Sports Med 2007; 37 (6): 519-532

REVIEW ARTICLE 0112-1642/07/0006-0519/$44.95/0

© 2007 Adis Data Information BV. All rights reserved.

The Role of Nutritional Supplements

in the Prevention and Treatment of
Resistance Exercise-Induced Skeletal
Muscle Injury
Richard J. Bloomer
Department of Health and Sport Sciences, The University of Memphis, Memphis,
Tennessee, USA

Contents
Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 519
1. Skeletal Muscle Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 521
2. Nutritional Supplements to Reduce Skeletal Muscle Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 522
2.1 Antioxidants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 522
2.2 β-Hydroxy-β-Methylbutyrate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 528
2.3 Miscellaneous Supplements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 529
3. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 530

Abstract The topic of exercise-induced skeletal muscle injury has received considerable
attention in recent years. Likewise, strategies to minimise the injury resulting
from heavy resistance exercise have been studied. Over the past 15 years, several
investigations have been performed focused on the role of nutritional supplements
to attenuate signs and symptoms of muscle injury. Of these, some have reported
favourable results, while many others have reported no benefit of the selected
nutrient. Despite these mixed findings, recommendations for the use of nutritional
supplements for the purposes of attenuating muscle injury are rampant within the
popular fitness media and athletic world, largely without scientific support. Those
nutrients include the antioxidant vitamin C (ascorbic acid) and vitamin E (tocoph-
erol), N-acetyl-cysteine, flavonoids, L-carnitine, astaxanthin, β-hydroxy-β-
methylbutyrate, creatine monohydrate, essential fatty acids, branched-chain
amino acids, bromelain, proteins and carbohydrates. A discussion of all published
peer-reviewed articles in reference to these nutrients and their impact on resis-
tance exercise-induced skeletal muscle injury is presented, in addition to a brief
view into the potential mechanism of action for each nutrient.
Based on the current state of knowledge, the following conclusions can be
made with regard to nutritional supplements and their role in attenuating signs and
symptoms of skeletal muscle injury occurring as a consequence of heavy resis-
tance exercise: (i) there appears to be a potential role for certain supplements
(vitamin C, vitamin E, flavonoids, and L-carnitine); (ii) these supplements cannot
520 Bloomer

effectively eliminate muscle injury, only attenuate certain signs and symptoms;
(iii) it is presently unclear what the optimal dosage of these nutrients is (whether
used alone or in combination); (iv) it is unclear what the optimal pretreatment
period is; and (v) the effectiveness is largely specific to non-resistance trained
individuals.
Ultimately, because so few studies have been conducted in this area, it is
difficult to recommend with confidence the use of selected nutrients for the sole
purpose of minimising signs and symptoms of resistance exercise-induced muscle
injury, in particular with regard to resistance-trained individuals.

The subject of exercise-induced skeletal muscle
injury has received considerable attention in recent
years and has been the focus of several reviews.[1-6]
This is perhaps fuelled by the increased use of heavy
resistance exercise as a means to improve muscular
strength, size, athletic performance and overall
physical conditioning. In fact, resistance exercise
has grown in popularity to include individuals from
all fitness backgrounds, ranging from sedentary old-
er adults with no formal exercise experience to
world class athletes. However, regardless of the
level of conditioning, one fact remains: high-force
resistance exercise has the ability to induce skeletal
muscle injury. This injury is often accompanied by
signs and symptoms that manifest in the minutes to
days following the acute exercise bout, including
muscle pain and impaired physical performance.
As a result of this observation, methods to mini-
mise the injury resulting from resistance exercise
have been investigated in recent years. These have
included the performance of prior exercise in an
attempt to condition the muscle, massage and the
use of NSAIDs and/or nutritional supplements. Of
these, prior exercise appears to be the best defence
against muscle injury resulting from future bouts of
heavy resistance exercise, in accordance with the
well described ‘repeated bout effect’.[7] The use of
massage and NSAIDs has been met with mixed
results,[2,8,9] and when demonstrating effectiveness,
has primarily resulted in decreased muscle soreness.
To date, 19 investigations have been published in
peer-reviewed articles in which nutritional supple-
ments were used in an attempt to attenuate the injury
response to heavy resistance exercise. These studies
have employed a wide variety of exercise protocols
(e.g. pure eccentric, mixed concentric/eccentric,
high and low volume, large and small muscle group)
as well as nutritional supplements (e.g. antioxidant
vitamins, amino acids, essential fatty acids, proteins,
carbohydrates) and have yielded mixed results. In
fact, the findings appear dependent as much upon
the marker studied as the nutritional supplement
being used in the investigation. Therefore, interpre-
tation and comparison of findings across studies can
be difficult. Unfortunately, popular fitness publica-
tions (in particular bodybuilding) and nutritional
supplement companies exaggerate the effect of nu-
tritional supplements with regard to their role in
decreasing muscle injury and improving recovery
following resistance exercise-induced muscle inju-
ry. This article presents an objective, scientific view
of studies that have focused on the use of nutritional
supplements to suppress resistance exercise-induced
skeletal muscle injury. Based on the continued inter-
est within this area among exercise scientists, sport
nutritionists, fitness trainers and athletes, it appears
that a review is warranted, especially considering
the widespread recommendation and use of certain
nutrients with the primary goal of favourably im-
pacting the muscle injury response following heavy
resistance exercise.
This article discusses the potential role of nutri-
tional supplements in attenuating resistance exer-
cise-induced muscle injury. It does not include nu-
trient intervention studies that have used aerobic
training modes as the exercise stimulus (e.g. step-
ping, downhill running), as this topic has been previ-
ously reviewed.[10] This may be considered a limita-
tion of the current review as not all studies conduct-
ed using nutrients to combat exercise-induced

© 2007 Adis Data Information BV. All rights reserved. Sports Med 2007; 37 (6)
Nutrients and Muscle Injury
muscle injury are included. Therefore, readers are
cautioned that the data presented apply specifically
to resistance exercise. It is possible that the positive
or negative findings for a given nutrient may have
differing results when applied in the context of
aerobic exercise. However, a review of the literature
on this topic concludes that results obtained from
studies using nutritional supplements (primarily an-
tioxidants) to attenuate muscle injury resulting from
aerobic exercise have been mixed, with potential
noted for vitamin E (tocopherol) to stabilise muscle
cell membranes resulting in lower creatine kinase
(CK) release into the circulation.[10] Readers inter-
ested in the role of nutrients to minimise muscle
injury resulting from aerobic exercise are referred to
Goldfarb.[10]
While aerobic exercise certainly has the ability to
cause muscle damage (often measured by muscle
protein release into the blood), the extent of damage
with lower intensity, longer duration aerobic exer-
cise is often less than with higher intensity heavy
resistance exercise, as used in the studies presented
here. Including only those studies utilising heavy
resistance exercise allows for the study pool to re-
main more homogeneous, without extrapolating
findings from one form of exercise to another, per-
haps allowing for more specific conclusions to be
drawn. This article includes a brief discussion of the
proposed mechanism(s) of action of those nutrients
for which data are presently available in relation to
attenuating muscle injury resulting from resistance
exercise, in addition to the specific findings from
peer-reviewed research articles. The review con-
cludes with a synopsis of the current state of knowl-
edge related to the role of nutritional supplements in
attenuating resistance exercise-induced muscle inju-
ry.
1. Skeletal Muscle Injury
In order to fully understand the methods of action
of the nutritional supplements in attenuating signs
and symptoms of muscle injury, as well as their
limitations to do so, it is first necessary to briefly
describe the process of skeletal muscle injury. Read-
ers are referred to the following excellent reviews on
© 2007 Adis Data Information BV. All rights reserved.
521
the topic for a more detailed understanding of the
processes involved.[1-4,6]
It is clear from the available evidence that strenu-
ous, unaccustomed exercise, typically involving ec-
centric actions in which the muscle is actively
lengthened, damages muscle in a fibre-specific man-
ner (e.g. the actively engaged fibres are damaged,
with selective sarcomeres being targets of dam-
age[4]). While both type 1 (slow) and type 2 (fast)
fibres experience injury, there appears to be a type 2
fibre bias, as demonstrated previously in animals.[11]
It is believed that the eccentric muscle actions in-
volve fewer motor units, less muscle fibre involve-
ment and greater force production. In this way, more
stress is placed on the engaged fibres, leading to
damage. Higher training intensity, an increase in
angular velocity, longer duration of eccentric ac-
tions and longer fibre lengths as they are subjected
to the stress[12] contribute to greater injury. It ap-
pears that the initial mechanical insult produces
damage that occurs rapidly (i.e. within 15 min-
utes[13]) and sporadically throughout the fibre (i.e.
focal injury). This initial mechanical trauma gives
rise to a host of biochemical changes within the
affected area, which may lead to increased genera-
tion of inflammatory cytokines and reactive oxygen
species (ROS) that may further degrade muscle pro-
teins and contribute to delayed injury.
Both direct and indirect markers of muscle fibre
injury often accompany the damage. These include
direct markers of tissue damage (e.g. cytoskeleton
disruption and/or magnetic resonance imaging
[MRI] of the affected muscle), in addition to multi-
ple indirect markers including: delayed-onset mus-
cle soreness (DOMS), decreased muscle force (both
isometric and dynamic) and decreased range of mo-
tion (ROM), increased muscle girth (probably medi-
ated by inflammation), increased urinary markers of
protein degradation (e.g. 3-methylhistidine
[3-MH]), increased blood markers of muscle cell
membrane disruption (CK and lactate
dehydrogenase [LDH]) and increased inflammatory
biomarkers (C-reactive protein and interleukin-6
[IL-6]). Related to these markers, the time course of
peak change varies greatly from one to another.
Sports Med 2007; 37 (6)
522
Fortunately, the extent of muscle damage is general-
ly minor. Based on the fact that most studies have
used muscle soreness and CK as dependent vari-
ables, it is possible to state with some degree of
confidence that these variables typically peak from
48 to 72 hours following exercise and may remain
significantly elevated for 7–10 days, after which
time they return to baseline values (in most cases).
Not enough data are available in reference to other
dependent measures to make statements of certainty
concerning their time course of change. It should be
noted that the magnitude of damage is reduced sig-
nificantly by conditioning of the muscle through
prior activity of a similar nature (i.e. a repeated bout
effect[14]).
2. Nutritional Supplements to Reduce
Skeletal Muscle Injury
Considering the characteristics of the initial
mechanical trauma imposed on activated muscle
fibres by heavy resistance exercise, it appears as
though nutritional supplements would function to
minimise the secondary or delayed-onset damage.
As a result of the variety of events associated with
changes in the signs and symptoms of muscle injury,
it is unlikely that any one specific nutrient (or com-
bination of nutrients) would function to effectively
eliminate muscle injury. Rather, the degree of dam-
age may simply be reduced. To identify published
peer-reviewed articles within this area of research, a
detailed search of PubMed, Google Scholar, Info-
Trac and the Internet (Google) was conducted be-
tween 28 and 31 March 2006 using the following
keywords in multiple combinations: ‘nutritional
supplements’, ‘nutrients’, ‘antioxidants’, ‘vitamins’,
‘muscle damage’, ‘muscle injury’, ‘resistance exer-
cise’, ‘eccentric exercise’, ‘exercise’, ‘strength
training’ and ‘soreness’. Nineteen studies were iden-
tified that have been presented in peer-reviewed
articles using a combination of heavy resistance
exercise to induce muscle injury and nutritional
supplements to combat the injury (table I).
© 2007 Adis Data Information BV. All rights reserved.
Bloomer
2.1 Antioxidants
It has been suggested that ROS may play a role in
both the initiation and the progression of muscle
fibre injury.[34-37] This injury may result from tempo-
rary periods of ischaemia followed by reperfusion
and the generation of xanthine oxidase. Moreover,
neutrophil respiratory burst activity may give rise to
ROS either during or following strenuous exer-
cise.[38] ROS may promote oxidation of various pro-
teins, including those responsible for calcium re-
lease such as ryanodine receptors associated with
the sarcoplasmic reticulum. In addition, the activity
of calcium adenosine triphosphatase is inhibited
with exposure to ROS. Impairments in calcium re-
lease and re-uptake may lead to decreased muscle
contractile ability and force production. This, cou-
pled with sarcolemma destruction due to extensive
lipid peroxidation and oxidative damage to structur-
al and contractile proteins within skeletal muscle,
can lead to impaired muscle performance. It is be-
lieved that antioxidant therapy may function to at-
tenuate signs and symptoms of muscle injury, per-
haps by minimising the damaging effects of ROS.[10]
While numerous antioxidants are present in
whole foods and available as nutritional supple-
ments, those that have been most well investigated
in relation to exercise-induced muscle injury include
the water-soluble vitamin C (ascorbic acid) and lip-
id-soluble α tocopherol. While most studies in the
literature using vitamin E have used α tocopherol
exclusively, it should be understood that four
isoforms each of tocopherol and tocotrienol are pre-
sent in vitamin E. These include α, β, δ and γ. Of
these, α tocopherol has the greatest antioxidant ac-
tivity in vivo and is widely sold in isolation as a
nutritional supplement. However, exploration into
the beneficial properties of these other forms of
vitamin E is currently underway. In addition to these
vitamins, investigators have recently studied the role
of more novel antioxidant nutrients such as astax-
anthin,[17] flavonoids[23] and carnitine.[32] Collective-
ly, and when compared with all other nutrient clas-
ses, the antioxidants appear to be most effective in
relation to attenuating resistance exercise-induced
Sports Med 2007; 37 (6)
Nutrients and Muscle Injury 523

Table I. Effect of nutritional supplements on markers of exercise-induced skeletal muscle injury. Reproduced from Bloomer and Goldfarb,[15]
with permission from Alliance Communications Group, a division of Allen Press, Inc.

Reference Supplementationa Subjects Exercise Marker Effect

Avery et al.[14] Vitamin E (tocopherol) 18 untrained men Full body resistance CK ↑
[1200 IU/d] for 21d before exercise protocol DOMS –
exercise and during 10d of MIF –
recovery Muscle power –

Beaton et al.[16] Vitamin E (1200 IU/d) for 30d 16 untrained men 240 eccentric actions of CK ↓
before exercise knee flexion/extension DOMS –
MIF –
Concentric torque –
Inflammatory cells –
Cytoskeleton –
disruption

Bloomer et al.[17] Astaxanthin (4 mg/d) 20 trainedb men 10 sets of 7–10 reps at CK –

for 3wk before exercise and 85% eccentric 1-RM with LDH –
during 4d of exercise recovery knee extensors DOMS –
MIF –
Concentric 1-RM –
Dynamic force –

Bloomer et al.[18] Vitamin C (ascorbic acid) 18 untrained 48 maximal eccentric CK ↓

(1g/d), vitamin E (400 IU/d) and women muscle actions with elbow DOMS ↓
selenium (90 μg/d) for 14d flexors ROM –
before exercise and during 4d MIF –
of exercise recovery

Childs et al.[19] Vitamin C (12.5 mg/kg/d) 14 untrained men 30 eccentric actions at CK ↑

NAC (10 mg/kg/d) for 7d after 80% eccentric 1-RM with LDH ↑
exercise elbow flexors IL-6 –
DOMS –
ROM –

Hoffman et al.[20] HMB (3 g/d) for 10d of 26 trained men Two-a-day sessions (pre- CK –
pre-season football training season football training) Soreness –
Kaminsky and Boal[21] Vitamin C (3 g/d) for 3d before 19 untrained men 15 min of cyclic plantar DOMS ↓
exercise and during 4d of and women flexion and extension
exercise recovery exercise
Kreider et al.[22] HMB (3 or 6 g/d) for 4wk 40 trained men Full body resistance CK –
concurrently with exercise training protocol for 4wk LDH –
(6.9 ± 0.7 h/wk)
Lenn et al.[23] Fish oil (1.8 g/d) or isoflavone 16 untrained men 50 maximal eccentric CK –
(120 mg/d soy isolate: genistein and women muscle actions with elbow DOMS –
and daidzein in 1.3 : 1 ratio) for flexors Circumference –
30d before exercise and during ROM –
7d of exercise recovery MIF –
IL-6 –
McBride et al.[24] Vitamin E (1200 IU/d) for 2wk 12 trained men Full body resistance CK ↓
before exercise training protocol at 50% DOMS –
1-RM (24 sets in total)
Nissen et al.[25] HMB (1.5 or 3 g/d) for 41 untrained men Full body resistance CK ↓
3wk concurrently with exercise training protocol (3d/wk) for LDH –
3wk 3-MH ↓

Continued next page

© 2007 Adis Data Information BV. All rights reserved. Sports Med 2007; 37 (6)
524 Bloomer

Table I. Contd
Reference Supplementationa Subjects Exercise Marker Effect
Paddon-Jones et al.[26] HMB (40 mg/kg/d) for 6d before 17 untrained men 24 maximal eccentric DOMS –
exercise and during 10d of muscle actions with elbow Circumference –
exercise recovery flexors MIF –
Concentric torque –
Eccentric torque –
Phillips et al.[27] Mixed tocopherols (300 mg/d), 40 untrained men 30 eccentric actions at CK –
DHA (800 mg/d) and flavonoids 80% eccentric 1-RM with LDH –
(300 mg/d) for 7d before elbow flexors DOMS –
exercise and during 7d of ROM –
recovery CRP ↓
IL-6 ↓
Rawson et al.[28] Creatine monohydrate (20 g/d) 23 untrained men 50 eccentric actions with CK –
for 5d before exercise elbows flexors LDH –
DOMS –
MIF –
ROM –
Circumference –
Shafat et al.[29] Vitamin C (500 mg/d) and 12 untrained men 300 maximal eccentric DOMS –
vitamin E (1200 IU/d) for 30d muscle actions with knee MIF ↑
before exercise and during 7d extensors E-stim muscle force ↑
of exercise recovery
Shimomura et al.[30] Isoleucine (1g) + leucine (2.3g) 30 untrained men 7 sets of 20 reps of squats DOMS
+ valine (1.2g) 15 min before and women (load unspecified) women ↓
exercise men –
Stone et al.[31] Bromelain (900 mg/d) 19 untrained men Flexion/extension exercise DOMS –
immediately and for 4d after and women using standardised loaded ROM –
exercise dumbbell with elbow Concentric peak –
flexors to failure torque
Volek et al.[32] L-carnitine (2 g/d) for 3wk 10 trained men 5 sets of 15–20 reps of CK ↓
before exercise and during 4d squats at 50% concentric DOMS ↓
of exercise recovery 1-RM MRI-assessed ↓
tissue damage
Wojcik et al.[33] CHO (1.25 g/kg) or CHO and 26 untrained men 100 eccentric actions at CK –
PRO mix (0.875 g/kg CHO and 120% of 1-RM with DOMS –
0.375 g/kg PRO) immediately quadriceps Isokinetic peak –
and 2h after exercise torque –
IL-6 –
3-MH
a A placebo condition was included for comparison in each investigation.
b ‘Trained’ refers to resistance trained.
1-RM = one-repetition maximum; 3-MH = 3-methlylhistidine; CHO = carbohydrate; CK = creatine kinase; CRP = C-reactive protein; DHA =
docosahexanoate; DOMS = delayed-onset muscle soreness; E-stim = electrical stimulation; HMB = β-hydroxy-β-methylbutyrate; IL-6 =
interleukin-6; LDH = lactate dehydrogenase; MIF = maximal isometric force; MRI = magnetic resonance imaging; NAC = N-acetyl-cysteine;
PRO = protein; reps = repetitions; ROM = range of motion; – indicates no difference from placebo; ↑ indicates higher vs placebo, ↓
indicates lower vs placebo.

muscle injury. However, there are still relatively few
studies demonstrating benefits.
The earliest study to investigate the role of anti-
oxidants in relation to resistance exercise-induced
muscle damage was performed by Kaminsky and
Boal[21] in 1992. In a double-blind, crossover design,
19 untrained men and women ingested either 3 g/
day of vitamin C or placebo for 3 days before
exercise and during the 4 days following exercise. It
is believed that vitamin C possesses anti-inflam-
matory properties, maintains vitamin C in the re-
duced and active form and acts to scavenge hydrox-
yl radical in the aqueous phase. Collectively, these
effects may serve to decrease ROS-mediated dam-

© 2007 Adis Data Information BV. All rights reserved. Sports Med 2007; 37 (6)
Nutrients and Muscle Injury
age to cellular components related to muscle func-
tion (e.g. structure proteins and contractile pro-
teins).[39] In this study, individuals performed 15
minutes of cyclic (i.e. 15 seconds on and 15 seconds
off) isotonic plantar flexion exercise. DOMS was
measured using a 10cm visual analogue scale. Indi-
viduals recorded their muscle soreness before and
for up to 96 hours post-exercise. DOMS was noted
to be lower in the vitamin C group at the 48-, 58- and
72-hour timepoints, with the greatest difference ob-
served at the 58-hour timepoint (e.g. individuals
receiving placebo reported a mean rating of 6.3/10
while individuals receiving vitamin C reported a
mean rating of 3.5/10). While these findings were of
statistical significance, it should be noted that a high
degree of variability existed among individuals with
regard to DOMS attenuation with vitamin C treat-
ment, indicating that some individuals were ‘re-
sponders’ while others were ‘non-responders’.
Therefore, caution is advised when interpreting
these data.
The findings of Kaminsky and Boal[21] differ
from those of Childs et al.[19] In this investigation, 14
untrained men ingested either a placebo drink mix or
a drink mix containing 12.5mg of vitamin C and
10mg of the antioxidant N-acetyl-cysteine per kilo-
gram of body mass immediately after exercise and
each day following exercise for 7 days, in a double-
blind design. The dosage of vitamin C used was
roughly one-third of the amount used in the Kamin-
sky and Boal[21] study. The exercise protocol includ-
ed three sets of ten repetitions performed at 80% of
the individuals’ eccentric one-repetition maximum
with the elbow flexors. While certain antioxidant
enzymes (e.g. superoxide dismutase and glutathione
peroxidase) were higher with the antioxidant treat-
ment, no difference was noted in DOMS between
conditions. Neither ROM nor IL-6 were affected by
the antioxidant treatment. The two most commonly
used markers of sarcolemma integrity, CK and
LDH, were higher in individuals in the antioxidant
treatment group, suggesting that supplementation
might have exacerbated the damage response.
It is possible that the damaging nature of the
eccentric exercise could have led to an increase in
© 2007 Adis Data Information BV. All rights reserved.
525
free iron, which could have reacted with the vitamin
C to form the ascorbate radical and Fe2+, ultimately
reacting with hydrogen peroxide to form the highly
reactive hydroxyl radical. The hydroxyl radical is
known to react with membrane lipids, promoting the
chain reaction sequence of lipid peroxidation, lead-
ing to impaired membrane integrity.[40] This may
help to explain the findings of increased enzyme
release from within the muscle. Unlike the Kamin-
sky and Boal[21] study, the antioxidant treatment in
this investigation was administered after the eccen-
tric exercise. This suggests that prophylactic use of
vitamin C may have greater protective properties
than intake following the insult. The timing of sup-
plementation in relation to the exercise bout needs to
be considered in future research.
Neither of these investigations measured muscle
performance, which has been suggested to best re-
present the extent of muscle damage following exer-
cise.[41] Therefore, it is presently unknown whether
or not vitamin C supplementation alone can
favourably alter muscle performance characteristics.
Whether moderate- to high-dose vitamin C would
have a beneficial or detrimental use in a practical
setting, where muscle force decrements may be of
greatest concern, remains to be determined.
Aside from vitamin C supplementation, other
investigations have focused on the role of vitamin E
in attenuating exercise-induced muscle injury. The
proposed mechanism of action of vitamin E appears
to be sarcolemma stabilisation, while functioning as
a chain-breaking antioxidant to inhibit lipid perox-
idation owing to ROS generation. Beaton et al.[16]
supplemented individuals with either placebo or
1200 IU/day of vitamin E for 30 days prior to
performing 24 sets of ten repetitions of knee flexion/
extension exercise, in a double-blind manner. Both
direct and indirect markers of muscle damage were
assessed before and through 7 days of exercise re-
covery. With the exception of a lower CK activity at
3 days following exercise, vitamin E supplementa-
tion had no effect on any measured variable, includ-
ing the direct assessment of tissue damage, cytos-
keletal disruption. Moreover, vitamin E did not af-
fect muscle force. It is possible that the extreme
Sports Med 2007; 37 (6)
526
volume employed in this investigation (e.g. 240
repetitions) created so much trauma that any poten-
tial effect of vitamin E may have been overcome by
the extent of the injury. However, in opposition to
this hypothesis, a study by Shafat et al.[29] using a
slightly greater exercise volume (e.g. 300 repeti-
tions) demonstrated a benefit. However, it should be
noted that individuals in this trial received a combi-
nation of vitamins E and C, as opposed to vitamin E
treatment alone, and continued supplementation
during the 7-day recovery period. It is possible that
combination therapy in relation to resistance exer-
cise-induced muscle injury provides additional pro-
tection above and beyond vitamin E therapy alone
(perhaps due to the ability of vitamin C to reduce
vitamin E into its active form following oxidation),
but this remains to be investigated in randomised
double-blind trials.
McBride et al.[24] noted no difference in DOMS
following a full body resistance exercise protocol
between individuals consuming placebo and those
consuming 1200 IU/day of vitamin E for 2 weeks
prior to exercise. However, individuals receiving the
vitamin E treatment demonstrated a lower CK activ-
ity compared with those receiving placebo. Unlike
most studies in this area, individuals in this investi-
gation were regularly performing resistance train-
ing, and because of this, may have already been
‘protected’ by their body’s own endogenous antioxi-
dant defence system, in addition to the muscular and
neural adaptations that serve to decrease the extent
of muscle injury during subsequent exercise bouts.[7]
These adaptations likely exceed any benefit to be
gained through supplemental antioxidant therapy
and may have contributed to the findings of Mc-
Bride et al.[24]
Beaton et al.[16] and McBride et al.[24] demonstrat-
ed that vitamin E could attenuate CK activity while
having no impact on other markers of muscle dam-
age. However, it was recently reported that 1200 IU/
day of vitamin E for 3 weeks prior to exercise
actually increased CK activity compared with place-
bo.[14] The authors suggested that the high degree of
variability in CK response among individuals could
have accounted for this finding. Moreover, no dif-
© 2007 Adis Data Information BV. All rights reserved.
Bloomer
ferences were noted between treatment groups for
DOMS, muscle force or muscle power.
Considering these studies, it appears that vitamin
E supplementation alone at dosages as high as 1200
IU/day has no favourable impact on markers of
muscle injury, with the possible exception of blunt-
ed CK activity. Furthermore, because the findings of
lower CK activity may simply represent the ability
of vitamin E to stabilise the sarcolemma leading to
less membrane disruption, caution should be used
when considering CK alone as a reliable index of
muscle injury. This is especially true in light of the
fact that CK does not correlate well with other
markers of muscle injury, including the direct mark-
er of cytoskeletal damage.[41]
Other investigators have used a combination of
vitamins C and E in an attempt to combat muscle
injury. These antioxidants function within different
body compartments (aqueous for vitamin C vs lipid
for vitamin E). Despite this, these antioxidant vita-
mins have multiple and synergistic biological activi-
ties that likely complement each other in vivo, as
vitamin C can assist in maintaining vitamin E in the
reduced and active state.[39] Bloomer et al.[18]
randomised 18 untrained women to either placebo or
an antioxidant mixture (vitamin C 1g, vitamin E
400IU, selenium 90μg) each day for 14 days before
exercise and during 4 days of exercise recovery.
Both CK and DOMS were lower in the days follow-
ing exercise in the antioxidant treatment group com-
pared with placebo. The antioxidant treatment had
no effect on maximal isometric force (MIF) or
ROM. Using a similar combination of nutrients,
Shafat et al.[29] reported no difference in DOMS
following eccentric exercise. However, the authors
did note an attenuated strength loss in untrained men
consuming a combination of vitamin C (500 mg/
day) and vitamin E (1200 IU/day) for 30 days before
exercise and during 7 days of exercise recovery.
Considering all studies using vitamins C and E,
there appears some evidence for an effect with vita-
min C alone[21] and in conjunction with vitamin
E.[18,29]
Aside from vitamins C and E, other antioxidants
have been used in recent years for the purposes of
Sports Med 2007; 37 (6)
Nutrients and Muscle Injury
minimising resistance exercise-induced muscle inju-
ry. Carnitine is a derivative of the amino acid lysine
(technically classified a vitamin BT), manufactured
in the body and consumed in the diet primarily from
red meat, and exists in the active form as L-carni-
tine. Its primary role is to assist in the transfer of
activated fatty acids into the mitochondrial matrix to
undergo β oxidation and adenosine triphosphate
production and may serve to prevent ROS-mediated
damage resulting from enhanced mitochondrial res-
piration. It has been shown to have antioxidant
properties both in vivo and in vitro, and may act as a
radical scavenger and iron chelator to decrease the
negative consequences of ROS. A recent report pro-
vides in vitro evidence for increased antioxidant
gene and protein expression with carnitine incuba-
tion.[42] In addition, transient ischaemia in endotheli-
al cells can promote carnitine release, oxidative
stress owing to xanthine oxidase production and
impaired blood flow. Therefore, supplemental carni-
tine may serve to maintain normal blood flow and
minimise the extent of ischaemia and ROS produc-
tion.
Volek et al.[32] studied the impact of L-carnitine
on markers of muscle damage following squat exer-
cise. Ten trained men were assigned to either place-
bo or L-carnitine (2 g/day) for 3 weeks before per-
forming five sets of squats for 15–20 repetitions at
50% of their one-repetition maximum and during 4
days of exercise recovery. Individuals receiving the
L-carnitine treatment experienced lower CK,
DOMS and MRI-assessed tissue damage compared
with placebo, suggesting a positive role for this
supplement. It is possible that L-carnitine treatment
in this study could have provided antioxidant bene-
fits as already described in addition to maintenance
of blood flow and adequate oxygen to active muscle
tissue. To lend support to this hypothesis, both hy-
poxanthine and xanthine oxidase were lower follow-
ing exercise in individuals receiving L-carnitine ver-
sus placebo. This is the first study to provide mech-
anistic data related to L-carnitine supplementation
and the attenuation of resistance exercise-induced
muscle injury. Based on these preliminary data, it is
possible that L-carnitine may provide benefits in
© 2007 Adis Data Information BV. All rights reserved.
527
relation to attenuating muscle injury in individuals
involved in heavy resistance exercise.
The carotenoid astaxanthin is another antioxidant
that has received attention recently and may provide
cell membrane stability, scavenge free radicals and
function to decrease inflammation.[43,44] It was re-
cently reported that astaxanthin can attenuate aero-
bic exercise-induced damage in mouse skeletal and
heart muscle, including the associated neutrophil
infiltration that may potentiate further injury.[45] To
determine if similar benefits would be present in
humans following eccentric resistance exercise,
Bloomer et al.[17] supplemented trained men with 4
mg/day of astaxanthin for 3 weeks before exercise
and during 4 days of exercise recovery. In contrast
to the animal study performed by Aoi et al.,[45]
which only measured CK as a marker of muscle
injury, Bloomer et al.[17] observed no benefit for
astaxanthin in relation to CK, LDH, DOMS or mus-
cle performance. Taken together, these initial find-
ings provide no evidence that astaxanthin can
favourably impact the muscle injury response in
humans following resistance exercise.
Isoflavones have grown in popularity in recent
years, are believed to have antioxidant properties[46]
and have been shown to reduce proinflammatory
cytokines.[47] In addition, the omega-3 fatty acids
found in fish oil have been associated with reduced
production of proinflammatory mediators, possibly
leading to less muscle swelling and pain following
damaging exercise. Lenn et al.[23] studied the inde-
pendent effects of isoflavones (120 mg/day soy iso-
late: genistein and daidzein in 1.3 : 1 ratio) and fish
oil (1.8 g/day) for 30 days before exercise and
during 7 days of exercise recovery. When compared
with a placebo condition, no differences were noted
between any of the groups for CK, DOMS, circum-
ference, ROM, MIF or IL-6. A higher dosage of
flavonoids (quercetin 200 mg/day + hesperetin 100
mg/day) in conjunction with 300 mg/day of mixed
tocopherols and 800 mg/day of docosahexanoate
was used in a study by Phillips et al.[27] Forty un-
trained men were supplemented with the above mix-
ture or placebo for 7 days before eccentric exercise
and during 7 days of recovery. Results demonstrated
Sports Med 2007; 37 (6)
528
a reduction in the inflammatory markers C-reactive
protein and IL-6 in individuals receiving the supple-
ment compared with those receiving placebo. How-
ever, no group differences were noted for CK, LDH,
DOMS or ROM. These data suggest that while the
combination of flavonoids, mixed tocopherols and
docosahexanoate aided in minimising inflammation,
supplementation did not lead to a change in other
more commonly assessed markers of muscle dam-
age.
Taken together, the data on antioxidants, either
alone or in combination, are mixed. The different
findings may be partly explained by the wide dis-
crepancies in the type and form of antioxidant pro-
vided, the timing and dosage of supplement admin-
istration, as well as the actual degree of training of
the individuals. Furthermore, although all protocols
used resistance exercise, the volume, intensity and
specific movements have differed across some stud-
ies. In relation to individuals training status, many
authors report that individuals are ‘recreationally
active’, are non-resistance trained or have not per-
formed formal resistance training in the 6 months
prior to participating. While the role of prior exer-
cise in providing a protective effect on muscle has
been well described,[7] care must be taken to selec-
tively screen individuals for the extent of their par-
ticipation in prior resistance exercise (e.g. type of
movements, intensity, volume), whether using
‘trained’ or ‘untrained’ individuals. Such screening
will allow for a more homogenous population. It is
possible that the degree of previous training per-
formed by individuals either within or across studies
could confound results and make interpretation of
the overall findings difficult.
Considering these factors, when administered for
a period of days prior to exercise, vitamin C appears
to reduce DOMS in untrained individuals, either
alone at 3 g/day (although a great degree of individ-
ual variability exists)[21] or at a lower dosage (1 g/
day) when taken in combination with vitamin E.[18]
With the exception of one study demonstrating an
attenuated strength loss following vitamins C and E
combination therapy,[29] no other investigators have
reported a positive effect of these antioxidants on
© 2007 Adis Data Information BV. All rights reserved.
Bloomer
muscle function. Therefore, this finding should be
taken with caution. Favourable results for other de-
pendent variables following vitamin C and/or E
supplementation have been either mixed (e.g. CK)
or nonexistent. Flavonoids (quercetin 200 mg/day +
hesperetin 100 mg/day) in conjunction with 300 mg/
day of mixed tocopherols and 800 mg/day of
docosahexanoate may reduce markers of inflamma-
tion in untrained individuals, but have no effect on
other markers of muscle injury. Finally, one isolated
study has demonstrated that L-carnitine (2 g/day)
can reduce CK, DOMS and MRI-assessed tissue
injury in trained men.
2.2 β-Hydroxy-β-Methylbutyrate
Apart from antioxidants, the leucine metabolite
β-hydroxy-β-methylbutyrate (HMB) is the next
most widely recommended and studied nutritional
supplement in relation to exercise-induced muscle
injury. It is believed that HMB possesses anti-cata-
bolic actions and can decrease nitrogen loss by
inhibiting muscle proteolysis, which in turn may
lead to a more rapid recovery. Aside from the scant
evidence indicating this to be the case (in untrained
individuals), there have been no other mechanisms
described in the literature related to the role of HMB
in altering other markers of muscle injury.
The first human trial to study the effects of HMB
on markers of muscle damage was performed by
Nissen et al.[25] In this investigation, 41 untrained
men were given 0, 1.5 or 3 g/day of HMB for 3
weeks concurrently with a full body resistance exer-
cise programme. Supplementation produced only a
modest reduction in urinary 3-MH, a crude marker
of protein breakdown, and CK when measured at the
end of weeks 2 and 3 of training. The study results
could have been somewhat confounded by the inclu-
sion of a protein beverage in addition to the HMB
treatment (i.e. individuals received various dosages
of protein along with HMB). Therefore, based on
these data alone, it is difficult to conclude that HMB
is effective in reducing the degree of muscle damage
associated with resistance exercise. In another study
using HMB alone, muscle force, circumference and
DOMS were measured following a bout of eccentric
Sports Med 2007; 37 (6)
Nutrients and Muscle Injury
exercise in untrained men assigned to either placebo
or HMB at 40 mg/kg/day for 6 days before exercise
and during 10 days of exercise recovery.[26] No
effect was noted for any of the dependent variables
following HMB supplementation.
Two investigations focused on HMB have used
resistance-trained individuals. Kreider et al.[22] stud-
ied the impact of HMB to decrease muscle catabol-
ism and damage following resistance exercise. Forty
men with >1 year of resistance training experience
consumed 0, 3 or 6 g/day of HMB in a meal replace-
ment drink for 28 days, while performing their nor-
mal resistance training routines (e.g. 6.9 ± 0.7 hour/
week). Both CK and LDH were assessed before and
following 4 weeks of training and no differences
were noted between any of the three conditions for
these variables. Recently, Hoffman et al.[20] studied
the effect of HMB supplementation at 3 g/day for 10
days of pre-season football training on muscle sore-
ness and CK in college football players. Results
demonstrated no difference between HMB- and pla-
cebo-treated individuals in reference to these vari-
ables.
Collectively, the data in relation to HMB supple-
mentation suggest little or no benefit with this amino
acid derivative in terms of minimising signs and
symptoms of exercise-induced muscle injury. With
the exception of lower urinary 3-MH and a moderate
reduction in CK at certain times following training
as reported by Nissen et al.,[25] there exists no evi-
dence of any benefit associated with the use of this
supplement related to attenuating muscle injury. It is
possible that the training status of individuals could
be partly responsible for the differing results. In
addition, as with the antioxidant studies, the vast
difference in exercise protocols used and dependent
variables measured in these investigations may have
impacted upon the findings. Therefore, with the
possible exception of minimal benefits related to
decreased protein breakdown in untrained individu-
als, evidence in support of the use of HMB for
purposes of favourably altering other markers of
muscle injury, or providing any benefit in resis-
tance-trained individuals, is presently unavailable.
© 2007 Adis Data Information BV. All rights reserved.
529
2.3 Miscellaneous Supplements
While other nutritional supplements (specifically
amino acids) have been used in relation to acute
bouts of heavy resistance exercise for purposes of
stimulating protein anabolism and decreasing prote-
olysis as reviewed previously,[48] only four other
studies using nutritional supplements to attenuate
skeletal muscle injury following resistance exercise
have been identified in peer-reviewed articles.
These have included the use of creatine monohy-
drate,[28] protein and carbohydrate,[33] branched-
chain amino acids (BCAA),[30] and bromelain.[31]
While these supplements have been recommended
for their selective benefits (e.g. to improve exercise
performance, increase protein anabolism and muscle
mass, and enhance glycogen resynthesis following
strenuous exercise), they do not appear to have any
benefit when it comes to retarding the negatives
consequences of heavy resistance exercise.
Rawson et al.[28] studied 23 untrained men receiv-
ing either placebo or creatine monohydrate at 20 g/
day for 5 days before a bout of eccentric elbow
flexion exercise. It was hypothesised that due to the
ability of creatine to bind to the polar phospholipid
heads of the sarcolemma, it would provide stabilisa-
tion, decreasing membrane fluidity and minimising
events leading to degradation and loss of muscle
function. While CK was slightly lower for individu-
als in the creatine condition, the difference was not
statistically different from individuals in the placebo
condition. Furthermore, no difference was noted
between conditions for LDH, DOMS, ROM, MIF or
circumference, suggesting that prophylactic supple-
mentation with creatine monohydrate does not
favourably impact upon the muscle damage re-
sponse to eccentric resistance exercise.
The effects of post-exercise carbohydrate and
protein ingestion on markers of muscle injury were
investigated by Wojcik et al.[33] Twenty-six un-
trained men performed ten sets of ten repetitions of
unilateral eccentric quadriceps actions at 120% of
their isometric one-repetition maximum, followed
by consumption of a carbohydrate, carbohydrate and
protein or placebo beverage immediately and 2
hours’ post-exercise. As a result of the high concen-
Sports Med 2007; 37 (6)
530 Bloomer

tration of amino acids in the carbohydrate and prote- mentation, which resulted in lower DOMS in wo-
in condition, it was believed that muscle proteolysis men during the 4 days’ post-exercise in one investi-
would be decreased, while protein synthesis would gation.[30]
be favourably affected. This, in turn, was hy-
pothesised to lead to a decrease in 3-MH and possi- 3. Conclusion
bly alter other signs and symptoms of the muscle Based on the available evidence, it appears that
injury. However, no differences were noted between selected nutrients may have efficacy in relation to
conditions for 3-MH, muscle force, DOMS, IL-6 or minimising the extent of injury following strenuous
CK, suggesting no effect of immediate post-exercise resistance exercise (table II). While the data are
protein and carbohydrate consumption on attenuat-
ing markers of muscle damage. Table II. Nutritional supplements and markers of exercise-induced
[30] skeletal muscle injury: evidence for effect
Shimomura et al. investigated the impact of
Variable Evidence for Nutrient(s)
BCAA supplementation following squat exercise to effecta
decrease DOMS in untrained men and women using Cytoskeleton disruption None
a crossover design (compared with placebo). Five MRI-assessed tissue Weak L-carnitine (2 g/d)
grams of a BCAA mixture was provided 15 minutes disruption

prior to performing seven sets of 20 repetitions of Muscle force Weak Vitamin C (ascorbic
acid) [500 mg/d] +
squat exercise (load unspecified). As with HMB and vitamin E (tocopherol)
protein/carbohydrate supplementation, the proposed [1200 IU/d]
mechanism of action with the BCAA is attenuation combination
IL-6, CRP Weak Mixed tocopherols,
of exercise-induced protein breakdown and stimula- DHA, flavonoids
tion of protein synthesis. Results indicated that (combination)
DOMS was less in women during the 4 days’ post- DOMS Weak Vitamin C (1–3 g/d)
exercise following BCAA treatment compared with Weak Vitamin E (400 IU/d)
placebo, with the greatest difference seen 1 and 2 [in combination with
vitamin C]
days’ post-exercise. This difference was not appar- Weak BCAA (5 g/d) – women
ent for men, and the authors speculate that the only
smaller relative dosage provided to the men could Weak L-carnitine (2 g/d)
help explain the discrepancy in findings. CK and LDH Weak Vitamin E (400–1200
IU/d)
Finally, a study by Stone et al.[31] investigated the Weak Vitamin C (1–3 g/d)
effect of the pineapple stem extract bromelain com- Weak HMB (1.5–3 g/d)
pared with placebo on DOMS, ROM and concentric Weak L-carnitine (2 g/d)
peak torque in untrained men and women following Girth None
arm curl exercise to failure. Bromelain is suggested ROM None
as a potential anti-inflammatory agent that may se- 3-MH Weak HMB (1.5–3 g/d)
lectively decrease thromboxane generation, possibly a Strength of evidence is based on outcome as well as number
of studies demonstrating benefit. If there is evidence for an
resulting in less muscle soreness and ROM loss effect in one to two studies for a given variable, the effect is
following strenuous exercise. Despite the proposed listed as weak. If there is evidence for an effect in three to
effect of this supplement, no impact was observed in five studies for a given variable, the effect is listed as
moderate. If there is evidence for an effect in more than five
individuals receiving bromelain for any dependent studies for a given variable, the effect is listed as strong.
variable through 96 hours’ post-exercise. 3-MH = 3-methlylhistidine; BCAA = branched-chain amino acid; CK
= creatine kinase; CRP = C-reactive protein; DHA =
Collectively, there appears to be no effect of any
docosahexanoate; DOMS = delayed-onset muscle soreness; HMB
of these miscellaneous supplements on markers of = β-hydroxy-β-methylbutyrate; IL-6 = interleukin-6; LDH = lactate
skeletal muscle injury following resistance exercise. dehydrogenase; MRI = magnetic resonance imaging; ROM = range
of motion.
The only possible exception is for BCAA supple-

© 2007 Adis Data Information BV. All rights reserved. Sports Med 2007; 37 (6)
Nutrients and Muscle Injury
indeed sparse and more investigations are needed to
corroborate the initial findings, the following con-
clusions may be made based on the current state of
knowledge:
1. There is evidence for an effect with vitamin C
alone and in conjunction with vitamin E, flavonoids
when taken with mixed tocopherols and docosahex-
anoate, and HMB in untrained individuals. Regard-
ing resistance-trained individuals, there is evidence
for blunted CK with vitamin E treatment, as well as
blunted CK, DOMS and tissue injury with L-carni-
tine treatment. However, it should be noted that the
evidence for all of these nutrients, because of the
limited study pool, is scant at best.
2. Nutritional supplements do not eliminate muscle
injury, but only attenuate certain signs and symp-
toms.
3. It appears that nutritional supplements need to be
consumed for a period of days to weeks prior to the
exercise stress in order to be effective. However, no
individual study has compared pretreatment with
post-exercise treatment, nor has any study compared
different durations of pretreatment. Therefore, it is
unknown whether or not an optimal pretreatment
period exists.
4. It is presently unclear what the optimal dosage of
these nutrients is because no individual study has
compared different dosages of the same supplement,
with the exception of those focused on HMB.
5. Aside from the potential for blunted CK following
vitamin E treatment, with the exception of L-carni-
tine, the effectiveness of nutritional supplements to
reduce muscle injury is specific to non-resistance-
trained individuals. As such, these findings should
not be generalised to resistance-trained individuals.
While studies have chosen to use nutrients in
isolation or in minimal combinations (e.g. vitamins
C and E), it is unknown what potential effect would
be observed if several nutrients were used in con-
junction (e.g. vitamins C and E, L-carnitine, HMB).
Because the potential mechanisms of action differ
among these nutrients, supplementation of such a
combination may provide maximal protection.
However, such a hypothesis is merely speculative at
the present time.
© 2007 Adis Data Information BV. All rights reserved.
531
While the nutritional supplements discussed in
this article may be recommended and used because
they have been shown to have efficacy within a
resistance or aerobically trained population for other
purposes (e.g. energy production, glycogen
resynthesis, enhanced immune function), they may
yield little or no benefit when it comes to minimis-
ing muscle injury resulting from heavy resistance
exercise. Unless additional data become available
providing evidence for an effect in attenuating mus-
cle injury, nutritional supplements, with few excep-
tions, should not be recommended for this specific
purpose alone.
Acknowledgements
No sources of funding were used to assist in the prepara-
tion of this review. The author has no conflicts of interest that
are directly relevant to the content of this review.
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161F Elma Neal Roane Fieldhouse, Memphis, TN
38152–3480, USA.
E-mail: rbloomer@memphis.edu
Sports Med 2007; 37 (6)