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The Prevention and Treatment of Exercise-Induced Muscle Damage



Exercise-induced muscle damage (EIMD) can be caused by novel or unaccustomed exercise and results in a temporary decrease in muscle force production, a rise in passive tension, increased muscle soreness and swelling, and an increase in intramuscular proteins in blood. Consequently, EIMD can have a profound effect on the ability to perform subsequent bouts of exercise and therefore adhere to an exercise training programme. A variety of interventions have been used prophylactically and/or therapeutically in an attempt to reduce the negative effects associated with EIMD. This article focuses on some of the most commonly used strategies, including nutritional and pharmacological strategies, electrical and manual therapies and exercise. Long-term supplementation with antioxidants or beta-hydroxy-beta-methylbutyrate appears to provide a prophylactic effect in reducing EIMD, as does the ingestion of protein before and following exercise. Although the administration of high-dose NSAIDs may reduce EIMD and muscle soreness, it also attenuates the adaptive processes and should therefore not be prescribed for long-term treatment of EIMD. Whilst there is some evidence that stretching and massage may reduce muscle soreness, there is little evidence indicating any performance benefits. Electrical therapies and cryotherapy offer limited effect in the treatment of EIMD; however, inconsistencies in the dose and frequency of these and other interventions may account for the lack of consensus regarding their efficacy. Both as a cause and a consequence of this, there are very few evidence-based guidelines for the application of many of these interventions. Conversely, there is unequivocal evidence that prior bouts of eccentric exercise provide a protective effect against subsequent bouts of potentially damaging exercise. Further research is warranted to elucidate the most appropriate dose and frequency of interventions to attenuate EIMD and if these interventions attenuate the adaptation process. This will both clarify the efficacy of such strategies and provide guidelines for evidence-based practice.
Sports Med 2008; 38 (6): 483-503
© 2008 Adis Data Information BV. All rights reserved.
The Prevention and Treatment of
Exercise-Induced Muscle Damage
Glyn Howatson
and Ken A. van Someren
1 School of Human Sciences, St Mary’s University College, Twickenham, UK
2 English Institute of Sport, St Mary’s University College, Twickenham, UK
Abstract ....................................................................................483
1. Proposed Mechanisms of Muscle Damage .................................................485
1.1 Primary Damage ....................................................................485
1.2 Secondary Damage .................................................................485
1.3 The Occurrence of Damage ..........................................................486
2. Preventative and Therapeutic Interventions to Attenuate Exercise-Induced Muscle Damage ....486
2.1 Antioxidants ........................................................................486
2.2 Carbohydrate and Protein ..........................................................489
2.3 β-Hydroxy-β-Methylbutyrate .........................................................490
2.4 NSAIDs.............................................................................491
2.5 Stretching ..........................................................................492
2.6 Massage...........................................................................492
2.7 Electrotherapeutic Modalities ........................................................493
2.8 Cryotherapy .......................................................................494
2.9 Exercise............................................................................495
2.10 Repeated Bout Effect ...............................................................496
3. Conclusion ..............................................................................498
Exercise-induced muscle damage (EIMD) can be caused by novel or unaccus-
tomed exercise and results in a temporary decrease in muscle force production, a
rise in passive tension, increased muscle soreness and swelling, and an increase in
intramuscular proteins in blood. Consequently, EIMD can have a profound effect
on the ability to perform subsequent bouts of exercise and therefore adhere to an
exercise training programme. A variety of interventions have been used prophy-
lactically and/or therapeutically in an attempt to reduce the negative effects
associated with EIMD. This article focuses on some of the most commonly used
strategies, including nutritional and pharmacological strategies, electrical and
manual therapies and exercise. Long-term supplementation with antioxidants or
β-hydroxy-β-methylbutyrate appears to provide a prophylactic effect in reducing
EIMD, as does the ingestion of protein before and following exercise. Although
the administration of high-dose NSAIDs may reduce EIMD and muscle soreness,
it also attenuates the adaptive processes and should therefore not be prescribed for
long-term treatment of EIMD. Whilst there is some evidence that stretching and
massage may reduce muscle soreness, there is little evidence indicating any
performance benefits. Electrical therapies and cryotherapy offer limited effect in
484 Howatson & van Someren
the treatment of EIMD; however, inconsistencies in the dose and frequency of
these and other interventions may account for the lack of consensus regarding
their efficacy. Both as a cause and a consequence of this, there are very few
evidence-based guidelines for the application of many of these interventions.
Conversely, there is unequivocal evidence that prior bouts of eccentric exercise
provide a protective effect against subsequent bouts of potentially damaging
exercise. Further research is warranted to elucidate the most appropriate dose and
frequency of interventions to attenuate EIMD and if these interventions attenuate
the adaptation process. This will both clarify the efficacy of such strategies and
provide guidelines for evidence-based practice.
Eccentric contractions occur when an external cific strength.
In addition, eccentric work occurs
force is greater than that being exerted by the muscle
at a lower metabolic cost than does concentric work
and hence lead to the muscle lengthening, whilst
and therefore a lower cardiovascular stress is in-
tension is generated.
In addition, the torque gener-
volved, which makes this mode of exercise attrac-
ated by maximal eccentric contractions is sizeable
tive to populations such as the elderly, who retain
and may greatly exceed maximal voluntary isomet-
greater levels of eccentric strength with age, and
ric contractions.
Although the torque produced
those with cardiovascular pathologies.
during eccentric contractions far exceeds that pro-
The culmination of benefits from eccentric
duced in other contraction types,
the metabolic
muscle actions provide compelling rationale for
cost and neural activation is less per unit of tor-
their inclusion in exercise and training regimens;
however, the damaging effects of eccentric muscle
Exercise-induced muscle damage (EIMD) is a
actions, thought necessary for adaptive remodel-
phenomenon that occurs as a result of novel or
can affect subsequent exercise sessions
unaccustomed exercise; the severity of the damage
due to residual muscle pain, restriction of movement
and the extent of discomfort are exacerbated over
and reduced capacity to exercise at an intensity that
time and can last for several days when the exercise
may be beneficial for the exerciser. Therefore, any
bout encompasses an eccentric component.
intervention that may alleviate the negative symp-
damage manifests itself as a temporary decrease in
toms of temporary EIMD may be beneficial to a
muscle function (force production and rise in pas-
range of exercising populations, from elite athletes
sive tension), increased muscle soreness, an in-
to the elderly and chronically diseased. A number of
creased swelling of the involved muscle group and
investigations have examined various interventions
an increase in intramuscular proteins in blood. Al-
in an attempt to reduce these negative effects. These
though these variables are commonly used to assess
investigations vary considerably in exercise modali-
EIMD, the methods employed can vary considera-
ty, muscle group used, duration and frequency of
bly between investigations and have been reviewed
treatments and population size, which can make
Most damage occurs when the exer-
conclusions sometimes difficult to make. This re-
cise bout is both novel and eccentric in nature.
view is not exhaustive; however, its purpose is to
Although eccentric contractions are potentially
provide the reader with a current overview of the
damaging, there are a number of benefits in con-
literature that examines interventions administered
ducting this muscle action; they produce greater
as a prophylactic or as a therapy to alleviate the
gains in hypertrophy than concentric contrac-
negative effects of EIMD.
and increase eccentric contraction-spe-
© 2008 Adis Data Information BV. All rights reserved. Sports Med 2008; 38 (6)
Muscle Damage: Prevention and Treatment 485
1. Proposed Mechanisms of EIMD occurring from eccentric biased exercise and
Muscle Damage may be limited to exercise of a long duration.
The mechanical hypothesis relates to the damage
Despite substantial research contributions to
that occurs as a direct consequence of the mechani-
EIMD, the exact mechanisms responsible for dam-
cal loading on the myofibres. Eccentric contractions
age, repair and adaptation from eccentric muscle
are capable of generating more force than isometric
actions remain inconclusive. A number of reviews
and concentric contractions and require less energy
have attempted to explain the mechanisms of EIMD
expenditure per unit of torque;
and for a more detailed overview of these the reader
lengthening of sarcomeres is non-uniform under
is directed to previous literature.
This article
eccentric conditions, which results in some myofila-
further simplifies the damage model and has divided
ments being stretched and no longer able to overlap
it into two general areas: (i) the initial phase or
within the sarcomere.
Consequently, when the
primary damage that occurs during the exercise
filaments are stretched beyond the point of overlap,
bout; and (ii) secondary damage that propagates
due to sarcomere inhomogeneity, passive structures
damage through processes associated with the in-
assume more tension and undergo what is termed
flammatory response.
and results in Z-band streaming.
The excessive tension that is placed upon these
1.1 Primary Damage
passive structures (such as desmin, synemin and
The initial events that occur as a direct outcome
titin) from repeated eccentric contractions may
of eccentric exercise may be further subdivided into
cause failure of the structure and is manifested as a
two possible pathways: metabolic and mechani-
reduction in the muscle’s ability to generate force,
Metabolic muscle damage has been pro-
which has been reviewed in detail elsewhere.
posed to result from ischaemia or hypoxia during
exercise of a prolonged nature.
Ischaemia is
1.2 Secondary Damage
thought to cause changes in ion concentration, meta-
bolic waste accumulation and adenosine triphospha-
The processes that follow the primary phase of
te deficiency, which ultimately result in dam-
damage appear to be initiated by a disruption of the
similar to that seen in EIMD.
intracellular Ca
homeostasis. An increase in the
Some previous literature examining marathon intracellular [Ca
] is thought to derive from ex-
running have reported the occurrence of damage and tracellular sources,
and consequently lead to fur-
this may be a function of reduced metabolite clear- ther myofibrillar damage in skeletal muscle.
however, marathon running has a substan- Eccentric exercise has been shown to lead to a loss
tial eccentric contraction component and the asso- of sarcoplasmic reticulum membrane integrity and
ciated mechanical stress may be the main cause of flux of Ca
into intracellular areas in rats, which
damage and any ischaemia may only exacerbate the culminates in skeletal muscle damage.
In addi-
damage from the eccentric contractions.
Compar- tion, a recent contribution to the literature has shown
isons of uphill and downhill running further support that there is a disruption in calcium homeostasis
this, with uphill running showing a higher metabolic resulting from changes in the sarcoplasmic reticu-
cost and no evidence of damage when compared lum following lengthening contractions in
with downhill running, which displayed a high inci- humans.
The influx of the Ca
into the cytosol
dence of damage at a lower metabolic cost.
More initiates a cascade of events that further damage the
recently, Beltman et al.
showed a reduced meta- cell by causing alterations to the cytoskeleton,
bolic cost during electrically stimulated lengthening sarcoplasmic reticulum, mitochondria and myofila-
contractions when compared with concentric and ments.
The Ca
-mediated responses appear to
isometric contractions in rats. Therefore, metabolic be manifested by the activation of proteolytic and
factors seem to be unlikely candidates as a basis for lipolytic pathways that lead to degradation of the
© 2008 Adis Data Information BV. All rights reserved. Sports Med 2008; 38 (6)
486 Howatson & van Someren
cell membrane and sarcolemma, cell infiltration and longer muscle lengths.
The muscle generates
subsequent activation, production of reactive oxy- excessive strain during lengthening, due to
gen species, fibre necrosis
and ultimately regen- sarcomere inhomogeneities,
and the tension from
eration of the fibres some days later.
The loss of within the muscle is derived to a larger extent from
membrane integrity allows for the ‘leakage’ of intra- passive structures and less from active tension in the
muscular proteins, both structural and cytosolic, ‘descending limb’ of the length-tension relationship,
which can be seen in blood for many days post- consequently extensive myofibrillar disruption can
However, there has recently been evi- occur.
Based on the current evidence, ec-
dence to show that necrosis may not occur after centric contractions, regardless of the speed or in-
damaging eccentric exercise in humans.
This tensity of the contraction, tend to cause damage
work and subsequent investigations from this group when the exercise bout is novel.
suggest that the tissue undergoes adaptation and
Eccentric muscle actions have been shown to be
regeneration rather than necrosis and therefore areas
beneficial to a number of populations; they are inte-
of increased cellular activity reflect synthesis and
gral to many sports and exercise activities and are
often exaggerated by some exercisers and athletes in
The exact mechanisms that underlie the initial order to promote adaptation. Any intervention used
phases in muscle damage are not completely under- either as a prophylactic or as a therapy that could
stood and it may be possible that initial damage is a help to attenuate the negative effects of these muscle
function of anomalies in excitation-contraction un- actions could prove beneficial for pain reduction,
or that passive structures within the maintaining training intensity and exercise adher-
sarcomere are compromised,
but there are ence. This review will consider human studies that
most likely contributions from both areas.
have investigated interventions to attenuate the neg-
There are convincing data to suggest that the exer- ative effects of EIMD.
cise-damage-repair process is associated with the
2. Preventative and Therapeutic
primary phase and is further exacerbated by the
Interventions to Attenuate
secondary phase,
although the extent to which
Exercise-Induced Muscle Damage
each is responsible remains debatable.
1.3 The Occurrence of Damage
2.1 Antioxidants
Investigations examining direct evidence of dam- The initial events caused by unaccustomed ec-
age immediately post-exercise have provided con- centric exercise that manifest muscle damage elicit
vincing data of myofibrillar disruption resulting an inflammatory response in which phagocytosis
from eccentric contractions,
which appear to and neutrophil respiratory burst result in the produc-
be focused within fast-twitch fibres, although more tion of reactive oxygen species (ROS), thereby im-
recent evidence suggests that some damage also posing an oxidative stress upon the tissue.
occurs to some slow-twitch fibres.
Furthermore, ROS have been implicated in the secondary damage
there is also evidence that damage may be exacer- that follows the primary mechanical disruption.
bated during faster eccentric contractions, which However, the exact nature of the relationship be-
may be due to reduced crossbridge formation that tween ROS production, EIMD and muscle soreness
occurs at higher speeds and thereby increasing the is unclear as highlighted in a recent review.
force per crossbridge and causing failure of the ary antioxidants have been proposed to reduce ROS
contractile apparatus.
However, eccentric con- production and therefore oxidative stress-imposed
tractions do not have to be maximal in nature to damage; the use of antioxidants to reduce symptoms
elicit damage,
although more damage tends to associated with EIMD has been extensively re-
occur when exercise is maximal and is carried out at viewed.
Most of the research to date has focused
© 2008 Adis Data Information BV. All rights reserved. Sports Med 2008; 38 (6)
Muscle Damage: Prevention and Treatment 487
on the effects of the antioxidant vitamins C creases the intracellular antioxidant glutathione)
(ascorbic acid) and E (tocopherol), which forms the 10 mg/kg administered for 7 days following 30
basis of this article with studies summarized in table eccentric contractions of the elbow flexors.
I. addition, supplementation with vitamin C 1000 mg
2 hours before and for 14 days following downhill
Vitamin C has been reported to have antioxidant
running delays the recovery of muscle function de-
and a number of studies have demon-
spite being effective in elevating plasma ascorbate
strated attenuated muscle damage and soreness
and attenuating the increase in MDA and conse-
when high doses are administered prophylactical-
quent ROS.
Supplementation with 3000 mg/day for 14
days prior to 70 eccentric contractions of the elbow Vitamin E is another antioxidant that has been
flexors and for 4 days post-exercise has been shown suggested to reduce intramuscular protein efflux by
to significantly reduce muscle soreness for the first increasing membrane integrity.
Reduced CK con-
24 hours post-exercise; thereafter a non-significant centrations in blood following muscle damaging
reduction in soreness was evident until 96 hours exercise when supplementing with vitamin E have
Furthermore, significant attenua- been reported.
These studies used prophylactic
tion of the glutathione ratio, which is used as a doses of 1000 IU/day for 12 weeks and 1200 IU/day
marker of oxidative stress, was observed for 24 for 14 days, respectively, demonstrating attenuated
hours post-exercise, indicating that vitamin C was CK responses following damaging exercise. In con-
effective in reducing oxidative stress, which may trast, however, another study found that despite vita-
have accounted for the reduced soreness. Whilst this min E 1200 IU/day taken for 30 days prior to 240
study demonstrated a non-significant attenuation of maximal eccentric contractions manifesting a
creatine kinase (CK) between 48 and 96 hours post- 2.8-fold increase in serum vitamin E concentration,
exercise, there were no effects of supplementation there was no effect on serum CK, Z-band disruption,
on maximal isometric force or range of motion muscle torque or muscle soreness.
It is possible,
(ROM). This study supported the findings of Ka- therefore, that longer-term supplementation periods
minsky and Boal,
demonstrating that 3000 mg/ (i.e. >30 day) may be required to confer a protective
day administered for 3 days prior to and for 4 days effect on muscle. The effects of vitamin E supple-
post-exercise (15 minutes of cyclic plantar flexion mentation on muscle damage and soreness have
and extension) decreased muscle soreness. In addi- been recently reviewed.
tion, Thompson et al.
have previously shown that
A number of studies have investigated the syner-
supplementation with 400 mg/day for 12 days prior
gistic effects of combined vitamin C and E supple-
to 90 minutes of intermittent running significantly
mentation. Shafat et al.
reported that a dosage of
reduced muscle soreness and plasma interleukin
vitamin C 500 mg/day and vitamin E 1200 IU/day
(IL)-6, although there was no effect on CK,
taken for 37 days attenuated the decline in eccentric
malondialdehyde (MDA) or muscle function.
torque during 300 maximal eccentric contractions of
In contrast, a recent study has shown supplemen- the knee extensors and in muscle function for 2 days
tation with vitamin C 3000 mg/day for 3 days prior post-exercise compared with a control. Furthermore,
and 5 days following eccentric exercise to have no females taking a daily dose of vitamin C 1000 mg
effect on strength loss, muscle soreness or ROM.
and vitamin E 400 IU for 14 days prior to and for 2
Furthermore, some studies have found supplementa- days following eccentric exercise of the elbow flex-
tion with vitamin C to be contraindicated in the ors has demonstrated decreased blood protein car-
reduction of EIMD. Increases in CK and lactate bonyls and MDA, indicative of reduced oxidative
dehydrogenase (LDH), indicative of reduced mem- stress and damage.
These findings contradict re-
brane integrity, have been reported with vitamin C cent work
in which prior supplementation with
12.5 mg/kg and N-acetyl-cysteine (NAC, which in- vitamin C 1000 mg/day and vitamin E 300 mg/day
© 2008 Adis Data Information BV. All rights reserved. Sports Med 2008; 38 (6)
488 Howatson & van Someren
Table I. Studies reporting effects of antioxidant supplementation on markers of exercise-induced muscle damage
Study Supplementation Exercise protocol Effects post-exercise
(compared with control group)
Bryer and Goldfarb
Vit C (3000 mg/d) for 14 d prior and 70 elbow flexor eccentric CK
4 d post-exercise contractions DOMS
Glutathione ratio
Muscle force
Kaminsky and Boal
Vit C (3000 mg/d) for 3 d prior and 15 min cyclic plantar flexion and DOMS
4 d post-exercise extension
Thompson et al.
Vit C (400 mg/d) for 12 d prior 90 min intermittent shuttle CK, Mb
running MDA
Muscle force
Connolly et al.
Vit C (3000 mg/d) for 3 d prior and 40 elbow flexor eccentric DOMS
5 d post-exercise contractions Muscle force
Childs et al.
Vit C (12.5 mg/kg/d) and NAC 30 elbow flexor eccentric CK
(10 mg/kg/d) for 7 d post-exercise contractions LDH
Close et al.
Vit C (1000 mg/d) 2 h prior and 14 d 30 min downhill running MDA
post-exercise Muscle force
Sacheck et al.
Vit E (1000 IU/d) for 12 wk prior 45 min downhill running CK in younger men
iPF(2α) in older men
McBride et al.
Vit E (1200 IU/d) for 14 d prior Whole-body resistance exercise CK
Beaton et al.
Vit E (1200 IU/d) for 30 d prior exercise 240 knee flexor and extensor CK
eccentric contractions Muscle force
Z-band disruption
Shafat et al.
Vit C (500 mg/d) and vit E (1200 IU/d) 300 knee extensor eccentric Decline in torque during
for 30 d prior and 7 d post-exercise contractions exercise
Muscle force
Goldfarb et al.
Vit C (1000 mg/d) and vit E (400 IU/d) 48 elbow flexor eccentric MDA
for 14 d prior and 2 d post-exercise contractions Plasma protein carbonyls
Glutathione status
Mastaloudis et al.
Vit C (1000 mg/d) and vit E (300 mg/d) 50 km ultramarathon run CK
for 6 wk prior LDH
Muscle force
Petersen et al.
Vit C (500 mg/d) and vit E (400 mg/d) 90 min downhill running IL-6
for 14 d prior and 7 d post-exercise CK
Lymphocytes (CD4
, CD8
Jakeman and Maxwell
Vit C (400 mg/d) or vit E (400 mg/d) 60 min box stepping Vit C: LFF, muscle force
for 21 d prior and 7 d post-exercise Vit E: LFF, muscle force
CK = creatine kinase; CRP = C-reactive protein; DOMS = delayed-onset muscle soreness; IL-6 = interleukin-6; iPF(2α) = iso-prostaglandin
2α; LDH = lactate dehydrogenase; LFF = low frequency fatigue; Mb = myoglobin; MDA = malondialdehyde; NAC = N-acetyl-cysteine; NK =
natural killer cells; ROM = range of motion; vit C = vitamin C (ascorbic acid); vit E = vitamin E (tocopherol); indicates decrease;
indicates increase; indicates no change.
© 2008 Adis Data Information BV. All rights reserved. Sports Med 2008; 38 (6)
Muscle Damage: Prevention and Treatment 489
for 6 weeks had no effect on markers of muscle supplementation (14 days) with either vitamin C or
E alone, or in combination, may reduce signs and
damage (LDH, CK) or hamstring or quadriceps
symptoms of EIMD through the reduction of ROS
function following a 50-km ultra-marathon. It is
following muscle damage.
possible that this difference in findings reflects dis-
parities in the nature of prolonged running and ec-
centric specific contractions; however, this study did
2.2 Carbohydrate and Protein
demonstrate significant increases in markers of
Muscle glycogen resynthesis has been shown to
muscle damage, thereby justifying comparison. The
be impaired following high-intensity eccentric exer-
role of ROS in perpetuating the inflammatory re-
Compared with a contralateral limb control,
sponse has recently been challenged.
significantly lower glycogen resynthesis in the
et al.
showed that supplementing 500 mg/day of
quadriceps was identified following eccentric knee
vitamin C and 400 mg/day of vitamin E for 14 days
extensor contractions followed by 60 minutes of
prior to, and for 7 days following 90 minutes of
cycling at 70% maximal oxygen uptake
downhill running increased plasma vitamin concen-
It was concluded that the lower carbo-
trations; however, there was no response on prolifer-
hydrate uptake in the eccentrically exercised limb
ation of cytokine or lymphocyte subpopulations.
was possibly due to inflammatory cells competing
Only one study has directly compared the effects
with muscle cells for blood glucose; however, high
of vitamins C and E in attenuating muscle dam-
dietary carbohydrate for 3 days after eccentric exer-
This work compared supplementation of vi-
cise did increase intramuscular carbohydrate stor-
tamin C 400 mg/day and vitamin E 400 mg/day for
These observations have been supported by
21 days prior to and 7 days following 60 minutes of
subsequent studies.
When eccentric contrac-
box-stepping exercise. Vitamin C significantly at-
tions were performed following glycogen-depleting
tenuated the decline in the 20/50 Hz ratio following
exercise (comprising 6 × 15-second sprints and 1-
exercise (this represents reduced low frequency fa-
hour submaximal ruining) not only was muscle gly-
tigue, which may be a consequence of attenuated
cogen reduced further in the 2 hours following exer-
muscle damage) and a trend for greater recovery in
cise, muscle glycogen resynthesis was also signifi-
muscle force in the 24-hour period post-exercise; no
cantly attenuated over the subsequent 48-hour
effects were found for vitamin E. A recent contribu-
This supports a previous investigation,
tion to the literature has examined the impact of tart
which also identified that the deficit in glycogen
cherry juice on the attenuation of symptoms of exer-
content peaked at 72 hours post-exercise, which
cise-induced muscle damage.
A daily dose of
may coincide with the delayed inflammatory re-
0.682 L (24 fl oz) for 4 days prior and 4 days
sponse that occurs after the initial myofibrillar dis-
following eccentric contractions of the elbow flex-
ruption from damaging exercise. Close et al.
ors reduced muscle soreness and attenuated the loss
compared high-carbohydrate (77%) and low-carbo-
in muscle force. Although this is the only study to
hydrate (11%) diets adopted for 48 hours prior to 30
have examined this supplement, the findings are
minutes of downhill running. There was no signif-
promising and suggest a requirement for further
icant difference in muscle soreness, CK, MDA,
research, not least to elucidate the mechanisms by
glutathione or muscle function; interestingly, how-
which any benefit may be conferred.
ever, the high-carbohydrate diet demonstrated
In summary, the literature is equivocal with re-
trends for higher soreness and CK at 24 and 48 hours
spect to the effects of antioxidant supplementation
post-exercise. Further evidence refuting the efficacy
on EIMD. Differences in dose, supplementation
of carbohydrate in attenuating muscle damage has
period and exercise interventions adopted in pre-
been presented
with no differences between gly-
vious studies confound the drawing of definitive
cogen-depleted and glycogen-repleted states for
conclusions; however, it is suggested that long-term muscle soreness, maximal isometric force, relaxed
© 2008 Adis Data Information BV. All rights reserved. Sports Med 2008; 38 (6)
490 Howatson & van Someren
knee angle and thigh circumference following 15 muscle damage (muscle function, plasma IL-6, or
urinary-3 methyl-histidine).
minutes of downhill running.
Whilst there is evidence that muscle glycogen
There is very little research that has examined the
resynthesis is impaired by exercise-induced muscle
role of protein supplementation in preventing or
damage, it appears that carbohydrate administration
alleviating symptoms of EIMD. Shimomura et al.
has little or no effect in attenuating signs and symp-
recently reported that a 5-g supplement of branched-
toms of muscle damage. There is, however, some
chain amino acids administered 15 minutes prior to
evidence that protein supplementation and the si-
squat exercise reduced muscle soreness for 4 days
multaneous ingestion of carbohydrate and protein
post-exercise in women, but not men. It is possible
may confer protection against exercise-induced
that the discrepancy between sexes was attributable
muscle damage; whether the co-ingestion of protein
to the lower relative dose in the men, as suggested
and carbohydrate provides any benefit over the in-
by the authors. Another recent study
gestion of protein alone is a question that has not yet
the effects of two amino acid supplementation strat-
been investigated and warrants research.
egies. Whilst supplementation with 3.6 g taken 30
minutes prior and immediately following exercise
(900 arm-curl repetitions) had no effect on any
2.3 β-Hydroxy-β-Methylbutyrate
markers of muscle damage, when supplementation
was extended for 4 days post-exercise (providing a
β-Hydroxy-β-methylbutyrate (HMB) has recent-
total dose of 36 g) there was a significant reduction
ly gained popularity as a dietary supplement in
in CK, blood myoglobin and muscle soreness. It is
humans, particularly among strength athletes.
clear that further research is required to elucidate the
HMB is a metabolite of the branched-chain amino
role of protein supplementation in the prevention
acid leucine and its ketoacid, α-ketoisocaproate,
and treatment of EIMD.
and has been proposed to have a prophylactic effect
in attenuating muscle protein degradation and exer-
The co-ingestion of protein and carbohydrate
cise-induced damage during intense physical train-
may also provide synergistic effects in attenuating
ing. Although no direct evidence exists as to exact
muscle damage.
Using a protocol of repeated-
mechanisms for these effects, HMB has been hypo-
cycle trials to exhaustion (the first at 75% peak
thesised to act as a precursor for cholesterol synthe-
oxygen uptake [
], the second at 85%
sis via its metabolism to β-hydroxy-β-methyl-
12–15 hours later), compared with carbo-
glutaryl CoA (HMG-CoA), thus providing a carbon
hydrate alone, the ingestion of a carbohydrate-pro-
source for cholesterol synthesis.
An increase in
tein beverage during and immediately after exercise
intracellular cholesterol could enhance cell mem-
significantly attenuated CK concentrations and sig-
brane integrity and therefore reduce muscle damage
nificantly improved performance (106.3 ± 45.2 and
following unaccustomed or intense exercise.
43.6 ± 12.5 minutes vs 82.3 ± 32.6 and 31.2 ± 8.7
other hypothesis is that HMB serves as a structural
minutes, for carbohydrate-protein and carbohydrate
component within the cell membrane.
trials, respectively). These findings indicate that the
co-ingestion of carbohydrate and protein increases
Supplementation with dosages of between 1.5
time to exhaustion and reduces muscle damage in
and 3.0 g/day has been shown to reduce muscle
prolonged endurance exercise. Small reductions in
protein degradation with consequent increases in
CK levels following eccentric exercise (100 quadri-
muscle mass and strength following resistance exer-
ceps eccentric contractions) performed in a glyco-
cise training performed for between 3 and 8
gen-depleted state have been reported as a result of
however, there is some evidence that
ingesting a carbohydrate-protein mix 2 hours and
these benefits are not observed in well trained sub-
immediately prior to exercise;
however, in con-
In addition, blood CK activity has also
trast, this study found no effect on other markers of
been shown to be reduced by HMB supplementation
© 2008 Adis Data Information BV. All rights reserved. Sports Med 2008; 38 (6)
Muscle Damage: Prevention and Treatment 491
following resistance training
and prolonged reduced muscle inflammation and CK following 20
minutes of strenuous stepping performed on the 15th
day of supplementation, thus indicating reduced
To date, only two studies have examined the
muscle damage.
Furthermore, ibuprofen taken
effects of HMB supplementation on muscle damage
before and after exercise (2400 mg) attenuates
resulting from a single bout of eccentric resistance
exercise. Paddon-Jones et al.
found that 6 days muscle damage as demonstrated by reduced CK
of HMB supplementation with 40 mg/kg body mass/
appearance in blood.
Performance benefits of
day provided no attenuation of symptoms associated
NSAID administration are, however, less clear.
with exercise-induced muscle damage following 24
Tokmakidis et al.
prescribed 400 mg ibuprofen
maximal eccentric contractions of the elbow flexors.
every 8 hours for 48 hours following eccentric leg-
In contrast, longer-term supplementation (3 g/day
curl exercise; although there was significantly less
for 14 days) prior to a single bout of eccentric
muscle soreness at 24 hours and CK at 48 hours,
resistance exercise has been reported to attenuate the
there was no effect on maximum strength, vertical
decrement in muscle function, the CK response and
jump performance or knee ROM. In contrast, some
limb swelling.
The evidence therefore suggests
studies have found NSAIDs to have no effect on
that supplementation with HMB for >6 days prior to
inflammation or muscle soreness. Donnelly et al.
exercise may attenuate symptoms of EIMD; how-
reported that doses of 1200 mg ibuprofen adminis-
ever, it should be noted that this conclusion is based
tered prior to 45 minutes of downhill running, to-
on studies examining responses in relatively un-
gether with a further 600 mg every 6 hours for 72
trained individuals who are unaccustomed to eccen-
hours post-exercise, had no effect on muscle sore-
tric exercise.
ness or strength; however, higher CK responses
were measured following supplementation. Gulick
2.4 NSAIDs
et al.
found 1200 mg of oxaprozin taken every 24
hours for 72 hours post-exercise had no effect on
NSAIDs, e.g. ibuprofen, aspirin (acetylsalicylic
indices of muscle damage. Similarly, Peterson et
acid), naproxen, diclofenac, flurbiprofen and keto-
used over-the-counter maximum doses of
profen, are perhaps the most widely known therapy
ibuprofen (1200 mg/day) and paracetamol (aceta-
in the treatment of muscle damage and delayed-
minophen) [4000 mg/day] following damaging ex-
onset muscle soreness (DOMS). NSAIDs inhibit the
ercise with no effect on the inflammatory response
synthesis of prostaglandin, a potential mediator of
24 hours post-exercise.
oedema and pain during acute inflammation, by
Evidence is currently equivocal for the use of
inhibiting the metabolism of arachidonic acid via the
NSAIDs in the prevention and/or reduction of the
cyclo-oxygenase (COX) pathway.
signs and symptoms associated with EIMD. The use
studies have investigated the effects of NSAIDs in
of higher doses of NSAIDs in future research has
animal models; however, this review focuses only
been advocated,
although caution should be
on studies in humans. The prophylactic and thera-
exercised as the habitual or long-term use of
peutic use of NSAIDs to alleviate the symptoms of
NSAIDs may produce adverse effects causing fur-
EIMD has been recently reviewed.
ther medical complications.
Prophylactic administration of ketoprofen has
inflammation is the body’s natural response to
been shown to significantly attenuate soreness and
EIMD and the use of pharmacological agents may
enhance the recovery of muscle function following
inhibit protein synthesis;
thus inhibiting the
maximal eccentric exercise;
with doses of 25 and
damage-repair-adaptation cycle of skeletal muscle
100 mg reducing soreness by 19% and 10%, respec-
to eccentric exercise. Evidence of suppressed tissue
tively, and enhancing muscle function by 9% and
protein synthesis following high-intensity eccentric
16%, respectively. Similarly, 150 mg diclofenac
exercise as a result of over-the-counter doses of
sodium (‘Voltaren’) administered orally for 27 days
© 2008 Adis Data Information BV. All rights reserved. Sports Med 2008; 38 (6)
492 Howatson & van Someren
ibuprofen and paracetamol administration (1200 effect on muscle soreness and maximal force
mg/day and 4000 mg/day, respectively) has recently or the CK response.
It is important to note that
been shown.
Indeed, there is evidence of inhib- both of these studies used female participants; it is
ited muscle regeneration and hypertrophy following therefore possible that sex difference may account
NSAID administration in animal models.
for these findings. It has been widely reported that
Given the equivocal acute effects of NSAIDs, the estrogen provides protection against damage in skel-
lack of performance benefits reported, and the nega- etal muscle and that females respond to damaging
tive long-term consequences of administration, the exercise in a different manner to males, dependent
use of NSAIDs is not recommended as an effective upon menstrual cycle phase.
However, High et
strategy to prevent or treat symptoms of EIMD. al.
have also reported static stretching to have no
effect on muscle soreness in a mixed sex sample
following eccentric exercise; this study compared
2.5 Stretching
stretching, warm-up and stretching with warm-up
Stretching is proposed to decrease the passive or
protocols, with no intervention having any effect. In
active stiffness of skeletal muscle, making it more
contrast, by employing five rapid arm extensions
compliant to eccentric contractions and thereby re-
following eccentric exercise, passive stiffness and
ducing the amount of primary mechanical damage.
muscle soreness has been shown to be temporarily
Accordingly, pre-exercise static stretching has been
reduced; however, passive stiffness was seen to
suggested as a possible intervention to attenuate the
increase over the following hour.
magnitude of muscle damage.
A brief meta-
Current literature reporting the efficacy of
analysis of five studies
found stretching to re-
stretching to prevent or reduce EIMD suggests only
duce soreness in the 72 hours following exercise by
minimal effect in reducing muscle soreness and no
2 mm on a visual analogue scale of 100 mm, but
effect on performance. It has, however, been pre-
suggested that this magnitude of change is too small
viously highlighted that other as yet un-investigated
to be worthwhile. LaRoche and Connolly
stretching protocols, such as proprioceptive neuro-
ed that long-term stretching (4 weeks of static or
muscular facilitation, ballistic or dynamic stretching
ballistic stretching) maintained ROM and stretch
techniques may be of benefit, and therefore present a
tolerance in the days following eccentric exercise,
direction for future research.
but had no effect on muscle soreness. Pizza et al.
have shown that passive stretching performed prior
2.6 Massage
to eccentric exercise reduces the inflammatory re-
sponse, thus suggesting that prior stretching may Massage is a widely used therapy in the treatment
protect the muscle cell against exercise-induced of athletic muscle soreness and micro-injury and
muscle damage. Indeed, Koh and Brooks
have many athletes are convinced by its potential to alle-
reported passive stretching to provide protection viate muscle soreness. Tiidus
highlighted a lack
against muscle damage when damaging exercise is of consensus in the literature as to the effects of and
performed 2 weeks later; furthermore, the magni- mechanisms by which massage might be effective;
tude of this protection was approximately 50% of however, there is now some literature base to sup-
that afforded by prior eccentric exercise (i.e. the port its use in the treatment of exercise-induced
repeated-bout effect [RBE], as discussed in section muscle soreness.
2.10). Reduced CK activity and attenuated losses in
Massage performed 2 hours following eccentric
force have been shown when stretching is performed
exercise has shown significant reductions in muscle
in combination with warm-up and post-exercise
soreness and CK appearance in blood.
effects may be explained by the physical disruption
In contrast, static stretching performed prior to of neutrophil accumulation within muscle and a
eccentric exercise has been shown to no have no consequent reduction in prostaglandin production
© 2008 Adis Data Information BV. All rights reserved. Sports Med 2008; 38 (6)
Muscle Damage: Prevention and Treatment 493
and pain.
Similar findings have been reported for which suggests that presynaptic pain fibres are in-
10 minutes of deeply applied clearing techniques 3
hibited by stimulation of large sensory fibres in the
hours post-exercise, significantly reducing muscle
Such findings are supported by those of
soreness, CK and limb circumference; however, no
Denegar and Perrin,
demonstrating that TENS
effects were found for muscle strength or ROM.
applied 48 hours following eccentric exercise signif-
These findings confirm those of Hilbert et al.,
icantly reduced muscle soreness in females. In addi-
who also found reduced soreness, but no change in
tion, this study identified that whilst TENS had no
muscle function (strength or ROM) when 20 min-
effect on ROM, when applied in conjunction with
utes of massage was applied 2 hours following max-
cold application ROM was increased; TENS had
imal eccentric exercise; however, in contrast to the
only a non-significant effect on muscle strength.
conclusions of Smith et al.,
no reduction in neu-
A similar modality to TENS, microcurrent elec-
trophil count was observed.
Performance bene-
trical neuromuscular stimulation, however, appears
fits have, however, been demonstrated alongside
to have no effect on muscle function or pain when
reduced muscle soreness when female collegiate
applied immediately after and at 24 hours post-
volleyball and basketball players were treated with
and no effect on muscle soreness or
effleurage, petrissage and vibration massage during
ROM when applied at 24, 48 and 72 hours post-
pre-season training, 2 days after intense training
In contrast, electro-membrane
As previously highlighted, mas-
microcurrent therapy significantly attenuates the in-
sage provided in combination with warm-up and
crease in CK and the decrease in ROM and muscle
stretching can also attenuate losses in force follow-
strength at 24 hours; although perhaps surprisingly,
ing eccentric exercise.
has no effect on muscle soreness.
The mechan-
The majority of the evidence to date points to-
isms for these observations are not known, although
wards massage being effective in alleviating muscle
it is proposed that disturbances in calcium homeo-
soreness, although its effect on muscle function and
stasis that are inherent with eccentric exercise may
performance is less clear. This may in part be due to
be reduced by such treatment.
a number of methodological limitations in the litera-
Another electrotherapeutic modality examined is
ture, (e.g. inadequate therapist training, different
high-voltage pulsed current (HVPC), which is ap-
massage techniques used, insufficient duration of
plied via a short pulse duration monophasic
treatment) that have been highlighted in previous
waveform directly through electrodes. HVPC has
been demonstrated in animal models to alleviate
muscle soreness by reducing oedema accumulation;
2.7 Electrotherapeutic Modalities
however, the only two studies that have examined
HVPC in humans
have shown no effects on
Electrical modalities have been used in the treat-
muscle soreness or function (strength and ROM).
ment of injury and are extensively utilized for the
rehabilitation of a range of musculoskeletal prob-
Ultrasound converts electrical energy into sound
lems; however, the use of electrical therapies to
waves that penetrate the skin and is proposed to
reduce symptoms associated with muscle damage
increase circulation, accelerate metabolism and con-
has not been extensively examined.
trol the sensation of pain.
There is evidence that
ultrasound treatment applied for 20 minutes at 24
Trancutaneous electrical nerve stimulation
hours following stepping exercise significantly
(TENS) is used for pain control and to elicit an anti-
reduces muscle soreness.
Ultrasound therapy
inflammatory response.
Denegar et al.
and the administration of an anti-inflammatory
ined pulsed TENS application in females experienc-
cream may have synergistic effects, with signifi-
ing DOMS, demonstrating a significant attenuation
cantly less muscle soreness reported when both
of pain and the reduction in ROM. These effects
treatments were used when compared with ultra-
were attributed to the ‘Pain Gate Control Theory’,
© 2008 Adis Data Information BV. All rights reserved. Sports Med 2008; 38 (6)
494 Howatson & van Someren
sound alone.
It was proposed that the combined ROM in females following eccentric exercise.
treatment allowed for increased blood flow to the
These studies indicate that single treatments of ice
damaged tissue whilst reducing the inflammatory
massage provide limited, if any, alleviation of
response and consequent oedema and secondary
damage. The paucity of experimental research in-
Repeated applications of ice massage following
vestigating the effects and mechanisms of ultra-
eccentric exercise have demonstrated non-signif-
sound therapy has been previously highlighted.
icant decreases in muscle strength and ROM and
In summary, electrical therapies show some
non-significant increases in muscle soreness and
promise in the treatment of EIMD and muscle sore-
CK, thereby identifying possible contraindications
ness; however, these electrical mediums require spe-
of ice massage in the treatment of EIMD.
cialist training to administer and the equipment itself
study was, however, limited by sample sizes of only
can be expensive. There are currently no evidence-
5–6 participants in treatment groups. Ice massage
based guidelines on the dose and frequency of appli-
administered immediately after and at 24-hour inter-
cation concerning electrical therapies. Robertson
vals for 48 hours following eccentric exercise has
has stated that guesswork is currently used in the
been shown to attenuate CK efflux at 72 hours post-
dose-response treatment using ultrasound. There-
but to have no effect on muscle sore-
fore, further research is required to elucidate the
ness or function.
efficacy of electrical therapies using standardized
Repeated cryotherapy application in the form of
guidelines based on documented evidence. How-
cold water immersion has also been unsuccessful in
ever, given that these therapies target isolated mus-
alleviating muscle soreness and EIMD. Paddon-
cles, the application of such findings may be of
Jones and Quigley
adopted a protocol of 20-min-
limited value in an athletic environment, in which
ute cold water immersions (5 ± 1°C), separated by
individuals rarely experience such isolated muscle
60 minutes and repeated five times following eccen-
damage and soreness.
tric exercise; it is possible that such an aggressive
approach may have elicited the Hunting Reaction.
2.8 Cryotherapy
This phenomenon is brought about when tissue tem-
perature falls below 18°C and there is periodic vaso-
Cryotherapy is the application of cold for thera-
dilation and warming of the tissue, which may elimi-
peutic purposes. It is usually applied during the
nate any potential benefits of cryotherapy. A less
acute stage of trauma and is proposed to diminish
intense treatment regimen involving immersion in
the undesirable effects of soft tissue injury
water of 15°C for 15 minutes, every 12 hours for 3
reducing the inflammatory response, swelling, oede-
days following eccentric exercise resulted in a sig-
ma, haematoma and pain.
The therapeutic
nificantly greater relaxed elbow angle (indicative of
effects are proposed to be a consequence of analge-
reduced passive stiffness) and lower CK levels in
sia of the injured tissue, hypometabolism of the
blood, but with no effects on muscle soreness or
tissue, and a vascular response whereby blood flow
and haematoma formation is retarded. strength.
Beneficial effects of cold water immer-
sion following eccentric exercise have also been
Single treatments of ice massage appear to have
reported by Yanagisawa et al.
A single treatment
very limited efficacy in treating muscle damage and
immediately post-exercise and repeated treatments
soreness, with only a short-term reduction in DOMS
immediately following and at 24 hours post-exercise
when ice massage was applied immediately follow-
of 15 minutes at 5°C both significantly reduced
ing exercise; importantly, however, this was mir-
soreness at 48 hours post-exercise and the increase
rored by a reduction in muscle force.
in magnetic resonance-T2 weighted image, which is
single ice massage applications of 15 minutes ap-
a measure of relaxation time, at 96 hours post-
plied either immediately post-exercise, or at 24 or 48
exercise. A recent study has examined the practice
hours post-exercise have no effect on DOMS or
© 2008 Adis Data Information BV. All rights reserved. Sports Med 2008; 38 (6)
Muscle Damage: Prevention and Treatment 495
of intermittent ice-water immersion, which has be- heat passive warm-up, high-heat passive warm-up,
come a popular practice amongst athletes in many
active warm-up, and no warm-up prior to eccentric
Immersion in ice-water (5°C) repeated
exercise and a control. The investigators concluded
three times and interspersed with 1-minute periods
that passive warm-up may be more beneficial than
out of the water resulted in no changes in CK,
an active warm-up in reducing swelling; however, it
muscle function or swelling; however, the interven-
does not attenuate any other damage indices or
tion did result in significantly greater muscle pain.
resolve symptoms of EIMD.
These investiga-
Cryotherapy appears an attractive strategy to
tions have a methodological design that make the
combat the signs and symptoms of EIMD because it
application to athletic and exercising populations
offers a quick, simple and if required, whole-body,
difficult; consequently they appear to lack external
intervention. Indeed, there are many anecdotal re-
validity. Perhaps a protocol with more external
ports of the widespread use of part or whole-body
application should be employed in future investiga-
cold water immersion following competition and
tions to elucidate the prophylactic effects of prior
training by athletes in an attempt to enhance recov-
ery. In contrast, however, the evidence regarding the
Hasson et al.,
who examined therapeutic ex-
effects of cryotherapy on muscle function and sore-
ercise, showed that high-speed voluntary contrac-
ness is equivocal, with perhaps the more effective
tions carried out 24 hours after eccentric stepping
treatment strategies comprising conservative and re-
exercise had some positive effects. Despite demon-
peated applications of cold media.
strating less soreness and an attenuation of torque at
48 hours post-exercise, it is not clear why these
2.9 Exercise
high-speed contractions may be of benefit when
has suggested exercise to be the
other investigators using exercise interven-
most effective strategy to alleviate DOMS; how-
have not.
ever, it seems that the analgesic effect is only tempo-
A recent addition to the literature
had subjects
and pain tends to resume after exercise has
complete one of three conditions (passive recovery,
Indeed physical therapists prescribe
running at 50%
, and electromyostimulation
light exercise in the presence of muscle soreness;
carried out at 30 minutes, 24, 48 and 96 hours post-
however, the appropriate mode, intensity and dura-
exercise). Each trial was separated by 3 weeks, in a
tion have yet to be elucidated.
randomized, crossover design. No differences were
ported that increased blood flow removed noxious
found between conditions; however, these data
waste products and increased endorphin release,
should be treated with some caution as this experi-
thereby causing an analgesic effect. However, the
mental design is likely to be confounded by the fact
research-based evidence pertaining to the efficacy
that all subjects completed all conditions and there
of exercise as a treatment in attenuating symptoms
was insufficient provision to account for the RBE,
of EIMD remains equivocal.
which has been shown to last for >12 weeks
Nosaka and Clarkson
showed that fatiguing
and is discussed in section 2.10. It would appear that
concentric exercise conducted immediately prior to
exercise conducted as a prophylactic intervention or
eccentric muscle actions significantly attenuated
as a therapy is of limited value in attenuating symp-
damage markers. One might expect that the fatigu-
toms associated with EIMD, and therefore other
ing concentric exercise would affect the production
areas are perhaps more worthwhile to explore.
of eccentric force; however, the eccentric torque
Having said this, there are some limitations within
during the damaging exercise was similar to the
the literature that could be addressed in order to
control group. A more recent investigation
elucidate the value of exercise administered before
amining the prophylactic effects of warm-up on
markers of muscle damage compared groups of low- and/or after potentially damaging exercise.
© 2008 Adis Data Information BV. All rights reserved. Sports Med 2008; 38 (6)
496 Howatson & van Someren
2.10 Repeated Bout Effect muscle function. More recent investigations support
earlier work concerning the RBE and demonstrate
The signs and symptoms of EIMD following
compelling and conclusive evidence of an attenua-
eccentric exercise can be greatly attenuated follow-
tion of the signs and symptoms of EIMD following a
ing a second bout of a similar magnitude. This
repeated bout or eccentric exercise.
protection or adaptation is commonly referred to as
Most investigations allow sufficient time for
the RBE
and has been demonstrated in both
markers of damage to return to pre-exercise levels
and humans using the lower
before exposing the muscle to a further insult of
and the upper limbs.
exercise, which usually occurs within 2 weeks.
RBE not only provides protection that seems to
However, some investigators have examined the
occur within a few days,
but has also been
RBE prior to the recovery of soreness and function,
reported to last for several months in humans.
which often occurs in sporting populations that may
The damage response has a tendency to be great-
conduct several potentially damaging exercise bouts
er in the upper limb than the lower limb, probably
over a short epoch. Nosaka and co-workers have
due to the lower limb being exposed to regular prior
made considerable contributions to the literature in
bouts of eccentric exercise for day-to-day locomo-
the field of muscle damage and adaptation. One such
tion such as descending stairs. The upper limb is
investigation examined whether repeated bouts of
non-weight bearing and most individuals are unac-
eccentric exercise would exacerbate damage when
customed to high-intensity eccentric loading using
repeated 2 and 4 days after the initial bout. The
this limb. Upper-limb exercise may lack specificity
repeated bouts did not exacerbate damage or impede
when making inference to many sports and exercise,
the time to recovery, which has subsequently been
but can provide a valuable insight into the damage-
supported by more recent work.
This is possibly
repair-adaptation response of human skeletal muscle
due to focal damage occurring to stress-susceptible
to EIMD. Several theories have been mooted as
fibres during the initial bout and therefore further
potential mechanisms for the RBE; these include
damage could not occur during the repeated bouts.
mechanical, cellular, neural, enhanced excitation-
In addition, the ability to generate force during bouts
contraction coupling as well as a growing body of
two and three was inhibited considerably; almost
evidence of an altered inflammatory response and/or
certainly as a result of the damage inflicted from the
change in reactive oxidative species during and after
initial bout and therefore the force generated during
the repeated bout; for a concise review of these
subsequent bouts was insufficient to elicit any fur-
possible theories, the reader is directed to Mc-
ther damage.
Our review uses examples of the RBE and
examined repeated bouts of eccentric
focuses on more recent contributions to the literature
exercise 3 days after the initial bout. Subjects com-
that provide information on factors that influence
pleted 30 maximal eccentric contractions followed 3
the protection of skeletal muscle from a single bout
days later by 30 or 70 maximal eccentric contrac-
of eccentric contractions.
tions using the elbow flexors. Damage was evident
Early investigations have clearly demonstrated
in all groups and was not exacerbated after the
the RBE by showing an attenuation of indirect dam-
second bout, even in the groups that completed more
age indices such as muscle soreness, CK and muscle
contractions in the repeated bout, which concur with
function following the repeated bout using upper-
the findings of Nosaka and Newton.
and lower-limb models.
Direct evi-
more, in Chen’s investigation
the second bout
dence for the RBE has also been demonstrated;
was conducted when initial damage was still evident
biopsy revealed reduced focal damage to the my-
and less torque could be generated (38% less in the
ofibrils in two-thirds of subjects at day two follow-
repeated bout of the 30 repetition group); therefore,
ing the repeated bout and all subjects showed mini-
it is perhaps unsurprising that no further damage
mal soreness, CK elevations and decrement in
© 2008 Adis Data Information BV. All rights reserved. Sports Med 2008; 38 (6)
Muscle Damage: Prevention and Treatment 497
occurred. From an applied standpoint, it seems that Another variable that can be manipulated is exer-
if the skeletal muscle has residual damage from
cise intensity. Nosaka and Newton
showed less
eccentric contractions, then further insults of exer-
damage in an initial bout of submaximal exercise
cise are unlikely to incur further detriments in per-
when compared with maximal exercise. Although it
formance or inhibit the recovery process. However,
would appear that whilst the initial bout does not
if the purpose of further exercise bouts (prior to full
have to cause appreciable damage (evident from
recovery) is to induce greater adaptation, then the
reduced volume), it does have to be of a maximal
exercise stimulus from the repeated bout might be
intensity to confer protection against subsequent
insufficient to induce additional benefits, although
maximal bouts. Nosaka and Newton
further research should be conducted to examine this
the effects of 8 weeks of submaximal (50% isomet-
ric one repetition maximum) concentric or eccentric
training on damaging maximal eccentric exercise
It is also possible that an adaptation or prophylac-
carried out at the end of the training period. Both
tic effect on subsequent bouts may be manifested by
eccentric and concentric training failed to provide a
an initial bout that causes only minimal damage and
protective effect; therefore, in order to confer pro-
soreness. Protection is conferred from bouts of a low
tection from EIMD the exercise should be muscle
volume on subsequent bouts of higher volume ec-
group and intensity specific. Having said this, lower
centric contractions,
which suggests
intensity eccentric exercise does appear to protect
that the RBE may occur from a relatively low stimu-
against subsequent bouts of a similar low volume
and intensity.
Clarkson and Tremblay
have shown that 24
Muscle length during the initial bout of contrac-
maximal eccentric contractions of the forearm flex-
tions may also affect the RBE. Eccentric muscle
ors (that induced modest damage) could attenuate
actions carried out at shorter muscle lengths, i.e. the
damage from a subsequent bout of 70 maximal
ascending limb of the length tension curve, provide
contractions. Since this investigation, others
or no protection
against a subsequent
have reported similar findings using the lower-limb
bout at longer muscle lengths. This is probably
model, where subjects performed 10, 30 or 50 maxi-
because there is little or no initial damage at short
mal eccentric contractions followed by a second
muscle lengths due to a substantial overlap within
bout of 50 contractions, carried out 3 weeks later.
the sarcomeres and hence active tension can be
The ten-repetition regimen caused appreciably less
generated by contractile elements within the myofi-
initial damage compared with 30 or 50 repetitions.
laments. Consequently, there is less mechanical
However, all groups showed significant attenuation
stress and adaptive stimulus imposed on structures
after the repeated bout, which demonstrates that a
responsible for passive tension, which occurs at
maximal low volume bout provides protection from
longer muscle lengths. Therefore, exercisers would
maximal higher volume bouts. Likewise, others
be prudent to consider this and conduct muscle
have further corroborated these findings and have
actions over the entire anatomical range to maxi-
showed evidence of a RBE after an initial bout of
mize the prophylactic potential of the initial bout.
only 2 and 6 maximal eccentric contractions, using
Lastly, the adaptation itself has been reported to last
elbow flexors, prior to a repeated bout of 24 contrac-
from between 6 to 9 months,
although anecdotal-
and most recently that ten maximal eccen-
ly, many strength and conditioning coaches report
tric contractions provides protection from a bout of
that athletes tend to experience muscular soreness
45 maximal eccentric contractions conducted 2
and reduced function after far shorter lay-off periods
weeks later;
although the magnitude of the pro-
between bouts. Nosaka et al.
have, however,
tection appears to be less from a lower volume bout
compared with a high volume bout. suggested that some dependent variables have a
© 2008 Adis Data Information BV. All rights reserved. Sports Med 2008; 38 (6)
498 Howatson & van Someren
reduced attenuation after 8 weeks, which is perhaps cise have been consistently shown to elicit a prophy-
more representative of applied observations. lactic effect on subsequent bouts of potentially dam-
aging exercise; conversely, many other treatments
The RBE is a phenomenon that has been consist-
have shown some promise, but the research evi-
ently demonstrated by various investigators using
dence remains equivocal, which may be due to
upper- and lower-limb models. This adaptive re-
inconsistencies in the dose, frequency and intensity
sponse to a single bout of eccentric exercise is
of the intervention. Very often there is little or no
probably the only intervention that has consistently
evidence-based practice in applying these interven-
shown a positive prophylactic effect in attenuating
tions and hence it is difficult to ascertain an appro-
EIMD; although a number of factors should be
priate strategy to combat the negative effects of
considered when prescribing potentially damaging
EIMD. Further research is warranted to elucidate the
exercise, particularly when the exerciser is expected
most appropriate dose, frequency and intensity of
to complete further bouts of eccentric biased exer-
these interventions in order to determine ‘best evi-
cise. If the exercise bout is novel, it would seem
dence-based practice’. Furthermore, it is unclear
prudent to start with a low-volume, high-intensity
how these interventions affect the adaptation pro-
bout in order to: (i) reduce the negative effects of
cess and it might transpire that treatments are being
eccentric exercise after the initial bout to allow
prescribed that actually attenuate adaptation; there-
minimum interference with further training bouts;
fore, there is a pressing need to ascertain the full
and (ii) to confer a RBE against a subsequent high-
implication of these interventions on their ability to
volume bout.
reduce the negative effects of EIMD and the impact
of prophylactic and therapeutic interventions on ad-
3. Conclusion
Eccentric muscle actions form an integral part of
human locomotion and have been demonstrated to
benefit a wide number of populations. Eccentric
No sources of funding were used to assist in the prepara-
contractions require a lower metabolic cost per unit
tion of this review. The authors have no conflicts of interest
of torque compared with concentric and isometric
that are directly relevant to the content of this review.
contractions, making them an appealing mode of
exercise for a variety of clinical and special popula-
tions. Furthermore, athletic populations employ ec-
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... A variety of recovery methods to attenuate EIMD have been suggested and can be divided into three categories: (1) therapeutic, (2) pharmacological, and (3) nutritional interventions [12]. Passive stretching, foam rolling, and vibrating foam rolling are therapeutic interventions, which have been previously researched [14][15][16][17]. Meanwhile, non-steroidal anti-inflammatory drugs (NSAIDs) are an example of a pharmacological intervention used to treat muscle damage [12,14]. ...
... Passive stretching, foam rolling, and vibrating foam rolling are therapeutic interventions, which have been previously researched [14][15][16][17]. Meanwhile, non-steroidal anti-inflammatory drugs (NSAIDs) are an example of a pharmacological intervention used to treat muscle damage [12,14]. Nutritional interventions are an alternative to therapeutic and pharmacological interventions [12,14]. ...
... Meanwhile, non-steroidal anti-inflammatory drugs (NSAIDs) are an example of a pharmacological intervention used to treat muscle damage [12,14]. Nutritional interventions are an alternative to therapeutic and pharmacological interventions [12,14]. Exercise can cause oxidative stress, which occurs when there is an imbalance between reactive oxygen species (ROS) production and antioxidant defenses [18]. ...
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The aim of this study was to investigate the effects of a tart cherry supplement on recovery from exercise-induced muscle damage. Seventeen recreationally active women (mean age ± SD = 22.2 ± 3.3 years, height = 162.0 ± 6.0 cm, body mass = 65.1 ± 11.1 kg, BMI = 24.7 ± 3.5 kg·m 2) supplemented with 1000 mg of concentrated tart cherry or a placebo for eight consecutive days. An overload protocol of 8 sets of 10 repetitions of maximal effort concentric and eccentric muscle actions of the leg extensors at a velocity of 60 • ·s −1 was performed on the fourth day of supplementation. Testing sessions consisted of a muscle function test (MFT) to examine pre-and post-testing peak torque, peak power, total work, time-to-peak torque, mean power, muscle activation of the quadriceps, and muscle soreness at baseline and post-testing at 0 h, 24 h, 48 h, and 72 h. A second trial of testing was repeated two weeks later using the opposite supplement to the one assigned for the first trial. No significant interaction for time × condition × velocity (p = 0.916) and no significant main effect for condition (p = 0.557) were demonstrated for peak torque. However, there were main effects for time and velocity for concentric quadriceps peak torque (p < 0.001). For muscle soreness, there was no two-way interaction for time x condition (p > 0.05) and no main effect for condition (p > 0.05), but there was a main effect for time (p < 0.001). In conclusion, a tart cherry supplement did not attenuate losses in isokinetic muscle peak torque, peak power, total work, time-to-peak torque, muscle soreness, or quadriceps muscle activation.
... Elite-level athletic participation necessitates recovery from many physiological stressors, including fatigue to the musculoskeletal, nervous and metabolic systems [18]. Athletic participation may also result in exercise-induced muscle damage (EIMD), which may lead to delayed-onset muscle soreness (DOMS) and decrements in subsequent performance [19]. Different studies have demonstrated the effectiveness of whole-body cryostimulation (WBC) in supporting recovery processes. ...
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The present study investigated the effects of a series of 10 whole-body cryostimulation (WBC) sessions (3 min; −110 °C) on physiological and thermal responses to a submaximal exercise test in 17 elite athletes. Participants performed an exercise test twice at similar levels of intensity before and after a series of ten WBC sessions. Before and during the test, each participant’s oxygen uptake (VO2), heart rate (HR), internal temperature (Ti), and skin temperature in selected areas of the skin were measured, and the mean arterial pressure (MAP), physiological strain index (PSI), and mean skin temperature (Tsk) were calculated. The results show that during exercise, increases in Ti and the PSI were significantly lower after the WBC sessions, and although there were no significant changes in HR or the MAP, the Tsk was significantly higher. Following exercise, an increase in skin temperature asymmetry over the lower-body muscles was detected. A series of WBC sessions induced a tendency toward a decrease in temperature asymmetry over the thigh muscles. In conclusion, a series of ten WBC sessions does not induce significant modifications in physiological variables but does influence the PSI and Ti during exercise. Moreover, a series of ten WBC sessions influences the distribution of skin temperature and the magnitude of temperature asymmetries in the early phase of recovery.
... Eight of 25 subjects exhibited a decrease of more than 10%, whereas 12 subjects exhibited a decrease that was less than 10% and 5 subjects exhibited increases. Perhaps, these results reflect variability in training experience and exercise-induced muscle damage, which is a result of unaccustomed exercise (11,25). For example, while all subjects self-identified as performing resistance training at least 2 times per week, eccentric exercise training habits were not recorded. ...
Neltner, TJ, Sahoo, PK, Smith, RW, Anders, JPV, Arnett, JE, Ortega, DG, Schmidt, RJ, Johnson, GO, Natarajan, SK, and Housh, TJ. Effects of high-intensity, eccentric-only muscle actions on serum biomarkers of collagen degradation and synthesis. J Strength Cond Res 37(9): 1729-1737, 2023-The purpose of this study was to examine the effects of high-intensity, eccentric-only muscle actions of the leg extensors on (a) serum biomarkers of collagen degradation (hydroxyproline [HYP] and C-terminal telopeptide of type I collagen [C1M]) and synthesis (pro-c1α1) and (b) the time course of changes in maximal voluntary isometric contraction (MVIC) and ratings of muscle soreness after the eccentric-only exercise bout. Twenty-five recreationally active men (mean ± SD: age = 21.2 ± 2.0 years) completed 5 sets of 10 bilateral, eccentric-only dynamic constant external resistance muscle actions of the leg extensors at a load of 110% of their concentric leg extension 1 repetition maximum. Analysis of variances (p < 0.05) and a priori planned pairwise comparisons using Bonferroni corrected (p < 0.0167) paired t tests were used to examine mean changes in blood biomarkers from baseline to 48 hours postexercise as well as in MVIC and soreness ratings immediately, 24 hours, and 48 hours postexercise. There were increases in HYP (3.41 ± 2.37 to 12.37 ± 8.11 μg·ml-1; p < 0.001) and C1M (2.50 ± 1.05 to 5.64 ± 4.89 μg·L-1; p = 0.003) from preexercise to 48 hours postexercise, but no change in pro-c1α1. Maximal voluntary isometric contraction declined immediately after the exercise bout (450.44 ± 72.80 to 424.48 ± 66.67 N·m; p = 0.002) but recovered 24 hours later, whereas soreness was elevated immediately (6.56 ± 1.58; p < 0.001), 24 hours (3.52 ± 1.53; p < 0.001), and 48 hours (2.60 ± 1.32; p = 0.001) postexercise. The eccentric-only exercise bout induced increases in collagen degradation but had no effect on collagen synthesis. These findings provide information for clinicians to consider when prescribing exercise after an acute injury or surgery.
... There is naturally a small amount of lactate dehydrogenase in plasma, a significant amount for which is released in the blood following a myocardial infarction, liver disease, or muscle and tissue damage. The use of nutritional and dietary supplements can also be a good way to prevent cell damage and increase inflammatory markers [8][9][10]. Beta-hydroxy betamethylbutyrate (HMB) is, also, one of the supplements that help to maintain muscle mass by reducing cell protein degradation and providing cell membrane cholesterol synthesis precursors and it functions as a potential candidate for increasing anabolic hormones, mass development and muscle growth under various conditions. ...
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Lactate is a glycolysis product that can be produced continuously by large cells at rest and even under sufficient oxygen conditions. It is suggested for extensive research to be conducted on the effects of HMB supplementation in human and animal samples. The aim of this study was to investigate the interactive effects of eccentric exercise and supplement HMB-FA on LDH in adult male rats. The 24 adult male rats split into four groups: control group (n=6), HMB (n=6), exercise (n=6) and Sport and HMB (n=6). After three familiarity session for experimental groups with training and obtain their 1RM, to supplement daily was administered weekly for two weeks. Then of course full load, eccentric resistance exercise was carried out. Upon completion of the exercise protocol blood of rats was carried out using LDH was measured by ELISA. Finally, data were analyzed using statistical software SPSS version 18. The finding no significant effect of supplementation with HMB-FA and eccentric resistance exercise on these variables have not found and the Conclusions this study found that in contrast to the results obtained in previous studies HMB-FA supplementation and eccentric resistance exercise no significant impact on the levels of LDH in adult male.
... 5,6 Although the exact mechanism of EIMD is not yet fully understood, 2 main phases are mentioned to describe this event. 7 First, damage to sarcomeres leads to a change in Z bands and a decrease in energy production. 8,9 Second, disturbance in redox balance and acute inflammatory response lead to muscle damage. ...
Context: Several meta-analyses have been conducted on the effect of nutritional interventions on various factors related to muscle damage. However, the strength of the evidence and its clinical significance are unclear. Objectives: This umbrella review aimed to provide an evidence-based overview of nutritional interventions for exercise-induced muscle damage (EIMD). Data sources: PubMed, Scopus, and ISI Web of Science were systematically searched up to May 2022. Data extraction: Systematic reviews and meta-analyses of randomized controlled trials investigating nutritional interventions' effects on recovery following EIMD were included. The certainty of the evidence was rated using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE). Results: Fifty-three randomized controlled trial meta-analyses were included, evaluating 24 nutritional interventions on 10 different outcomes. The results revealed a significant effect of hydroxymethylbutyrate (HMB) supplementation and l-carnitine supplementation for reducing postexercise creatine kinase; HMB supplementation for reducing lactate dehydrogenase; branched-chain amino acids and leaf extract supplementation for reducing the delayed onset of muscle soreness; and l-carnitine, curcumin, ginseng, polyphenols, and anthocyanins for reducing muscle soreness, all with moderate certainty of evidence. Conclusions: Supplementation with HMB, l-carnitine, branched-chain amino acids, curcumin, ginseng, leaf extract, polyphenols, and anthocyanins showed favorable effects on some EIMD-related outcomes. Protocol registration: PROSPERO registration no. CRD42022352565.
... • A single bout of resistance exercise stimulates a range of acute physiological responses which reduce muscle function and performance (Howatson & Van Someren, 2008). As such, a variety of strategies have been developed to reduce these perturbations with the aim of enhancing exercise recovery. ...
... 2 The rate of recovery following exercise-induced muscle damage (EIMD) has been studied in relation to training experience, 4 age, 5 and gender, 6 while many studies explored efficient ways to facilitate recovery and to shed light on the individual recovery mechanisms. [7][8][9] These studies notwithstanding, the variability in recovery rate between and within participants remains uncertain. More in-depth and accurate tools for tracking muscle state are therefore needed to increase the sensitivity to early/pre-symptomatic muscle damage and facilitate muscle recovery after acute damage. ...
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Purpose: Postexercise recovery rate is a vital component of designing personalized training protocols and rehabilitation plans. Tracking exercise-induced muscle damage and recovery requires sensitive tools that can probe the muscles' state and composition noninvasively. Methods: Twenty-four physically active males completed a running protocol consisting of a 60-min downhill run on a treadmill at -10% incline and 65% of maximal heart rate. Quantitative mapping of MRI T2 was performed using the echo-modulation-curve algorithm before exercise, and at two time points: 1 h and 48 h after exercise. Results: T2 values increased by 2%-4% following exercise in the primary mover muscles and exhibited further elevation of 1% after 48 h. For the antagonist muscles, T2 values increased only at the 48-h time point (2%-3%). Statistically significant decrease in the SD of T2 values was found following exercise for all tested muscles after 1 h (16%-21%), indicating a short-term decrease in the heterogeneity of the muscle tissue. Conclusion: MRI T2 relaxation time constitutes a useful quantitative marker for microstructural muscle damage, enabling region-specific identification for short-term and long-term systemic processes, and sensitive assessment of muscle recovery following exercise-induced muscle damage. The variability in T2 changes across different muscle groups can be attributed to their different role during downhill running, with immediate T2 elevation occurring in primary movers, followed by delayed elevation in both primary and antagonist muscle groups, presumably due to secondary damage caused by systemic processes.
... In addition, exercise-induced muscle damage (EIMD) has been shown to negatively affect functional performance for several days in female athletes tested in the luteal phase (Keane et al. 2015). There is some evidence, from research conducted on males, that the consumption of protein and the simultaneous ingestion of carbohydrates and protein offer protection against exercise-induced muscle damage (Howatson and van Someren 2008). Only a small number of studies have been conducted using endurance-trained, resistance-trained, and team sport female athletes and the post-exercise ingestion of whey protein versus casein protein (Wilborn et al. 2013), whey versus soy protein (Tara et al. 2013), carbohydrate versus carbohydrate/protein (Green et al. 2008), and whey protein versus maltodextrin ) on perceptions of muscle damage, strength, and biomarkers of muscle damage and inflammation. ...
A number of nutrients, foods, and supplements have the potential to augment health, exercise performance, and/ or recovery, particularly in women, due to the fluctuation of sex hormones, or reductions thereof. Some of these for which significant amounts of research have provided evidence include: Carbohydrate (CHO) loading can overcome lower resting muscle glycogen in the follicular phase but an increase in total energy intake may be required. Pre-exercise feeding and/or CHO ingestion can negate the estrogen-induced reduction in gluconeogenesis during endurance exercise. Increased protein during recovery may help offset the increase in protein catabolism in the luteal phase. Special attention to not overhydrating and replacing sodium losses in the luteal phase of the menstrual cycle may help reduce the increased risk of hyponatremia that is due to differences in fluid and electrolyte handling and thirst in this phase. Supplementing with dietary sources of antioxidants may be prudent in those with amenorrhea or in menopause and, thus, low estrogen, as estrogen enhances the antioxidant capacity. However, this may not fully compensate for the lack of estrogen. Fish oil (omega-3 fatty acid source) may aid in inflammatory disorders such as dysmenorrhea and those associated with menopause. Vitamin D and calcium influence fertility, possibly dysmenorrhea, as well as bone health; however, supplementation cannot fully compensate for the lack of estrogen. Branched-chain amino acid oxidation may be greater when estrogen is low; this may have dietary implications for those with amenorrhea or in menopause, particularly when training regularly and or on low energy diets. Pre- and probiotics have the potential to help with dysmenorrhea and menopause as well as bone health; however, a healthy microbiota is largely influenced by the diet as a whole. In general, it is acknowledged that the dietary matrix is important to the effects of specific dietary components and that supplementing with a single component rarely achieves the same outcome as when eating a complement of foods, containing myriad phytochemicals and nutrients.KeywordsFemalesDietary supplementsMenstrual cycleDietNutritionEstrogenReactive oxygen speciesAntioxidants
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Purpose: To identify the effects of leucine, β-hydroxy β-methylbutyrate (HMB) and branched chain amino acid (BCAA) on post-exercise cytokine responses in females and males. Methods: Males (n=53) and females (n=37) completed 100 drop jumps and consumed either no supplement, leucine (3g/d), HMB (3g/d) or BCAA (4.5g/d) from 1d pre to 14d post-exercise. Muscle soreness, squat jumps, chair rises and creatine kinase (CK) were measured at pre, post, 24h, 48h, 7 and 14d. Blood lactate (pre, post), 10 cytokines (pre, 24h, 48h, 7d) and oestradiol (pre, 7d) were also measured. Results: Without supplementation post-exercise, soreness was induced in both males (6-fold) and females (5-fold). With supplementation, there were no increases in CK or oestradiol in females and no impact on muscle soreness, performance, or function in both sexes. In males, CK was elevated in untreated (48%) and leucine (69%) conditions vs baseline, but these were suppressed with HMB and BCAA. IL-7 was elevated in females vs males at baseline (6.3-fold), leucine increased IL-7 concentrations in females at 24h (17.0-fold), 48h (5.1-fold) vs males. With HMB, TNFr1-α increased in females at 24h (2.2-fold), 48h (2.3-fold) and 7d (2.3-fold) vs males. In males with BCAA, TNFr1-α decreased (P=0.06) from pre to 24h (6.8-fold), then increased (P<0.05) from 24 to 48h (8.0-fold). Conclusion: Although supplements were without effect on soreness following exercise, the cytokine response was evoked by exercise and impacted significantly by leucine, HMB and BCAA in females vs males. This improved cytokine response in females could lead to improved resistance to damage.
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The mechanisms that account for the strength loss after contraction-induced muscle injury remain controversial. We present data showing that (1) most of the early strength loss results from a failure of excitation-contraction coupling and (2) a slow loss of contractile protein in the days after injury prolongs the recovery time. Keywords: strength, damage, calcium, contractile protein, sarcoplasmic reticulum, plasmalemma
Experiments were conducted to test the hypothesis that injury to skeletal muscle in rats resulting from prolonged downhill running is prevented to a greater extent by prior downhill training than by either uphill or level training. Changes in plasma creatine phosphokinase (CPK) activity and glucose-6-phosphate dehydrogenase (G-6-PDase) activity in the soleus (S), vastus intermedius (VI), and medial head of triceps brachii (TM) muscles were evaluated as markers of muscle injury 48 h after 90 min of intermittent downhill running (16 m . min -1). Prior to this acute downhill run, groups of rats were trained by either downhill (-16 degrees), level (0 degrees), or uphill (+16 degrees) running (16 m . min -1) for 30 min/day. Training duration was either 5 days or 1 day. A training effect (i.e., reduced muscle injury) was indicated if muscle G-6-PDase or plasma CPK activity in a trained group following the 90-min downhill run was not different from that of nonexercised control animals and/or if it was lower than that of nontrained runners. A significant training effect was achieved in all three muscles with 5 days of either downhill or level training, but only in S after 5 days of uphill training. Elevation of plasma CPK activity was prevented by 5 days of training on all three inclines.(ABSTRACT TRUNCATED AT 250 WORDS)
The primary purpose of the study was to examine circulating neutrophils and monocytes and their plasma membrane expression of CD64, CD11b, and CD18 after two bouts (B1 and B2) of eccentric exercise. Subjects (n = 10) performed 25 forced-lengthened contractions of the forearm flexors on two occasions separated by 3 wk. Blood samples were obtained before exercise and at 1.5, 6, 12, 24, 48, 72, and 96 h of recovery. CD64, CD11b, and CD18 expression was determined via direct immunofluorescence and used as an indicator of neutrophil and monocyte activation. Creatine kinase activity (B1 = 1,390, B2 = 108 U/l), myoglobin (B1 = 163, B2 = 41, ng/dl), and muscle soreness and tenderness were higher (P < 0.01) after B1 compared with B2. Neutrophils at 6, 12, and 96 h were higher (P < 0.05) for B1 vs. B2. CD11b expression on neutrophils was 2.7-fold higher at 72 h for B1 vs. B2. CD64 expression on neutrophils at 72 and 96 h was 1.4- and 1.9-fold higher, respectively, for B1 vs. B2. At 72 and 96 h, CD18 and CD64 expression on monocytes was 1.3-fold higher for B1 vs. B2. The observed changes were not significantly correlated with changes in creatine kinase activity or myoglobin. In conclusion, the adaptation to eccentric arm exercise was associated with a reduction in circulating neutrophils and a lower state of neutrophil and monocyte activation.
Perceived muscle soreness ratings, serum creatine kinase (CK) activity, and myoglobin levels were assessed in three groups of subjects following two 30-min exercise bouts of downhill running (-10 degrees slope). The two bouts were separated by 3, 6, and 9 wk for groups 1, 2, and 3, respectively. Criterion measures were obtained pre- and 6, 18, and 42 h postexercise. On bout 1 the three groups reported maximal soreness at 42 h postexercise. Also, relative increases in CK for groups 1, 2, and 3 were 340, 272, and 286%, respectively. Corresponding values for myoglobin were 432, 749, and 407%. When the same exercise was repeated, significantly less soreness was reported and smaller increases in CK and myoglobin were found for groups 1 and 2. For example, the percent CK increases on bout 2 for groups 1 and 2 were 63 and 62, respectively. Group 3 demonstrated no significant difference in soreness ratings, CK activities, or myoglobin levels between bouts 1 and 2. It was concluded that performance of a single exercise bout had a prophylactic effect on the generation of muscle soreness and serum protein responses that lasts up to 6 wk.
The purpose of this study was to determine the effects of ultrasound and phonophoresis using an anti-inflammatory–analgesic cream (trolamine salicylate) on delayed-onset muscle soreness (DOMS). Repeated eccentric contractions were used to induce DOMS in the elbow flexors of 40 college-aged women. Subjects were then assigned randomly to one of four groups: (1) group 1 (n=10) received sham ultrasound using placebo cream, (2) group 2 (n=10) received sham ultrasound using trolamine salicylate cream, (3) group 3 (n=10) received ultrasound using placebo cream, and (4) group 4 (n=10) received ultrasound using trolamine salicylate cream. Subjects were treated on 3 consecutive days. Muscle soreness and active elbow range of motion were assessed daily prior to each treatment. The subjects in group 3 experienced an increase in DOMS, whereas no increase in soreness was observed in the subjects in group 4. The authors concluded that ultrasound enhanced the development of DOMS but that this enhancement was offset by the anti-inflammatory–analgesic action of salicylate phonophoresis. These findings suggest that salicylate phonophoresis may be useful in clinical situations in which it is desirable to administer ultrasound without increasing inflammation.
This study examined the effects of supplemental beta-hydroxy-beta-methylbutyrate (HMB) on muscle damage as a result of intense endurance exercise. Subjects (n = 13) were paired according to their 2-mile run times and past running experience. Each pair was randomly assigned a treatment of either HMB (3 g/day) or a placebo. After 6 wk of daily training and supplementation, all subjects participated in a prolonged run (20-km course). Creatine phosphokinase and lactate dehydrogenase (LDH) activities were measured before and after a prolonged run to assess muscle damage. The placebo-supplemented group exhibited a significantly greater (treatment main effect, P = 0.05) increase in creatine phosphokinase activity after a prolonged run than did the HMB-supplemented group. In addition, LDH activity was significantly lower (treatment main effect, P = 0.003) with HMB supplementation compared with the placebo-supplemented group. In conclusion, supplementation with 3.0 g of HMB results in a decreased creatine phosphokinase and LDH response after a prolonged run. These findings support the hypothesis that HMB supplementation helps prevent exercise-induced muscle damage.