ArticlePDF AvailableLiterature Review

The role of cherries in health and exercise: A review

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  • Nicholas Institute of Sports Medicine and Athletic Trauma Lenox Hill Hospital

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Recently, cherries and cherry products have received growing attention within the literature with regards to their application in both exercise and clinical paradigms. Reported to be high in anti-inflammatory and anti-oxidative capacity, cherries and their constituents are proposed to provide a similar, but natural alternative akin to over-the-counter non-steroidal anti-inflammatory drugs (NSAID’s) or analgesics. Within exercise paradigms, concern has been raised with regards to the use of products which inhibit such inflammatory or oxidative actions, due to the possibility of the blunting of physiological training adaptations. Despite this, numerous scenarios exist both within exercise and clinical populations where a goal of optimal recovery time is more important than physiological adaptation. This review critically evaluates and discusses the use of cherries as a supplementation strategy to enhance recovery of muscle function, inhibit exercise-induced inflammation, oxidative stress and pain primarily; furthermore the potential application of cherries to clinical populations is discussed
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Review
The role of cherries in exercise and health
P. G. Bell1, M. P. McHugh2, E. Stevenson1, G. Howatson1,3
1Department of Sport, Exercise and Rehabilitation, Faculty of Health and Life Sciences, Northumbria University, Newcastle upon
Tyne, UK, 2Nicholas Institute of Sports Medicine and Athletic Trauma, Lenox Hill Hospital, New York, New York, USA, 3Water
Research Group, School of Environmental Sciences and Development, Northwest University, Potchefstroom, South Africa
Corresponding author: Glyn Howatson, PhD, Faculty of Health and Life Sciences, Northumbria University, Northumberland Building,
Newcastle upon Tyne NE1 8ST, UK. Tel: +44 (0)191 243 7018, Fax: +44 (0)191 227 4713, E-mail: glyn.howatson@northumbria.ac.uk
Accepted for publication 26 April 2013
Recently, cherries and cherry products have received
growing attention within the literature with regard to
their application in both exercise and clinical paradigms.
Reported to be high in anti-inflammatory and anti-
oxidative capacity, cherries and their constituents are
proposed to provide a similar but natural alternative
akin to over-the-counter non-steroidal anti-inflammatory
drugs (NSAIDs) or analgesics. Within exercise para-
digms, concern has been raised with regard to the use of
products, which inhibit such inflammatory or oxidative
actions, because of the possibility of the blunting of
physiological training adaptations. Despite this, numer-
ous scenarios exist both within exercise and clinical
populations where a goal of optimal recovery time is
more important than physiological adaptation. This
review critically evaluates and discusses the use of cher-
ries as a supplementation strategy to enhance recovery of
muscle function, inhibit exercise-induced inflammation,
oxidative stress, and pain primarily; furthermore, the
potential application of cherries to clinical populations is
discussed.
Research into supplementation with “functional foods”
in health and exercise science has gained momentum in
recent years. Beetroot juice (Bailey et al., 2009, 2010;
Ferreira & Behnke, 2010; Vanhatalo et al., 2010;
Lansley et al., 2011a,b), purple sweet potatoes (Chang
et al., 2007, 2010), blueberries (Sanchez-Moreno et al.,
2008; McAnulty et al., 2011), pomegranate juice
(Trombold et al., 2010, 2011), green tea (Eichenberger
et al., 2010; Jowko et al., 2011), lychee extract
(Nishizawa et al., 2011; Kang et al., 2012), and cherries
(Connolly et al., 2006; Ducharme et al., 2009; Howatson
et al., 2010, 2011a, b; Kuehl et al., 2010; Bowtell et al.,
2011) have received varying degrees of attention in rela-
tion to their purported applications. The last of these,
cherries, have provided several avenues for research
because of the high levels of bioactive compounds
present within them and have been compared favorably
with other functional foods. More specifically, both
sweet and tart cherries contribute to dietary fiber intake
and contain high levels of antioxidants such as melato-
nin, carotenoids, hydroxycinnamates, and several fla-
vonoid groups including anthocyanins, as well as the
flavonol quercetin (McCune et al., 2011). Bioavailability
of these potent phytochemicals has been shown to differ
depending upon food source and dose (Manach et al.,
2005). Reports suggest that quercetin metabolites have a
slow elimination rate, with half-lives ranging from 11 to
28 h reported, and as a result, plasma accumulation may
be possible with multiple doses (Manach et al., 2005).
Conversely, anthocyanins are rapidly absorbed with poor
efficiency and are quickly eliminated (Manach et al.,
2005). Although it has been suggested that anthocyanins
may be efficiently absorbed into the gastrointestinal tract
tissue efficiently, with the subsequent transport into the
circulation being the point at which overall dose effi-
ciency decreases (Wallace, 2011). Additionally, the food
matrix and gut microflora may also play a significant
role in the metabolism, absorption, and subsequent bio-
availability of anthocyanins (Manach et al., 2005;
Wallace, 2011). A detailed review has recently been pro-
vided by McCune et al. (2011) outlining specific nutri-
tional properties of cherries.
Such antioxidants have been demonstrated to be: (a)
proficient in the reduction of cell damaging oxidative
stress (Wang et al., 1997, 1998, 1999; Boyle et al., 2000;
Bitsch et al., 2004; de Boer et al., 2005; Traustadottir
et al., 2009); (b) high in anti-inflammatory capacity
(Howatson et al., 2010; Kelley et al., 2006; Seeram
et al., 2001); and (c) inhibit uric acid production (Jacob
et al., 2003), which, although is a powerful antioxidant,
is also implicated in the development of gouty arthritis
(Schlesinger & Schlesinger, 2012; Zhang et al., 2012;
Kelley et al., 2013). Resultantly, cherries have been
implicated in their use as a natural nutritional supplement
Scand J Med Sci Sports 2013: ••: ••–••
doi: 10.1111/sms.12085
© 2013 John Wiley & Sons A/S.
Published by John Wiley & Sons Ltd
1
for the treatment of chronic inflammatory and hemato-
logical diseases, cancer, cardiovascular disease, and dia-
betes. To date, only a single clinical trial (Schumacher
et al., 2011) has been conducted to support such implica-
tions; however, several anecdotal reports dating back as
early as 1950 have promoted cherry supplementation in
the treatment of chronic inflammatory disease (Blau,
1950; Jacob et al., 2003; Schlesinger & Schlesinger,
2012; Kelley et al., 2013).
While cherry supplementation has received attention
for its application in clinical populations (Jacob et al.,
2003; Kang et al., 2003; Kim et al., 2005; Kelley et al.,
2006; Traustadottir et al., 2009; Pigeon et al., 2010;
Howatson et al., 2011a, b), a growing body of research
has investigated its use within the exercise domain. The
ability to recover quickly and efficiently after exercise is
important to athletes, and as a result, several interven-
tions have been investigated within the literature.
Reports have suggested that both tart Montmorency and
sweet cherries reduce inflammation (Kelley et al., 2006;
Howatson et al., 2010). Meanwhile, oxidative stress,
muscle soreness, and improved recovery of muscle func-
tion have been demonstrated using the tart Montmorency
cherry cultivar, each of which are desirable to the
exercising/recovering athlete (Connolly et al., 2006;
Ducharme et al., 2009; Traustadottir et al., 2009;
Howatson et al., 2010; Kuehl et al., 2010; Bowtell et al.,
2011). Concerns have been raised with regard to inhib-
iting inflammation and oxidative stress because of the
possible blunting of adaptive responses after antioxidant
supplementation (Gomez-Cabrera et al., 2005, 2006,
2008a). The cited studies used vitamin C or allopurinol
supplementation to blunt oxidative stress using human
(Gomez-Cabrera et al., 2006) and/or animal cohorts
(Gomez-Cabrera et al., 2005, 2008b); however, there is a
lack of evidence demonstrating attenuated adaptation
using cherry or any other functional food products. In
support of this notion, Yfanti et al. (2010) demonstrated
that 12 weeks of vitamin C and E supplementation had
no negative effects upon adaptations to endurance train-
ing. Additionally, polyphenols have also been suggested
to enhance adaptation in animal models, where
resveratrol-fed rats showed an ~21% improvement in
endurance performance (Dolinsky et al., 2012). A recent
review with regard to antioxidant supplementation and
adaptation has suggested that despite a number of studies
demonstrating attenuated oxidative stress, implications
upon exercise-induced muscle damage and performance
have not been consistently demonstrated (Peternelj &
Coombes, 2011). Lastly, there are several scenarios
where optimal recovery is more important than physi-
ological adaptation, e.g., tournament scenarios, where
the ability to perform on a daily basis may be required.
The focus of this review is to evaluate research evidence
of cherries and their derivatives within exercise para-
digms and its potential applications in clinical
populations.
Muscle function
Disruption of the structures in exercising muscle leads to
a cascade of events resulting in impaired muscular func-
tion (Proske & Morgan, 2001). Eccentric muscle actions,
particularly prominent in downhill running (Eston et al.,
1996), plyometrics (Byrne & Eston, 2002a, b), and mul-
tiple repeat sprint-based exercise (Thompson et al.,
1999; Twist & Eston, 2005; Howatson & Milak, 2009)
are accepted as the source of mechanical stress that
causes primary muscle damage (Proske & Morgan,
2001; Howatson & van Someren, 2007; Howatson et al.,
2007; Cockburn et al., 2008) and the subsequent second-
ary inflammatory cascade and impaired muscle function
(Howatson & van Someren, 2008). Connolly et al.
(2006) was the first to investigate the application of
cherry juice supplementation in a damaging exercise
model. The supplementation consisted of freshly pre-
pared tart Montmorency cherry juice mixed with apple
juice in a proprietary ratio, with each serving containing
~50–60 tart cherries. In a single blind crossover design,
participants completed 9 days of supplementation span-
ning 4 days pre-exercise on the day of exercise and 4
days post-exercise, consuming two 237-ml servings per
day (am/pm). In the 96 h following eccentrically biased
contractions of the elbow flexors, maximal isometric
strength loss was attenuated with the tart Montmorency
cherry juice blend vs placebo (4% vs 22%); conse-
quently, recovery was accelerated with the tart Mont-
morency cherry juice blend. Furthermore, recent
research supported these findings using a similar study
design with a damaging bout of knee extensor exercise;
Bowtell et al. (2011) reported faster recovery of isoki-
netic knee extensor force when supplementing with a tart
Montmorency cherry juice concentrate vs isoenergetic
placebo. Creatine kinase (CK) showed a trend to be
raised in the placebo trial when compared to cherries,
although this did not reach statistical significance. Simi-
larly, Ducharme et al. (2009) found trends of increased
post-exercise muscle damage indices in horses. In the
days following an exhaustive exercise test, horses
supplemented with tart Montmorency cherry juice blend
showed lower values of CK in comparison to a placebo
(P=0.054), although only six horses were used in this
crossover design. A secondary muscle damage biomar-
ker (aspartate aminotransferase, AST) showed treatment
effects, whereby the tart Montmorency cherry juice
supplementation resulted in less AST activity during
both exercise and recovery periods.
Despite the three previously mentioned studies pro-
viding positive results in relation to attenuated muscle
damage, caution should be used when interpreting these
data. Each study utilized a crossover design where the
protocol was repeated in the second trial. Crossover
studies using eccentric exercise are subject to repeated
bout effect, whereby a protective effect is shown on
subsequent bouts of damaging exercise following just a
Bell et al.
2
single bout of damaging exercise (Newham et al., 1987;
Nosaka et al., 1991; McHugh et al., 1999; McHugh,
2003; Howatson et al., 2007), thereby confounding
results in subsequent trials. The Connolly et al. (2006)
and Bowtell et al. (2011) studies have attempted to
resolve the issue associated with the repeated bout effect
through the use of the contralateral limb. However,
recent work has indicated that a contralateral repeated
bout effect may be present (Howatson & van Someren,
2007; Starbuck & Eston, 2011) in which the adaptive
effect is carried over to the non-exercising limb, albeit
to a lesser extent. Despite this, the use of randomized
or counterbalanced treatment order in these studies
could conceivably wash out any potential contralateral
repeated bout effects. As a result, the findings of these
studies suggest efficacy in the use of tart Montmorency
cherry juice for reducing muscle damage symptoms.
Like the aforementioned research, improvements
in isometric strength recovery have been found follow-
ing marathon running after consumption of tart
Montmorency cherry juice supplementation vs placebo
(Howatson et al., 2010). Using a placebo-controlled,
independent groups design, other muscle damage
indices, delayed onset of muscle soreness (DOMS), CK,
and lactate dehydrodgenase (LDH) were not different
between conditions. However, although there are
acknowledged limitations in determining the magnitude
of damage from CK measures, similar to the aforemen-
tioned studies, a trend toward lower CK values was
apparent in the tart Montmorency cherry juice group. For
example, peak CK values at 24 h post-exercise showed a
21% lower value for tart Montmorency cherry juice vs
placebo (2227 IU/L vs 2814 IU/L). High levels of inter-
individual variability of CK have been reported, with the
causes of the variability being explained by inherent high
and low responders, muscle fiber composition, and size
and training status (Brancaccio et al., 2007). Subse-
quently, it is unsurprising that significant differences in
CK between groups or conditions within the cherry
supplementation literature have not been found, with
high data scedasticity and only a small number of studies
conducted in the field.
It is unlikely that that cherry juice exerts its protective
effect through directly impacting upon the primary
mechanical stress caused during exercise. Mechanical
damage caused through eccentric muscle actions are
thought to cause so-called sarcomere “popping”
(Morgan, 1990) due to excessive strain and sarcomere
inhomogeneities (Julian & Morgan, 1979). As a result,
the function of affected sarcomeres is compromised and
a cascade of events takes place, leading to secondary
damage. Additionally, post-exercise maximum voluntary
contraction is generally the same, suggesting that
primary damage alone is not responsible for perfor-
mance decrement. This is demonstrated by Howatson
et al. (2010) and Bowtell et al. (2011), following mara-
thon running and eccentric knee extensor exercise,
respectively, who showed strength loss was not different
between cherry juice and placebo treatments in the
immediate post-exercise period. However, subsequent
recovery of strength was more rapid with the cherry juice
treatments (Howatson et al., 2010; Bowtell et al., 2011).
These results point to protection against the secondary
damage response. The bioactive food components of
cherry juice do not provide any rationale for the preven-
tion of the initial primary damage, and more relevance
should be placed upon secondary damage in the form of
oxidative stress and inflammation. Circulating reactive
oxygen/nitrogen species (RONS), resulting from exer-
cise, theoretically may cause oxidative damage to
muscle cell membranes (Girotti, 1985) providing a
vehicle for the leakage of intracellular proteins and
membrane-bound proteins to be attacked by RONS
(Powers & Jackson, 2008). Although there is a lack of
conclusive evidence for any direct interaction of antioxi-
dants with cell membranes, reducing the magnitude of
oxidative stress and inflammation through antioxidant
supplementation may attenuate the proteolytic and
lipolytic response, lowering the subsequent secondary
inflammatory cascade. However, it has been postulated
that fat-soluble antioxidants may stabilize muscle mem-
branes via their action with membrane phospholipids
(Van Der Meulen et al., 1997). Vitamin E has been sug-
gested to protect against membrane damage following a
reduced serum CK response to exercise in rats (Van Der
Meulen et al., 1997; McGinley et al., 2009), although
conversely, it has been speculated that lipid peroxidation
does not contribute to muscle membrane damage
(Warren et al., 1992).
Oxidative stress
Increasing the bioavailability of antioxidants through
cherry ingestion could be desirable in preventing oxida-
tive damage from RONS, commonly referred to as free
radicals. RONS are produced endogenously as a result
of biological metabolism and may also be brought
into the body through exogenous sources such as
smoking (Valavanidis et al., 2009). Exercise increases
the endogenous production of RONS above resting
levels, altering the cellular pro-oxidative : antioxidative
ratio (Gomez-Cabrera et al., 2006) or redox balance.
Disruptions in redox balance can result in altered cell
signaling (Powers & Jackson, 2008; Powers et al., 2010),
degradation of cellular performance (Powers & Jackson,
2008; Powers et al., 2010; McAnulty et al., 2011), and as
aresult,causeadecrementinphysicalperformance
(Vollaard et al., 2005; Hillman et al., 2012). Conse-
quently, when RONS outweigh the antioxidative capac-
ity of an organism, free radical species attack lipids,
proteins, and DNA, challenging the functionality and
structural integrity of these materials (Wang et al.,
1999). Additionally, RONS have been implicated in the
fatigue of muscle because of decreased myofibrillar
Cherries, exercise, recovery, and health
3
calcium sensitivity (Lamb & Westerblad, 2011) and may
impact upon muscle glucose uptake (Bashan et al., 2009;
Merry et al., 2009). It has been postulated, however, that
a moderate increase in oxidative stress (i.e., an increase
in pro-oxidative : antioxidative ratio) is beneficial to the
exercising muscle, although excessive levels might
reduce muscle function (Reid et al., 1993; Andrade
et al., 1998; Reid, 2001). Reid et al. (1993) demonstrated
increased muscular twitch force in rat diaphragm muscle
through increasing oxidative stress, while increased anti-
oxidant infusion significantly decreased twitch charac-
teristics. Further work by Andrade et al. (1998) supports
this, with findings showing increased force of mouse
muscle fibers following brief exposure to oxidative
stress. In the same report, it was found that prolonged
exposure to a pro-oxidative environment resulted in pro-
gressive decline in force output (Andrade et al., 1998).
Despite research suggesting that cellular damage from
oxidative stress only occurs when exercise is exhaustive
(Gomez-Cabrera et al., 2006), others have demonstrated
increased biomarkers indicative of damage, following
high-intensity (Powers & Jackson, 2008; Bowtell et al.,
2011) or prolonged duration exercise (Powers &
Jackson, 2008; Howatson et al., 2010); hence, attenuat-
ing such damage with antioxidant supplementation has
received attention in the literature (Gomez-Cabrera
et al., 2006; Powers & Jackson, 2008).
Ducharme et al. (2009) was the first to investigate the
effects of cherry juice supplementation upon indices of
oxidative stress, following damaging exercise in thor-
oughbred horses. The exhaustive treadmill exercise
increased plasma thiobarbituric acid reactive species
(TBARS), a measure of lipid peroxidation. While there
were significant elevations in TBARS indicating oxida-
tive stress, there were no differences between tart Mont-
morency cherry juice and placebo conditions. TBARS
have been criticized as a measure of lipid peroxidation
because it lacks specificity in human studies (Urso &
Clarkson, 2003), as the assay also reacts with both satu-
rated and unsaturated non-functional aldehydes, carbo-
hydrates, and prostaglandins (Alessio, 2000).
The first human study to examine the influence of
cherry juice on oxidative stress and inflammatory vari-
ables after exercise-induced damage was carried out by
Howatson et al. (2010). Oxidative stress was induced via
both mechanical and metabolic pathways through the
completion of a marathon. Participants who were
supplemented twice per day for 120 h prior to and 48 h
post-marathon with tart Montmorency cherry juice
showed significantly lower levels of TBARS than
their placebo-fed counterparts at 48 h post-marathon
(21.4 mmol/L vs 30.2 mmol/L). Interestingly, plasma
total antioxidative status (TAS), a measure encompass-
ing all biological components with antioxidant activity
(Randox, 2013), of the placebo group fell below baseline
measures at 48 h, suggesting that the maintained TAS
(and, hence, redox balance) of the cherry juice group
may have contributed to staving off any associated oxi-
dative stress. Protein carbonyls (PC), a marker of protein
oxidation, showed no significant elevation above pre-
exercise levels in either group following the marathon
run. Oxidative stress was also measured by Bowtell et al.
(2011) following tart Montmorency cherry juice supple-
mentation; although, in contrast to Howatson et al.
(2010), the exercise protocol used in this study placed a
relatively low metabolic cost (eccentric exercise) on par-
ticipants. Following eccentrically biased knee exten-
sions, participants given tart Montmorency cherry juice
showed a trend (P=0.079) of lower levels of PC 24-h
post-exercise (Bowtell et al., 2011). Although this
finding provides limited support for the antioxidative
actions of tart Montmorency cherry juice, the use of PC
as a measure of oxidative stress in in vivo human studies
has been criticized as unreliable, non-specific, and,
whether it represents a good marker of protein oxidation
in exercise paradigms, is somewhat controversial (Urso
& Clarkson, 2003). Carbonyl groups are formed when
RONS attack protein side chains (Dalle-Donne et al.,
2003) and amino acids (Urso & Clarkson, 2003);
however, the formation of such groups is not restricted to
protein structures. Carbonyl groups may also be formed
with protein through secondary reactions with aldehydes
produced during lipid peroxidation (Dalle-Donne et al.,
2003), making it difficult to discriminate between the
sources of oxidative damage through the measure of
protein carbonyls alone.
Interestingly, tart Montmorency cherry juice supple-
mentation for 14 days has been applied in a non-
exercising ischemia/reperfusion (I/R) model that was
used to initiate acute oxidative stress (Traustadottir
et al., 2009). Following I/R, oxidative stress (plasma
F2-isoprostanes) was attenuated in the tart Montmorency
cherry juice condition compared to a placebo. F2-
isoprostanes are considered the “gold standard” measure
(Michel et al., 2008) of lipid peroxidation when ana-
lyzed by liquid chromatography mass spectrometry. No
differences between baseline measures of F2-isprostanes
were found after the 14-day loading phase of tart
Montmorency cherry juice or placebo, suggesting that
cherries had no impact upon basal F2-isoprostane levels.
Additional measures showed lowered basal levels
urinary 8-oxo-2-deoxyguanosine and 8-oxo-guanine
(markers of DNA and RNAoxidation, respectively) after
tart Montmorency cherry juice consumption. Three sug-
gestions were proposed to explain how the phytonutri-
ents in tart Montmorency cherry juice may exert their
protective effects: (a) direct free radical scavenging; (b)
formation of cyaniding–DNA complexes resistive to oxi-
dative damage; and (c) the activation of protective xeno-
biotic responses (Traustadottir et al., 2009). The direct
neutralization of free radicals by cherry anthocyanins is
possible; however, the absorption of anthocyanins from
other foods has been shown to be poor (Bitsch et al.,
2004; Charron et al., 2007; Charron et al., 2009), with
Bell et al.
4
fast clearance (Felgines et al., 2003; Kurilich et al.,
2005; Traustadottir et al., 2009). However, the dose-
response of tart Montmorency cherry anthocyanins has
yet to be elucidated, so this explanation remains a pos-
sibility. The formation of cyanidin-DNA complexes
resistive to oxidative damage is a second theory
(Traustadottir et al., 2009), although this mechanism
does not account for any changes in lipid peroxidation or
protein oxidation, meaning a further mechanism may be
possible. Third, the activation of xenobiotic responses,
up-regulating the expression of endogenous antioxi-
dants, may be responsible for the protective effects (Shih
et al., 2007; Traustadottir et al., 2009). Finally, a syner-
gistic effect of all three theories remains a possibility.
The mechanism by which cherries exert their protec-
tive effect against oxidative stress is unclear and requires
further investigation. However, it is apparent that the role
of cherries in attenuating oxidative stress does not appear
to be selective to the type of oxidative stress caused by
the exercise mode (mechanical or metabolic challenges),
although the methods used to assess these indices in the
aforementioned studies have limitations. Conceivably,
the pathway for mechanical and metabolic oxidative
stress may be different; however, this has yet to be estab-
lished as no exercise study using a purely metabolically
challenging protocol has been conducted.
Inflammation
The use of an antioxidant supplementation strategy to
limit inflammation after exercise may be a desirable
outcome in order to maintain muscular function and
attenuate pain. However, the pro-inflammatory response
to exercise and its implication on resulting protein syn-
thesis and subsequent adaptation remains a point of con-
jecture (Trappe et al., 2002; Krentz et al., 2008). In the
acute phase, it has been proposed that protein fractional
synthesis rate (FSR) may be attenuated through the
down-regulation of the inflammatory cascade associated
with stressful exercise (Trappe et al., 2002), although it
has been demonstrated in elderly participants that
non-steroidal anti-inflammatory drugs (NSAID) admin-
istration does not affect muscle protein synthesis rate
following low-grade inflammation (Petersen et al.,
2011). Chronically, Krentz et al. (2008) demonstrated
that muscle hypertrophy was not inhibited through
NSAID ingestion over a 6-week training study, whereas
a review by Schoenfeld (2012) stated that long-term
NSAID use may be detrimental to hypertrophy.
Alternatively, pro-inflammatory cytokines have been
proposed as inhibitors of protein synthesis (Caiozzo
et al., 1996; Frost et al., 1997) and, as such, may play a
negative role in recovery from damaging bouts of exer-
cise. Nemet et al. (2002) demonstrated attenuated
plasma levels of insulin-like growth factor-1 (IGF-1) in
adolescents following a single intense exercise session.
Additionally, increases in inflammatory cytokines
interleukin-6 (IL-6), tumor necrosis alpha (TNF-a), and
interleukin-1-beta (IL-1b) were found. These findings
suggest a reduced anabolic environment in the presence
of inflammatory cytokines in the early stage of training
(Nemet et al., 2002). Conversely, however, it has been
postulated that increases in systemic inflammation and
oxidative stress are necessary for gaining the beneficial
physiological adaptations to training or exercise
(Trappe et al., 2002; Soltow et al., 2006; Gomez-Cabrera
et al., 2006, 2008a, b; Powers et al., 2011). Soltow
et al. (2006) demonstrated reduced hypertrophy of 50%
in overload trained rats with 14 days of NSAID admin-
istration. Nevertheless, there are numerous sporting
paradigms where adaptation is not important and the
critical element is to facilitate recovery and, hence,
the ability to compete in subsequent competition and
training.
An in vitro study identified cherry anthocyanins as
being inhibitors of cyclooxygenase-1 and -2 (COX-1,
COX-2) activity (Seeram et al., 2001). Inhibition of
COX-2 is believed to be mainly responsible for anti-
inflammatory actions (Masferrer et al., 1994) and has
been shown to dampen the inflammatory response within
skeletal muscle (Bondesen et al., 2004). Sweet cherry,
Balaton tart cherry, and Montmorency tart cherry antho-
cyanins were shown to reduce COX-2 activity by 47.4%,
38.3%, and 36.6%, respectively, which was similar to the
actions of the NSAIDs ibuprofen and naproxen that
showed reductions in COX-2 activity of 39.8% and
41.3%, respectively (Bondesen et al., 2004). Subse-
quently, research has focused on the effects of cherries
and their anthocyanins on inflammation in vivo.
Several studies have investigated the impact of cherry
supplementation on inflammatory responses to exercise.
In Ducharme et al.’s (2009) study on horses, serum
amyloid A (SAA), an indicator of inflammation, showed
no differences between tart Montmorency cherry juice
and placebo-supplemented groups. However, overall
SAA was only marginally elevated by the exercise inter-
vention, so SAA may not be a good marker of equine
exercise-induced inflammation. In horses, SAA is typi-
cally used as a marker of inflammation secondary to
infection (Pepys et al., 1989). Moreover, markers of
muscle damage showed great variation among horses,
making it increasingly unlikely that significant differ-
ences would be found within the secondary inflamma-
tory response. Further to this, horses were not
supplemented throughout the recovery period where the
secondary inflammatory and oxidative stress variables
are likely to be greatest. Additionally, the repeated bout
effect (McHugh et al., 1999; McHugh, 2003; Howatson
et al., 2007; Howatson & van Someren, 2007) may have
influenced the results due to the crossover design of the
protocol.
Using human participants, Howatson et al. (2010)
demonstrated attenuation in inflammatory variables fol-
lowing marathon running using tart Montmorency
Cherries, exercise, recovery, and health
5
cherry juice supplementation. IL-6 and C-reactive
protein (CRP) were both significantly reduced with tart
Montmorency cherry juice vs placebo consumption.
Serum IL-6 showed immediately post-race values of
41.8 pg/mL vs 82.1 pg/mL, and CRP was reported to be
lower at 24 and 48 h in tart Montmorency cherry juice-
fed participants (see Fig. 1).
Bowtell et al. (2011) were unable to detect any effects
of tart Montmorency cherry juice concentrate on high
sensitivity CRP (hsCRP) following eccentrically biased
knee extensions. The protocol did not significantly
elevate hsCRP from baseline, although the authors did
report a tendency for hsCRP to be higher in the placebo
group in the hours following the exercise protocol. Kelley
et al. (2006) showed decreases in circulating plasma
levels of hsCRPusing healthy participants supplementing
their diets with Bing sweet cherries. Reductions of 8%
and 25% were found for CRP following 14 and 28 days of
supplementation (280 g/day), respectively. Further evi-
dence for the anti-inflammatory actions of cherries was
provided by Jacob et al. (2003), who showed trends of
decreased circulating CRP in healthy women following
two servings (280 g each) of Bing sweet cherries. These
early results provide a good evidence base for further
research into the anti-inflammatory actions of cherries
and their constituent anthocyanins.
Pain
In the hours and days following intense physical activity,
muscular pain is regularly reported in exercise tasks that
are heavily eccentric biased. Following these types of
exercise task, muscular pain has been shown to increase
in the following 24–96 h, with peak muscle soreness
(DOMS) usually occurring at 24–48 h (Semark et al.,
1999; Marginson et al., 2005; Twist & Eston, 2005;
Twist et al., 2008; Davies et al., 2009). The origin of
what causes pain is not established; however, it is con-
ceivable that it is related to inflammation of the sur-
rounding area (Howatson & van Someren, 2008). Cherry
anthocyanins were first shown to inhibit pain by Tall
et al. (2004). Using anthocyanins extracted from Balaton
tart cherries, inflammation-induced pain, as measured by
thermal hyperalgesia, mechanical hyperalgesia, and paw
edema was significantly suppressed in rats when com-
pared to a control saline solution. Results showed that
the administration of Balaton tart cherry anthocyanins
provided similar pain inhibiting effects as indomethacin
(NSAID). These findings in an animal model provided
a template for the future work conducted in human
populations.
Several aforementioned studies reported pain scores
following supplementation with cherry juice. Connolly
et al. (2006) reported that the development of pain in the
elbow flexors was significantly attenuated in a tart Mont-
morency cherry juice supplemented trial vs a placebo,
assessed using a visual analog scale (VAS) with scores
averaged over 96 h. Additionally, peak pain scores
occurred at 24 h in the cherry juice trial as opposed to
48 h in the placebo trial. In contrast to VAS results,
pressure pain threshold (PPT) was not found to be dif-
ferent between cherry juice and placebo groups. The
PPT results from Bowtell et al.’s (2011) study showed a
trend towards lowered pain following tart Montmorency
cherry juice supplementation vs a placebo, although the
results did not reach significance 48 h after exercise.
Further research conducted by Kuehl et al. (2010) pro-
vided support for the analgesic effects of tart Mont-
morency cherry juice. Participants completed a distance
running event (average distance completed 26.3 km) and
those supplemented with tart Montmorency cherry juice
blend provided significantly lower pain (VAS) following
the race, although it should be noted that the time
between completing the run and pain assessment was not
standard across participants due to the relay-based nature
of the race. No further measurements of pain were taken
by the authors, which may have provided further evi-
dence for pain relief, given that the onset of post-exercise
inflammation and subsequent peak of pain would be
unlikely to have manifested until 24–48 h post-exercise.
IL-6 (pg/mL)
Pre-
supplement
Pre-race Post-race
Time
24 h 48 h Pre-
supplement
Pre-race
*
*
*
Post-race
Time
24 h 48 h
140
Cherry juice
Placebo
Cherry juice
Placebo
120
100
80
60
40
20
0
CRP (mg/L)
40
35
30
25
20
15
10
5
0
Fig. 1. Serum interleukin (IL)-6 and C-reactive protein (CRP) concentrations for tart Montmorency cherry juice and placebo groups
following marathon running (taken from Howatson et al., 2010).
Bell et al.
6
Conversely, Howatson et al. (2010) reported no differ-
ence in pain scores between tart Montmorency cherry
juice and placebo groups up to 48-h post-marathon
running. The inconsistent results between these studies
immediately after exercise seem surprising given the
similarity in exercise task and participant demographic.
Given the results of these aforementioned studies, it
appears there may be a beneficial effect of cherry juice
and cherry anthocyanins on post-exercise pain. However,
results are not consistent in the literature currently avail-
able, leaving scope for further research to investigate
both analgesic effects of cherries and the possible
mechanistic cause of any effects.
Dosage strategies
The majority of research into cherry supplementation
has provided positive findings; however, there appears to
be little rationale provided for the dosing strategies
employed in the literature. In human exercise studies,
dosing strategies range from 7 days pre-exercise through
to 4 days post-exercise inclusive; and in animal studies
up to 14 days of pre-exercise dosing has been used
(Ducharme et al., 2009). Non-exercising studies have
used longer loading phases, implementing up to 28 days
(Kelley et al., 2006) of cherry or cherry analog consump-
tion (Table 1). Although efficacy has been demonstrated
using a range of dosing strategies, it would seem prudent
to identify an optimal strategy in order to confidently
prescribe supplementation.
The pharmacokinetic nature of cherry anthocyanins
has yet to be elucidated; however, dose–response studies
of other functional food anthocyanins have shown low
bioavailability (Bitsch et al., 2004; Manach et al., 2005;
Charron et al., 2009), as shown by limited absorbance
efficiency recovery of <0.05% (Charron et al., 2009) and
rapid excretion (Kurilich et al., 2005; Hollands et al.,
2008). Timings of systemic anthocyanin concentration
appear to be consistent across these studies, with peaks
in plasma concentrations being reported at 1.5–2 h post
dose despite differences in dose volume and anthocyanin
magnitude. Additionally, the clearance of systemic
anthocyanins appears to be fast, with returns to baseline
values typically occurring by 8-h post-dose. Charron
et al. (2009) suggested the dose volume range (76–
380 mmol) of anthocyanins provided in their study
may be reasonable, given previous work showed antho-
cyanin absorption mechanisms to be saturated at higher
amounts (Kurilich et al., 2005). It must be noted,
however, that findings from these papers might not be
generalizable to all plant or food stuffs containing antho-
cyanins as bioavailability and metabolism may be
affected by the plant matrix (Charron et al., 2009). It is
unclear whether there is biological storage of anthocya-
nins, although it has been suggested that due to the
discovery of anthocyanin metabolites in 24-h urine
samples (Felgines et al., 2003), there may be potential
for some minor tissue accumulation (Kay et al., 2004). A
further complication with regard to anthocyanins bio-
availability is the influence of microbiota during trans-
port in the large intestine. Flavonoids have been
suggested to be degraded to low-molecular-weight aro-
matic compounds through the actions of colonic micro-
biota (Serra et al., 2012). Such effects could make
assessment of anthocyanins bioavailability troublesome
as such compounds may exhibit variance with regard to
metabolism and systemic bioavailability.
The bioavailability of cherry anthocyanins may
impact upon dosing strategy for optimizing recovery
from exercise. If the high RONS scavenging ability of
anthocyanins (Wang et al., 1999; Seeram et al., 2001;
Ducharme et al., 2009) is responsible for the protective
effects of cherries, it would be reasonable to suggest that
a dosing strategy resulting in optimal systemic anthocya-
nin concentration at the point of peak oxidative stress
would be appropriate. However, if cherry anthocyanins
have pharmacokinetic properties similar to other foods,
it would mean supplementing ~2 h prior to exercise,
possibly interfering with dietary routines and raising the
potential for gastrointestinal distress during exercise. At
the very least, a period of supplementation-exercise
habituation would be recommended prior to embarking
on such a dosage strategy. Despite this, Howatson et al.
(2010) reported significant increases in total antioxidant
status (TAS) following 5 days (2 times per day) of pre-
exercise supplementation, in conjunction with decreased
inflammation, oxidative stress, and faster recovery of
isometric strength, suggesting this dosing strategy is
appropriate prior to exercise. However, this measure
does not discriminate between antioxidants, so the sys-
temic level of anthocyanins may not have been optimal.
Additionally, dosing continued for 2 days post exercise,
making it difficult to differentiate between the effects of
the cherry supplement pre- and post-exercise.
As previously discussed, the ability of anthocyanins to
form cyanidin–DNA complexes resistive to oxidative
damage and/or the activation of xenobiotic responses has
been proposed as mechanism for the protective effects of
cherries (Kong et al., 2003; Sarma & Sharma, 1999;
Traustadottir et al., 2009). The time-course for the for-
mation of cyanidin-DNA complexes has not been
reported in human studies; however, an in vitro study has
shown that 1 min following the mixing of anthocyanins
(cyanidin) with calf thymus DNA (ctDNA), oxidative
stress was diminished (Sarma & Sharma, 1999) when
compared with anthocyanins or ctDNA alone. Similarly,
the activation of xenobiotic responses has not been
assessed through human in vivo study, although Shih
et al. (2007) showed that treating rat liver cells with
anthocyanins for 24 h increased the cells’ expression of
endogenous antioxidants.
The mechanism by which cherries exert their protec-
tive effects is still unclear, and as a result, it is difficult
to definitively prescribe a dosage strategy. Regarding
Cherries, exercise, recovery, and health
7
Table 1. Summary of human and animal studies investigating the effects of supplementation with cherry or cherry products
Authors Participant cohort Exercise Supplement type Supplementation
strategy
Change in
antioxidant status
Muscle damage/
function/pain
Inflammation Oxidative
stress
Tall et al. (2004) 32 male rats N/A Tart cherry anthocyanins
(400 mg/kg)
3 days pre Not reported Pain (thermal
hyperalgesia)N/A N/A
Connolly et al.
(2006)
14 male students 2 ¥20 maximum eccentric
elbow flexions
Tart cherry juice blended
with apple juice (12 fl oz,
2/day)
4 days pre,
4 days post
Not reported Iso strength
recovery
Pain*
N/A N/A
Kelley et al.
(2006)
18 healthy
volunteers (16
female, 2 male)
N/A Bing sweet cherries
(280 g/day)
28 days Not reported N/A CRP* N/A
Ducharme et al.
(2009)
6 horses Stepwise incremental
treadmill test until horses
unable to maintain speed
Tart cherry juice blend
(1.42 L/day)
14 days pre Not reported AST* N/A N/A
Traustadottir
et al. (2009)
12 volunteers
(6 male, 6 female)
Pre-supplement and post
supplement
Ischemia/Reperfusion
(3 ¥10 min ischemia using
blood pressure cuff inflated
to 200 mm Hg, with 2 min
reperfusion of upper arm)
Tart cherry juice blend
(240 mL, 2/day)
14 days pre Not reported N/A N/A F2-isoprostane
response to I/Ra
Howatson et al.
(2010)
20 recreational
marathon runners
(13 male, 7 female)
Marathon Tart cherry juice blend
(8 fl oz, 2/day)
5 days pre,
2 days post
TASIso strength
recovery* IL-6CRP
Uric acid*TBARS*
Kuehl et al.
(2010)
54 healthy runners
(36 male, 18 female)
Running (mean
26.3 !2.5 km over 2 days)
Tart cherry juice mixed with
apple juice in propriatary
ratio (355 mL)
7 days pre Not reported VAS painN/A N/A
Bowtell et al.
(2011)
10 well-trained
males
10 ¥10 single-leg–knee
extensions at 80% 1 RM,
with elongated eccentric
phase
Tart cherry juice (30 mL,
2/day)
7 days pre,
2 days post
No difference MVC recovery* N/A PC*
*P<0.05.
P<0.01.
P<0.001.
AST, asparate aminotransferase; CRP, C-reactive protein; IL-6, interleukin 6; I/R, ischemia-reperfusion; MVC,maximum voluntary contraction; N/A, not applicable; PC, protein carbonyl; TBARS, thiobarbituric acid reactive
species; VAS, visual analog scale.
Bell et al.
8
dosage volume, bioavailability studies suggest anthocya-
nin volume per supplement should not exceed 380 mmol
(322.7 mg) due to diminishing efficiency in absorbance
(Charron et al., 2007; Charron et al., 2009). In relation to
the frequency and timing of dosage, it appears likely that
supplementation should begin at some point prior to
exercise; although in exercise studies, it is unclear as to
whether pre or post exercise dosing alone would provide
any differences in results. Furthermore, it has not been
established as to whether multiple doses are necessary to
gain the same beneficial effects. Additionally, the above
speculation requires cherry anthocyanins to act as per
other functional food anthocyanins, which has yet to be
confirmed. Clearly, further work is warranted to identify
an optimal dosing strategy to gain the beneficial effects
of cherries. Despite this, cherry supplementation has
showed a degree of efficacy in all exercise and recovery
paradigms regardless of loading phase or post-exercise
dosing. It remains to be elucidated whether such pro-
longed phases are necessary to gain the beneficial effects
associated.
Clinical application
The anti-inflammatory and antioxidative capacity of
cherries has led to focus on supplementation for a
number of pathologies. Inflammation and oxidative
stress is associated with numerous pathologies such as
cancer, cardiovascular disease, diabetes (McCune et al.,
2011), arthritis (Wang et al., 1999), and acceleration of
the aging process (Golden et al., 2002; Vollaard et al.,
2005; McAnulty et al., 2011). Cherries compare favor-
ably with other functional foods in terms of anthocyanin
(Table 2) and antioxidative capacity (Fig. 2), and as a
result, increasing exogenous antioxidant availability
through cherry consumption has become of interest to
researchers investigating methods of reducing inflamma-
tion and oxidative stress in clinical populations.
Tart Montmorency cherry juice has been suggested as
a benefit for those suffering from chronic inflammatory
diseases such as osteoarthritis (Schumacher et al., 2011).
Recent data from Schumacher et al. (2011) demonstrated
significant reductions of the inflammatory marker CRP
in patients diagnosed with osteoarthritis given twice
daily servings of tart cherries. In association with this,
participants reported lower scores of pain and WOMAC
(Western Ontario and McMaster Universities Arthritis
Index). Whole Bing sweet cherries have been shown to
lower systemic plasma urate concentration (Jacob et al.,
Table 2. Anthocyanin concentration of various fruit juices [adapted from
Clifford (2000)]
Food Anthocyanin content (mg/L)
Montmorency tart cherry juice 9117 (Biosciences 2010)
Blackberry 1150
Blueberry 825–4200
Grape (Red) 300–7500
Sweet cherry 20–4500
Strawberry 150–350
Cranberry 600–2000
0
10
20
30
40
50
60
Pomegranate
juice
Red
wine
Concord
grape juice
Blueberry
juice
Black
cherry juice
Tart cherry
juice
Acai juice Cranberry
juice
Orange
juice
Apple
juice
Iced green
tea
ORAC (µmol of TE/mL)
Bevera
g
e
Fig. 2. Comparison of antioxidant status of fruit juice beverages as assessed through oxygen radical absorbance capacity [ORAC;
values sourced from Seeram et al. (2008) and Howatson et al. (2010)].
Cherries, exercise, recovery, and health
9
2003), suggesting the incidence of gout may be reduced.
Gout occurs as the result of crystallization of uric acid in
joints, causing tenderness, swelling, and pain in the asso-
ciated areas. In this study, asymptomatic participants
consumed a single dose of 280 g of whole Bing sweet
cherries. Results showed significantly lower measures of
plasma urate 5-h post-dose following Bing sweet cherry
consumption, although the observed mean decrease of
14.5% maintained values in the normal range expected
within humans (Jacob et al., 2003). Additionally, trends
of lowered CRP were found; however, they did not reach
statistical significance. Supporting this, Kelley et al.
(2006) showed that following multiple dosages (280 g/
day for 28 days) of Bing sweet cherries lowered circu-
lating levels of CRP. These early findings provide a
foundation for further research into gout using symptom-
atic participants. It is conceivable to expect that using a
concentrated tart Montmorency cherry juice supplement
may be of greater benefit due to the higher concentration
of anthocyanins present.
Recent work has shown further positive results for
cherry supplementation in the management of sleep
(Pigeon et al., 2010; Howatson et al., 2011a). Chronic
sleep disruption has been associated with the stimula-
tion of inflammatory responses (Irwin et al., 2008) and
may increase the risk of several chronic disorders such
as atherosclerosis, diabetes mellitus, Crohn’s disease,
and rheumatoid arthritis (Walsh et al., 2011). More
recently, Cohen et al. (2009) found that adults reporting
sleep of less than 7 h per night were approximately three
times more likely to develop symptoms of upper respi-
ratory tract infections. Furthermore, despite the knowl-
edge of disturbed sleep impairing both physical
(Mougin et al., 1991) and mental performance (Alhola
& Polo-Kantola, 2007), sleep is often overlooked in its
contribution to recovery and recuperation (Halson,
2008). Additionally, studies have found reductions in
endurance exercise performance following one night of
sleep deprivation (Oliver et al., 2009), and associations
between over-reached soccer players and sleep quality
have also been established (Brink et al., 2012). With
regard to cherries, in addition to their high anti-
inflammatory and antioxidative capacity, tart Mont-
morency cherries contain high quantities of melatonin
(Burkhardt et al., 2001), a compound associated heavily
with regulation of the sleep–wake cycle (Hughes et al.,
1998). Howatson et al. (2011a) showed significant
increases in total sleep time, sleep efficiency and time in
bed in tart Montmorency cherry juice fed asymptomatic
participants. These results support the findings of
Pigeon et al. (2010) who, following anecdotal reports of
improved sleep during an unrelated tart Montmorency
cherry juice study (Connolly et al., 2006), conducted a
pilot study supplementing insomniacs with a tart Mont-
morency cherry juice blend. The authors reported
improvements in insomnia severity with tart Mont-
morency cherry juice compared to a placebo group,
although the effect sizes were reported as “modest.” The
application of improved sleep spans a range of sce-
narios, including shift workers, insomniacs, time-zone
travelers, and those suffering from disturbed sleep.
These initial studies provide foundation for further work
to be conducted investigating the use of cherries as a
sleep regulator.
Perspectives
Cherries and their constituents have received growing
attention for application in sport and exercise and other
potential clinical populations; the beneficial effects
appear promising and are supported with a growing body
of evidence regarding its efficacy. The food science,
animal, and human literature currently available clearly
demonstrates the anti-inflammatory and antioxidative
effects of cherries. The research suggests that there are
benefits of cherry consumption in enhancing recovery
from exercise and sleep regulation and lends itself well
to further investigation into numerous clinical scenarios.
Currently, the mechanisms of action are somewhat
speculative with regard to recovery from exercise, and as
a result, confident prescription of the optimal supple-
mentation strategy is troublesome, although efficacy for
a loading phase has been established. Despite this, no
negative effects of supplementation with cherries have
been reported. As a result, the use of any of the dosing
strategies in the reviewed papers may be deemed appro-
priate, although there is conjecture regarding the
manipulation of the stress responses to exercise (inflam-
mation and oxidative stress), with a suggestion that
adaptation may be blunted as a result of down-regulating
the stress response (Gomez-Cabrera et al., 2005, 2006,
2008b). However, it should be noted that such negative
adaptive effects have not been reported in cherry studies
or any other functional foods and perhaps warrant
further investigation. It should also be noted that the
specific compounds responsible for any beneficial
effects of cherry juice may not be limited to anthocya-
nins and their metabolites. As discussed, quercetin has
also been implicated in antioxidative actions and should
therefore not be forgotten in the future study of cherries.
In summary, cherries appear to provide an efficacious
option for assisting with recovery from damaging bouts
of exercise. Possibly of greater importance is the poten-
tial for application within clinical pathologies. In par-
ticular, chronic inflammatory conditions where the
option of natural remedies may be more desirable than
the use of pharmacological interventions such as
NSAIDs, although research is required prior to prescrip-
tion of such a strategy.
Key words: recovery, muscle function, antioxidants,
inflammation, oxidative stress, Montmorency tart
cherries.
Bell et al.
10
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... Tart cherry has also been investigated for its health benefits in clinical trials associated with cardiovascular disease, muscle recovery, sleep quality, and osteoarthritis [14][15][16][17][18]. In addition to these reported health benefits, tart cherry juice has been shown to decrease biomarkers of inflammation, such as high sensitivity C-reactive protein (hsCRP), as well as indicators of oxidative stress such as thiobarbituric acid reactive species (TBARS) [15,[19][20][21][22][23]. ...
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