Tart Cherry Supplementation for Muscle Recovery

BSc(Hons)Sport & Exercise Science Ryan Till
66-6920-00L-A-20145 Project 22008862
Faculty of Health and Wellbeing Sheffield Hallam University
Page 1
Table of Contents
Acknowledgements ..................................................................................................................... 3
Abstract ...................................................................................................................................... 3
CHAPTER 1: Introduction .......................................................................................................... 4-5
CHAPTER 2: Literature Review..................................................................................................4-16
2.1 The causes of Muscle Damage which results in DOMS............................................................... 4
2.2 Mechanically Induced Muscle Damage..................................................................................... 5
2.3 Metabolically Induced Muscle Damage..................................................................................... 6
2.4 Tart Cherries Mechanism of Action .......................................................................................... 7
2.5 Clinical Practice to Sport Science.............................................................................................. 7
2.6 The Effects of Tart Cherries on Muscular Performance .............................................................. 8
2.7 The Effects of Tart Cherries on Muscle Damage ........................................................................ 9
2.8 Inflammation.........................................................................................................................10
2.9 Oxidative Stress .....................................................................................................................12
2.10 Perceived Muscle Soreness...................................................................................................13
2.11 Dosage Strategy...................................................................................................................14
2.12 Participants..........................................................................................................................15
2.13 Hypothesis...........................................................................................................................16
CHAPTER 3: Methods.............................................................................................................17-21
3.1 Participants ...........................................................................................................................17
3.2 Experimental Design...............................................................................................................17
3.3 Nutritional Supplements.........................................................................................................17
3.4 Experimental Protocol............................................................................................................18
3.5 VAS Questionnaire.................................................................................................................19
3.6 Serum CK Blood Analysis ........................................................................................................20
3.7 Isokinetic Dynamometer.........................................................................................................20
3.8 Data Collection/Analysis.........................................................................................................20
CHAPTER 4: Results................................................................................................................22-26
4.1 Delayed Onset Muscle Soreness..............................................................................................22
4.2 Maximum Voluntary Contraction............................................................................................24
4.3 Creatine Kinase......................................................................................................................25
CHAPTER 5: Discussion...........................................................................................................26-33
5.1 Functional Recovery...............................................................................................................26
5.2 Perceived Muscle Soreness.....................................................................................................30

66-6920-00L-A-20145 Project 22008862
Page 2
5.3 Limitations.............................................................................................................................31
CHAPTER 6: Conclusion ...............................................................................................................33
CHAPTER 7: References..........................................................................................................34-40
APPENDICES 1. Progress Record Form ..........................................................................................41
2. Participant Information Sheet ..............................................................................43
3. Medical Health Questionnaire...............................................................................46
4. Informed Consent Form........................................................................................49
5. VASQuestionnaire ……………………………………………………………………………………………….. 50
6. Risk Assessment Form..........................................................................................52
7. EthicsForms ……….……………………………………………………………………..………………………… 55

66-6920-00L-A-20145 Project 22008862
Page 3
The effects of tart cherry supplementation on muscle damage, muscle force regeneration and
perceived muscle soreness in untrained males and females following isokinetic dynamometry
i. Acknowledgments
I would like to thank the participants who actively engaged in the present study. I also wish to
extend my gratitude to Sheffield Hallam University, for the use of their laboratory facilities and
to the physiology laboratory technicians for their technical support during the investigation.
Finally I would like to thank Dr Mark Hopkins for academic support and guidance throughout
the course of the project.
ii. Abstract
Background: Tart cherries phytochemical content namely, anthocyanins and flavonoids elicit
potent antioxidant and anti-inflammatory effects. By increasing antioxidant defence systems
and reducing inflammation it’s believed we can accelerate muscle function recovery and
reduce perceived pain following exercise induced muscle damage. Objective: previous
research into tart cherries have shown positive effects in speeding up the recovery process in
well-trained/recreationally active individuals. Therefore, we aimed to investigate whether these
effects would be identical when tested using untrained participants. Methods: 6 untrained
participants completed two trials, consisting of 5 sets of 12 maximal eccentric hamstring
contractions on an isokinetic dynamometer (60⁰-secˉ¹).Trials were separated by a 6 day wash
out period. Participants consumed each supplement (Cherry Active or Cherry Cordial) 5 days
pre, on the day and 2 days post. CK was measured before and 48 hours post-exercise, MVC
was measured before, after and 48 hour post-exercise whilst a VAS was given before, after
and 24-72 hours post-exercise. Results: No significant differences were seen between
conditions on measures of CK or MVC, but clear trends of reduced CK and accelerated force
regeneration were seen in the tart cherry group 48 hours post exercise. CK: (78% vs 340% of
pre-ex values, MVC: (91% vs 80% of pre-ex values). Perceived soreness of the hamstring
group was significantly reduced in the tart cherry condition, compared to the placebo (P =
0.045) whilst there was also a significant time*condition interaction effect (P = 0.006).
Conclusion: The consumption of 2 tart cherry drinks per day (~90-100 cherries) decreased
perceived muscle soreness and identified trends of reduced muscle damage (CK) and
accelerated muscle force recovery in untrained participants which may be due to the
phytochemical content of cherries reducing oxidative stress and tissue damage whilst blunting
the inflammatory response to muscle damage and exercise. Keywords: Maximum Voluntary
Contraction (MVC), Creatine Kinase (CK), Visual Analog Scale (VAS).

66-6920-00L-A-20145 Project 22008862
Page 4
1. Introduction
Delayed onset muscle soreness is prevalent throughout each extreme of the performance
pyramid with both well trained and novice performers experiencing the delayed soreness post
exercise bout (Cheung et al. 2003). Whilst it’s difficult to obtain statistics on the incidence of
delayed onset musclesoreness due to the majority of individuals not seeking medical attention
(Kedlaya, 2014) it is however, more prevalent following eccentric exercise (Cheung et al.
2003).
Exercise induced muscle damage following an unaccustomed bout of exercise is caused by
inadequately conditioned skeletal muscle which leads to injury within the muscle fibres;
typically after a bout of eccentric exercise(Armstrong et al. 1991). The structuraldamage often
results in pain or soreness, which has been termed Delayed Onset Muscle Soreness (DOMS)
(Kuipers, 2008). Delayed onset muscle soreness results in a loss of contractile force (Hamlin
and Quigley, 2001) which may be due to the loss of Creatine Kinase (CK) and the release of
inflammatory enzymes (Haramizu et al. 2011). Other consequences of DOMS include
negative impacts on performance due to impaired motor control, negatively impacting sense
of position, co-ordination and as a result performance (Serinken et al. 2013) whilst muscle
glycogen storage is reduced in muscles damaged through eccentric exercise when compared
to limbs not exercised (Costill et al. 1990).
DOMS is suggested to be caused by the inflammation response to muscle damage and can
last for up to 96 hours, with levels of soreness suggested to peak by 48 hours (Connolly et al.
2003). The hypothesis used to explain the formation of muscle damage has been attributed to
either mechanical or metabolic causes (Armstrong et al. 1991, Tee et al. 2007, Kuipers, 2008,
Penailillo et al. 2013). The mechanical cause has being more widely accepted but neither
hypothesis has been characterised sufficiently (Tee et al. 2007). The mechanical cause of
muscle damage attributes the structural damage to high tension contractions which cause the
myofibril to tear and calcium to flood into the tissue causing inflammation (Morgan and Proske,
2004). The metabolic cause of muscle damage on the other hand, suggests muscle damage
occurs from a cascade of events whereby adenosine triphosphate (ATP) and glycogen stores
are depleted leaving muscles morevulnerable to mechanicalmuscledamage whilst also being
exposed to greater Reactive Oxygen Species (ROS) which scavenge electrons from local
tissues which cause muscle damage (Tee et al. 2007).
Supplementation with functional foods has become increasingly popular due to evidence
indicating that such food or supplements may speed up the recovery process (Bell et al.
2014a). Cherries have lately been of debate on their effectiveness on a variety of conditions
from enhanced sleep through elevating melatonin (Howatson et al. 2012), to inflammation

66-6920-00L-A-20145 Project 22008862
Page 5
conditions of the body’s tissue (Jacob et al. 2003, Kelley et al. 2006; Kelley et al. 2013). Tart
cherries are of interest due to their high antioxidant content and anti-inflammatory properties.
Wang et al. (1999), identified cherries had similar antioxidant activity to commercial
antioxidants and had greater anti-inflammatory effects than aspirin. It is proposed that tart
cherry supplementation blunts the primary and secondary response to muscle damage
associated with inflammation, following the initial onset of muscle damage suspected to be
caused by the previously discussed mechanical and metabolic processes; whilst improving
antioxidant defence systems to neutralise Reactive Oxygen Species (ROS)(Bell et al. 2014b).
Previous research using tart cherry supplementation has found beneficial effects on DOMS
following long distance running (Kuehl et al. 2010) and muscle force regeneration following
eccentric resistance training (Connolly et al. 2006; Bowtell et al. 2011) .
However, no study currently exists which focuses specifically on the effects of tart cherry
supplementation on untrained subjects. As a result, these positive results may have been
found because the participants were accustomed and protected from the damage of eccentric
contractions due to, regular training causing adaptations in sarcomere lengths (Morgan and
Proske, 2004). Furthermore, it is important to focus on untrained individuals for numerous
reasons such as; pain being a common barrier to exercise and causing avoidance behaviour
(Letham et al. 1983; Dalle-Grave et al. 2010) and the poorer antioxidant defence system in
inactive individuals (Kruk, 2011). Therefore, this study aims at investigating whether tart cherry
supplementation produces desirable effects on; subjective ratings of musclesoreness,muscle
force regeneration and CK markers of muscle damage in an untrained population, following
unaccustomed eccentric exercise in the lower extremities.
2. Literature Review
2.1 The causes of muscle damage which results in DOMS.
Muscle damage and inflammation, connective tissue damage, lactic acid accumulation and
enzyme efflux theories are the potential mechanisms which cause DOMS (Cheung et al.
2003). However, theories such as the lactic acid accumulation have found limited success in
explaining DOMS, whilst it’s generally accepted muscle damage is the main cause of DOMS,
but a combination of all theories may best explain DOMS (Gulick and Kimura, 1996). As briefly
discussed structural damage of the muscle fibre, which commonly occurs following a bout of
eccentric exercise causes the formation of pain 1-5 days post exercise (Armstrong, 1984)
which may be due to the inflammation phase of musclerecovery (Liu et al. 2006). The process
in which muscle damage occurs has been associated with both mechanical and metabolic
stress models which are outlined below.

66-6920-00L-A-20145 Project 22008862
Page 6
2.2. Mechanically induced muscle damage
Mechanically induced muscledamage occurs due to musclefibres weakening. Human motion
consists of two types of contractions which co-exists; these include eccentric contractions and
concentric contractions (Tee et al. 2007). Therefore, when exercise is manipulated to be
completely eccentric it is no surprise muscle damage is observed as it’s been demonstrated
several or single bouts of eccentric contractions result in micro-injury (Cheung et al. 2003)
caused by the stress in the fibre being greater than the components strength (Armstrong et al.
1991). This causes the contractile proteins to fail due to excessive force on the cross-bridges
(Tee et al. 2007). Morgan and Proske (2004) proposed a popping sarcoplasm hypothesis,
suggesting when sarcomeres are stretched to points in which are beyond optimum length, it
would result in damage to the sarcomere due to it being stretched more rapidly. Due to the
weakest sarcomeres being at different points of each myofibril, the eccentric nature of the
stretch results in tears of the myofibril and these tears result in an increase in calcium which
causes a pro-inflammation response (Morgan and Proske, 2004). However, it is important to
note that stretches 50% of optimum length have resulted in increased calcium concentration
yet with no damage to the surface membrane, suggesting the muscle may not always be
structurally damaged when inflammation occurs (Butterfield, 2010). Liu et al. (2006) proposed
a three phase hypothesis of DOMS composed of the stages; inflammation, proliferation and
maturation. It was suggested inflammation occurred 0-5 days post muscle damaging exercise
and as a result, may infer muscle damage and inflammation is the predominant cause of
DOMS as pain is typically felt 1-5 days post exercise (Connolly et al. 2003).
2.3. Metabolically induced muscle damage
Insufficient mitochondrial respiration and free radical production are hypothesised to be
attributing factors to metabolically induced muscle damage (Armstrong et al. 1991). Whilst
exercising humans switch through the various energy systems to produce the equivalent
adenosine triphosphate (ATP) to the amount of ATP expended during activity. Therefore Tee
et al. (2007) suggests it is possible that muscle damage can be a direct effect of insufficient
amounts of ATP, especially when coincided with severe glycogen depletion due to a reduction
of high energy phosphates during muscular contractions, which may create a vulnerability to
mechanical muscle damage, or increase the cellular damage due to the greater consumption
of oxygen resulting in an increased number of reactive oxygen species (ROS) (Kruk, 2011).
These ROS readily oxidize with lipid molecules and can cause tissue damage when
overcoming antioxidant defence systems (Mylonas and Kouretas, 1999). Therefore, an
increased number of ROS following exercise would equate to greater muscle damage. Tee et
al. (2007) elicited on a final mechanism which could potentially explain metabolic muscle

66-6920-00L-A-20145 Project 22008862
Page 7
damage in the absence of mechanical stress through the reduction in activity of adenosine
triphosphatase which prevents the removal of calcium causing muscle fibre damage and
inflammation. However, like the mechanical stress model the metabolic stress model is not
without its limitations, as eccentric contractions have a reduced cost of ATP when compared
with concentric contractions, yet seem to significantly induce greater muscle damage (Tee et
al. 2007). As a result, a combination of both models may best explain muscle damage, whilst
these micro-injuries and the inflammation response to these injuries may best explain the
DOMS phenomenon (Gulick and Kimura, 1996).
2.4. Tart Cherries Mechanism of Action
Tart cherries also known as sour cherries or Prunus cerasus L have been of interest due to
their high phytochemical contents such anthocyanins which have seen values as high as 80.4
mg/100g in tart cherries (Blando et al. 2004). Anthocyanins and quercetin content of tart
cherries is known to inhibit cyclooxygenase (COX) found responsible for the inflammation
response, whilst the flavonoid content has been shown to reduce oxidative stress (McCune et
al. 2011). As previously discussed the causes of DOMS are suspected to be associated with
muscle damage and inflammation (Cheung et al. 2003). Therefore, tart cherries may be a
suitable supplement to use to prevent DOMS and muscledamage due to the anti-inflammatory
properties to supress the inflammation stage which occurs 0-5 days following muscle damage
(Liu et al. 2006) which is commonly associated with muscle soreness (Connolly et al. 2003).
Furthermore, tart cherries may improve the antioxidant defence systems due to the
anthocyanin and flavonoid content which may reduce the extent of muscle damage through
metabolic stress by neutralising ROS. The most recent proposed mechanism of tart cherries
is that it improves antioxidant defences, which leads to a reduction in cell damage following
metabolically induced muscle damage and therefore, less primary and secondary
inflammation (Bell et al. 2014b). Subsequently tart cherries are suggested to blunt the
secondary inflammation response and reduce the oxidative stress in exercise high in
mechanical stress and low in metabolic stress (Bowtell et al. 2011). Therefore, if there is less
overall damage or a decrease in inflammation it would be feasible to suggest; there would be
a decrease in serum CK, muscle pain would be significantly reduced and as a direct result
muscular performance in terms of force production would remain closer to baseline levels.
2.5. Clinical practise to Sport Science
Tart cherry supplementation was originally tested and used in clinical application (Bell et al.
2014a). Jacob et al. (2003) investigated the effects of cherry supplementation on uric acid in
healthy women which lead to the conclusion that adopting a dietary intake of 45-50 cherries
per day, in which the cherries were consumed in under 10 minutes was successful in

66-6920-00L-A-20145 Project 22008862
Page 8
decreasing uric acid production by 14.5%. This is of importance as uric acid has been
identified to cause inflammatory conditions such as gout (Zhang et al. 2012) and suggests a
role for tart cherries in decreasing uric acid and subsequent inflammation. However, Jacob et
al. (2003) failed to establish a placebo group, whilst the control of the study was lost after 3
hours where participants were free to do as they wished before returning on the 5th
hour for
more post measures.As a result, it is possible participants may have consumed extra sources
of antioxidants and anti-inflammatories over estimating the ability of cherries.Furthermore with
the participants being healthy, the results cannot be readily generalised to patients with
inflammatory conditions. However, this initial research into cherries reinforced the original
work by Wang et al (1999) who identified in vitro that the phytochemicals in cherries such as
the anthocyanins and flavonoids were successful in preventing inflammation enzymes
(cyclooxygenase) and reducing oxidative stress. As a direct result of the positive findings in
clinical application, tart cherries have more recently become popular in the sport science
domain due to the antioxidant properties and anti-inflammatory affects originally discussed by
Wang et al. (1999). It is hypothesised that tart cherries will be of benefit in sport specifically to
reduce muscle damage and muscle pain following a bout of vigorous exercise by reducing
oxidative tissue damage (metabolic muscle damage) whilst reducing the inflammatory
response to muscle damage which occurs following eccentric exercise (mechanical muscle
damage) (Connolly et al. 2003). Therefore, if the muscle is protected from damage and pain
is supressed we would expect muscle function to remain around a normal capacity.
2.6. The Effects of Tart Cherries on Muscular Performance
The evidence on muscle force regeneration following tart cherry supplementation has been
positive in the three studies which have measured muscular performance. Connolly et al.
(2006) was first to identify supplementation over a period of 9 days with 2 cherry drinks per
day, which consisted of approximately 45-50 cherries, was successful in maintaining muscle
function. Connolly et al (2006) identified only a 4% reduction in muscle strength in the tart
cherry group in comparison to a 22% reduction in the placebo group following maximum
eccentric contractions of the elbow. However, they found no difference in range of movement
and muscle tenderness between the placebo and tart cherry group, which infers muscular
strength may be the greatest variable to measure. Consistent with these findings, Bowtell et
al. (2011) also found that tart cherry may speed up the recovery of muscle function. Bowtell et
al. (2011) adopted a different dosage strategy opting to use a 10 day supplementation period;
7 days loading, on the day of exercise and 2 days post, with 2 drinks consumed a day. Bowtell
et al. (2011) found that tart cherry supplementation significantly attenuated strength loss, as
Maximum Voluntary Contraction (MVC) was 6% closer to baseline MVC levels in the cherry

66-6920-00L-A-20145 Project 22008862
Page 9
group when compared to the placebo after 24 hours whilst also being closer to normal after
48 hours (92.9% vs 88.5%) following knee extension exercises and MVC to induce muscle
damage. However, both studies have the same methodological limitation of utilizing a cross
over design where by participants complete both conditions and as a result are subject to the
repeat bout effect. The repeated bout effect creates a protective effect following a single bout
of exercise, which may be due to; cellular adaptations which make the surface membrane
greater resistant to future damage (Howatson et al. 2007) or through increased recruitment of
muscle fibres (Tee et al. 2007). Furthermore, both Connolly et al. (2006) and Bowtell et al.
(2011) failed to gain strict control on diet and physical activity suggesting any positive results
in strength regeneration may have been down to differences in diet or training from one trial
to the other. However, the significant findings from these studies infer tart cherry
supplementation may be beneficial in speeding up the recovery process and maintaining
muscle function close to normal values following muscle damaging exercise. With muscular
strength being proposed to be the most accurate indirect marker of muscle damage (Xin et al.
2014) it suggests that tart cherry supplements may effectively speed up the recovery process
and prevent a greater extent of muscle damage. It is important to note, the previously
mentioned studies showed force regeneration following eccentric resistance training
consisting of high mechanical stress and low metabolic stress (Connolly et al. 2006; Bowtell
et al. 2011). Unlike Connolly et al. (2006) and Bowtell et al. (2011), Howatson et al. (2010)
induced muscle damage through the mechanical and metabolic stress processes during
marathon running and like the aforementioned studies also found greater force regeneration
when compared to a placebo, identifying muscle force was back to normal values after 48
hours in the tart cherry condition whereas, the placebo group was still recovering after the 48
hour mark. From the growing base of literature we can conclude; tart cherry supplementation
may offer beneficial effects in speeding up the recovery of muscular force following muscle
damaging exercise.
2.7. The Effects of Tart Cherries on Muscle Damage
The literature on the effects of tart cherry supplementation on serum creatine kinase (CK)
markers of muscle damage have demonstrated slight improvement when supplementing tart
cherry in comparison to a placebo. Howatson et al. (2010) initially demonstrated that 20
marathon runners who completed the London marathon following an 8 day supplementation
period (5 day prior to the marathon, on the day and 2 days post), consuming approximately
100-120 cherries per day had lower values of CK than those in the placebo group at 24 and
48 hour post marathon. Whilst the values did not meet statistical significance they still
demonstrated tart cherry may have had an effect on attenuating serum CK, as CK was 23%

66-6920-00L-A-20145 Project 22008862
Page 10
(at 24 hours) and 28% (at 48 hours) lower in the cherry group when compared to placebo. In
addition, Bell et al. (2014b) identified attenuated CK 48 hours post repeated sprint cycle
exercises in 16 well trained participants who consumed tart cherries when compared with
placebo. There was a significant 42% decrease in CK from placebo to tart cherry and more
importantly the values of CK 48 hours after exercise were now lower than initial baseline
measurements. However, both of the studies adopted an independent measures design.
Therefore, any change observed may be due to individual physiological differences, as some
individuals may be trained and adapted better to eccentric exercise than others (Morgan and
proske, 2004). Whilst it’s also been demonstrated that different individuals of similar age and
training status doing the same exercise produce different amounts of CK (Baird et al. 2012).
In contrast to the aforementioned studies, Bowtell et al. (2011), adopted a cross over design
using the same 10 well trained participants in each testing condition and found no significant
difference between trials and unlike the previous studies identified an overall trend of CK
activity being greater during the tart cherry trial following eccentric knee extension exercises
at 80% of the participants 1RM. Therefore, from Bowtell et al. (2011) findings we could
conclude that tart cherry supplementation has no significant effect on serum CK. However,
the use of CK as an indirect marker of muscle damage is highly debated. Baird et al. (2012)
discuss how CK may leave muscle cells to allow for a regeneration period and may not be
strictly associated with physical/structural damage but instead a restriction in energy
processes. Therefore, unlike MVC, CK may not be the greatest indirect marker of muscle
damage to be used. However, currently only one study using tart cherry supplementation has
found increased levels of CK following eccentric resistance training of the knee flexor (Bowtell
et al. 2011).
2.8. Inflammation
The phytochemicals which exist in tart cherries; specifically the anthocyanin and flavonoid
content have been studied in vitro (Wang, 1999) and in healthy females (Jacobs et al. 2003)
and found to have anti-inflammatory effects. Cherries are suggested to have one of the
greatest concentration of flavanols and quercetin (Bentz, 2009). Studies on quercetin indicate
it has a long half-life ranging from 3 hours (Moon et al. 2008) to 11-28 hours (Manach et al.
2005) and as a result constant loading could allow for accumulation of these flavonoids to
maximise the anti-oxidant and anti-inflammatory effects (Nieman, 2010; Bell et al, 2014a).
Therefore, cherries may offer a valuable role in the recovery process from exercise induced
muscle damage, by supressing both primary and secondary inflammation responses to the
initial muscle damage caused by mechanical and metabolic stress (Howatson et al. 2010;
Bowtell et al. 2011).

66-6920-00L-A-20145 Project 22008862
Page 11
The development from Jacobs et al. (2003) initial study which demonstrated a decrease in uric
acid, plasma C-reactive proteins (CRP) and nitric oxide (NO) has been slow. Currently only
three studies exist on the consumption of cherries on inflammatory indices. Howatson et al.
(2010), found significantly reduced serum interleukin 6 (IL-6), CRP and uric acid in the tart
cherry supplement group when compared to the placebo group following marathon running.
However, the study also identified individuals in the placebo group started with a greater uric
acid content suggesting the participants in the placebo group may have been more prone to
inflammation initially. However, both IL-6 and CRP were reduced in the tart cherry group when
compared to placebo during the study. In addition, Bowtell et al. (2011), identified that highly
sensitive C-reactive proteins tended to be lower in the cherry supplement group when
compared to the placebo fruit cordial group. Although, the resistance knee extension training
Bowtell et al. (2010) adopted, failed to significantly increase the response of highly sensitive
C-reactive proteins. More recently Bell et al. (2014b) identified both IL-6 and hsCRP were
reduced following cherry supplementation when compared to a placebo after repeated cycle
sprint trials. This reduction in inflammatory markers post exercise when compared to the
placebo group, in combination with the greater increase between trials 2 and 3 in the placebo
group formed the conclusion that cherries play a role in blunting a secondary inflammation
response from the initial muscle damage.
However, in blunting the inflammatory process it has been argued physiological adaptation
may be hampered. Schoenfeld (2012) emphasised the need for inflammation for long-term
hypertrophy adaptations. Its suggested inflammation is needed to increase swelling which
accumulates fluid and plasma protein in the localised tissue which results in greater protein
synthesis, therefore, when cell swelling is reduced optimal protein synthesis is inhibited
(Schoenfeld 2012). Currently no research exists to indicate tart cherry supplementation
inhibits physiological adaptations (Bell et al. 2014a) and the need to study its effects on
possible blunting of physiological adaptations is needed. Research on NSAIDs which inhibit
COX-2, like tart cherries (Seeram et al. 2001) have reduced the satellite cell response
(Bamman, 2007) which are responsible for muscle growth as individuals with higher satellite
cell pools saw greater muscle growth following exercise (Parise, 2014). To conclude, if we
adopt a loading strategy similar to either Howatson et al. (2010) or Bell et al. (2014b), we
should also expect an anti-inflammatory response following exercise inducing muscle
damage; however, in doing so muscular hypertrophy may be hindered.

66-6920-00L-A-20145 Project 22008862
Page 12
2.9. Oxidative stress
Bell et al. (2014b) suggest that the primary and secondary anti-inflammatory responses
following tart cherry consumption was due to the reduced oxidative stress tissue damage. In
contrast, Mastaloudis et al. (2004) concluded a supplementation period of 6 weeks using
vitamin E and C failed to attenuate inflammation in ultramarathon runners. Therefore, it
suggests either tart cherries may offer greater antioxidant benefits than vitamin E and C or the
metabolic cost of the sprint exercises was far lower than ultra-marathon running which meant
there was significantly less reactive oxygen species (ROS) due to the lower oxygen
consumption in sprints, compared to an ultra-marathon. It is widely acknowledged that
exercise increases the proportion of ROS which often results in the scavenging of electrons
from muscle tissue causing muscle damage (Kruk, 2011). Therefore, it is proposed increasing
the number of antioxidants ingested would overcome this muscle damage by neutralising
radicals, which may therefore, be why tart cherries offer a viable method of reducing muscle
damage and speeding up the recovery process (Bell et al. 2014a). However, research has
indicated the blunting of muscle damage by reducing oxidative stress as much as possible
can have negative effects on physiological adaptation. Peternelj and Coombes (2011)
reported antioxidant intake greater than usual dietary consumption can interfere with
physiological processes related to ROSsuch as insulin signalling and vasodilation. In the case
of cherry supplementation no current study exists which has studied or demonstrated impaired
physiological adaptation following a period of cherry supplementation (Bell et al. 2014a).
Currently only 3 human studies exist on the effects of tart cherry supplementation on oxidative
stress. Howatson et al. (2010) was the initial human study which found attenuated oxidative
stress following cherrysupplementation 5 days prior to a marathon, on the day of the marathon
and 2 days post marathon. The study identified a significant increase in thiobarbituric acid
reactive species (TBARS) 48 hours post marathon in the placebo group whereas the cherry
group did not significantly increase. In contrast, Bowtell et al. (2011) adopted an exercise
which induced muscle damage primarily through the mechanical stress model, but still
identified Protein carbonyls (PC) were significantly reduced throughout the protocol in the tart
cherry condition. Therefore, it’s suggested tart cherries successfully reduce oxidative stress
following both exercise high in metabolic and mechanical stress. Bell et al (2014b) reinforces
this conclusion, as a significant decrease in lipid hydroperoxides was seen throughout the trial
in the cherry group when compared to placebo following a 7 day supplementation period
following sprint cycle exercises. However the role in which anthocyanins play is not clear.
Studies have found poor bioavailability of anthocyanins in food choices such as red wine and
grape juice (Bitsch et al. 2004) which are typically high in antioxidants (Seeram et al. 2008).

66-6920-00L-A-20145 Project 22008862
Page 13
Fang (2014), identified diets high in milk, carbohydrates and other flavonoids tended to prevent
absorption; whilst anthocyanins could be excreted from the system in the form of bile or urine
without being metabolized. This suggests the anthocyanins content of tart cherries may not
directly reduce oxidative damage but indirectly cause a greater antioxidant defence to reactive
oxygen species due to the aforementioned studies finding reductions in markers of oxidative
stress. From the literature we can conclude cherry supplements may be more beneficial in
reducing oxidative stress in exercise which has a high metabolic content. However, more
research needs to be done on the effects of tart cherry supplementation and the possible
negative impacts on physiological adaptation. Finally, more research needs to be done on the
effects of oxidative stress following mechanical muscle damage as Bell et al (2014b)
suggested PC used to measure oxidative stress by Bowtell et al. (2011) was a poor marker of
oxidative stress.
2.10. Perceived muscle soreness
As a result of the anti-inflammatory and antioxidant content of the tart cherry juice, it would be
expected that pain would significantly be reduced, if the musclefibres were less damaged and
still able to perform near normal forceful contraction. However, the literature on the
effectiveness of tart cherry on subjected ratings of perceived pain/soreness are conflicted.
Attenuated pain ratings were initially reported by Connolly et al. (2006) following a bout of
maximal contractions of the elbow flexor. Connolly et al (2006) identified pain was scored 0.8
higher in the placebo group than the cherry group when measured on a 1-10 scale, with pain
also peaking at 24 hours in the cherry group whilst taking 48 hours in the placebo group.
Similarly, Bowtell et al. (2011) adopted a similar DOMS inducing exercise; (maximal knee
extension exercises) and found that cherry juice was beneficial in reducing pain following
pressure pain threshold testing. However, results failed to reach significance but a clear trend
of reduced pain was seen in the cherry group.
In contrast, to the aforementioned studies which induced DOMS primarily through the
mechanical stress methods,Howatson et al. (2010) induced DOMS through marathon running
provoking both mechanical and metabolic stress processes. Howatson et al. (2010) identified
trends of higher perceived soreness ratings measured using a VAS questionnaire 24 and 48
hours after the marathon whilst both the cherry and placebo group were rated equal in
perceived soreness after the marathon. This result is surprising when Howatson et al. (2010)
also recorded reduced CK and increased MVC in the cherry group than placebo. This may
indicate pain is an unsuitable marker for measures of physiological recovery. However, pain
should not be ignored and efforts should be made to reduce pain especially amongst untrained
individuals as indeed, pain is commonly associated with a negative emotional response which

66-6920-00L-A-20145 Project 22008862
Page 14
can often result in avoidance behaviour (Letham et al.1983) and drop outs of exercise
programs (Dalle-Grave et al. 2010). Furthermore, Howatson et al. (2010) may have caused
significantly more muscle damage by exhausting the muscle fibres metabolically and
mechanically, as a result too much muscle damage may have occurred for any supplement to
be of benefit in reducing the perception of pain.
Kuehl et al. (2010) studied the effects of cherry supplementation on muscle pain following
endurance running (26.3 km). The study identified a 50.1% reduction in perceived muscle
soreness post-race when measured on a VAS questionnaire, but failed to follow up with
measures 24 and 48 hour post-race. As a result, we cannot identify if tart cherry
supplementation attenuates pain days after the race or made pain peak earlier in the
aforementioned study, which has been demonstrated in DOMS inducing exercises high in
mechanical stress (Connolly et al. 2006; Bowtell et al. 2011). To conclude, the literature
suggests cherry supplementation has proven effective in reducing perceived pain in well
trained subjects following exercise high in mechanical stress (Bowtell et al. 2011), whilst
exercise high in both mechanical and metabolic stress have yielded conflicted results,
identifying the need for future research in the area in terms of greater studies inducing muscle
damage through metabolic stress, and more studies on mechanical muscle damage in
untrained subjects.
2.11. Dosage strategy
Currently no dose-response study in terms of; dosage or loading strategy of cherries exist and
whilst the studies which exist have found positive outcomes, the reasoning behind the dosage
utilized is not fully understood (Bell et al. 2014a). Jacobs et al. (2003) initial study indicated
that 45 cherries per day was beneficial in reducing inflammatory markers. However, more
recent studied increased the dosage by double the amount with a loading period. Connolly et
al. (2006) adopted a dosage strategy of 100-120 cherries per day, 4 days before the exercise,
on the day and 3 days after. This dosage strategy saw beneficial results in terms of force
regeneration and reduced perception of pain. Kuehl et al. (2010), adopted a 7 day loading
strategy of 90-100 cherries per day, before the race, which resulted in positive effects on
perceived muscle soreness post-race. However, the study’s failed to measure markers of
inflammation and oxidative stress and therefore, we cannot see how the dose adopted directly
affected markers of inflammation and oxidative stress and can only infer the anthocyanins and
flavonoids were successfulinaiding recovery. Howatson et al. (2010) adopted a loading period
5 days before the marathon, on the day and 2 days after, consuming approximately 100-120
cherries per day. This method saw the greatest effects in reducing inflammation and oxidative
stress as IL-6 and CRP were significantly reduced in the cherry group when compared to the

66-6920-00L-A-20145 Project 22008862
Page 15
placebo group throughout the trial. Therefore, a loading strategy, 5 days before, on the day
and 2 days prior consuming approximately 100-120 cherries may be successful in reducing
inflammation and oxidative stress due to sufficient phytochemicals being absorbed, aiding the
recovery process in terms of; muscledamage, force regeneration and pain. However, no study
has followed another’s dosage strategy therefore, it may be beneficial in the future to replicate
the dosage used in previous studies, in order to see if it yields the same results. Currently it is
unknown how lower or higher doses of cherries will affect the recovery process, but adopting
a similar dosage strategy to Howatson et al. (2010) may produce beneficial results in speeding
up the recovery process. Interestingly Kuehl et al. (2010) adopted to consume 20-30 cherries
less than Howatson et al. (2010) and identified attenuated pain whereas Howatson et al.
(2010) found the placebo had lower perceived soreness ratings. Therefore, the need for
research around an optimal and cost effective dose of cherries per day is needed, especially
when attempting to make it a viable option for untrained individuals who are looking to become
active and avoid the feeling of pain which is accompanied with unaccustomed or vigorous
exercise.
2.12. Participants
No study which currently exists to our knowledge focuses on specifically untrained subjects.
Two studies focused specifically on recreational level marathon runners (Howatson et al.
2010) and distance runners (Kuehl et al. 2010), whilst two studies focused on well-trained
participants (Bowtell et al. 2011; Bell et al. 2014b). A few studies opted for a full male sample
(Connolly et al. 2006; Bowtell et al. 2011; Bell et al. 2014b) in case of any specific gender
effects on muscle damage and recovery. However, Dannecker et al (2003) showed females
only reported more pain to experimental stimuli such as electro-neuromuscular stimulation.
Furthermore, Rinard et al. (2000) studied a larger sample of males and females and found no
significant difference in soreness ratings using similar eccentric exercise protocols. The
repeated bout effect is a phenomena well known which produces a protective effect against
muscle damage (Xin et al. 2014) and as a result any positive results seen in the previous
studies may have been due to the participants already having some form of protection from
muscle damage and its debilitative symptoms. Therefore, future research needs to be
conducted on untrained participants in order to see if tart cherry supplementation still has
beneficial effects on individuals who have no physiological adaptation to muscle damage.
Furthermore, it is also important to focus on reducing the time to recover and more importantly
the pain response to muscle damage in the untrained population in order to overcome this
potential barrier to exercise. Letham et al. (1983) suggested pain is often accompanied by a
negative emotional response leading to avoidance behaviour. Dalle-Grave et al. (2010)

66-6920-00L-A-20145 Project 22008862
Page 16
reinforce this view finding pain was a common barrier to obese individuals exercising, whilst
more recently Van Schijndel-Speet (2014) identified pain and physical discomfort were
barriers to exercise in elder individuals. Hopefully by blunting the pain response, individuals
will not display avoidance behaviour and may decide to adopt an active lifestyle; to overcome
the pandemic proportion of physical inactivity which is currently the fourth leading cause of
death worldwide (Kohl et al. 2012).
2.13. Hypothesis
From reviewing the literature we hypothesis that tart cherry supplementation for a period of 8
days (5 days prior, on the day and 2 days post) will have a positive impact on recovery from
exercise induced muscledamage, due to the anti-inflammatory nature and antioxidant content
of the phytochemicals in cherries. By adopting this loading strategy proven to absorb sufficient
phytochemicals to reduced inflammation and oxidative stress (Howatson et al. 2010) we
expect to see a number of benefits when using tart cherry supplementation in an untrained
population following eccentric contractions on an isokinetic dynamometer. The benefits we
expect to occur in our untrained participants throughout the study are as follows.
1) We expect to see significantly improved muscle force regeneration in the tart cherry group
when compared to placebo, with values of force being closer to baseline values 48 hours post
DOMS exercise, which has been demonstrated in previous studies.
2) We do not expect to see any significant differences between groups, on markers of CK, 48
hours post exercise due to it being a poorer marker of muscle damage, whilst research has
shown both raised and reduced CK following tart cherry supplementation when compared to
a placebo group.
3) Finally, we expect to see a reduction in perceived muscle soreness following the ingestion
of tart cherry juice. We expect pain to be lower in the tart cherry group when compared to
placebo for 24, 48 and 72 hours post DOMS exercise.

66-6920-00L-A-20145 Project 22008862
Page 17
3. Methods
3.1. Participants
Six untrained participants, (male n = 5, female n = 1, age = 20.5 ± 2.3 yr, weight = 81.6 ± 21.8
kg, height = 175.9 ± 8.7 cm) completed the study. Untrained participants were defined as
individuals who had not participated in competitive sporting events within the past 3 months
and who were not currently training for competition. Participants were recruited via a
questionnaire to ensure participants fell within our untrained category. The study was
approved by Sheffield Hallam University. All participants were made aware of the experimental
protocol via a written participant information sheet (see Appendix 2) which included the
procedure, potential risks, benefits and rights as a participant. A medical health questionnaire
(see Appendix 3) was completed to assess whether participants could participate in the study.
Signed consent forms were obtained (see Appendix 4). Exclusion criteria for the study
included; those currently competing in sport or training for a sporting event, individuals with
known allergies to cherry juice, individuals with known co-morbidities and individuals injured
or prone to injury in the lower limbs.
3.2. Experimental design.
The experiment adopted a randomised, counter-balanced cross over design where
participants completed two main trials which were separated by a 6 day wash out period.
Participants consumed either Cherry active juice concentration (CA) or a commercially
available cherry cordial (CC) for 8 days in each trial. In each trial, participants completed a
DOMS inducing exercise protocol on day 6 of the supplementation period (5 sets of 12
maximal effort eccentric hamstring exercises on an isokinetic dynamometer). Measures of CK
were taken before the DOMS exercise and 48 hours after the exercise. MVC was measured
using eccentric peak torque before the DOMS exercise, after the DOMS exercise and 48 hours
after the DOMS exercise, whilst VAS questionnaires were completed pre, post and up to 72
hours after the DOMS inducing exercise to measures perceived musclesoreness.Participants
returned to the lab at the same time in a fasted state to standardise each testing condition.
Participants were instructed to keep records of diet and physical activity from the start of
supplement consumption, up until 48 hours after the DOMS exercise and asked to replicate
during the second trial.
3.3. Nutritional supplements.
A 15 ml serving of Cherry Active Concentrate Juice is equivalent to 40-50 cherries per drink.
Therefore, participants in the cherry active group consumed 90-100 cherries per day by
consumingtwo 15 ml serving per day. The Cherry Active juice used was the samesupplement

66-6920-00L-A-20145 Project 22008862
Page 18
used in Bowtell et al. (2011) study. Therefore, each 15ml of Cherry Active juice combined with
half a pint of water contained approximately 4.558 mgImL of anthocyanins with an oxygen
radical absorbance capacity (ORAC) of 137.5 mmolIL. The cherry cordial placebo was
adopted to have similar taste and appearance but without the phytochemical properties of the
tart cherry group. Both CA and CC supplements were consumed for a total of 8 days,
consuming two 15 ml supplements per days. The nutritional information of each supplement
can be found in table 1. Participants were asked to consume one drink in the morning and
another before they went to bed.
Table 1. Nutritional content of each nutritional supplement.
Cherry Active
(Per 30 ml)
Cherry Cordial Placebo
(per 30ml)
Energy 102 Kcal 30 Kcal
Protein 1.1g 0g
Carbohydrate 24.5g 7.7g
Fat 0g 0g
Fibre 2.6g 0g
Salt 0g 0g
Anthocyanin 9.117 mgIML Trace
ORAC 275 mmolIL Trace
3.4. Experimental protocol (Figure 1).
Participants arrived at the lab in a fasted state on the 6th
day of supplementation and were
seated. Participants were given a Visual Analog Scale (VAS) questionnaire (see Appendix 5)
to complete to account for a measure of perceived soreness before any capillary blood
sample, power testing or DOMS inducing exercise was complete. Once participants
completed the VAS questionnaire a capillary blood sample was taken following the WHO
guidelines (WHO, 2010) and analysed via a Photometer (Reflotron, Boehringer Mannheim
GMBH, Germany) to give a baseline measure of CK. After the baseline blood analysis, a
baseline MVC measure was taken using an isokinetic dynamometer (Biodex stystem 3). The
procedure used has previously been shown to provide reliable measures of torque (Drouin et
al. 2004). The isokinetic dynamometer was set at an angular torque of 60 degrees.secˉ¹, with
range of motion set from 90 degrees until participants felt their hamstrings tightening.
Participants were then given 3 attempts with a brief 30 second rest between efforts and the
greatest force reading was taken. After a 3 minute rest period the DOMS inducing exercise
was completed.

66-6920-00L-A-20145 Project 22008862
Page 19
All participants warmed up for 5 minutes on a cycle ergometer (824E, Monarch AB, Sweden)
with self-selected weight and cadence to achieve 60% Age Predicted Heart rate max
(APHRM) (Polar Electro OY, FS1, Finland). Following the warm up participants were
introduced to the isokinetic dynamometer to carry out the eccentric hamstring exercise on the
right leg. Isokinetic dynamometer was set at an angular peak torque of 60 degrees.secˉ¹. The
exercise was performed maximally over a period of 5 sets consisting of 12 reps each set with
a one minute rest period between sets. The range of motion was set at; 90 degrees towards
limit whilst the away limit was set at a point in which the participant noted tightening in the
hamstring muscle group.
Immediately after the DOMS inducing exercise another VAS questionnaire was completed
and 3 minutes after the exercise another MVC was completed on the isokinetic dynamometer.
Again the participants were allowed 3 attempts with a brief 30 second rest period between
efforts and the highest force reading was taken.
Participants then returned to the lab at the same time in a fasted state, 48 hours after the
DOMS inducing exercise to have post measurements completed. Participants arrived with a
completed VAS questionnaire for 24 and 48 hours after the exercise, which were both
completed in the morning. A capillary blood sample was taken again to see the level of CK 48
hours post exercise and again another 3 MVC were completed following the same protocol. A
final VAS questionnaire was completed 72 hours after the DOMS inducing exercise.
After a 6 day wash out period the second trial began. The experimental protocol stayed exactly
the same, targeting the right leg due to a repeated contralateral bout effect existing (Xin et al.
2014) and to prevent results being effected by leg dominance effects.
3.5. VAS questionnaire.
A VAS questionnaire (0-100 mm) (see Appendix 5) was completed for the; quadricep,
hamstring, tibialis anterior and calf muscle groups, where 0mm was ‘no pain’ to 100mm
‘severe pain’. The VAS was given before DOMS test, after the DOMS test, 24-72 hours after
the test to assess perceived ratings of muscle soreness. The VAS questionnaire was
completed in the morning after waking up to standardise the measure of perceived soreness
for all days excluding the DOMS inducing exercise day. The VAS scale was used due to its
validity and reliability in measuring acute pain (Bijur et al. 2003) and the ratio level data it
produces making it a more favourable method than Likert scales (Williamson and Hoggart,
2005).

66-6920-00L-A-20145 Project 22008862
Page 20
3.6. Serum CK blood analysis.
CK was measured through obtaining a capillary blood sample from participant’s finger tips on
their desirable finger. The blood samples were collected from participants following an
overnight fast. Approximately 20 µl of blood was collected, which was then analysed using a
Photometer (Reflotron, Boehringer Mannheim GMBH, Germany), before the test and 48 hours
after the test to assess markers of muscle damage following the DOMS inducing exercise.
Serum CK was measured before the MVC to get a baseline value of serum CK before the
experimental protocol was conducted.
3.7. Isokinetic dynamometer.
The isokinetic dynamometer (System 3 pro, Biodex medical systems inc. USA) was set at an
angular velocity of 60 degrees.secˉ¹ for both the MVC and DOMS inducing exercise and
always performed on the right leg throughout the study. The ranges of motion were set at: 90⁰
towards limit, whilst the away limit was set when participants noted a tightening of the
hamstring group. The MVC consistedof 3 reps, with a 30 second rest in between efforts, whilst
the DOMS inducing exercise consistedof 5 sets of 12 reps with a 1 minute rest period between
sets. Both protocols were completed with maximal effort and participants were given verbal
encouragement to perform maximally. The DOMS inducing exercise was performed once per
trial on the 6th
day of supplementation. MVC was performed 3 times per trial; before, after and
48 hours after the DOMS inducing exercise. Eccentric peak torque was collected during the
MVC to account for changes in muscular force production from baseline following eccentric
hamstring exercise.
3.8. Data Collection/analysis.
Data was collected from baseline, after testing, 1-3 days post DOMS inducing exercise. The
greatest MVC value over each 3 attempts was used as the participants maximum force
exerted. MVC, CK and VAS were reported as mean values with standard deviations following
statistical analysis. Statistical analysis was performed using SPSS statistics for Windows,
Version 22.0. Normality of the data was assessed using the Sharpiro-Wilk test, before
conducting a two way repeated measures ANOVA, treatment (tart cherry vs placebo) by time
(Before, after, 24 48, 72 hours post DOMS exercise) to identify any statistical significance of
treatment or time on the studies dependent variables (CK,MVC and VAS of perceived muscle
soreness). Testing for homogeneity of variance was done using a Mauchly sphericity test.
Greenhouse-Geisser adjustment was used for violations of the assumptions of sphericity. The

66-6920-00L-A-20145 Project 22008862
Page 21
accepted alpha level of the study was set at 0.05 to test for statistical significance. Cohen’s d
was used to calculate effect size for visual trends.
Figure 1. Schematic diagram of the experimental protocol. For the second trial this procedure
was replicated following a 6 day wash out period, with participants swapping supplement
groups. Experimental testing took place between 12:00 – 4:00 PM. (CK; Creatine Kinase,
MVC; Maximum voluntary contraction, VAS; Visual Analog Scale Questionnaire).
Day 1 – 5 Day 6
5 sets of 12 reps at
maximal effortMVC MVC
Day 7 Day 8
MVC
VAS VAS
CK
VAS VAS
Day 9
Tart Cherry or Placebo supplementation Day 1- 8
VAS
CK

66-6920-00L-A-20145 Project 22008862
Page 22
4. Results
4.1. Delayed onset muscle soreness.
Table 2. Perceived muscle soreness descriptive statistics, measured using a Visual Analog
Scale (VAS) questionnaire over 5 time points.
Pre-Exercise Post-Exercise 24 h 48 h 72 h
Hamstrings
DOMS*** (mm)
Tart
Cherry 6 ± 8 25 ± 26 35 ± 22 27 ± 22 17 ± 22
Placebo 5 ± 6 49 ± 21 56 ± 29 65 ± 22 45 ± 23
Quadriceps DOMS
(mm)
Tart
Cherry 6 ± 9 15 ± 22 13 ± 20 6 ± 8 1 ± 1
Placebo 5 ± 6 22 ± 19 15 ± 22 13 ± 25 11 ± 26
Calf DOMS (mm)
Tart
Cherry 5 ± 12 24 ± 27 18 ± 25 7 ± 9 1 ± 1
Placebo 20 ± 27 24 ± 20 7 ± 13 7 ± 13 4 ± 10
Tibialis Anterior
(mm)
Tart
Cherry 2 ± 4 15 ± 22 14 ± 25 2 ± 2 1 ± 1
Placebo 12 ± 19 13 ± 14 10 ± 15 12 ± 15 6 ± 14
Data is presented as mean ± standard deviation.
There was a main effect of time for Hamstrings DOMS (P = < 0.01)*.
The increase in Hamstrings DOMS tended to be reduced in the Tart Cherry group (condition
main effect, P = 0.045)*, with a significant time and condition interaction (Time*Condition
interaction effect, P = 0.006)*.
DOMS; delayed onset muscle soreness.

66-6920-00L-A-20145 Project 22008862
Page 23
There was only significant increases in perceived muscle soreness in the Hamstrings muscle
group. Table 2, identifies that all muscle groups excluding hamstrings peaked pre-exercise
and began to return to baseline levels. Figure 2 identifies muscle soreness in the hamstring
group peaked at 24 hours in the tart cherry group whereas, soreness peaked at 48 hours in
the placebo. The large standard deviations indicate variability in perceived soreness ratings
between participants. There was a main effect of time (F (4, 20) = 16.993, P = < 0.01),
demonstrating the experimental protocol induced delayed onset muscle soreness in the
targeted hamstring muscle group, from pre-exercise values up until 72 hours post-exercise.
There was also a condition effect which identified pain reduction in the hamstring during the
tart cherry condition (F (1, 5) = 7.079, P = 0.045). Furthermore, there was an increase in
perceived muscle soreness of the hamstring post-exercise – 72 hours post in the placebo
condition when compared to the tart cherry condition (interaction effect, F (4, 20) = 5.065, P =
0.006).
Figure 2. VAS perceived soreness values represented as change from pre-DOMS inducing
exercise values. There was a significant main effect of time (P = < 0.01) and condition (P =
0.045) along with a significant time*condition interaction effect (P = 0.006). All data points had
a significant time effect from pre-exercise values.
0
200
400
600
800
1000
1200
1400
1600
1800
Pre-ex Post-ex 24 h 48 h 72 h
VAS(%ofpre-exVAS)
Percieved musclesoreness in the Hamstring musclegroup
Tart cherry Placebo

66-6920-00L-A-20145 Project 22008862
Page 24
4.2. Maximum Voluntary Contraction (MVC)
Table 3. Maximum Voluntary Contraction (MVC) indirect marker of muscle recovery,
descriptive statistics.
Pre-Exercise Post-Exercise 48 h
MVC (N.mˉ¹)*
Tart Cherry 158.9 ± 67.6 130.1 ± 40.8 138.1 ± 48.5
Placebo 151.9 ± 45.6 123.6 ± 31.2 121.6 ± 47.4
Data is presented as mean ± standard deviation.
There was a main effects of time for MVC (P = 0.038)*
MVC; Maximum Voluntary Contraction
MVC of the hamstring muscle group was reduced on average to 84% of values pre-DOMS
inducing exercise and were still reduced to 85% 48 hours post-DOMS inducing exercise.
There was a significant main effect of time (F (2, 10) = 4,629, P = 0.038), this significant
difference occurred between pre and 48 hours post-exercise (P = 0.021). There was no
significant difference in MVC between conditions (main effect of condition, F (1, 5) = 1.998, P
= 0.217) and there was no significant difference in force recovery over time between condition
(interaction effect, F (1.017, 5.086) = 0.193, P = 0.683). However, trends identified muscular
force recovery tended to be increased in the tart cherry group with levels returning to 91% ±
12% compared to 80% ± 13% in the placebo group 48 hours post-DOMS inducing exercise
(figure 3). Cohen’s effect size value (d=0.38) indicated a small positive effect of tart cherry
juice on muscle force recovery when compared to placebo. Cohen’s effect size (d = 0.39)
indicated there was a small difference in force from pre-exercise to 48h post-exercise in the
tart cherry group when compared to a larger effect (d = 0.71) in the placebo identifying greater
reductions in force.

66-6920-00L-A-20145 Project 22008862
Page 25
Figure 3. MVC values represented as change from pre-DOMS inducing exercise values. There
was no significant main effect of condition (P = 0.217), or time*condition interaction effect (P
= 0.683). However, the graph displays force recovery tended to be improved in the tart cherry
condition 48h post exercise.
4.3. Creatine Kinase
Table 4. Serum Creatine Kinase marker of muscle damage, descriptive statistics.
Pre-Exercise 48 h
CK (µ/l, n = 5)
Tart Cherry 130 ± 115. 9 101 ± 67. 5
Placebo 55.3 ± 35.8 188.6 ± 177. 4
Data reported as mean and standard deviation.
CK: Creatine Kinase.
CK data was based on 5 participants; 1 participant failed to complete blood analysis
throughout the study. The descriptive statistics identify CK was reduced by 22% 48 hours
post-DOMS inducing exercise in the tart cherry group whilst the placebo group increased by
around 240% compared to pre-exercise values. There was no significant increase in serum
CK 48 hours post-DOMS inducing exercise (main effect of time, F (1, 4) = 2.221, P = 0.210).
The differences between tart cherry and placebo conditions werealso insignificant (main effect
of condition, F (1, 4) = 0.020, P = 0.894). Changes in CK from pre-exercise values were not
statistically significant between tart cherry and placebo condition (Interaction effect, F (1, 4) =
2.217, P = 0.211). However, a clear trend that CK activity was greater in the placebo condition
is observed as the tart cherry groups serum CK was reduced to 78% of the baseline value
0
20
40
60
80
100
120
BL after 48 hours
MVC(%ofpre-exMVC) Maximum Voluntary Contraction (MVC)
Tart Cherry
Placebo

66-6920-00L-A-20145 Project 22008862
Page 26
whereas, the placebo group had increased to 340% of the baseline value (Figure 4). Cohen’s
effect size value (d = 0.97) suggests there was a larger baseline value of CK in the tart cherry
group, whilst 48 hours post-exercise effect size values (d = -0.73) indicates there was
moderate significance in the tart cherry group to reduce CK when compared to placebo.
Furthermore, Cohen’s effect size value (d = 0.34) suggests there was a small positive effect
of tart cherries on CK reduction, 48 hours post-exercise when compared to a large negative
effect (d = -1.16) seen 48 hours post-exercise in the placebo group to reduce CK.
Figure 4. CK values represented as change from pre-DOMS inducing exercise values. There
was no significant main effect of condition (P = 0.894), or time*condition interaction effect (P
= 0.211). However, the graph displays trends that CK was greater in the placebo group when
compared to tart cherry group which was reduced from pre-exercise values.
5. Discussion
The main finding of this study was the reduction in perceived musclesoreness ofthe hamstring
group following maximal eccentric hamstring contractions when consuming tart cherry juice 5
days pre, on the day, and 2 days post eccentric exercise. This improvement in perceived
muscle soreness was combined with trends of increased muscle force regeneration and
decreases CK in the tart cherry group 48 hours post-eccentric exercise when compared to the
placebo group. However, no significant increases in CK and decreases in MVC post-exercise
question the amount of muscle damage induced by the eccentric exercise protocol.
Furthermore, there was no significant reduction in perceived soreness of either; quadriceps,
calf or tibialis anterior muscle groups between tart cherry and placebo trials. This may be due
to the relatively low ratings of soreness in the aforementioned muscle groups.
0
200
400
600
800
1000
1200
BL 48 hours
CK(%ofpre-exvalues)
Creatine Kinase (CK)
Tart Cherry
Placebo

66-6920-00L-A-20145 Project 22008862
Page 27
5.1 Functional recovery
The findings of this study in terms of trends of greater muscle force regeneration in the tart
cherry group is also demonstrated in previous literature as, Connolly et al. (2006), Howatson
et al. (2010) and Bowtell et al. (2011) all identified muscle force returned closer to baseline
values 48 hours post-eccentric exercise and marathon running. This study identifies muscle
force returned closerto baseline values during the tart cherry condition 48 hours post exercise,
whilst the force in the placebo group continued to decrease from baseline values. This study
produced similardecreases in strength post activity (~84% of pre-ex values) between both tart
cherry and placebo groups which was also found by Howatson et al. (2010) and Bowtell et al.
(2011) following marathon running and knee extension exercises, with greater increases in
muscular strength 48 hours post-exercise in the tart cherry group. This led to the belief that
tart cherries do not work by preventing the structural damage of muscle tissue following bouts
of eccentric or strenuous exercise but instead reduces the local inflammatory response
following the onset of muscle damage (Howatson et al. 2010, Bowtell et al. 2011).
Unfortunately this study failed to measure markers of inflammation. However, Howatson et al.
(2010) identified IL-6 markers of inflammation were closely correlated with serum CK.
Therefore, from this association we may be able to use serum CK as an indirect marker of
muscle damage and inflammation.
This study demonstrated serum CK markers of muscle damage were reduced by 22% from
baseline values, 48 hours post-eccentric exercise when consuming tart cherries, compared to
a 240% increase in the placebo group. This was accompanied with a marked increase (80%)
in baseline CK values in the tart cherry group, indicating participants may have failed to
standardise their activity between trials. Therefore, if IL-6 is closely associated with CK as
Howatson et al. (2010) identified it would suggest either; tart cherries successfully worked at
blunting a secondary inflammation response by inhibiting inflammatory enzymes (COX), or
the experimental protocol failed to induce muscledamage and as a result no subsequent local
inflammation occurred. Unfortunately this study only utilised one follow-up serum CK blood
sample after 48 hours to identify change from baseline. Therefore, we cannot identify whether
the experimental protocol did in fact, cause muscle damage. Though the study demonstrated
both tart cherry and placebo groups muscular force after 48 hours was still decreased from
baseline. The tart cherry group reached 91% of baseline MVC values whereas placebo only
achieved 80% or pre-exercise MVC values, which may best indicate muscle recovery (Xin et
al. 2014) due to CK having a large variability because of high and low responders (Tajra et al.
2014) which is evident in the present study due to the large standard deviation in the placebo
group 48 hours post exercise.

66-6920-00L-A-20145 Project 22008862
Page 28
Kasapis and Thompson (2005) systematic review identified muscle damage did not have to
occur for a marked increase in inflammatory marker IL-6. The increases in IL-6 were greater
but shorter in duration in the absence of muscle damage. Furthermore, Clarkson et al. (1992)
proposed the idea that range of motion was inhibited post exercise bout when CK was still
significantly decreased due to the accumulation of calcium. This theory has been reinforced
by the findings of Butterfield (2010) who identified calcium caused an inflammatory response
even when no structural muscle damage occurred. This could explain the studies positive
findings in terms of greater trends towards improved muscle force recovery in the tart cherry
group when compared to placebo. Like Howatson et al. (2010) and Bowtell et al. (2011), tart
cherry supplementation may have supressed the inflammatory response to either; muscle
damage, or the inflammatory response associated with muscular contractions (Kasapis and
Thompson, 2005). In agreement with Howatson et al. (2010) this study identifies trends of
reduced CK in the tart cherry group when compared to placebo. However, both Howatson et
al. (2010) and Bowtell et al. (2011) identified increased CK 48 hours post-exercise when
compared to baseline values, whilst this study identified a reduction in CK 48 hours post-
exercise in the tart cherry group. The difference in results from this study comparedto previous
studies may be due to the experimental protocol and participants used. Howatson et al. (2010)
adopted to induce muscle damage through marathon running whilst Bowtell et al. (2011)
adopted knee extension exercises, similar to the present protocol. It is possible the present
findings showed no significant increase in CK due to participants being untrained compared
to Bowtell et al. (2011) well trained participants. Well trained participants can work at higher
capacity over a prolonged period of time due to the strength adaptations from training, whilst
untrained participants fatigue and are unable to produce forceful muscular contractions for a
prolonged duration (Shimano et al. 2006). Furthermore, Friden and Lieber (2000) suggest,
humans work at submaximal intensities rather than maximally during eccentric contractions
due to the feeling of pain. Although participants were asked and verbally encouraged to
perform maximally, it’s highly unlikely they were capable of doing so, due to the perception of
pain. This perception of pain may have been of greater magnitude in this study compared to
Bowtell et al. (2011) due to participants having limited adaptation to eccentric lengthening
contractions. If participants are not working maximally there would be less stress in the muscle
fibre limiting muscle damage caused from the DOMS-inducing exercise (Armstrong et al.
1991, Tee et al. 2007). In addition, the study failed to measure total work, which may have
provided an explanation to why CK decreased in the tart cherry condition. Participants may
have produced more total work in the placebo condition when compared to tart cherry which
would explain why CK was reduced by 22% 48 hours post-eccentric exercise whilst the
placebo saw a 240% increase from baseline.

66-6920-00L-A-20145 Project 22008862
Page 29
Unlike, Howatson et al. (2010), Bowtell et al. (2011) and Bell (2014b) this study failed to
measure markers of oxidative stress. Whilst oxidative stress is predominantly observed in
aerobic activity, its effects on resistance exercise is conflicted (Bowtell et al. 2011). Deminice
et al. (2010) identified oxidative stress was induced following 3 sets of 10 reps at a moderate
intensity, identifying a 45% increase in TBARS which was statistically significant, concluding
resistance exercise can induce oxidative stress. Therefore, our study may have induced
oxidative stress due to the greater numbers of sets and higher intensity than the
aforementioned study. This study adopted a loading strategy utilized by Howatson et al. (2010)
due to positive findings on reduced IL-6, CRP and TBARS. As a result, greater trends of
muscle function recovery in the tart cherry group when compared to the placebo group may
have been identified due to a reduction in oxidative stress from consuming tart cherries.
Howatson et al. (2010), identified TBARS in the tart cherry group were approximately 10
uMol/L less than the placebo group after 48 hours, whilst it was important to note total
antioxidant status (TAS) was sufficient in reducing oxidative stress up until 24 hours in the
placebo group. There was also no increase in TBARS following marathon running when
participants consumed the tart cherry juice. Bowtell et al. (2011) also identified PC markers of
oxidative stress weredecreased 24 hours post eccentric exercisesuggesting tart cherries may
prevent oxidative stress even in exercise low in metabolic stress. The possible reduction in
oxidative tissue damage may not only explain why muscle function recovery was greater in
the tart cherry group at 48 hours, whilst the placebo groups force continued to decrease, but
may also explain the decreases in serum CK in the present study. If there is less oxidative
stress, then less muscular damage would occur because of the reduction in ROS scavenging
electrons from muscletissue,and in turn would yield a reduction in CK.This was demonstrated
by Bell et al. (2014b) who found lower CK values after the third cycling trial when compared
with pre-exercise CK values during a cycle trial predominantly causing metabolic stress. This
decrease in CK was attributed to the tart cherries improving antioxidant defence systems;
leading to reduced cell damage and inflammation. Therefore, supplementing with tart cherries
may have prevented fluctuations in TAS and protected participants from oxidative stress and
tissue damage, leading to reduced inflammation; accelerating muscle force regeneration and
reducing serum CK in this studies untrained participants.
However, whilst the study aimed at recruiting untrained participants, the definition used in this
study was individuals inactive from sporting competition and training for a period of 3 months.
Nosaka et al. (2001) suggested adaptive effects from training supress muscledamage caused
by eccentric exercise when performed no more than 6 months apart. Therefore, problems with
the sample selection may have caused a repeated bout effect, preventing a significant
increase in serum CK. Furthermore, it has been identified that even a single bout of eccentric

66-6920-00L-A-20145 Project 22008862
Page 30
exercise markedly decreases the levels of CK when performing the same exercise over a
period of 2 weeks due to the rapid motor unit recruitment adaptations (Clarkson et al. 1992).
Therefore, this studies 6 day wash-out period (7 days from the last MVC) was not sufficient to
reduce the repeated bout effect, which may have prevented significant increases in serum CK.
Future research should look to use the contralateral leg, with larger sample sizes so the study
can be counter-balanced for limb dominance effects.
5.2 Perceived muscle soreness
The initial studies into tart cherry juice by Connolly et al. (2006) and Kuehl et al. (2010)
identified those who consumed tart cherry juice for a 3 day period before eccentric elbow
exercises and 4 days after and 7 days before a long distance (26 km) race was successful at
reducing subjective ratings of pain. This present study reinforces the findings of the
aforementioned studies as there was a significant reduction in hamstring soreness following
the consumptions of tart cherry juice 5 days before, on the day and 2 days post eccentric
hamstring exercise when compared to a placebo group, in untrained participants. This finding
was not surprising when accompanied with reduced CK and increased muscle force
regeneration 48 hours post-exercise when compared to the placebo group. Like Kuehl et al.
(2010), this study demonstrates a decrease in subjective ratings of soreness immediately after
exercise in the tart cherry group. The placebo group had a 96% higher musclesoreness rating
than the tart cherry group immediately after exercise. Furthermore, like Connolly et al. (2006)
the present study identified hamstring soreness peaked at 24 hours post eccentric exercise in
the tart cherry group whereas the placebo did not peak until 48 hours post exercise. The large
standard deviation in the study indicates the great variability in either perceived soreness or
individual’s interpretation of the visual analog questionnaire, which in itself is a limitation of the
subjective nature of the visual analog scale.
These results in attenuated perceived soreness ratings contrastthe findings of both Howatson
et al. (2010) and Bowtell et al. (2011) who identified no significant reduction in subjective
ratings of soreness. Howatson et al. (2010) identified significant reductions in inflammation,
oxidative stress and improvements in force regeneration following marathon running.
Therefore, it’s surprising that no reduction in soreness was accompanied with such findings
and in fact greater values of muscle soreness were seen in the tart cherry group. Bowtell et
al. (2011), utilized a protocol to induce muscle damage mechanically through knee extension
resistance exercise, which was similar to the protocol utilized in the present study. However
unlike this study’s findings, Bowtell et al. (2011) identified no significant differences in pain
pressure threshold. Whilst Bowtell et al. (2011) identified no significant findings, clear trends
of reduced soreness were seen in the tart cherry group 24 and 48 hours after exercise as

66-6920-00L-A-20145 Project 22008862
Page 31
values started to return to baseline values whilst the placebo group’s soreness continued to
increase up to 48 hours post-eccentric exercise which was found in the present study. All
studies apart from Howatson et al (2010) have shown reduced soreness to some extent.
However, the marathon running protocol utilized by Howatson et al. (2010) is greater in
duration than the protocol utilized in this study and all previously published studies (Connolly
et al. 2006, Kuehl et al. 2010, Bowtell et al. 2011, Bell et al. 2014b) whichinduced considerable
metabolic stress causing a greater magnitude of muscle damage (CK), compared to the
present study and Bowtell et al. (2011) knee extensor exercises. Therefore, from the present
findings and the previous research into tart cherries it suggestes cherries may have a
beneficial effect on post-exercise muscle soreness in not only trained individuals but also
those untrained and unaccustomed to eccentric exercise when moderate amounts of muscle
damage are induced. This reduction in pain in the present study was accompanied with
decreased serum CK and increased force regeneration inferring; tart cherries and specifically
the anthocyanin and flavonoid content may have reduced tissuedamage from oxidative stress
and subsequently reduced the inflammatory response to muscledamage, reducing the feeling
of soreness.
5.3 Limitations
Whilst the findings of this study demonstrate tart cherries significantly decreased perceived
soreness following eccentric exercise, whilst showing trends of increased force regeneration
and decreased serum CK in untrained participants, we cannot attribute all these finding to tart
cherry supplementation due to several methodological limitations. Firstly, the differences
between the tart cherry supplement and placebo in terms of appearance, odour and taste may
have made it easy for participants to discern the tart cherry group. As a result, this may have
created demand characteristics from the participants to over-estimate their soreness in the
placebo condition, and under-estimate their soreness in the tart cherry condition. Furthermore,
the difference in calorie and macronutrient content (table 1) may have had an effect when
participants were completing the study in a fasted state. Whilst carbohydrate status before
exercise has found to have no effect on DOMS and muscledamage (Closeet al. 2005), protein
before exercise is known to increase protein synthesis post-exercise which may have caused
a measurable decrease in muscle damage (Pasiakos et al. 2014). Whilst the contents of each
supplement were not vastly different, future studies should look to match the energy and
macronutrient contents of each supplement. No restrictions were placed on medication such
as NSAIDS which are known anti-inflammatories to work on DOMS (Schoenfeld, 2012) and
other sources of antioxidants, whilst there is no guarantee individuals adhered to consuming
the supplements.As a result, future researchneeds to gain greater control on individual’s diets

66-6920-00L-A-20145 Project 22008862
Page 32
to reduce antioxidant/anti-inflammatory content to be able to attribute the findings solely to tart
cherry juice.
The elevated pre-exercise values of CK in the tart cherry trial indicates participants did not
replicate their activity logs successfullybetween trials. Therefore, this cofounding variable may
have affected the results and caused the decrease in CK 48 hours post exercise along with
the reduced perception of pain and increased force regeneration, because of a repeated bout
effect (Clarkson et al. 1992, Nosaka et al. 2002). This was likely the case for one participant
who had a CK value of 301µ/l before the initial trial had begun, arguing how untrained the
participants of the study were. This participant’s decrease in CK to 194 µ/l would likely be
caused by the repeated bout rather than tart cherry supplementation as studies have shown
activity, even concentric in nature reduced serum CK (Kim et al. 2010). Furthermore, this
increase in baseline CK may have caused a considerable effect as the isokinetic
dynamometers away range of motion was reset for each trial. Therefore, participants with
higher baseline CK values may have felt their hamstrings tightening quicker in one trial
compared to the other due to the decreases in range of motion typically observed following
muscle damaging activity (Connolly et al. 2006) due to the calcium accumulation and
subsequent discomfort (Clarkson et al. 1992, Butterfield, 2012). As a result, participants
muscle fibres may have been stretched considerably less in one trial compared to another,
which maybe why reductions in CKwere found in the tart cherry trial due to no muscledamage
being induced because the fibres may not have been stretched beyond optimum length to
cause micro-injury (Morgan and Proske, 2004). Furthermore, failing to measure total work
between trials means participants could have simply completed less work in the tart cherry
group producing less muscle damage. Therefore, future research needs to be more stringent
on methods to standardise participant’s activity from one trial to the other, whilst using the
same range of motion on the isokinetic dynamometer to ensure the muscle fibres are being
stretched to the same extent. Total work should also be noted to identify whether the same
amount of effort was produced in each trial.
Finally, limitations with the sample used, may not only have affected the results as previously
discussed with participants potentially being untrained for as little as 3 months and being
protected from the effects of eccentric exercise due to the repeated bout effect. But may also
make the sample unable to generalise to a wider untrained population. The increase in
baseline CK from one trial to the other and the large baseline difference between individuals
in the study indicates someparticipants may be currently training or greater trained to exercise
than they believe. As a result, improved sampling methods are needed to recruit untrained
participants. Future research should look to obtain objective measures through measuring

66-6920-00L-A-20145 Project 22008862
Page 33
aerobic capacity (Dogra et al. 2013) and 1 repetition max (Shimano et al. 2006) to assess the
participants training status, whilst recruiting individuals unaccustomed to eccentric exercise
may not be sufficient as concentric muscle contractions also supress the CK muscle damage
response due to the repeated bout effect (Kim et al. 2010). Future samples should look to
recruit more participants and be made up of more females. In the present study only one
female participant was included, meaning the results cannot be generalised to untrained
females due to the male bias sample, whilst the small sample size means we can only infer
significance and trends as the sample size is too small to prove significant effects of tart
cherries on recovery of muscle function and soreness.
6. Conclusion
In conclusion, the consumption of 2 tart cherry drinks per day (~90-100 cherries), 5 days pre,
on the day and 2 days post-eccentric hamstring exercise, supressed the perception of
soreness in the hamstring muscle group, whilst showing trends of accelerated force and
muscle recovery in untrained participants. We infer these improvements occurred in the tart
cherry condition due to the anti-inflammatory and anti-oxidative stress properties of the
phytochemicals found in tart cherries. Future research should look to measure inflammation
and oxidative-stress along with functional recovery and perceived soreness to identify whether
tart cherries do significantly reduce oxidative stress and inflammation in untrained participants
which could only be inferred in this present study. Future research should also focus on the
consequences of blunting post-exercise muscle damage and inflammation with tart cherries
and its effects on physiological adaptations such as muscular hypertrophy, whilst a dose
response study may be beneficial on eliciting an optimal dose and loading period for
accelerated recovery from unaccustomed or strenuous exercise.
Word Count: 11994 / 12100

66-6920-00L-A-20145 Project 22008862
Page 34
7. References:
ARMSTRONG, R.B., et al. (1991). Mechansims of exercise-induced muscle fibre injury.
[online]. Journal of sports medicine, 12 (3), 184-207.
ARMSTRONG, R.B. (1984). Mechanisms of exercise-induced delayed onset muscular
soreness: a brief review. [online]. Journal of medicine and science in sport and exercise, 16
(6), 529-538.
BAIRD, Marianne F., et al. (2012). Creatine-kinase- and exercise-related muscle damage
implications for muscle performance and recovery. [online]. Journal of nutrition and
metabolism, 2012 , 960363, 1-13.
BAMMAN, Marcas M. (2007). Take two NSAIDs and call on your satellite cells in the morning.
[online]. Journal of applied physiology, 103 (2), 415-416.
BELL, P. G., et al. (2014a). The role of cherries in exercise and health. [online]. Scandinavian
journal of medicine & science in sports, 24 (3), 477-490.
BELL, Phillip G., et al. (2014b). Montmorency cherries reduce the oxidative stress and
inflammatory responses to repeated days high-intensity stochastic cycling. [online]. Nutrients,
6 (2), 829-843.
BENTZ, Alexandra. (2009) A review of quercetin: chesmity, antioxidant properties, and
bioavailability. [online]. Journal of young investigators, 2009 April.
BIJUR, P. E., SILVER, W. and GALLAGHER, E. J. (2001). Reliability of the visual analog scale
for measurement of acute pain. [online]. Academic emergency medicine: official journal of the
society for academic emergency medicine, 8 (12), 1153-1157.
BLANDO, Federica., et al. (2004). Sour cherry (prunus cerasus l) anthocyanins as ingredients
for functional foods. [online]. Journal of biomedicine and biotechnology, 5, 253-258.
BOWTELL, Joanna L., et al. (2011). Montmorency cherry juice reduces muscle damage
caused by intensive strength exercise. [online]. Medicine and science in sports and exercise,
43 (8), 1544-1551.
BITSCH, Roland, et al. (2004). Bioavailability and biokinetics of anthocyanins from red grape
juice and red wine. [online]. Journal of biomedicine and biotechnology, 2004 (5), 293-298.

66-6920-00L-A-20145 Project 22008862
Page 35
BUTTERFIELD, T., et al. (2010) Eccentric exercise in vivo: strain-induced muscle damage
and adaptation in a stable system. [online]. Exercise sport science review, 32 (2), 51-60.
CHEUNG, Karoline., et al. (2003) Delayed onset muscle soreness. [online]. Journal of sports
medicine, 33 (2), 145-164.
CLARKSON, Priscillia., et al. (1992) Muscle function after exercise-induced muscle damage
and rapid adaptation. [online] Medicine and science in sport and exercise, 24 (5), 512-521.
CLOSE, G., et al. (2005). Effects of dietary carbohydrate on delayed onset muscle soreness
and reactive oxygen species after contraction induced muscle damage. [online] British journal
sports medicine, 39 (12), 948-953.
COHEN, J. (1977). Statistical power analysis for behavioral sciences (revised ed.). New York:
Academic Press.
CONNOLLY, Declan A. J., et al. (2003). Treatment and prevention of delayed onset muscle
soreness. [online]. Journal of strength and conditioning research, 17, 197-208.
CONNOLLY, D. A. J., et al. (2006). Efficacy of a tart cherry juice blend in preventing the
symptoms of muscle damage. [online]. British journal of sports medicine, 40 (8), 679-683.
COSTILL, D., et al. (1990). Impaired muscle glycogen resynthesis after eccentric exercise.
[online]. Journal of applied physiology, 69, 46-60.
DANNECKER, E. A., et al. (2003). Sex differences in delayed onset musclesoreness.[online].
The journal of sports medicine and physical fitness, 43, 78-84.
DALLE-GRAVE, Riccardo, et al. (2011). Cognitive-behavioral strategies to increase the
adherence to exercise in the management of obesity. [online]. Journal of obesity, 2011,
348293, 1-11.
DEMINICE, R., et al. (2010). Blood and salivary oxidative stress biomarkers following an acute
session of resistance exercise in humans. [online]. International journal of sports medicine, 31
(9), 599-603.
DOGRA, Shilpa, et al. (2013). Oxygen uptake kinetics in endurance-trained and untrained
postmenopausal women. [online]. Applied physiology, nutrition, and metabolism, 38 (2), 154.

66-6920-00L-A-20145 Project 22008862
Page 36
DROUIN, Joshua M., et al. (2004). Reliability and validity of the biodex system 3 pro isokinetic
dynamometer velocity, torque and position measurements. [online]. European journal of
applied physiology, 91, 22-29.
DUCHARME, Norm G., et al. (2008). Effect of a tart cherry juice blend on exercise-induced
muscle damage in exercising horses. [online]. Medicine & science in sports & exercise, 40,
239-240.
FANG, Jim (2014). Bioavailability of anthocyanins. [online]. Drug metabolism reviews, 46 (4),
508-520.
FRIDEN, J and LIEBER, R (2000). Serum creatine kinase level is a poor predictor of muscle
function after injury. Scandinaval journal medicine science sports, 11, 126-127.
GULICK, Dawn and KIMURA, Iris. (1996) Delayed onset muscle soreness: what is it and how
do we treat it? [online]. Journal of sports rehabilitation, 5, 234-243.
HAMLIN, Michael J. and QUIGLEY, Brian M. (2001). Quadriceps concentric and eccentric
exercise 1: Changes in contractile and electrical activity following eccentric and concentric
exercise. [online]. Journal of science and medicine in sport, 4, 88-103.
HARAMIZU, Satoshi, et al. (2011). Catechins attenuate eccentric exercise-induced
inflammation and loss of force production in muscle in senescence-accelerated mice. [online].
Journal of applied physiology, 111 (6), 1654-1663.
HOWATSON, G., et al. (2007). Repeated bout effect after maximal eccentric exercise. [online].
International journal of sports medicine, 28 (7), 557-563.
HOWATSONG, SOMEREN, K. Van. (2007). Evidence of a contralateral repeated bout effect
after maximal eccentric contractions. [online]. European journal of applied physiology, 101,
207–214.
HOWATSON, G., et al. (2010). Influence of tart cherry juice on indices of recovery following
marathon running. [online]. Scandinavian journal of medicine & science in sports, 20 (6), 843-
851.
HOWATSON, Glyn and MILAK, Adi (2009). Exercise-induced muscledamage following a bout
of sport specific repeated sprints. [online]. Journal of strength and conditioning research, 23
(8), 2419-2424.

66-6920-00L-A-20145 Project 22008862
Page 37
IBM Corp. Released 2013. IBM SPSS Statistics for Windows, Version 22.0. Armonk, NY: IBM
Corp.
JACOB, Robert A., et al. (2003). Consumption of cherries lowers plasma urate in healthy
women. [online]. The journal of nutrition, 133 (6), 1826-1829.
KEDLAYA, Divakara. (2014). Postexercise muscle soreness. [online]. Last updated May 8,
2014. http://emedicine.medscape.com/article/313267-overview.
KELLEY, Darshan S., et al. (2013). Sweet bing cherries lower circulating concentrations of
markers for chronic inflammatory diseases in healthy Humans. [online]. The journal of
nutrition, 143 (3), 340-345.
KELLEY, Darshan S., et al. (2006). Consumption of bing sweet cherries lowers circulating
concentrations of inflammation markers in healthy men and women. [online]. The journal of
nutrition, 136 (4), 981-986.
KIM, J-S, et al. (2010). Post-eccentric exercise blunted hGH response. [online]. International
journal of sports medicine, 31 (2), 95-100.
KOHL, 3rd, Harold W., et al. (2012). The pandemic of physical inactivity: Global action for
public health. [online]. Lancet, 380 (9838), 294-305.
KRUK, Joanna (2011). Physical exercise and oxidative stress. [online]. Romanian sports
medicine journal, 15, 30-40.
KRUSTRUP, P., et al. (2006) Muscle and blood metabolites during a soccer game:
implications for sprint performance. [online]. Journal of medicine science sport exercise, 38
(6), 1165-74.
KUEHL, Kerry S., et al. (2010). Efficacy of tart cherry juice in reducing muscle pain during
running: A randomized controlled trial. [online]. Journal of the international society of sports
nutrition, 7 (17), 1-6.
KUIPERS, H. (2008). Exercise-induced muscle damage. [online]. International journal of
sports medicine, 15 (3), 132-135.
LETHEM, J., et al. (1983). Outline of a fear-avoidance model of exaggerated pain perception.
[online]. Behaviour research and therapy, 21 (4), 401-408.

Tart Cherry Supplementation for Muscle Recovery

Tart Cherry Supplementation for Muscle Recovery

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Viewers also liked

Viewers also liked (7)

Similar to Tart Cherry Supplementation for Muscle Recovery

Similar to Tart Cherry Supplementation for Muscle Recovery (20)

Tart Cherry Supplementation for Muscle Recovery