest training
run (miles)
Cherry juice 7/3 37 13 1.77 0.06 72.9 9.8 3:41:00 0:26:01 3:48:04 0:48:58 33.0 11.6 20.9 2.6 7 9
Placebo 6/4 38 5 1.75 0.09 73.8 9.5 3:56:40 0:40:37 4:15:48 1:01:22 31.7 8.2 19.3 3.1 2 7
Values are mean SD;
510 per group. There were no statistical differences between groups for any variable.
Howatson et al.
elevated post-race and at 24h in the placebo group
with no increase in the cherry juice group (P0.006).
TAS, as a percentage of baseline, was significantly
higher in the cherry juice group vs placebo (group –
510.938, Po0.001; group by time – P50.053,
Fig. 5.). The 5-day supplementation increased TAS
in the cherry juice group (pre-race 111% of baseline,
Po0.01) with no change in the placebo group (101%
of baseline, P50.75). TAS was increased in both
groups after the marathon (cherry juice group 124%
of baseline, Po0.01; placebo 112% of baseline,
Po0.01), and remained elevated in the cherry juice
group at 24 h (114% of baseline, Po0.01) but not in
the placebo group (103% of baseline, P50.21). By
48 h post-race TAS was below baseline in the placebo
group (90%, Po0.01) but not different from baseline
in the cherry juice group (99% of baseline, P50.82).
The TBARS response to the Marathon was different
between groups (group by time – F
P50.018, Fig. 6.) with significantly higher values
for the placebo group vs the cherry juice group at
48 h post-exercise (30.2 vs 21.4 mmol/L, Po0.01).
The PC response to the Marathon was not different
between groups (Table 2) with no post-race eleva-
tions evident in either group.
Following the investigation subjects were asked to
report if they knew what supplement they had been
given. Half (n55) of the cherry juice group guessed
correctly, the remainder of this group reported that
they did not know what supplement they were
taking. In the placebo group 20% (n52) thought
they were on a placebo, the remainder did not know
or thought they were taking the cherry juice. In
addition, the food diaries provided by the partici-
pants did not allow for accurate quantification of
antioxidants; however, we attempted to quantify the
total number of food portions that may contain
Table 2. Indices of muscle function, damage and protein carbonyls for the cherry juice and placebo groups before and following Marathon running
Pre-supplement Pre-race Post-race 24 h 48 h
DOMS (mm)
Cherry juice N/A 0 115 52 91 39 58 39
Placebo N/A 0 115 60 82 45 46 28
Cherry juice N/A 432 114 310 88 387 94 435 109
Placebo N/A 384 112 276 69 313 74 349 96
Cherry juice 187 126 109 40 586 315 2227 1486 1118 905
Placebo 201 164 187 220 912 663 2814 2235 1487 1180
Cherry juice 477 96 487 120 1084 358 828 265 591 173
Placebo 557 88 483 97 1072 344 761 179 712 234
PC (mmol/L)
Cherry juice 24 11 12 11 17 6158176
Placebo 21 9186167167184
DOMS, muscle soreness; MVIC, maximal voluntary isometric contraction; CK, creatine kinase; LDH, lactate dehydrogenase; PC, protein carbonyls.
Significantly more force in the cherry juice group than the placebo (
o0.05); values are mean SD (
510 per group).
IL-6 (pg/mL)
Cherry Juice
Pre-race 24hPost-race
Fig. 2. Serum interleukin 6 (IL-6) concentrations for the
cherry juice and placebo groups before and following
Marathon running.
Significantly lower serum IL-6 in the
cherry juice group than the placebo immediately post-race
(Po0.05); values are mean SD (n510 per group).
CRP (mg /L)
Cherry Juice
Post-race 24hPre-race
Fig. 3. Serum C-reactive protein (CRP) concentrations for
the cherry juice and placebo groups before and following
Marathon running.
Significantly lower serum CRP in the
cherry juice group than the placebo at 24 and 48 h post-race
(Po0.05); values are mean SD (n510 per group).
Cherry juice supplementation and Marathon running
antioxidant compounds in the time before the race.
The mean number of portions was 20 vs 21 portions
for the cherry juice and placebo groups, respectively,
and was not significantly different between groups.
It was hypothesized that consumption of a tart
cherry juice blend would reduce markers of muscle
damage, inflammation and oxidative stress in re-
sponse to running a Marathon. With respect to
markers of muscle damage, the cherry juice group
had a more rapid return of isometric knee extension
strength than the placebo group with no differences
between groups in CK, LDH or muscle soreness.
Despite this, markers of inflammation showed eleva-
tions in IL-6, CRP and uric acid to be significantly
smaller in the cherry juice group compared with the
placebo group. Finally, with respect to oxidative
stress, total antioxidant capacity was increased and
lipid peroxidation was decreased in the cherry juice
group compared with the placebo group; however,
serum protein carbonyl concentration was not dif-
ferent between groups.
The fact that post-race strength loss was similar
between groups, with a more rapid return of strength
in the cherry juice group vs placebo, indicates that
consumption of the cherry juice may have served to
blunt the secondary muscle damage response. With
exercise-induced muscle damage the initial injury is a
mechanical disruption of myofibrils which triggers a
local inflammatory response that exacerbates the
initial damage (Pizza et al., 2002) and this is referred
to as the secondary damage response (Howatson &
van Someren, 2008). The IL-6, CRP and uric acid
data indicate that the inflammatory response to
running the Marathon was blunted by consuming
cherry juice and that this may have limited the
subsequent exacerbation of damage. While the
strength data support this interpretation, the CK,
LDH and DOMS data are less clear because these
markers were not different between the cherry juice
and placebo groups. However, there was an apparent
association between the inflammatory response and
the CK response. The post-race IL-6 elevation was
correlated with CK elevation post-race (r50.58,
P50.007), at 24 h (r50.61, P50.006) and at 48 h
(r50.50, P50.026). Similarly, CRP elevation at
24 h was correlated with CK elevation at 24 h
(r50.56, P50.01) and CRP elevation at 48 h was
correlated CK elevation at 48 h (r50.52, P50.019).
The apparent beneficial effect of cherry juice con-
sumption on recovery of strength is consistent with
previous findings showing that consumption of
cherry juice markedly reduced strength loss after a
bout of high-intensity eccentric contractions of the
elbow flexors (Connolly et al., 2006). In contrast,
Connolly et al. (2006) also found that cherry juice
consumption reduced the pain response to the ec-
centric exercise. However, the effect on pain was not
as marked as the effect on strength. Additionally, the
pain response to isolated maximum eccentric con-
tractions typically peaks 24–48 h after the exercise
bout (Connolly et al., 2006; Howatson & van Som-
eren, 2007); while the muscle soreness reported in the
present study was highest immediately post-race.
Post-race elevations in IL-6 have been consistently
shown in Marathon runners (Ostrowski et al., 1999;
Starkie et al., 2001; Suzuki et al., 2003). In only one
of those investigations (Starkie et al., 2001) was IL-6
measured for a longer period than 24 h after the race;
at 24 h, values were markedly lower than post-race.
Similarly, in the present study IL-6 had returned to
baseline by 24 h. Elevations in CRP (Weight et al.,
Uric Acid (mg/dL)
Cherry Juice
Pre-race Post-race 24h
Fig. 4. Serum uric acid concentrations for the cherry juice
and placebo groups before and following Marathon run-
Significantly lower serum C-reactive protein in the
cherry juice group than the placebo immediately post-race
and at 24 h post-race (Po0.05); values are mean SD
(n510 per group).
TAS (% change)
Cherry Juice
Pre-race Post-race 24h
Fig. 5. Total antioxidative status (TAS) for the cherry juice
and placebo groups before and following Marathon run-
Significantly higher TAS in the cherry juice group
than the placebo (Po0.05); values are mean SD (n510
per group).
Howatson et al.
1991) and uric acid (Rokitzki et al., 1994; Kratz
et al., 2002) have also been demonstrated in response
to running a Marathon. Similar to the present
results, CRP elevations were shown to peak 24 h
post-race and uric acid was shown to be elevated
immediately post-race and at 24 h. In our study, post-
race IL-6 elevation was 49% lower in the cherry juice
group compared with the placebo group while at 24 h
the CRP elevation was 34% lower in the cherry juice
group. These results are clear evidence of an anti-
inflammatory effect of the cherry juice.
While lower IL-6 values in the cherry juice group
are attributed here to an inflammatory effect others
have considered IL-6 as an anti-inflammatory cyto-
kine (Peters et al., 2001a; Steensberg et al., 2003;
Fischer et al., 2004). Infusion with recombinant hu-
man IL-6 has been shown to increase production of
IL-1ra and IL-10, which are both regarded as anti-
inflammatory cytokines (Steensberg et al., 2003).
Furthermore, prolonged (29 days) vitamin C
(500 mg/day) and vitamin E (400 IU/day) supplemen-
tation before concentric exercise (Fischer et al., 2004)
blunted the exercise-induced IL-6, IL-1ra and IL-10
responses. Of note this exercise did not induce eleva-
tions in CK activity and was not considered to have
caused muscle damage. High-dose vitamin C supple-
mentation (1500 mg/day) for 7 days before and 2
days following a 90 km run lowered the IL-1ra and
IL-10 responses and was interpreted as an attenua-
tion of the anti-inflammatory response (Peters et al.,
2001a). However, IL-6 values were not reported.
Furthermore, in an earlier study these authors
showed that vitamin C supplementation (1000 mg/
day) for 7 days before and 2 days following a 90 km
run resulted in an elevated CRP response compared
with a placebo which is consistent with a pro-inflam-
matory response (Peters et al., 2001b). The possibility
that IL-6 might be an anti-inflammatory cytokine
has caused some to question the benefit of a vitamin
supplementation regimen that blunts the normal IL-6
response because it might compromise the immune
system (Fischer et al., 2004). Neither IL-1ra or IL-10
were measured here so it is difficult to compare and
contrast the current results with these previous
studies. In the present study it is important to note
that in addition to having a blunted IL-6 response to
exercise the cherry juice group had a more rapid
recovery of knee extension strength compared with
placebo. The combination of improved function and
lower values for various blood markers (IL-6, CRP,
uric acid, TBARS) is consistent with an accelerated
recovery in the cherry juice group.
Elevations in uric acid after prolonged endurance
exercise have been shown consistently (Duthie et al.,
1990; Rokitzki et al., 1994; Kratz et al., 2002; Rønsen
et al., 2004), but the mechanism is not well under-
stood. Increased uric acid after Marathon running
may reflect (1) decreased clearance of uric acid,
secondary to dehydration (Suzuki et al., 2006), (2)
increased mobilization of uric acid as part of the
antioxidant defences (Mastaloudis et al., 2004;
Rietjens et al., 2007) or (3) increased production
of uric acid as part of the inflammatory process
(Kondo et al., 2005). Post-race weight loss was not
different between the cherry juice and placebo groups
(1.2 1.3 vs 1.7 1.5 kg, P50.49), therefore, it is
unlikely that the differences in uric acid were attri-
butable to dehydration effects. Previous studies have
attributed exercise-induced uric acid elevations to
antioxidant defence mechanisms (Mastaloudis
et al., 2004; Rietjens et al., 2007). Furthermore, uric
acid infusion has been shown to increase total anti-
oxidant capacity and decrease exercise-induced oxi-
dative stress (Waring et al., 2003). However, the
cherry juice group had an increased total antioxidant
capacity and decreased oxidative stress in the pre-
sence of lower uric acid levels compared with the
placebo group. Therefore, the uric acid changes in
response to running a Marathon were not reflective
of an enhanced antioxidant defence. A third inter-
pretation is that uric acid elevations reflected the
inflammatory response to running a Marathon. CRP
is correlated with uric acid in healthy subjects
(Kondo et al., 2005). In the present study detectable
levels of CRP were not evident until 24 and 48 h post-
Marathon. CRP at 24 and 48 h was correlated with
uric acid levels (r50.57, P50.009 and r50.45,
P50.048, respectively) lending some support to the
conclusion the uric acid elevations in response to
running a Marathon reflect the inflammatory re-
In previous studies TBARS were not elevated
immediately after or 24 h after a Marathon (Rokitzki
et al., 1994) or at any time point up to 5 days after a
half-Marathon (Duthie et al., 1990). In contrast,
TBARS (uMol/L)
Cherry Juice
Pre-race Post-race 24h
Fig. 6. Serum thiobarbituric acid reactive species (TBARS)
for the cherry juice and placebo groups before and following
Marathon running.
Significantly higher TBARS in the
placebo group at 48 h (Po0.05); values are mean SD
(n510 per group).
Cherry juice supplementation and Marathon running
following 3 weeks of multivitamin–mineral supple-
mentation an elevation in TBARS was reported in
the placebo, but not the treatment group, at 72 h
during a 7-day foot race (Marathon des Sables)
(Machefer et al., 2007). In the present study, TBARS
was not elevated immediately post-Marathon or at
24 h. However, at 48 h a marked increase in TBARS
was apparent in the placebo group but not in the
cherry juice group, which shows a similar response in
the elevation of TBARS following extended endur-
ance activity (Machefer et al., 2007). It is notable in
the present study that the increase in TBARS in the
placebo group occurred when total antioxidant ca-
pacity had fallen below baseline (89%). This indi-
cates that normal antioxidant defences may only be
effective at preventing oxidative stress up to 24 h after
Marathon running and that after that point an
augmentation in antioxidant capacity was required
to prevent oxidative stress. Consistent with this
summation, TAS at 48 h (percentage of baseline)
was negatively correlated (r50.49, P50.03) with
TBARS at 48 h (percentage of baseline).
While previous studies have measured changes in
TBARS as a marker of lipid peroxidation in response
to a half Marathon (Duthie et al., 1990), a Marathon
(Rokitzki et al., 1994) and an ultraendurance event
(Machefer et al., 2007) it is recognized that TBARS
lacks specificity (Urso & Clarkson, 2003). F
prostanes is perhaps a more specific marker of lipid
peroxidation that has been examined in ultramara-
thon events (Mastaloudis et al., 2004; McAnulty
et al., 2007). Antioxidant supplementation was
shown to reduce the elevation in F
after a 50 km race, but uric acid, CRP and IL-6
were unaffected by antioxidant supplementation
(Mastaloudis et al., 2004).
PC has been shown to be elevated after a 160 km
run (McAnulty et al., 2007), a soccer match (Ispirli-
dis et al., 2008) and a 30-min running (Bloomer et al.,
2006). Surprisingly, in this investigation, there was
no evidence of protein oxidation (based on PC data)
after the Marathon despite obvious signs of inflam-
mation and muscle damage.
The effects of the tart cherry juice on markers of
muscle damage, inflammation and oxidative stress
demonstrated in this study are most likely attribu-
table to the numerous different phytochemicals in
tart cherries that have been shown to have antiox-
idant and anti-inflammatory properties (Wang et al.,
1999; Seeram et al., 2001). The high-ORAC value for
the cherry juice (55 mmol/L Trolox equivalents)
compared with values reported for other available
juices (ranging from 31.7 to 9.1 mmol/L Trolox
equivalents) (Seeram et al., 2008) indirectly indicated
that the antioxidant phytochemicals in tart cherries
were unlikely to have been degraded by the proces-
sing and storage procedures, although it remains to
be determined if similar effect would be evident using
a concentrate.
Although it is likely that muscle damage, inflam-
mation and oxidative stress are important factors in
the adaptation process, minimizing these factors in
response to strenuous or prolonged exercise may be
important to the recovery process when subsequent
training and performance can be inhibited. For
example, the IL-6 response to the same bout of
exercise is more prolonged during a period of high-
intensity training compared with a period of low-
intensity training (Rønsen et al., 2001). Similarly, a
dramatic increase in training load to simulate over-
reaching was shown to increase TBARS in rats
(Zoppi & Macedo, 2008). Numerous studies have
examined the effects of various nutritional interven-
tions with antioxidants on markers of muscle da-
mage, inflammation and oxidative stress. While some
studies have demonstrated reductions in markers of
oxidative stress (Itoh et al., 2000; Mastaloudis et al.,
2004; Kingsley et al., 2005; Bloomer et al., 2006;
Machefer et al., 2007) and muscle damage (Rokitzki
et al., 1994; Itoh et al., 2000) other studies have
shown no effect on markers of oxidative stress
(Rokitzki et al., 1994; Kaikkonen et al., 1998; Daw-
son et al., 2002) or muscle damage (Kaikkonen et al.,
1998; Peters et al., 2001b; Dawson et al., 2002;
Kingsley et al., 2005; Mastaloudis et al., 2006;
Machefer et al., 2007). Additionally, antioxidant
interventions have generally shown to have little or
no positive effect with regards to elevations in mar-
kers of inflammation in response to prolonged run-
ning (Castell et al., 1997; Kaikkonen et al., 1998;
Peters et al., 2001b; Mastaloudis et al., 2004; Mache-
fer et al., 2007). However, reductions in neutrophilia
and IL-8 were evident following glutamine supple-
mentation (Castell & Newsholme, 1997) and vitamin
C supplementation was shown to decrease IL-6
following 90 min shuttle running (Thompson et al.,
2001), although there was no effect of vitamin C
supplementation on CRP, uric acid or markers of
muscle damage, and markers of oxidative stress were
not examined. In the present study clear reductions
in IL-6, CRP and uric acid were evident with the
cherry juice intervention. These findings have impor-
tant practical significance for distance runners con-
sidering that the inflammatory response to prolonged
endurance exercise (particularly IL-6) has been
linked to delayed recovery (Neubauer et al., 2008).
The 8-day supplementation period in this study is
markedly shorter than most investigations examining
the effects of dietary interventions on markers of
exercise stress. For example, reductions in markers of
oxidative stress and/or muscle damage following
ultraendurance running events (Mastaloudis et al.,
2004; Machefer et al., 2007), a Marathon race
(Rokitzki et al., 1994) or repeated days of running
Howatson et al.
(Itoh et al., 2000) occurred with 21–32 days supple-
mentation. The optimal dosage and supplementation
period for this cherry juice remains to be determined
but it is apparent that marked effects can be achieved
with a relatively short duration of supplementation.
In conclusion, when compared with a placebo,
cherry juice taken for 5 days before, the day of and
for 2 days after running a Marathon was effective at
accelerating recovery of strength, increasing total
antioxidant capacity, minimizing lipid peroxidation
and reducing IL-6, CRP and uric acid. This repre-
sents a broad spectrum of aiding recovery and
providing protection against the inflammation and
oxidative stress that is associated with prolonged
Various strategies are routinely used to accelerate
recovery following strenuous physical activity. Pre-
vious work (Connolly et al., 2006) has suggested that
tart cherry juice accelerates recovery following mus-
cle damaging exercise, which was speculated to be
attributable to the anti-inflammatory and antioxi-
dant phytochemicals contained within the juice. The
current investigation supports the supposition of
Connolly et al. (2006) and has demonstrated that
the cherry juice reduced oxidative stress and inflam-
mation and hence increases the rate of recovery. Tart
cherry juice appears to provide a feasible alternative
to pharmaceutical and therapeutic interventions in
aiding recovery following such exercise; in addition,
it may also prove useful where a number of strenuous
exercise bouts are required within a relatively short
period of time. Furthermore the marked reductions
in inflammation afforded by tart cherry juice may
also have implications for the management of other
clinical pathologies that display inherently high levels
of inflammation and oxidative stress, although this
remains to be elucidated.
Key words: recovery, inflammation, muscle damage,
antioxidants, Montmorency cherries.
The authors would like to thank the participants for their
commitment in completing this investigation. We would also
like to extend our gratitude to Julia Atkin, Dr. Lygeri
Dimitriou, John Eagle, Sarah Golding, Sunny Pottay, Louise
Ross and Natalie Ross for their valuable contributions on day
of the Marathon. We would also like to thank Dr. Marco
Cardinale from the British Olympic Association for procuring
technical support and St Mary’s University College Scholar-
ship and Research Support Fund for financial support of the
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Howatson et al.
... Importantly, studies concerning the antioxidant levels in U.S. grown Montmorency tart cherry extracts including juice demonstrate that processing and storage have minimal impact on antioxidant capacity [23]. This makes Montmorency tart cherries a useful source of antioxidants, and consumption on a regular basis may impact on oxidative damage and inflammatory processes [24]. As a source of these biologically active phytochemicals, tart cherry consumption may be of benefit to patients with chronic pain and other inflammatory diseases [24]. ...
... This makes Montmorency tart cherries a useful source of antioxidants, and consumption on a regular basis may impact on oxidative damage and inflammatory processes [24]. As a source of these biologically active phytochemicals, tart cherry consumption may be of benefit to patients with chronic pain and other inflammatory diseases [24]. Dietary interventions for patellofemoral pain have not received any attention in clinical literature, despite there being a growing body of evidence, indicating that cherries have significant antiinflammatory, antioxidant, and pain-mediating effects in musculoskeletal conditions [25][26][27]. ...
Full-text available
PURPOSE: This study aimed to explore the efficacy of U.S. Montmorency tart cherry in treating recreationally active individuals with patellofemoral pain. METHODS: Twenty-four recreationally active participants with patellofemoral pain were randomly separated into either placebo (males N = 8, females N = 4, age = 43.30 ± 7.86 yrs, mass = 72.10 ± 17.89 kg, stature = 171.16 ± 10.17, BMI = 24.31 ± 3.75 kg/m 2 , symptom duration = 30.18 ± 10.90) or Montmorency tart cherry (males N = 9, females N = 3, age = 41.75 ± 7.52 yrs, mass = 76.96 ± 16.64 kg, stature = 173.05 ± 7.63, BMI = 25.53 ± 4.03 kg/m 2 , symptom duration = 29.73 ± 11.88) groups. Both groups ingested 60 mL of either Montmorency tart cherry concentrate or taste matched placebo daily for 6-weeks. Measures of self-reported pain (KOOS PF), psychological wellbeing (COOP WONCA) and sleep quality (PSQI) alongside blood biomarkers (Creactive protein, uric acid, TNF alpha, creatinine and total antioxidant capacity) and knee biomechanics were quantified at baseline and 6-weeks. Differences between groups were examined using linear mixed effects models. RESULTS: There was 1 withdrawal in the cherry and 0 in the placebo group and no adverse events were noted in either condition. The placebo condition exhibited significant improvements (baseline = 67.90±16.18 & 6-weeks = 78.04±14.83) in KOOS PF scores compared to the tart cherry group (baseline = 67.28±12.55& 6-weeks = 67.55±20.61). No other statistically significant observations were observed. CONCLUSION: Tart cherry supplementation as specifically ingested in the current investigation, does not appear to be effective in mediating improvements in patellofemoral pain symptoms in recreationally active individuals.
... According to the results, short-term use of cherry juice supplement did not significantly change the total antioxidant capacity, hydrogen peroxide and creatine kinase in non-athletic men. Howatson et al (2010) showed that the average of antioxidant capacity increased by only 10% compared to control group in athletes. In addition, Su et al. (2008) reported that there was no reduction in total antioxidant capacity following by exhausting aerobic exercise (Su et al., 2008). ...
... In a study, Howatson et al. (2010) examined the consumption of cherry juice for 8 days on 20 Morton runners. The results showed aerobic exercises does not have an effect on the amount of creatine kinase in the blood. ...
Full-text available
Introduction: Oxidative stress is a condition in which the reactive oxygen species production exceeds the antioxidant system capacity to neutralize these peroxidases. In these situations, proteins, lipids, and nucleic acids are damaged. In this regard, the cherry can be noted as a food antioxidant which leads an increasing antioxidant capacity and reducing inflammation and damage muscle. Therefore, The purpose of this study was to determine the effect of cherry juice supplementation on total antioxidant capacity (TAC), creatine kinase (CK), hydrogen peroxide (H 2 O 2) in non-athlete men after an exhaustive aerobic exercise. Method: In this quasi-experimental research, ten untrained (UT) men were randomly selected. Then, they were divided into two equal groups: supplement group (cherry juice) and placebo group (commercial Cherry juice diluted with natural water). After eight days of supplementation period, all subjects were participated in aerobic exercise protocol (Bruce test run to the point of exhaustion) on the treadmill. Primary blood samples in the baseline were taken. The second was immediately after the Bruce test, third and fourth were six and twenty-four hours later were taken (5 ml). For analysis of the results. Analysis of variance with repeated measures was used at the significant level. Result: A significant effect of short-term cherry juice supplementation on TAC, H 2 O 2, and CK was observed (p≤0.05). Conclusions: In general, it can be concluded that probably eight days of cherry juice supplementation probably cannot prevent the adverse effects of oxidative stress caused by acute aerobic exercise.
... Physical activity that is novel, demanding, and high in volume often results in exercise-induced muscle damage (EIMD). 1 Eccentric muscle actions appear especially likely to induce damage. 1 Exercise of this nature may cause intracellular muscle damage, impair muscle function, lead to swelling and inflammation, and cause delayed onset muscle soreness (DOMS). 2,3 While the exact mechanisms of EIMD are unclear, both metabolic and mechanical pathways are likely contributory. 4 Tee et al. suggested that oxidative stress, a delayed inflammatory response, and impairment of excitation-contraction coupling represent a metabolic cascade resulting in EIMD. 4 Proske and Morgan described a mechanical pathway where sarcomere disruption occurs via high myofibrillar tension. ...
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Background Intense physical activity can result in exercise-induced muscle damage, delayed-onset muscle soreness, and decrements in performance. Phototherapy (PhT), sometimes referred to as photobiomodulation or low-level laser therapy, may enhance recovery from vigorous exercise. Purpose The purpose of this study was to assess the influence of phototherapy on functional movements (vertical jump, agility), and perceptions of muscle soreness following exercise-induced muscle damage caused by high volume sprinting and decelerations. Methods In a between-group design, 33 participants performed 40x15m sprints, a protocol intended to cause muscle damage. Immediately following sprinting and in the four days following, vertical jump and agility were assessed, as well as calf, hamstring, quadriceps, and overall perceptions of soreness. Sixteen subjects (age 20.6±1.6 yrs; BMI 25.8±4.6 kg.m-2) received PhT prior to testing each day, while 17 (age 20.8±1.3 yrs; BMI 26.2±4.5 kg.m-2) received sham PhT and served as a control (CON). Measurements were recorded during five days of recovery from the repeated sprint protocol, then compared to those recorded during three baseline days of familiarization. Area under the curve was calculated by summing all five scores, and comparing those values by condition via a two-tailed unpaired t-test for normally distributed data, and a two-tailed Mann-Whitney U test for nonparametric data (alpha level = 0.05). Results Calf soreness was lower in PhT compared to CON ( p = 0.02), but no other significant differences were observed between groups for vertical jump, agility, quadriceps, hamstring, and overall soreness ( p > 0.05). Discussion Phototherapy may attenuate soreness in some muscle groups following exercise-induced muscle damage, but may not enhance recovery after explosive, short-duration activities. Conclusion Phototherapy may not be a useful recovery tool for those participating in explosive, short-duration activities. Level of evidence 2c
... Strategies to attenuate inflammation after intense exercise regimens are becoming gradually popular. Dietary supplements with anti-inflammatory properties, such as turmeric, a derivative of curcuminoids, have been consumed for this purpose (Howatson et al., 2010). ...
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Dietary supplements are used to enrich the diet of athletes, and contribute to better adaptation on the part of athletes to their training, as well as quicker recovery from physical exercises. One such substance is turmeric, which has received widespread interest from medical, scientific and sports specialists due to its numerous benefits to human health and recovery. Curcumin is the most widely researched bioactive component of turmeric, but even curcumin-free turmeric is believed to be as effective as curcumin, and, therefore, this review concentrates on the effect of turmeric as a whole. Turmeric, also known as the 'golden spice', may help in the treatment of exercise-induced inflammation and muscle soreness, and, therefore, turmeric can enhance recovery in athletes. This current review focuses on the benefits of turmeric for athletes, including anti-inflammatory, antioxidant and muscle recovery activities exhibited by turmeric.
... Indeed, several studies have reported that supplementation with some anti-inflammatory substances is beneficial for attenuating exercise-induced muscle damage (EIMD) (D. Connolly, McHugh, & Padilla-Zakour, 2006;Howatson et al., 2010;Trombold, Barnes, Critchley, & Coyle, 2010), although some studies did not find such an effect (O'Fallon et al., 2012). ...
To quantify the effects of curcumin supplementation on exercise‐induced muscle damage, muscle soreness, inflammatory biomarkers, muscle strength, and joint flexibility via assessment of creatine kinase (CK), visual analogue scale (VAS) score, maximal voluntary contraction (MVC), and range of motion (ROM), respectively. Online databases, including PubMed, Google Scholar, and Scopus, were searched up to February 2021. RevMan® software (version 5.3) was used for assessing the risk of bias to assess the quality of studies. The mean differences (MD) and confidence intervals (95% CI) of CK activity (IU/L), VAS score, tumor necrosis factor (TNF‐α) (pg/ml), interleukin‐6 (IL‐6) (pg/ml), IL‐8 (pg/ml), MVC (nm) and ROM (degree) were pooled using a random‐ or fixed‐effect model. Between‐study heterogeneity was assessed using χ‐square or I2 statistic. Ten trials met the eligibility criteria and were included in the pooled analysis. Meta‐analysis showed that curcumin supplementation significantly reduced serum CK activity [WMD = −65.98 IU/L, 95% CI (−99.53 to −32.44)], muscle soreness [WMD = −0.56, 95% CI (−0.84 to −0.27)], and TNF‐α concentration [WMD = −0.22 pg/ml, 95% CI (−0.33 to −0.10)]. Also, curcumin supplementation elicited significant improvements in MVC [WMD = 3.10 nm, 95% CI (1.45–4.75)] and ROM [WMD = 6.49°, 95% CI (3.91–9.07)], although no significant changes in IL‐6 and IL‐8 levels were found. Dose–response analysis indicated that there is a significant non‐linear association between the daily dose and the final effect size regarding TNF‐α. Curcumin supplementation may improve some aspects of DOMS, including muscle damage, muscle soreness, inflammation, muscle strength, and joint flexibility. Further, well‐designed and high‐quality studies with larger sample sizes are needed to ascertain the long‐term effects and safety of curcumin supplementation.
... Montmorency tart cherries, blueberries, strawberries, cranberries, and blackcurrants [16] in particular have been shown to possess high levels of anthocyanins [17] although the majority of peer-reviewed literature has focused on tart cherries. Supplementation of anthocyanin-rich tart cherries has been shown to improve oxidative stress [18,19] and inflammation [19][20][21], and blackcurrant supplementation was also shown to enhance fat-oxidation rates [22]. Improved fat oxidation during rest and physical activity is linked to long-term changes in body mass and composition allied with improvements in insulin sensitivity [23]. ...
The current study aimed to investigate the influence of tart cherry and blueberry juices on cardiometabolic and other health indices following a 20-day supplementation period. Forty-five adults were randomly assigned to receive tart cherry, blueberry, or a placebo; of which they drank 60 mL per day for 20-days. The primary outcome; systolic blood pressure and secondary measures; anthropometric, energy expenditure, substrate oxidation, haematological, diastolic blood pressure/resting heart rate, psychological wellbeing and sleep efficacy were measured before and after the intervention. There were no statistically significant differences (P>0.05) for systolic blood pressure, however total and LDL cholesterol were significantly improved with blueberry intake (pre: total cholesterol=4.36mmol/L and LDL cholesterol=2.71mmol/L & post: total cholesterol=3.79mmol/L and LDL cholesterol=2.23mmol/L) compared to placebo (pre: total cholesterol=4.01mmol/L and LDL cholesterol=2.45mmol/L & post: total cholesterol=4.34mmol/L and LDL cholesterol=2.67mmol/L). Furthermore, psychological wellbeing indices measured using the Beck Depression Inventory, State Trait Anxiety Inventory and COOP WONCA improved statistically in the blueberry arm compared to placebo. Given the clear association between lipid concentrations and the risk of cardiovascular disease as well as the importance of psychological wellbeing to health-related quality of life, this investigation indicates that it could be a useful tool to help in managing cardiovascular diseases.
... More recently, Hooper and colleagues [105] found that daily intake of 500 mg/day of cherries can significantly reduce oxidative stress and markers of myocardial damage levels and central fatigue, by decreasing CK and creatine kinase amounts in cardiac muscle. In addition, the daily intake of 30 mL of their juice twice a day in trained men and women showed efficacy in improving recovery and reducing muscle soreness, IL-6, CRP, CK, uric acid, and TBARS concentrations [261,293,296,299,300]. Similar effects were observed at doses of 60, 100, and 240 mL/day [292,297,298,301]. ...
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In recent years, many efforts have been made to identify micronutrients or nutritional strategies capable of preventing, or at least, attenuating, exercise-induced muscle damage and oxidative stress, and improving athlete performance. The reason is that most exercises induce various changes in mitochondria and cellular cytosol that lead to the generation of reactive species and free radicals whose accumulation can be harmful to human health. Among them, supplementation with phenolic compounds seems to be a promising approach since their chemical structure, composed of catechol, pyrogallol, and methoxy groups, gives them remarkable health-promoting properties, such as the ability to suppress inflammatory processes, counteract oxidative damage, boost the immune system, and thus, reduce muscle soreness and accelerate recovery. Phenolic compounds have also already been shown to be effective in improving temporal performance and reducing psychological stress and fatigue. Therefore, the aim of this review is to summarize and discuss the current knowledge on the effects of dietary phenolics on physical performance and recovery in athletes and sports practitioners. Overall, the reports show that phenolics exert important benefits on exercise-induced muscle damage as well as play a biological/physiological role in improving physical performance.
Background Chronic inflammation has been classified as one of the most important threats to health. Scientists suggested that tart cherry (TC) can reduce plasma levels of inflammatory mediators. Therefore, the aim of this study was to summarize the effect of TC on circulating C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) among adult participants in non-exercise randomized clinical trials (RCTs). Methods and materials The eligible English-language RCTs were found by searching databases including PubMed, Web of Science, Cochrane Library, Scopus, and clinical up to May 2022, with no time limit. We used the mean change from baseline and its standard deviation for both intervention and comparison groups to calculate the effect size. The random-effects model proposed by DerSimonian and Laird was used to estimate the overall summary effect and the heterogeneity. We used PRISMA 2020 guidelines to report this study. Results Ten RCTs were included in this study. The results demonstrated that TC had a significant decreasing effect on plasma CRP level compared with the comparison group (weighted mean differences (WMD) = −0.55 mg/L; 95% confidence interval (CI): − 1.03, − 0.06; p = 0.029), but had no significant effect on plasma IL-6 compared with comparison group (WMD = 0.08 pg/mL; 95% CI: −0.02, 0.17; p = 0.10). The effect of TC consumption on plasma TNF-α level was evaluated in only three studies that showed no significant effects (p>0.05). Conclusion Our results confirmed a significant decreasing effect of TC on CRP. Regarding IL-6 and TNF-α, our study did not present any significant effect of TC.
Zur optimalen Sportlernahrung gibt es viele Ratgeber und Mythen. Braucht man wirklich Superfood? Was isst man nach dem Wettkampf? Wie sieht der Speiseplan nach dem Training aus? Und kann man mit der richtigen Auswahl der Nahrungsmittel die Regeneration unterstützen? Fragen über Fragen. Der Artikel gibt darauf Antworten.
Physical activity results in a series of proinflammatory reactions and innate immune responses, which occur postexercise. This is followed by antiinflammatory reactions that are critical for regeneration and healing. The severity of inflammation following exercise depends on the type, duration, and intensity of the exercise bout, as well as the training status of the individual. Interventions designed to reduce the inflammatory response following exercise may, in fact, be detrimental to adaptation, though they may positively impact performance and competition with short turnaround times. Although acute inflammation is critical for recovery, chronic inflammation—even low-grade systemic and tissue-specific simmering inflammation—appears to be a mechanism associated with the aging process and is related to many chronic diseases. It appears that regular, sustained physical activity, including endurance and resistance-type exercise, may provide a protective impact on chronic low-grade inflammatory conditions. General patterns of dietary intake and specific nutrients and other dietary constituents or supplements demonstrate promise for positively impacting this relationship. Many of the same cytokine and chemokine actors that are modulated by physical activity also are affected by diet. Many of the intercellular signaling systems modulated by physical activity are also regulated by various aspects of nutrition, including carbohydrate and fatty acid metabolism and oxidation. While much of the focus of this chapter is on exercise training among people at optimal ages for fitness, there are important and obvious implications for nonathletes across the lifespan, especially during childhood and among the elderly. Research into non-steroidal anti-inflammatory drugs also has implications for exploring the effect of diet in modulating inflammatory and immune responses in context of physical activity.
Participants in marathon races may require medical attention and the performance of laboratory assays. We report the changes in basic biochemical parameters, cardiac markers, CBC counts, and WBC differentials observed in participants in a marathon before, within 4 hours, and 24 hours after a race. The concentrations of glucose, total protein, albumin, uric acid, calcium, phosphorus, serum urea nitrogen, creatinine, bilirubin, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, total creatine kinase, creatine kinase-MB, myoglobin, and the anion gap were increased after the race, consistent with the effects of exertional rhabdomyolysis and hemolysis. The increase in WBC counts was due mainly to neutrophilia and monocytosis, with a relative decrease in circulating lymphocytes, consistent with an inflammatory reaction to tissue injury. A significant percentage of laboratory results were outside the standard reference ranges, indicating that modified reference ranges derived from marathon runners might be more appropriate for this population. We provide a table of modified reference ranges (or expected ranges) for basic biochemical, cardiac, and hematologic laboratory parameters for marathon runners.
Purpose: To compare the effects of two antioxidant formulas on biomarkers of oxidative stress before and after aerobic exercise. Methods: Aerobically trained men (N = 25) and women (N = 23) were assigned to one of three treatments: 400 IU of vitamin E + 1 g of vitamin C (V; N = 15), a fruit and vegetable juice powder concentrate (FV; N = 16), or a placebo (P; N = 17). Subjects ran for 30 min at 80% VO2max before, after 2 wk of supplementation, and after a 1-wk washout period. Blood samples were taken before and immediately after exercise and analyzed for protein carbonyls (PC), malondialdehyde (MDA), 8-hydroxydeoxyguanosine (8-OHdG), and vitamins C and E. Results: The V treatment increased plasma vitamin C and E after 2 wk (P <= 0.05), with no change in the FV or P. Postexercise PC values were elevated for all treatments after all exercise bouts (P < 0.0001). Both V and FV attenuated the exercise-induced increase in PC after 2 wk of supplementation (V = 21%, FV = 17%), and after the 1-wk washout (V = 13%, FV = 6%) compared with P (P < 0.05), with no differences between V and FV. MDA was unaffected by exercise and treatment. A treatment main effect for 8-OHdG was noted, with values for V lower than for FV and P (4.5 +/- 2.5, 5.5 +/- 2.7, and 6.0 +/- 2.5 ng(.)mL(-1), respectively; P = 0.0002). No exercise session or time main effect was noted for 8-OHdG, suggesting that the lower mean value for the V treatment group was not a result of the supplementation. Conclusion: These data suggest that V and FV supplementation for 2 wk can attenuate the rise in PC after 30 min of aerobic exercise, even after a 1-wk washout, without an impact on plasma MDA or 8-OHdG.
To test the effects of combined coenzyme Q10 (Q10) and d-α-tocopheryl acetate supplementation on exercise-induced oxidative stress and muscular damage we conducted a double-blind study in 37 moderately trained male marathon runners. These were randomly allocated to receive either an antioxidant cocktail: 90 mg of Q10 and 13.5 mg of d-α-tocopheryl acetate daily (18 men) or placebo (19 men) for three weeks before a marathon (42 km) run. Just before the run, plasma Q10 was 282% (p < 0.0001) and plasma vitamin E 16% (p < 0.007) higher in the supplemented group, than in the placebo group. Also the proportion of plasma ubiquinol of total Q10, an indication of plasma redox status in vivo, was significantly higher in the supplemented group. Furthermore, the susceptibility of the VLDL + LDL fraction, to copper-induced oxidation, was significantly reduced in the supplemented group, compared to the placebo group. The exercise increased lipid peroxidation significantly in both study groups, as assessed by the elevated proportion LDL- of LDL and the increased susceptibility of lipoproteins to copper induced oxidation. However, the supplementation had no effect on lipid peroxidation or on the muscular damage (increase in serum creatine kinase activity or in plasma lactate levels) induced by exhaustive exercise. Plasma ascorbate, Q10, whole blood glutathione and serum uric acid concentrations increased during the exercise, elevating significantly the TRAP value of plasma by 10.3% and the proportion of plasma ubiquinol of total Q10 by 4.9%. These results suggest that even though exercise increases plasma lipid peroxidation, it also elevates the antioxidative capacity of plasma, as assessed by the increased plasma TRAP and the proportion of Q10H2 of total Q10. However, prior supplementation with small doses of Q10 and d-α-tocopheryl acetate neither attenuates the oxidation of lipoproteins nor muscular damage induced by exhaustive exercise such as encountered in a marathon run.
: To study the effects of a single soccer game on indices of performance, muscle damage, and inflammation during a 6-day recovery period. : 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). : 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. : Twenty-four elite male soccer players (age, 20.1 +/- 0.8 years; height, 1.78 +/- 0.08 m; weight, 75.2 +/- 6.8 kg). : Muscle strength, vertical jumping, speed, DOMS, muscle swelling, leukocyte count, creatine kinase (CK), lactate dehydrogenase (LDH), C-reactive protein (CRP), cortisol, testosterone, cytokines IL-6 and IL-1b, thioburbituric acid-reactive substances (TBARS), protein carbnyls (PC), and uric acid (UA). : 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. : 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 indicate the need of sufficient recovery for elite soccer players after a game.
1. It has been suggested that the physiological consequences of strenuous exercise are analogous to those of the acute-phase response. 2. In 70 male and 20 female competitive distance runners, a marked, but transient, neutrophil leucocytosis occurred immediately after these athletes completed a standard (42 km) marathon race. Concomitant significant increases were noted in the plasma cortisol levels, creatine kinase activity, C-reactive protein level, total protein level and albumin level (P <0.01). 3. The plasma fibrinogen, C-reactive protein and total protein concentrations were markedly increased both 24 h and 48 h after exercise (P <0.01). The serum haptoglobin level was significantly decreased after exercise (P <0.01), and increased 48 h later (P <0.05). There was no change in the serum iron level, total iron-binding capacity, per cent saturation of transferrin and serum ferritin level. 4. A significant increase in interleukin-1-type activity was demonstrated immediately and 24 h after exercise (P <0.01). 5. It is concluded that the metabolic sequelae of sustained exercise are similar, but not analogous, to the acute-phase response, and interleukin-1 probably plays a significant role in linking the haematological and immunological changes observed after sustained strenuous exercise.
The relationship between prolonged exercise, oxidative stress, and the protective capacity of the antioxidant defense system has been determined. Venous blood samples were removed from seven trained athletes before and up to 120 h after completion of a half-marathon for measurements of blood antioxidants, antioxidant enzymes, and indices of lipid peroxidation. Plasma creatine kinase (CK) activity, an index of muscle damage, increased (P < 0.05) to a maximum 24 h after the race but this was not accompanied by changes in conjugated dienes and thiobarbituric acid reactive substances (TEARS), which are indices of lipid peroxidation. An increase (P < 0.05) in plasma cholesterol concentration (4%) immediately after the race was similar to the change in plasma volume (6%). However, transient increases (P < 0.05) immediately postrace in the plasma concentrations of uric acid (24%), vitamin A (18%), and vitamin C (34%) were only partly accounted for by the fluid shifts. The immediate postrace increases in α- and γ-tocopherol did not attain statistical significance. Erythrocyte antioxidant enzyme activities were unaffected by the exercise but the α- and γ-tocopherol concentrations progressively increased (P < 0.001 and P < 0.05, respectively) up to 48 h postrace. Paradoxically, 24 h after the race erythrocyte susceptibility to in vitro peroxidation was markedly elevated (P < 0.01). This enhanced susceptibility to peroxidation was maintained even at 120 h postrace and did not correspond to changes in the age of the red cell population. A decrease (P < 0.001) in total erythrocyte glutathione immediately after the half-marathon was mainly due to a reduction in the reduced form (GSH). The results show that when trained athletes run a comparatively short distance sufficient to result in some degree of muscle damage but which is insufficient to cause elevations in plasma indices of lipid peroxidation, significant alterations in erythrocyte antioxidant status do occur.
The aim of this study was to examine whether extreme endurance stress of trained athletes can influence lipid peroxidation and muscle enzymes. A randomized and placebo-controlled study was carried out on 24 trained long-distance runners who were substituted with alpha-tocopherol (400 I.U. d-1) and ascorbic acid (200 mg d-1) during 4.5 weeks prior to a marathon race. The serum concentrations of retinol, ascorbic acid, beta-carotene, alpha-tocopherol, malondialdehyde (TBARS) and uric acid as well as glutathione peroxidase (GSH Px) and catalase were measured 4.5 weeks before (A), immediately before (B), immediately after (C) and 24 h after (D) the course. After competition (C) TBARS serum concentrations of the athletes (n = 22) decreased in both groups (P < 0.0001). The ascorbic acid serum concentration increased significantly in the supplemented group from (A) to (B) (P < 0.01), from (B) to (C) (P < 0.001) and in the placebo group a significant increase from (B) to (C) (P < 0.01) was observed. The alpha-tocopherol serum concentration increased significantly in the supplemented group from (A) to (B) (P < 0.001) and from (B) to (C) (P < 0.05). The enzymes glutathione peroxidase (GSH Px) and catalase measured in erythrocytes as well as the serum selenium levels did not show significant differences at any time. A significant increase of CK concentration was observed from (C) to (D) in the supplemented group (P < 0.01) and in the placebo group (P < 0.001). The increase of CK serum concentration is remarkably lower in the supplemented group compared with the placebo group (P < 0.01). It is concluded that endurance training coupled with antioxidant vitamin supplementation reduces blood CK increase under exercise stress.
Strenuous exercise may be associated with immune suppression. However, the underlying mechanism is not known. A decrease in the plasma level of glutamine, which is utilised at a high rate by cells of the immune system, and an increase in the plasma level of some cytokines may impair immune functions such as lymphocyte proliferation after prolonged, exhaustive exercise. In two separate studies of the Brussels marathon, using similar protocols, the time course of the changes in the plasma concentrations of some amino acids (glutamine, glutamate, alanine, tryptophan and branched chain amino acids), acute phase proteins and cytokines (interleukins IL-1 alpha, IL-2, IL-6, tumour necrosis factor type a) was measured in male athletes. The numbers of circulating leucocytes and lymphocytes were also measured. Amino acid and cytokine concentrations have not previously been measured concomitantly in marathon runners; the measurement of some of these parameters the morning after the marathon (16 h) is novel. Another novel feature is the provision of glutamine versus placebo to marathon runners participating in the second study. In both studies the plasma concentrations of glutamine, alanine and branched chain amino acids were decreased immediately after and 1 h after the marathon. Plasma concentrations of all amino acids returned to pre-exercise levels by 16 h after exercise. The plasma concentration of the complement anaphylotoxin C5a increased to abnormal levels after the marathon, presumably due to tissue damage activating the complement system. There was also an increase in plasma C-reactive protein 16 h after the marathon. The plasma levels of IL-1 alpha were unaffected by the exercise, while that of IL-2 was increased 16 h after exercise. Plasma IL-6 was increased markedly (approximately 45-fold) immediately after and at 1 h after exercise. Neopterine, a macrophage activation marker, was significantly increased post-exercise. There was a marked leucocytosis immediately after the marathon, which returned to normal 16 h later. At the same time there was a decrease in the number of T-lymphocytes, which was further reduced within 1 h to below pre-exercise levels. Glutamine supplementation, as administered in the second study, did not appear to have an effect upon lymphocyte distribution.