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Sports Med 2003; 33 (2): 145-164
R
EVIEW
A
RTICLE
0112-1642/03/0002-0145/$30.00/0
Adis Data Information BV 2003. All rights reserved.
Delayed Onset Muscle Soreness
Treatment Strategies and Performance Factors
Karoline Cheung,1 Patria A. Hume1 and Linda Maxwell2
1 School of Community Health and Sports Studies, Auckland University of Technology,
Auckland, New Zealand
2 Department of Pathology, School of Medicine, University of Auckland, Auckland,
New Zealand
Contents
Abstract ....................................................................................145
1. Literature Reviewed ......................................................................146
2. Definition of Delayed Onset Muscle Soreness (DOMS) ........................................147
3. Mechanisms of DOMS ....................................................................147
4. Impact of DOMS on Athletic Performance ..................................................150
4.1 Perception of Functional Impairment ..................................................150
4.2 Joint Kinematics .....................................................................150
4.3 Strength and Power ..................................................................151
4.4 Altered Recruitment Patterns..........................................................151
4.5 Injury Risk Factors ....................................................................152
5. Treatment and Management Strategies for DOMS ..........................................153
5.1 Cryotherapy ........................................................................153
5.2 Stretching ...........................................................................154
5.3 Anti-Inflammatory Drugs ..............................................................155
5.4 Ultrasound ..........................................................................156
5.5 Electrical Current Techniques .........................................................156
5.6 Homeopathy ........................................................................157
5.7 Massage ............................................................................157
5.8 Compression ........................................................................158
5.9 Hyperbaric Oxygen Therapy ..........................................................158
5.10 Exercise ............................................................................159
6. Conclusions and Recommendations .......................................................160
Delayed onset muscle soreness (DOMS) is a familiar experience for the elite or
Abstract novice athlete. Symptoms can range from muscle tenderness to severe debilitating
pain. The mechanisms, treatment strategies, and impact on athletic performance
remain uncertain, despite the high incidence of DOMS. DOMS is most prevalent
at the beginning of the sporting season when athletes are returning to training
following a period of reduced activity. DOMS is also common when athletes are
first introduced to certain types of activities regardless of the time of year.
Eccentric activities induce micro-injury at a greater frequency and severity than
other types of muscle actions. The intensity and duration of exercise are also
important factors in DOMS onset. Up to six hypothesised theories have been
proposed for the mechanism of DOMS, namely: lactic acid, muscle spasm,
146 Cheung et al.
connective tissue damage, muscle damage, inflammation and the enzyme efflux
theories. However, an integration of two or more theories is likely to explain
muscle soreness. DOMS can affect athletic performance by causing a reduction in
joint range of motion, shock attenuation and peak torque. Alterations in muscle
sequencing and recruitment patterns may also occur, causing unaccustomed stress
to be placed on muscle ligaments and tendons. These compensatory mechanisms
may increase the risk of further injury if a premature return to sport is attempted.
A number of treatment strategies have been introduced to help alleviate the
severity of DOMS and to restore the maximal function of the muscles as rapidly as
possible. Nonsteroidal anti-inflammatory drugs have demonstrated
dosage-dependent effects that may also be influenced by the time of administra-
tion. Similarly, massage has shown varying results that may be attributed to the
time of massage application and the type of massage technique used. Cryotherapy,
stretching, homeopathy, ultrasound and electrical current modalities have demon-
strated no effect on the alleviation of muscle soreness or other DOMS symptoms.
Exercise is the most effective means of alleviating pain during DOMS, however
the analgesic effect is also temporary. Athletes who must train on a daily basis
should be encouraged to reduce the intensity and duration of exercise for 1–2 days
following intense DOMS-inducing exercise. Alternatively, exercises targeting
less affected body parts should be encouraged in order to allow the most affected
muscle groups to recover. Eccentric exercises or novel activities should be
introduced progressively over a period of 1 or 2 weeks at the beginning of, or
during, the sporting season in order to reduce the level of physical impairment
and/or training disruption. There are still many unanswered questions relating to
DOMS, and many potential areas for future research.
Following unaccustomed physical activity, a sen- thology.[2,5,17,23,24] It is not within the scope of this
paper to address in detail the proposed theories of
sation of discomfort, predominantly within the skel-
DOMS. This has been well reviewed by other inves-
etal muscle, may be experienced in the elite or
tigators.[2,5,17,25] Rather, the aim of this paper is to
novice athlete. The intensity of discomfort increases discuss the impact of muscular soreness on athletic
within the first 24 hours following cessation of performance and to review the current research on
exercise, peaks between 24 and 72 hours, subsides the treatment techniques and management strategies
and eventually disappears by 5–7 days post- of DOMS.
-exercise.[1-5] This exercise-induced phenomenon is
referred to as delayed onset muscle soreness 1. Literature Reviewed
(DOMS) and is perhaps one of the most common
and recurrent forms of sports injury. Literature was located using two computer
Numerous studies have attempted to identify pre- databases (Medline and SPORT Discus) in addition
vention strategies for DOMS.[5-22] The absence of a to manual journal searches. The computer databases
known preventative measure and the diverse range provided access to biomedical and sports-oriented
of treatment techniques available are largely due to journals, serial publications, books, theses, confer-
the lack of understanding surrounding the exact ence papers and related research published since
mechanisms of DOMS.[17] Currently, as many as six 1948. The keywords used included: muscle sore-
hypothesised theories have been proposed as poten- ness, DOMS, delayed onset muscle soreness, mus-
tial aetiological explanations for the muscular pa- cle injury, muscle strain, injury prevention and ec-
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
Delayed Onset Muscle Soreness 147
centric exercise. Excluding articles that were not ised by an elongation of the muscle during simulta-
published in English and/or in scientific journals, neous contraction. Thus, if the external load exceeds
refined the literature searches. Articles that focused the muscle’s ability to actively resist the load, the
on the psychological effects of DOMS, or the effect muscle is forced to lengthen and active tension is
of DOMS in special populations, were not included generated.[34] Cross bridges formed during eccentric
in the review. The criteria for inclusion were: actions must also be separated with greater force due
to the disruption of the actin-myosin bonds prior to
•the paper must have addressed at least one mech-
relaxation.[34] As a result, greater tension per active
anism and/or proposed treatment of prevention
motor unit is developed and there is an increased
for DOMS
risk of injury to the vulnerable myotendinous junc-
•the paper must have used normal, healthy partici- tion. Researchers investigating the mechanisms of
pants. Age, sex, fitness differences were not an DOMS have induced muscle soreness using exer-
excluding factor cise protocols consisting of predominantly eccentric
•DOMS may have been discussed in relation to activity, i.e. downhill running,[35-42] resisted cy-
other forms of muscle injury, e.g. muscle strain, cling,[43-46] ballistic stretching,[47] isokinetic dyna-
cramp mometry,[14,17,20,32,48-61] stepping[7,8,25,62-64] and/or ec-
•the paper may have been a review of previous centric resistance exercise.
research.
3. Mechanisms of DOMS
2. Definition of Delayed Onset Muscle
Soreness (DOMS) A number of theories have been proposed to
DOMS is classified as a type I muscle strain explain the pain stimulus associated with DOMS
injury[17,26] and presents with tenderness or stiffness including: lactic acid, muscle spasm, connective
to palpation and/or movement.[17] Although the pa- tissue damage, muscle damage, inflammation, en-
thology associated with DOMS is usually sub- zyme efflux theories and other proposed mod-
clinical,[27] the sensations experienced with this inju- els.[5,17] It is beyond the scope of this review to
ry can vary from slight muscle stiffness, which provide a detailed discussion of each theory. Rather,
rapidly disappears during daily routine activities, to it is the intention of the authors to provide a brief
severe debilitating pain which restricts movement. overview of the mechanisms and how they interre-
Tenderness is concentrated in the distal portion late so that a basic understanding of the possible
of the muscle[2,24,27-30] and becomes progressively mechanism(s) of soreness perception may be ob-
diffuse by 24–48 hours post exercise.[24] This local- tained.
isation of pain can be attributed to a high concentra- The lactic acid theory is based on the assumption
tion of muscle pain receptors in the connective tis- that lactic acid continues to be produced following
sue of the myotendinous region.[31] The myotendi- exercise cessation. For the lay public, the accumula-
nous junction is characterised by a membrane which tion of toxic metabolic waste product is thought to
is continuous, extensively folded and interdigitated cause a noxious stimulus and the perception of pain
with the muscle cells.[29] The oblique arrangement of at a delayed stage.[2,17,22] However, this theory has
the muscle fibres just prior to the myotendinous largely been rejected as the higher degree of met-
junction reduces their ability to withstand high ten- abolism associated with concentric muscle contrac-
sile forces.[29,32,33] As a result, the contractile ele- tions have failed to result in similar sensations of
ment of the muscle fibres in the myotendinous junc- delayed soreness.[65] In addition, lactic acid levels
tion is vulnerable to microscopic damage. return to pre-exercise levels within 1 hour following
DOMS is usually associated with unfamiliar, exercise and blood lactate levels measured before,
high-force muscular work and is precipitated by during and sporadically up to 72 hours after level
eccentric actions.[27] Eccentric activity is character- and downhill running have failed to show a relation-
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
148 Cheung et al.
ship between lactic acid levels and soreness rat- increased collagen synthesis or its degradation. Sub-
ings.[42] Therefore, lactic acid may contribute to the sequently, the specific mechanism leading to an
acute pain associated with fatigue following intense increase in HP and HL remains uncertain.
exercise, however, it can not be attributed to the The muscle damage theory, first proposed by
delayed pain that is experienced 24–48 hours post- Hough,[73] focuses on the disruption of the contrac-
exercise.[66] tile component of the muscle tissue, particularly at
The muscle spasm theory[67] was introduced fol- the level of the z-line, following eccentric exer-
lowing the observation of increased levels of resting cise.[2,4,71,75-78] The characteristic microscopic lesion
muscle activity after eccentric exercise.[17,68,69] It is a broadening, smearing or even total myofibrillar
was proposed that an increased resting muscle acti- disruption of the z-line,[79] in addition to more wide-
vation indicated a tonic localised spasm of motor spread disruption of sarcomere architecture.[39] This
units. This was thought to lead to a compression of damage is the result of increased tension per unit
local blood vessels, ischaemia and the accumulation area caused by a reduction in active motor units
of pain substances. In turn this initiated a ‘vicious during eccentric actions.[2] Mechanical disruption to
cycle’[70] as further stimulation of pain nerve end- the structural elements is increased, particularly
ings caused further reflex muscle spasms and pro- amongst the type II fibres which have the narrowest
longed ischaemic conditions.[68] However, investi- and weakest z-lines. Nociceptors situated in the
gations using both bipolar and unipolar electromy- muscle connective tissue and in the region of the
ography (EMG) have been inconclusive with some arterioles, capillaries and the musculotendinous
studies showing no increase in EMG activity in sore junction are also stimulated leading to the sensation
muscles,[1,25,71] whilst others have observed an in- of pain. Blood enzymes have been measured post-
crease in EMG, but no relation between its magni- exercise to support this theory. Creatine kinase (CK)
tude and the perception of soreness.[68] The use of is considered a reliable indicator of muscle mem-
bipolar and unipolar electrode techniques remains brane permeability as this enzyme is found exclu-
controversial with some researchers arguing that the sively within skeletal and cardiac muscle.[5] Thus,
former method lacks the sensitivity to record the disruption of the z-lines and damage to the sarco-
electrical activity in sore muscles,[72] whilst others lemma will enable the diffusion of soluble muscle
have argued the contrary.[25] enzymes, such as CK, into the interstitial fluid. In
normal resting conditions, plasma CK is approxi-
The connective tissue damage theory examines mately 100 IU/L.[71] However, following eccentric
the role of the connective tissue that forms sheaths exercise, circulating levels of CK have been known
around bundles of muscle fibres. The content and to rise to 40 000 IU/L,[71] indicating a significant
composition of connective tissue differs between increase in the permeability of the muscle cell mem-
muscle fibre types. Type I (slow twitch) fibres dis- branes following z-line disruption.[39,69,80,81] Yet
play a more robust structure than type II (fast twitch) there is a clear discrepancy between the time of peak
fibres. Subsequently fast twitch fibres may demon- serum CK levels and peak muscle soreness (up to 5
strate an increased susceptibility to stretch-induced days).[39,43,45,54,59,71,82,83] As a result, the muscle dam-
injury[34] and excessive strain of the connective tis- age theory can only be accepted as a partial explana-
sue may lead to muscle soreness.[73] Measurements tion for the onset of DOMS.
of urine excretion hydroxyproline (HP) and hydrox-
ylysine (HL) following exercise have been exa- The inflammation theory is based on the finding
mined to provide support for this theory.[74] HP and that aspects of the inflammatory response, i.e. oede-
HL amino acids are a component of mature collagen ma formation and inflammatory cell infiltration, are
and their presence in urine is the result of collagen evident following repetitive eccentric muscle ac-
degradation either by overuse or strain damage.[34] tion.[22,45,84] Muscle fibres contain proteolytic en-
However, HP and HL excretion can reflect either zymes which initiate the degradation of lipid and
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
Delayed Onset Muscle Soreness 149
protein structures of cells following injury. This aspects from the above theories and start with the
assumption that high tensile forces, associated with
rapid breakdown of damaged muscle fibres and con-
eccentric exercise, damage muscle tissue and con-
nective tissue in addition to the accumulation of
nective tissue initially. This is followed by an acute
bradykinin, histamine and prostaglandins, attracts
inflammatory response consisting of oedema forma-
monocytes and neutrophils to the injury site.[62] This
tion and inflammatory cell infiltration. An integra-
is followed by an influx of protein-rich fluid (exu-
tion of the models proposed by Armstrong,[2,81]
date) into the muscle via the increased permeability
Smith[84] and Smith and Jackson[85] can be described
of small blood vessels following eccentric exer-
as follows:
cise.[84] Ultimately, an osmotic pressure is exerted
and pain is produced if group IV sensory neurons are •High tensile forces produced during eccentric
activated.[32] However, only peak oedema levels (as muscle activity cause disruption of structural pro-
measured by limb volume and girth) appear to coin- teins in muscle fibres, particularly at the weak-
cide with peak muscle soreness;[14,17] the time course ened z-lines. This is accompanied by excessive
of inflammatory cell infiltration is less coinciden- strain of the connective tissue at the myotendi-
tal.[4,41] This may explain why some authors have nous junction and surrounding muscle fibres
chosen to address this mechanism simply as the (connective tissue damage theory and muscle
Tissue Fluid Theory.[17] Nonetheless, Smith[84] and damage theory).
Armstrong[2] have both argued that monocytes, •Damage to the sarcolemma results in the ac-
which convert into macrophages, accumulate at the cumulation of calcium that inhibits cellular respi-
injury site and produce substances which sensitise ration. ATP production is hindered and calcium
the type III and IV nerve endings within 24–48 homeostasis is disturbed. High calcium concen-
hours. Whether oedema formation, as well as in- trations activate calcium-dependent proteolytic
flammatory cell infiltration, are mechanisms re- enzymes that degrade the z-line of sarcomeres,
sponsible for DOMS remains controversial. troponin and tropomyosin (enzyme efflux theo-
ry).
The enzyme efflux theory proposed by Gulick •Within a few hours there is a significant elevation
and Kimura[17] is based on the assumption that calci- in circulating neutrophils (inflammation theory).
um, which is normally stored in the sarcoplasmic
reticulum, accumulates in injured muscles following •Intracellular components and markers of connec-
sarcolemmal damage.[2] This is thought to lead to an tive tissue damage and muscle damage (e.g. HP
inhibition of cellular respiration at the mitochondrial and CK) diffuse into the plasma and interstitium.
level causing adenosine triphosphate (ATP) regen- These substances serve to attract monocytes be-
eration, which is required for the active transport of tween 6–12 hours that in turn convert to macro-
calcium back into the sarcoplasmic reticulum, to phages. Mast cells and histamine production are
slow. In addition, calcium accumulation is also activated (inflammation theory). Within hours
thought to activate proteases and phospholipases, there is a significant elevation in circulating neu-
thus causing further injury to the sarcolemma with trophils at the injury site (inflammation theory).
the production of leukotrienes and pros- •Monocytes/macrophages peak in number at 48
taglandins.[2,81] As a result, muscle protein degenera- hours. Upon exposure to the inflammatory envi-
tion at the weakened z-lines increases and the chem- ronment, macrophages produce prostaglandin
ical stimulation of pain nerve endings occurs. (PGE2) that sensitises type III and IV nerve end-
ings to mechanical, chemical or thermal stimula-
The general consensus amongst researchers is tion (inflammation theory).
that a single theory cannot explain the onset of
DOMS. As a result, some researchers have proposed •The accumulation of histamine, potassium and
unique sequences of events in order to explain the kinins from active phagocytosis and cellular ne-
DOMS phenomenon.[2,85] These models integrate crosis in addition to elevated pressure from tissue
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
150 Cheung et al.
oedema and increased local temperature could et al.[90] observed a reduced joint proprioception and
then activate nociceptors within the muscle fibres an overestimation of force production in 12 partici-
and the muscle tendon junction (inflammation pants (six male, six female) following 50 maximal
theory). eccentric muscle actions of the elbow flexors. De-
spite being confident that the force sustained in the
•These events lead to the sensation of DOMS.
experimental arm was equal to that being supported
Soreness may be increased with movement as the
in the control arm, participants were consistently
increased intramuscular pressure creates a
producing 35% of the force of the experimental arm.
mechanical stimulus for pain receptors already
Participants were also unable to match the reference
sensitised by PGE2.
joint angle of the control arm following eccentric
At present, the above sequence of events remains exercise; instead constant overshooting of the refer-
hypothetical. It is evident that further research is ence angle was observed. These findings provide
warranted to validate the biochemical and cellular preliminary evidence to suggest that neuromuscular
events that occur leading up to the onset of muscle function is impaired by the performance of unaccus-
soreness. tomed eccentric exercise that induces muscle sore-
4. Impact of DOMS on ness.[90] Since proprioception is also dependent on
Athletic Performance afferent receptors located in the skeletal muscle and
tendons, this also suggests that muscle damage must
In addition to muscle soreness, structural damage have occurred during eccentric exercise.
to muscle and connective tissue incurred during
eccentric activity may result in alterations to muscle 4.2 Joint Kinematics
function and joint mechanics.[86] For the elite ath-
lete, these adaptations, together with any other com- Kinematic analyses of running gait following
pensatory mechanisms for soreness relief, may DOMS inducement have revealed varied findings.
cause significant alterations to, and a reduction in, Hamill et al.[91] reported statistically significant dif-
performance and/or a less than optimal training in- ferences in maximum ankle dorsiflexion and plantar
tensity. flexion during the support phase, a reduction in
maximum knee joint flexion in both swing and
4.1 Perception of Functional Impairment support phases, and a reduction in maximum hip
Past research has reported independent changes flexion at touch down in ten females following 30
in joint kinematics and muscle function during minutes of downhill running. It was hypothesised
DOMS.[15,77,87,88] However, minimal research has that these changes were a compensatory response to
focused on an individual’s perception of his/her the reduced range of motion in the muscle group
physical impairment. Impairment can be defined as most affected by DOMS (i.e. quadriceps). The re-
an objectively measurable alteration of anatomical, duced ability of the knee and hip joints to attenuate
physiological or psychological status of the human shock (as a result of the reduced range of motion of
being.[89] Examples of impairment include a de- the quadriceps muscle) was also thought to be com-
creased range of joint motion, decreased strength or pensated for by the ankle joint and was observed as
abnormal electromyographical patterns. A restric- increased dorsiflexion during support (23.1–25.3°).
tion or the lack of ability to perform an activity or Supporting this theory, Goff et al.[92] used acceler-
function within the range considered normal for an ometry data to report an increased attenuation of
individual can also be described as a functional shock in the legs and a reduced attenuation at the
limitation.[89] This may have important implications head in nine male runners during level running
during periods of muscle soreness as an athlete’s 24–120 hours following 30 minutes of downhill
incorrect perception of his/her temporary impair- running. The researchers attributed these findings to
ment may lead to an increased risk of injury. Saxton the body’s ability to adapt and protect the leg from
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
Delayed Onset Muscle Soreness 151
injury during running. In contrast, Harris et al.[88] eccentric peak torque of the elbow flexors at 0 hours
found no significant differences in hip or ankle (43.5%), 24 hours (38.8%) and 48 hours (–32%)
range of motion but reported a shortened stride following repetitive eccentric contractions using the
length and a reduced excursion of the lower limb at Biodex isokinetic dynamometer (60°/sec). By 336
various running speeds. hours (14 days), eccentric peak torque had returned
to normal. Other researchers have reported a
Significant reductions in joint range of motion
delayed return of eccentric peak torque of the elbow
have been reported by other researchers[22,55,93-96]
flexors following isokinetic eccentric exercise, with
following repetitive eccentric resistance exercise[55]
eccentric peak torque remaining at a value 15% less
and maximal voluntary eccentric contractions of the
than initial peak torque until 7 days post-DOMS
elbow flexors.[97] Jones et al.[97] attributed their find-
inducement.[100] Similar trends have also been ob-
ings to a shortening of the non-contractile elements
served with respect to the lower limb; Eston et al.[98]
(i.e. muscle connective tissue), which acts in parallel
measured isokinetic, eccentric and concentric knee
with the muscle fibres. In one participant, up to 70N
extension peak torque values of the dominant leg at
of force was required to forcibly straighten the arm.
0.52 and 2.83 radians/sec 2, 4 and 7 days following
The reduced joint range of motion was not accompa-
DOMS-inducing isokinetic exercise. The results
nied by a stretch receptor-induced increase in elec-
showed an immediate post-exercise loss in peak
trical activity in the primary muscles. Howell et
torque for both modes of exercise at slow and fast
al.[96] also failed to demonstrate any spontaneous
velocities up to day 4, and a return to normal levels
activity in the elbow flexors following repetitive
between days 4–7. Significant reductions in concen-
eccentric lowering of a weight (60–80% of maxi-
tric and eccentric peak torque in the lower limb 48
mum isometric load). As a result, the reduced joint
hours following DOMS-inducing exercise have also
range of motion/stiffness has not been attributed to
been reported in other studies.[62,63]
increased muscle activity, but to significant in-
creases in the swelling of affected tissues, particu- Yet despite these findings, the duration of
larly within the perimuscular connective tissue and strength recovery still remains equivocal. As these
regions of the myotendinous junction.[96] This swell- studies have shown, many researchers have failed to
ing is characteristic of an acute inflammatory re- collect data at regular intervals over the 48-hour
sponse to muscle damage or injury.[22,45,84] period or have only recorded on selected days fol-
lowing DOMS inducement. As a result, the time at
which peak torque returns to normal levels remains
4.3 Strength and Power uncertain. This may have important implications for
Significant reductions in strength and power pa- the athlete as an alteration in the strength ratio of
rameters during DOMS have been documented by agonist to antagonist muscle groups may contribute
numerous researchers.[15,37,54,55,62,63,80,98-100] These to an increased risk of injury.[103]
reductions are most notable in eccentric muscle ac-
tions, although concentric and isometric strength 4.4 Altered Recruitment Patterns
losses have also been reported.[15,37,54,55,62,63,80,98-100]
Peak torque deficits are most pronounced 24–48 Muscular injury can often be characterised by the
hours following DOMS-inducing exercise and are presence of muscle dysfunction, a term used to
more profound and persistent during eccentric test- describe unusual patterns of muscle recruitment dur-
ing.[47] The duration of strength reduction is also ing a prescribed set of movements.[104] Any injury to
greater following eccentric activity and may require the muscle or connective tissue during eccentric
up to 8–10 days to return to normal baseline exercise may lead to changes in recruitment patterns
levels,[101] whilst concentric and isometric strength or changes in the temporal sequencing of muscle
has been shown to recover within 4 days. Evans et activation patterns. Such alterations are significant
al.[102] observed significant decreases in isokinetic as they can result in changes in muscle co-ordination
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
152 Cheung et al.
and segment motion. Although this area has not that perform similar or opposing functions.[104] This
method of EMG assessment has been successful in
been well examined in past DOMS research, studies
the diagnosis of patellofemoral pain[108] and back
that have examined muscle activity following ec-
and neck muscular dysfunction,[104] and involves the
centric exercise have shown promising findings.
identification of compensatory increases in EMG
Miles et al.[105] reported a lengthening of the
activity (hyperactivity) in areas of the muscle which
triphasic EMG pattern of the elbow musculature are uninjured or in other muscle groups (synergists
during elbow flexion in ten non-weight trained fe- or antagonists). Whether this method can also be
males following 50 maximal velocity eccentric rep- used to identify muscular dysfunction during
etitions of elbow flexion through 0–90°. Specifical- DOMS warrants further investigation.
ly, numerous indicators of altered neuromuscular
control were recorded, including lengthening of mo- 4.5 Injury Risk Factors
tor time, time to biceps peak EMG, time to peak
velocity and slowing of peak velocity. These re- Although DOMS is presently a sub-clinical inju-
sponses persisted for up to 5 days and were attribut- ry that is privately tolerated, there is certainly poten-
ed to muscular fatigue and dysfunction at the level tial for DOMS to lead to more costly and debilitating
of the muscle due to the high force eccentric exer- injury. Due to the increasing emphasis on health and
cise. The slowing of peak velocity and the lengthen- fitness promotion, it is becoming commonplace for
ing of the triphasic pattern were thought to be related individuals to continue exercising during periods of
to the selective damage of fast twitch fibres during intense muscle soreness. Those striving to improve
high-force eccentric exercise. Alterations in the tem- or to maintain levels of fitness or performance regu-
poral sequencing of muscles may also be due to a larly adhere to the ‘no pain, no gain’ philosophy. As
lengthening of the electromechanical delay. The a result, the first instinct is to ‘work through the
electromechanical delay refers to the time lag be- pain’ as opposed to resting the affected areas.[47] The
tween the onset of myoelectrical activity and tension potential impact of such behaviour could be detri-
development in a muscle contraction and includes mental to weakened tissue and to any unaccustomed
the time required for the conduction of action poten- tissue structures that are forced to compensate dur-
tials, the release of calcium, the formation of cross ing the period of functional deficiency post-DOMS
bridges, the development of tension, and the stretch- inducement. The following risk factors should be
ing of the series elastic components.[106] Zhou et considered prior to returning to sport:
al.[106,107] reported an approximately 20 msec elon- •The cushioning effect from a full range of joint
gation of the electromechanical delay after fatiguing motion during landings in running, or landing
exercise of an isometric nature, and attributed the after a jump, may be reduced during DOMS. The
elongation to either impaired muscle conductive, reduced capacity to efficiently absorb shock at
contractile or elastic properties or an increased mus- impact places the joints and tissue structures
cle temperature. As similar damage has been report- under unaccustomed loading.[47] To compensate,
ed following eccentric exercise, an increase in the increased shock absorption will occur at other
electromechanical delay and alterations in the tem- joints causing unaccustomed strain to be placed
poral sequencing of muscles is also conceivable on other muscles, joints, ligaments and tendons.
during DOMS. This in turn may affect the temporal •Changes in co-ordination and segment motion
sequencing and co-ordination of muscles during may result from alterations in muscle sequencing
functional activity. However, further research is still caused by DOMS.[104] This may lead to unaccus-
needed to confirm these assumptions. tomed strain being placed on muscles, ligaments
and tendons during functional activity.
An alternative means of assessing muscular dys-
function using EMG techniques is to analyse the •A reduction in force output by an injured part of a
ratio of EMG amplitude between pairs of muscles muscle may lead to compensatory recruitment
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
Delayed Onset Muscle Soreness 153
from an uninjured area of a muscle, or from other 5.1 Cryotherapy
muscles.[104] This leads to a marked increase in
The initial treatment recommended for traumatic
EMG activity (hyperactivity), altered EMG ratios
soft tissue injuries is R.I.C.E (rest, ice, compression
and increased force production of the compensat-
and elevation). The superficial application of ice
ing muscles, causing unfamiliar stress to be
results in changes in skin, subcutaneous, intramus-
placed on the compensating muscle groups. cular and joint temperatures.[109] A decrease in tissue
•A reduction in strength and power during intense temperature stimulates cutaneous receptors to excite
muscle soreness may lead to an individual work- the sympathetic adrenergic fibres causing the con-
ing at a higher intensity than to which they are striction of local arterioles and venules. This results
normally accustomed.[47] An individual pre- in a reduction of swelling and a decreased rate of
scribed to work at a specific percentage of one metabolism which in turn reduces the inflammatory
repetition maximum for example, may continue response, vascular permeability and the formation of
to train at a pre-determined intensity during oedema.[15,109] However, studies to date have shown
DOMS. However, as a result of damaged and little or no attenuation of the magnitude of muscle
weakened muscle fibres following eccentric ac- soreness or the facilitation of its recovery following
tivity, the intensity is now relatively higher thus the application of cryotherapy.[17,21,110-113] Paddon-
increasing the risk of further injury. Jones and Quigley[15] observed DOMS in eight re-
•An increased incidence of injury may also be sistance-trained males after performing 64 eccentric
observed if there is an alteration in the strength actions of the elbow flexors. Immediately following
ratio of agonist and antagonist muscle the completion of the eccentric exercise session the
groups.[103] Whether DOMS can lead to signifi- experimental arm was subjected to five 20-minute
cant changes in the strength ratio of opposing ice water immersions, with 60-minutes recovery
muscle groups has not been extensively between each immersion. The results showed no
researched. significant differences in muscle soreness, isometric
torque, isokinetic torque or limb volume between
•An inaccurate perception of impairment may lead the experimental arm and the control arm at baseline
to an individual returning to high intensity activi- or following ice immersion. Similarly, no differ-
ty before adequate recovery. ences in the perception of muscle soreness were
reported following studies using single ice massage
5. Treatment and Management applications of 15 minutes duration either immed-
Strategies for DOMS iately, 24h or 48h post-exercise;[114] 20 minutes du-
ration immediately post-exercise[93] or following
The proposed mechanisms of DOMS have al- immersion of the experimental limb in an ice bath 25
lowed researchers to investigate various treatment minutes prior to exercise.[115] The lack of significant
strategies aimed at alleviating the symptoms of findings can not be attributed to the training status of
DOMS, restoring the maximal function of the mus- the participants as both trained[15] and untrained
cles as rapidly as possible and/or reducing the participants[93] were observed. This contradicts be-
magnitude of the initial injury.[17] Treatment strate- liefs that trained individuals are more resistant to
gies have been administered either prophylactically eccentric exercise-induced injury, more resistant to
as a preventative measure and/or therapeutically as a muscle damage and thus more likely to demonstrate
treatment measure. Treatment strategies have in- a positive response to cryotherapy.[15] Variations in
cluded cryotherapy, stretching, anti-inflammatory the frequency of cold application (either in multiple
drugs, ultrasound, electrical current techniques, ho- or single applications) and the timing of application
meopathy, massage, compression, hyperbaric oxy- (either pre- or post-exercise) also appear to have
gen and exercise. minimal effect on minimising muscle soreness and
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
154 Cheung et al.
muscle function. Whilst it is possible that an in- muscles. However, studies which have investigated
creased number of applications (more than five) and the effect of stretching prior to,[7,44,53,118] af-
an increased or decreased duration of ice application ter,[8,53,64,111,112,119] or before and after[120] eccentric
could be employed, their effect remains equivocal. exercise have shown no preventative effect of
These protocols would also be impractical for the stretching on DOMS. One explanation is that studies
individual to administer and applications of more that employ stretches of less than 30sec may be
than 20 minutes duration have not been recommend- limited by the stretch reflex response. When a mus-
ed (20 minutes is generally recommended in order to cle is stretched the muscle spindles are also stretch-
effectively lower deep muscle temperature, whilst ed, causing sensory impulses to be sent to the spinal
preventing nerve injury).[116] Thus, cold application, cord to indicate that a muscle is being stretched.
other than its analgesic effect, provides little benefit Efferent impulses are in turn sent back to the muscle
in the prevention and treatment of DOMS. This from the spinal cord causing the muscle to contract.
contrasts with the effectiveness of cryotherapy in If the stretch continues for at least 6sec, the Golgi
acute traumatic injury and may indicate that a differ- tendon organs send sensory impulses to the spinal
ent or a much smaller magnitude of inflammatory cord causing a reflex relaxation of the antagonist
response occurs during DOMS. muscle. This reflex relaxation allows the agonist
muscle to stretch through relaxation, reducing the
5.2 Stretching risk of damage to the muscle.[121] A short duration of
stretching thus limits the time available for the Golgi
Static stretching, pre or post-exercise, has been tendon organs to respond to the change in length and
recommended[53] as a preventative measure of tension of the muscles.[121] Interestingly, muscle
DOMS as it is thought to relieve the muscle spasm soreness can also be induced by stretching exercises
described in de Vries’ muscle spasm theory. Bob- alone. Smith et al.[118] reported that three sets of 17
bert et al.[68] later proposed that the static stretching 60-second stretches during 90 minutes of static and
of sore muscles post-exercise could also force the ballistic stretching induced significant increases in
dispersion of oedema which accumulates following muscle soreness perception and serum CK in 20
tissue damage. Repeated and held stretching reduces male participants. Static stretching produced signifi-
the tension on the muscle-tendon unit at any given cantly greater soreness on a 10-point scale (2.1 ±
length. This visco-elastic behaviour of the muscle- 1.4) than ballistic stretching (1.6 ± 1.0) throughout
tendon unit implies a combination of viscous the 120 hours post-exercise. Various muscles have
properties, where deformation is rate dependent, and been testing including quadriceps,[7,8,64,119,120] ham-
elastic properties, where deformation is load strings,[44,53,111] calves[64] and elbow flexors[113] us-
dependent.[117] A visco-elastic material when held at ing stepping,[7,8,64] isokinetic profiles,[44,53,120] elbow
the same tension will increase in length over time contractions[113] and squats.[119] Further research
(creep). Alternatively, if the visco-elastic material is should be directed at investigating the efficacy of
stretched to a new length and held constant, it will stretching in order to determine its role as a prevent-
decline in tension over time (stress-relaxation). This ative measure against, or a predisposing factor to-
visco-elastic behaviour could be beneficial in eccen- wards, DOMS. It is also important to emphasise that
tric exercise as a decrease in force production at a viscoelasticity is temperature-dependent.[30] There-
given elongation may lead to a reduction in the level fore, the intensity and duration of warm-up should
of damage to connective and muscle tissue.[53] Since
be individualised to the athlete’s physical capabili-
muscle damage also occurs at a critical level and rate
ties.[121] An increase in rectal temperature of at least
of tension during stretch, increased flexibility may
1–2°C is sufficient during a warm-up, although the
also prevent stretch-induced injury. This is of partic-
more practical observation of a mild sweating in
ular significance for two-joint muscles that are sub-
jected to greater levels of stretch than single-joint normal ambient conditions has also been relia-
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
Delayed Onset Muscle Soreness 155
ble.[26,121] Despite this, only minimal warm-ups (0–5 ings.[62] To test this hypothesis, the effect of prophy-
minutes) have been reported in stretching studies. lactic (prior to exercise) and therapeutic (post-exer-
cise) drug administration has been examined. Pro-
phylactic administration of ibuprofen (400mg three
5.3 Anti-Inflammatory Drugs
times a day for a total of 1200mg) resulted in greater
It has been proposed that the inflammatory pro- declines in muscle soreness than therapeutic admin-
cess and the accumulation of muscle oedema fol- istration.[62] Francis and Hoobler[22] also demonstrat-
lowing tissue injury can contribute significantly to ed a reduction in muscle soreness when 10g of
the development of DOMS.[22,45,84] As a result, the aspirin were administered four times daily from 4
efficacy of a number of nonsteroidal anti-inflam- hours prior to exercise until 48 hours post-exercise.
matory drugs (NSAIDs) and oral analgesics in When larger doses of NSAIDs have been adminis-
preventing or treating DOMS has been exa- tered the effect has been minimal.[37] Donnelly et
mined.[17,22,37,46,62,63,122] NSAIDs inhibit the met- al.[37] administered 1200mg of ibuprofen to 16 par-
abolism of arachidonic acid via the cyclo-oxygenase ticipants before 45 minutes of downhill running at a
pathway and thus prevent the production of en- speed that elicited 70% heart rate maximum, and
doperoxides and prostaglandins.[62,63] A reduction in then 600mg every 6 hours up to 72 hours post-
the inflammatory response leads to a reduction in exercise. The total dose administered was 8400mg,
the amount of muscle oedema and intramuscular i.e. 7-fold the dosage prescribed by Hasson et al.[62]
pressure; two factors which contribute to pain and However, despite the prophylactic and therapeutic
muscle soreness. Hasson et al.[62,63] reported signifi- administration in this study, the effect of the
cant reductions in the perception of muscle soreness NSAIDs was minimal compared with the placebo
at 48 hours post-exercise for an experimental group group of 16 participants. Ibuprofen did not affect
that received therapeutic or prophylactic administra- muscle soreness, muscle strength or 50% endurance
tion of ibuprofen, dexamethasone and aspirin com- time. Serum CK and urea were higher in the
pared with a placebo group that received ionto- ibuprofen group after both runs. Large doses can
phoresis, or a control group who received no treat- impede the production of myofibrillar protein and
ment. Maximum voluntary contraction, peak torque delay the healing process of damaged tissue.[93] This
and work were no different between the three groups was observed in a study investigating the effect of
at 48 hours. Fifty percent less change in elbow dexamethasone iontophoresis,[63] a method which
extension at both 24 hours (–14 ± 3 vs –8 ± 1°) and involves the introduction of charged compounds
48 hours (–30 ± 6 vs –14 ± 3°) has been reported in across the skin and into the tissue via an electrical
an aspirin group when compared with a placebo current (refer to section 5.4). The use of iontophore-
group after isokinetic elbow flexor action till ex- sis to administer NSAIDs resulted in a prolonged
haustion at 60°/sec.[22] Soreness of the aspirin group progression of muscle soreness between 24 and 48
was 25% less than the control at 48 hours. Both hours.
groups demonstrated reduced force production at 24 Diclofenac does not influence muscle damage,
and 48 hours. However, other researchers[17,37,46,123]
but may reduce soreness.[124] Twenty untrained male
have reported no effect on the perception of muscle
participants took diclofenac or placebo before, and
soreness following NSAID administration.
for 72 hours after, two 45 minute downhill runs 10
The inconsistency in findings may be attributed weeks apart. Diclofenac had no influence on the
to the timing of drug administration[62] and/or the
serum biochemical response to downhill running.
drug dosage administered.[93] Medication is general-
Overall, soreness was not affected by the drug, but
ly administered when an individual complains of
individual soreness was reduced by diclofenac for
pain, not before. It has therefore been suggested that
the first period of study. Gulick et al.[93] reported no
the consumption of an anti-inflammatory compound
significant differences in DOMS symptoms between
prior to an exercise event may alter these find-
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
156 Cheung et al.
treatments (NSAID total dosage of 5400mg over 72 showed a significant reduction in soreness after 48
hours, high velocity concentric exercise, ice mas- hours compared with the sham and control groups.
sage, 10 minutes stretching, arnica montana1 oint- In contrast, Ciccone et al.[127] reported an enhance-
ment and arnica montana pellets) for 70 untrained ment of DOMS symptoms following the application
participants who completed 15 sets of 15 isokinetic of ultrasound (1 MHz frequency, 1.5 W/cm2 intensi-
eccentric contractions of the forearm extensor mus- ty) in 40 females following bilateral DOMS-induc-
cles. The NSAID and arnica montana appeared to ing eccentric exercise of the elbow flexors. The
impede recovery of muscle function. Flurbiprofen purpose of this study was to determine the effects of
has been shown to have no effect on muscle soreness ultrasound (sham and real) and/or phonophoresis
48 hours post-exercise for six male cycle trained using an anti-inflammatory analgesic cream (place-
participants who completed three trials of 30 min- bo or cream) during DOMS. Phonophoresis is a
utes at 80% maximal oxygen uptake on a cycle method of drug administration that utilises ultra-
ergometer. Flurbiprofen or placebo was adminis- sound waves to enhance the delivery of pharmaco-
tered from the day before exercise until 4 days logical agents through the skin to the underlying
following exercise in a double-blind crossover pro- tissues. The results showed that although all groups
tocol. No effect of the drug on enzyme activity was experienced an increase in soreness 24 hours follow-
shown.[123] As a result of these findings, future re- ing DOMS-inducement, the group who was treated
search should be directed towards the use of with ultrasound alone experienced the only statisti-
NSAIDS as prophylactic or therapeutic interven- cally significant increase in muscle soreness at 48
tions for post-exercise pain and discomfort. Howev- hours when compared with the control arm. These
er, the encouragement of drug-use for such purposes increases were not observed in the group that was
can easily cross over to the casual abuse of other treated with ultrasound and trolamine salicylate
performance-related drugs, i.e. ergogenic aids and cream. Therefore salicylate phonophoresis may be
performance enhancers. The chronic overuse of indicated when ultrasound is required to improve
NSAIDs has also been related to certain adverse blood flow and tissue heating without promoting the
effects, i.e. an increased incidence of stomach ul- inflammatory response in musculoskeletal inju-
cers, kidney failure and liver damage.[125] Research- ries.[127] Pulsed ultrasound has also failed to dimin-
ers must therefore recognise the potential conse- ish DOMS symptoms whether delivered once or
quences of promoting NSAID use to the general twice daily.[128]
public in terms of the contraindications to anti-
inflammatory drug use, and must acknowledge their 5.5 Electrical Current Techniques
responsibility as educators against drug-abuse. The application of small electrical currents have
been used clinically to accelerate the healing of
5.4 Ultrasound wounds and fractures.[113] However, the efficacy of
this type of treatment technique on musculoskeletal
Ultrasound is thought to promote the inflam-
injuries is less known as only a few studies have
matory response via an increase in tissue heating
investigated the effect of microcurrent,[129] high-volt
and blood flow. Its success as a treatment regimen
pulsed current electrical stimulation[130] or tran-
has shown mixed results. Hasson et al.[126] compared
scutaneous electrical nerve stimulation (TENS)[131]
sham and real ultrasound treatment compared with a
on DOMS.
control group following 10 minutes of stepping ex-
ercise. Ultrasound given at 24 hours post-exercise to Weber et al.[87] compared the effectiveness of
the vastus lateralis and vastus medialis and pulsed at microcurrent electrical stimulation (30µA, gentle
a frequency of 1 MHz and an intensity of 0.8 W/cm2wave slope, 0.3Hz frequency, alternating polarity, 8
1Use of tradenames is for product identification purposes only and does not imply endorsement.
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
Delayed Onset Muscle Soreness 157
minutes duration) in minimising muscle soreness duced analgesia remains questionable. The authors
and force deficits immediately following and 24 proposed that continued use of this therapeutic mo-
hours after DOMS-inducing exercise of the elbow dality requires a more comprehensive understanding
extensors. The results showed no statistically signif- and that further investigation should include a con-
icant difference between the microcurrent electrical trol group to eliminate the placebo effect.[134] A
stimulation group and the control group. The effect recent double-blind, placebo-controlled study has
of low-volt microamperage stimulation (100µA, 0.3 shown that Acustat electro-membrane microcurrent
pulses/sec, alternating polarity for 20 minutes) has therapy can reduce the signs and symptoms of
also been explored following DOMS induce- DOMS after an eccentric exercise protocol for the
ment.[113,132] When low-volt microamperage stimu- arm compared with a matching placebo membrane
lation is combined with static stretching, and com- group.[137]
pared with a placebo treatment/static stretching 5.6 Homeopathy
group, no significant differences in concentric tor-
que, pain and range of motion between groups at 24, Homeopathy has been described as a form of
48, 72, 96 and 196 hours post-exercise were report- therapy based on the principle of ‘let like be cured
ed.[132] However, a transient analgesic effect was with like’, that is ‘practitioners prescribe in a low
noted at 24 and 48 hours immediately post-treatment dose whatever drug would cause symptoms similar
in the low-volt microamperage stimulation group to those in the patient were that drug to be taken in a
compared with the placebo group. In contrast, an high dose’.[16] The most popular homeopathic
earlier investigation by the same authors[133] using medicine of choice is arnica due to its analgesic,
TENS (low frequency, 2 pulses/sec, 300 µsec pulse antibiotic and anti-inflammatory properties.[93,138]
width, 30 minutes duration) showed a significant Recent studies,[16,93] which have investigated the
reduction in pain perception and an improvement in effect of arnica on DOMS, have shown minimal
range of elbow extension in eight female partici- benefit of the remedy. In a randomised, double-
pants 48 hours following DOMS-inducing exercise. blind, placebo-controlled trial, no statistical differ-
It has been proposed that TENS with low frequency ences were found in mean muscle soreness follow-
and long pulse duration can result in the release of β-ing DOMS-inducing bench stepping exercise be-
endorphin from the anterior pituitary gland. β-En- tween the placebo group and the arnica group (arni-
dorphin shares the pre-cursor hormone propiomela- ca 30c, Rhustox 30c and sarcolactic acid 30c).[16]
nocortin with corticotropin.[134] The latter results in Gulick et al.[93] reported similar results in their par-
the synthesis and release of cortisol from the adrenal ticipants who were instructed to take three pellets
cortex which stimulates gluconeogenesis, promotes (50g) of arnica montana in a sublingual form
glucose utilisation, protein synthesis, fatty acid every 8 hours for 3 days following DOMS-induce-
mobilisation and suppresses acute and chronic in- ment in the forearm extensors. When arnica was
flammatory responses.[131,135] Despite having a posi- administered in an ointment format, (4%, 0.5g dose,
tive effect on pain perception and range of motion, rubbed into the skin every 8 hours for 3 days) the
TENS treatment showed no significant increase in results were again ineffective in reducing the
serum cortisol concentration. Similar results were amount of muscle soreness when compared with a
obtained in a study using interferential current as the control group.
intervention (low beat frequency 10 beats per sec-
ond [bps] for 30 minutes vs high beat frequency 100 5.7 Massage
bps for 30 minutes).[134] Interferential current uses
medium frequencies which encounter less resistance The influx of calcium ions into the muscle fibres
at the skin and have a better conductance through and a subsequent disruption of the calcium homeo-
skin.[134,136] Despite these differences, the role of β- stasis following eccentric exercise[2,81] may be re-
endorphin in TENS and interferential current in- stored by increasing the amount of oxygenated
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
158 Cheung et al.
blood flow to the injured area.[2] It has been suggest- hours post-exercise).[21,142] Gulick et al.[93] reported
that massage was not effective in abating the signs
ed that an increased blood flow during vigourous
and symptoms of DOMS. The inconsistency in re-
massage hinders the margination of neutrophils[139]
search findings could be attributed to the large varie-
and reduces subsequent prostaglandin production,
ty of massage techniques and massage ther-
thus reducing any further damage associated with
apists.[143] The optimal duration of massage treat-
the inflammatory process. An increased delivery of ment also needs to be investigated as research to
oxygen also restores the mitochondrial regeneration date has only examined the effects of 5–30 minutes
of ATP and the active transport of calcium back into of massage treatment with varied findings. It is also
the sarcoplasmic reticulum.[2] However, studies that necessary to determine whether manual manipula-
have examined the effect of massage on local blood tion of injured tissue serves to encourage healing or
flow have shown varying results. An increase in impede it. The use of massage before exercise to
blood flow through the vascular bed during massage prevent DOMS has also not been examined.
was reported by some researchers.[140,141] Converse-
ly Tiidus[142] reported no differences in arterial or 5.8 Compression
venous blood flow during effleurage (stroking) mas-
sage of the quadriceps. Studies examining the effect Kraemer et al.[144] reported that continuous com-
of massage on the perception of DOMS also vary. pression was an effective therapeutic intervention in
No differences in soreness levels[14,87] or force defi- treating eccentric exercise-induced muscle soreness.
cits[87] have been reported between the massaged Fifteen healthy, non-strength-trained men were ran-
limb or the control limb using either petrissage domly placed in a control group or a continuous
(kneading),[14] or a combination of effleurage and compression-sleeve group. Two sets of 50 arm curls
petrissage massage (2 minutes effleurage, 5 minutes at 1 repetition maximum (RM) elbow flexion at 60
petrissage and 1 minute effleurage)[87] following degrees/sec were completed. The compression-
high intensity exercise. sleeve prevented loss of elbow extension, decreased
the participants’ perception of soreness, reduced
In contrast, Rodenburg et al.[20] observed small swelling and promoted recovery of force produc-
reductions in muscle soreness following a combina- tion. Further studies are required to confirm the
tion of eccentric exercise of the forearm, warm-up, initial benefits of compression on reducing DOMS
stretching and massage (6 minutes of skin and mus- symptoms.
cle effleurage, half a minute of tapotement/tapping,
5 minutes of petrissage and 1 minute of muscle 5.9 Hyperbaric Oxygen Therapy
effleurage with decreasing intensity). However, the
effects of massage in this study could not be isolated Several authors have investigated the effects of
from the effect of warm-up and stretching. Nonethe- hyperbaric oxygen therapy (HBOT) to enhance re-
less, a reduction in serum CK levels in participants covery from DOMS.[145-148] Harrison et al.[145] exa-
who were massaged (effleurage, petrissage and mined the role of HBOT in the treatment of exer-
shaking of the limb) for 30 minutes 2 hours follow- cise-induced muscle injury. Twenty-one college-
ing exercise have been reported.[139] Similar results aged males were assigned to three groups: control, 2
have been shown by Lin[119] who reported a reduc- hours or 24 hours post-exercise. All participants
tion in plasma CK level after exercise when the performed six sets (ten repetitions per set) of eccen-
participants in the massage group received the first tric repetitions with a load equivalent to 120% of
15-minute massage 2 hours after the exercise. This their concentric maximum. HBOT treatments con-
may suggest that the timing of massage intervention sisted of 100 minutes exposure to 2.5 atm and 100%
may be an influential factor. However, this remains oxygen with intermittent breathing of ambient air
equivocal as few studies have investigated the ef- (30 minutes at 100% O2, 5 minutes at 20.93% O2).
fects of early massage intervention (i.e. within 1–2 HBOT was not effective in the treatment of exer-
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
Delayed Onset Muscle Soreness 159
cise-induced muscle injury as indicated by isometric be due to the break up of adhesions in the sore
strength, forearm flexor cross-sectional area, serum muscles, an increased removal of noxious waste
CK levels, T2 relaxation time (via magnetic products via an increased blood flow or an increased
resonance imaging) and rating of perceived sore- endorphin release during activity.[73] The latter re-
ness. Mekjavic et al.[147] induced DOMS to the bi- sults in an analgesic effect that minimises the sensa-
ceps brachii and brachialis muscles of 24 healthy tion of DOMS. Elevated afferent input from large,
male participants. Twelve participants received low threshold sensory units (groups Ia, Ib and II
HBOT at 2.5 atm once a day for 7 days. The placebo fibres) may also interfere with the pain sensation
group was exposed to a normoxic gas mixture at 2.5 carried by group III and IV fibres, thus reducing
atm. There was no difference in perceived muscle pain.[149]
soreness or arm circumference, suggesting that Studies that have investigated the therapeutic ef-
HBOT therapy did not enhance recovery from fects of exercise on the development of DOMS have
DOMS. In contrast to Mekjavic et al.,[147] Staples et shown mixed findings. Upper arm ergometry per-
al.[148] suggested that HBOT may enhance recovery formed for 8[87]–10 minutes[93] immediately follow-
of quadriceps DOMS. Sixty-six untrained males had ing DOMS-inducing eccentric muscle activity of the
100% oxygen at 2 atm for 1 hour per day (HBOT) or elbow[87] and wrist extensors[93] revealed no statisti-
21% oxygen at 1.2 atm for 1 hour per day (placebo). cally significant differences in muscle soreness at
In phase one (four groups) there were no significant 24, 48 and/or 72 hours post-exercise when com-
differences found in pain-scores between the groups pared with a control group. The performance of 25
over time, but the eccentric torque from immed- submaximal eccentric contractions 1 day following
iately after exercise to 96 hours after exercise was a heavy eccentric DOMS-inducing exercise regimen
significantly (p = 0.021) better in the HBOT group for the forearm flexor and extensor muscles also
than in the other three groups. In phase two (three showed no effect on muscle soreness.[150] Hasson et
groups) there was no difference in pain-scores be- al.[151] reported a significant decrease in DOMS at
tween the groups, but when comparing the mean 48 hours following high velocity concentric
torque for the sham and the 5-day HBOT groups, a isokinetic exercise (6 × 20 maximum voluntary con-
significant difference (p = 0.023) was detected at the traction of the knee flexors and extensors at 5.23
final test of eccentric quadriceps torque. There were rad/sec) performed 24 hours following stepping ex-
no other significant differences noted between indi- ercise. The contrast in research findings was attrib-
vidual groups. Over-oxygenation would have result- uted to differences in exercise protocols, including
ed in oxygen toxicity, and under-oxygenation would type of exercise performed, timing of exercise and
have resulted in a lack of effect on the tissue. It was degree of effort (submaximal vs maximal).[93]
questioned whether the high-force eccentric Therefore studies using similar exercise parameters
workout was enough to induce sufficient oedema to need to be studied and compared in order to deter-
promote tissue hypoxia. The investigators did not mine the true effect of exercise on reducing the
use biochemical or radiological markers to test the magnitude and severity of muscle soreness. Re-
changes and only used measurement of the arm search aimed at investigating the training effect of a
circumference for testing oedema. single bout of eccentric exercise (downhill running)
has shown significantly diminished muscle soreness
5.10 Exercise and serum CK activity after exercise sessions re-
peated 3 and 6 weeks after the initial bout.[40]
Exercise is one of the most effective strategies for
It has been proposed that a continuous pool of
alleviating DOMS.[2] However, pain relief is also
stress-susceptible or fragile fibres are damaged by
temporary and rapidly resumes again following ex-
the initial bout of exercise and that this damage
ercise cessation.[47] It has been proposed that the
temporary alleviation of pain during exercise may manifests itself as muscle soreness, enzyme changes
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
160 Cheung et al.
and a temporary reduction in the pool of fragile creased risk of injury to unaccustomed tissues if an
fibres.[40] Therefore, subsequent work bouts result in individual returns to sport prematurely.
fewer stress-susceptible fibres being damaged and Numerous theories of DOMS have been pro-
hence reduced muscle soreness. However, due to the posed in the literature, with most criticism directed
dynamic degeneration-regeneration process that oc- at the lactic acid theory and muscle spasm theory. It
curs to replace damaged fibres, the reduction in is likely that a combination of theories can contrib-
muscle soreness and serum CK levels is also tempo- ute to DOMS with most emphasis being placed on
rary and exercise bouts performed at 9 weeks pro- the inflammatory response to connective tissue or
duced similar levels as the initial bout of exercise. muscle damage. Treatment mechanisms are also
This may have important implications for athletes plentiful, however only limited success has been
who train on a daily basis or who are preparing for reported in research to date. The most notable find-
an event that will comprise some eccentric activity. ings are those related to stretching; although stretch-
In particular, attention must be paid to the schedul- ing is publicly recommended as an injury prevention
ing of training programmes in order to minimise the measure, the rationale for stretching has yet to be
amount of muscle soreness experienced at or near validated by future research.
competition times. Future research should be direct- Future research should focus on clarifying the
ed towards the identification of pain relief strategies following points:
during exercise, and whether compensatory mecha- •Is the combination of models a valid explanation
nisms are adopted to help alleviate pain. Although for the mechanism of DOMS? The model draws
this may not be relevant to the recreational athlete numerous aspects from different theories, there-
who will most likely rest for 2–3 days following fore to assume that all these stages occur requires
strenuous exercise, the elite athlete, who must train further investigation. The time frame of specific
daily or twice daily, may be predisposed to further events also needs to be clarified.
injury if biomechanical adaptations are adopted to •Is DOMS preventable prior to exercise? Are ther-
help relieve intense muscle soreness. apeutic treatment strategies suitable as prophy-
lactic strategies? The administration of anti-in-
6. Conclusions and Recommendations flammatory drugs, stretching and physical train-
ing are currently performed prior to exercise and
DOMS can result from strenuous, unaccustomed have resulted in mixed findings. Can other forms
tasks of an eccentric nature. Symptoms of DOMS of treatment also be used prophylactically to pro-
can include: tenderness or stiffness to palpation duce positive findings?
(particularly at the musculotendinous junction), a •Is stretching a valid preventative measure? If
loss of range of motion, flexibility, force production static stretching can lead to DOMS in the absence
and mobility. Greater perception of muscle soreness of any exercise, should individuals perform
tends to be associated with high intensity exercise, stretching at all? The increasing interest in pro-
although duration also has a contributing effect. The prioceptive neuromuscular facilitation stretching
impact of DOMS on athletic performance has not warrants investigation.
been well researched. However, a reduction in joint •Past research has led to the assumption that
range of motion during periods of severe muscle DOMS induces temporary alterations in joint
soreness, and a reduction in shock attenuation have kinematics and muscle activation patterns. If so,
been observed. Significant reductions in peak torque when is the safest time to return to sport and what
can occur for up to 8 days following eccentric exer- are the biomechanical implications, if any, of
cise, and there are also alterations in muscle se- premature return?
quencing and recruitment patterns which occur as a
result of damage to the muscle fibres. Any compen- There are still many questions that remain unan-
satory mechanisms that occur may lead to an in- swered relating to DOMS, therefore numerous re-
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
Delayed Onset Muscle Soreness 161
14. Lightfoot JT, Char D, McDermott J, et al. Immediate post-
search directions can be pursued. This review has exercise massage does not attenuate delayed onset muscle
identified certain areas of research that may benefit soreness. J Strength Cond Research 1997; 11 (2): 119-24
15. Paddon-Jones DJ, Quigley BM. Effect of cryotherapy on muscle
both the elite and recreational athlete. However, it is soreness and strength following eccentric exercise. Int J Sports
important to note that DOMS is not exclusive to Med 1997; 18: 588-93
sport; it also has a prevalent occurrence in strenuous, 16. Vickers AJ, Fisher P, Smith C, et al. Homeopathy for delayed
onset muscle soreness: a randomised double blind placebo
unaccustomed activities of a non-sporting nature, controlled trial. Br J Sports Med 1997; 31: 304-7
i.e. activities of daily living. As a result, sports- 17. Gulick DT, Kimura IF. Delayed onset muscle soreness: what is
it and how do we treat it? J Sport Rehab 1996; 5: 234-43
related DOMS research may serve to benefit a wider
18. Sharkey J. Delayed onset muscle soreness. Ultrafit 1995; 5 (7):
audience than initially anticipated, with research 3
findings also applicable in other health industries. 19. Cleary MA. The time course of the repeated bout effect of
eccentric exercise on delayed onset muscle soreness. Philadel-
phia (PA): Temple University, 1995
Acknowledgements 20. Rodenburg JB, Steenbeek D, Schiereck P, et al. Warm-up,
stretching and massage diminish harmful effects of eccentric
The authors would like to acknowledge Sport Science exercise. Int J Sports Med 1994; 15 (7): 414-9
New Zealand for funding assistance in the preparation of this 21. Isabell WK, Durrant E, Myrer W, et al. The effects of ice
manuscript. The authors have provided no information on massage, ice massage with exercise, and exercise on the pre-
vention and treatment of delayed onset muscle soreness. J
conflicts of interest directly relevant to the content of this Athletic Train 1992; 27 (3): 208, 210, 212, 214, 216-7
review. 22. Francis KT, Hoobler T. Effects of aspirin on delayed muscle
soreness. J Sports Med Phys Fitness 1987; 27 (3): 333-7
23. Portero P, Maisetti O. A new treatment technique on delayed
References onset muscle soreness recovery: preliminary study on physio-
1. Talag T. Residual muscle soreness as influenced by concentric, logical mechanisms. 2000 Pre-Olympic Congress; 2000 Sep
eccentric, and static contractions. Res Q 1973; 44: 458-69 7-12; Brisbane, 58
2. Armstrong RB. Mechanisms of exercise-induced delayed onset 24. MacIntyre DL, Reid WD, McKenzie DC. Delayed muscle sore-
muscular soreness: a brief review. Med Sci Sports Exerc 1984; ness: the inflammatory response to muscle injury and its
16 (6): 529-38 clinical implications. Sports Med 1995; 20 (1): 24-40
3. Byrnes WC, Clarkson PM. Delayed onset muscle soreness and 25. Abraham WM. Factors in delayed muscle soreness. Med Sci
training. Clin Sports Med 1986; 5 (3): 605-14 Sport Exerc 1977; 9 (1): 11-20
4. Jones DA, Newham DJ, Round JM, et al. Experimental human 26. Safran MR, Seaber AV, Garrett JWE. Warm-up and muscular
muscle damage: morphological changes in relation to other injury prevention, an update. Sports Med 1989; 8 (4): 239-49
indices of damage. J Physiol 1986; 375: 435-48 27. Armstrong RB, Warren III GL. Strain-induced skeletal muscle
5. Cleak MJ, Eston RG. Delayed onset muscle soreness: mecha- fibre injury. In: Macleod D, editor. Intermittent high intensity
nisms and management. J Sports Sci 1992; 10 (4): 325-41 exercise: preparation, stresses and damage limitation. London:
6. Willoughby DS. Delayed onset muscle soreness: a possible E & FN Spon, 1993: 275-85
physiological etiology and practical implications for coaches. 28. Garrett JWE. Muscle strain injuries: clinical and basic aspects.
Texas Coach 1990; 35 (1): 34-6 Med Sci Sports Exerc 1990; 22 (4): 436-43
7. High DM, Howley ET. The effects of static stretching and warm 29. Noonan TJ, Garrett Jr WE. Injuries at the myotendinous junc-
up on prevention of delayed onset muscle soreness. Res Q tion. Clin Sports Med 1992; 11 (4): 783-806
Exerc Sport 1989; 60 (4): 357-61 30. Garrett J. Muscle strain injuries. Am J Sports Med 1996; 24 (6):
8. Maxwell S, Kohl S, Watson A, et al. Is stretching effective in S2-8
the prevention of or amelioration of delayed onset muscle 31. Newham DJ, Mills KR, Quigley R, et al. Muscle pain and
soreness? Aust J Sci Med Sport 1988; 20 (4): 22 tenderness after exercise. Aust J Sports Med Exerc Sci 1982;
9. Claps F. Soothe the burn: 11 ways to extinguish post-workout 14: 129-31
pain. Men’s Fitness 2000; 16 (5): 104-7
32. Friden J, Sfakianos PN, Hargens AR. Muscle soreness and
10. Nessel EH. Even my eyebrows hurt. American Swimming 1999; intramuscular fluid pressure: comparison between eccentric
(3): 2 and concentric load. J Appl Physiol 1986; 61 (6): 2175-9
11. Fell JW, Brown RB, Gaffney PT. Ibuprofin and creatine inter- 33. Tidball JG. Myotendinous junction injury in relation to junction
vention does not reduce the effect of exercise induced muscle structure and molecular composition. Exerc Sport Science Rev
damage or delayed onset muscle soreness. Fifth IOC World 1991; 19: 419-45
Congress on Sport Sciences; 1999 Oct 31-Nov 5; Sydney.
Sydney: Sports Medicine Australia, 1999 34. Stauber WT. Eccentric action of muscles: physiology, injury
and adaptation. In: Pandolf KP, editor. Exercise and sport
12. Brown RB, Fell JW, Gaffney PT. The influence of previous science reviews. Baltimore (MD): Williams and Wilkins,
aerobic activity levels on morphological and biochemical in- 1989: 157-86
dicators of exercise induced muscle damage [abstract]. Fifth
IOC World Congress on Sport Sciences; 1999 Oct 31-Nov 5; 35. Eston RG, Lemmey AB, McHugh P, et al. Effect of stride
Sydney. Sydney: Sports Medicine Australia, 1999 length on symptoms of exercise-induced muscle damage dur-
13. Birk TJ. Preventive interventions can minimize delayed onset ing a repeated bout of downhill running. Scand J Med Sci
muscle soreness. Sports Med Alert 1999; 5 (6): 47-9 Sports 2000; 10 (4): 199-204
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
162 Cheung et al.
36. Eston RG, Critchley N, Balzopoulos V. Delayed onset muscle 55. Francis K, Hoobler T. Delayed onset muscle soreness and
soreness, strength loss characteristics and creatine kinase ac- decreased isokinetic strength. J Appl Sport Sci Res 1988; 2 (2):
tivity following uphill and downhill running. UK sport: part- 20-3
ners in performance. The contribution of sport science, sports 56. Horswill CA, Layman DK, Boileau RA, et al. Excretion of
medicine and coaching to performance and excellence. 3-methylhistidine and hydroxyproline following acute weight-
Manchester: Sports Council, 1993: 10-11 training exercise. Int J Sports Med 1988; 9 (4): 245-8
37. Donnelly AW, Maughan RJ, Whiting PH. Effects of ibuprofen 57. Newham DJ, Jones DA, Gosh G, et al. Muscle fatigue and pain
on exercise-induced muscle soreness and indices of muscle after eccentric contractions at long and short length. Clin Sci
damage. Br J Sports Med 1990; 24 (3): 191-5 (Lond) 1988; 74: 553-7
38. Webber LM, Byrnes WC, Rowlands TW, et al. Serum creatine 58. Newham DJ, Jones DA, Clarkson PM. Repeated high-force
kinase activity and delayed onset muscle soreness in eccentric exercise: effects on muscle pain and damage. J Appl
prepubescent children: a preliminary study. Pediatr Exerc Sci Physiol 1987; 63 (4): 1381-6
1989; 1 (4): 351-9 59. Jones DA, Newham DJ. The effect of training on human muscle
39. Newham DJ, Jones DA, Edwards RHT. Plasma creatine kinase pain and damage. J Physiol 1985; 365: 76
changes after eccentric and concentric contractions. Muscle 60. Tiidus PM, Ianuzzo CD. Effects of intensity and duration of
Nerve 1986; 9: 59-63 muscular exercise on delayed soreness and serum enzyme
40. Byrnes WC, Clarkson PM, White JS, et al. Delayed onset activities. Med Sci Sports Exerc 1983; 15 (6): 461-5
muscle soreness following repeated bouts of downhill running. 61. Wilson RW. A review of methods used in research to induce,
J Appl Physiol 1985; 59 (3): 710-5 measure, and treat exercise induced delayed onset muscle
41. Schwane JA, Johnson SR, Vandenakker CB, et al. Delayed- soreness. Foil 1992; Fall: 11-4
onset muscular soreness and plasma CPK and LDH activities 62. Hasson SM, Daniels JC, Divine JG, et al. , Effect of ibuprofen
after downhill running. Med Sci Sports Exerc 1983; 15 (1): use on muscle soreness, damage, and performance: a prelimi-
51-6 nary investigation. Med Sci Sports Exerc 1993; 25 (1): 9-17
42. Schwane JA, Hatrous BG, Johnson SR, et al. Is lactic acid 63. Hasson SM, Wible CL, Reich M, et al. Dexamethasone ionto-
related to delayed-onset muscle soreness? Phys Sports Med phoresis: effect on delayed muscle soreness and muscle func-
1983; 11 (3): 124-7, 130-1 tion. Can J Sport Sci 1992; 17 (1): 8-13
43. Walsh B, Tonkonogi M, Malm C, et al. Effect of eccentric 64. Buroker KC, Schwane JA. Does postexercise stretching allevi-
exercise on muscle oxidative metabolism in humans. Med Sci ate delayed muscle soreness? Phys Sports Med 1989; 17 (6):
Sports Exerc 2001; 33 (3): 436-41 65-83
44. Johansson PH, Lindstrom L, Sundelin G, et al. The effects of 65. Asmussen E. Observations on experimental muscle soreness.
preexercise stretching on muscular soreness, tenderness and Acta Rheumatol Scand 1956; 2: 109-16
force loss following heavy eccentric exercise. Scand J Med Sci 66. Cazorla G, Petibois C, Bosquet L, et al. Lactate et exercice:
Sports 1999; 9 (4): 219-25 mythes et realites. Rev Sci Tech Activ Phys Sport (Grenoble)
45. Evans WJ, Meredit CN, Cannon JG, et al. Metabolic changes 2001; 22 (54): 63-76
following eccentric exercise in trained and untrained men. J 67. de Vries HA. Electromyographic observations of the effects of
Appl Physiol 1986; 61 (5): 1864-8 static stretching upon muscular distress. Res Q 1961; 32:
46. Janssen E, Kuipers H, Vertsappen F, et al. Influence of anti- 468-79
inflammatory drugs on muscle soreness. Med Sci Sport Exerc 68. Bobbert MF, Hollander AP, Huijing PA. Factors in delayed
1983; 15: 165 onset muscular soreness of man. Med Sci Sports Exerc 1986;
47. Smith LL. Causes of delayed onset muscle soreness and the 18 (1): 75-81
impact on athletic performance: a review. J Appl Sport Sci Res 69. Cleak MJ, Eston RG. Muscle soreness, swelling, stiffness and
1992; 6 (3): 135-41 strength loss after intense eccentric exercise. Br J Sports Med
48. Lund H, Vestergaard-Poulsen P, Kanstrup IL, et al. Isokinetic 1992; 26 (4): 267-72
eccentric exercise as a model to induce and reproduce patho- 70. de Vries HA. Quantitative EMG investigation of the spasm
physiological alterations related to delayed onset muscle sore- theory of muscle pain. Am J Phys Med 1966; 45: 119-34
ness. Scand J Med Sci Sports 1998; 8 (4): 208-15 71. Newham DJ, Mills KR, Edwards RHT. Large delayed plasma
49. Brown SJ, Child RB, Day SH, et al. Exercise-induced skeletal creatine kinase changes after stepping exercise. Muscle Nerve
muscle damage. J Sports Sci 1997; 15 (2): 215-22 1983; 6: 380-5
50. Housh TJ, Housh DJ, Weir JO, et al. Effects of eccentric-only 72. de Vries HA. Prevention of muscular distress after exercise. Res
resistance training and detraining. Int J Sports Med 1996; 17 Q 1960; 32 (2): 177-85
(2): 145-8 73. Hough T. Ergographic studies in muscular soreness. Am J
51. Sorichter S, Koller A, Haid C, et al. Light concentric exercise Physiol 1902; 7: 76-92
and heavy eccentric muscle loading: effects on CK, MRI and 74. Sydney-Smith M, Quigley B. Delayed onset muscle soreness:
Markers of Inflammation. Int J Sports Med 1995; 16: 288-92 evidence of connective tissue damage, liquid peroxidation and
52. Teague BN, Schwane JA. Effect of intermittent eccentric con- altered renal function after exercise. Report to the Australian
tractions on symptoms of muscle microinjury. Med Sci Sports Sports Commission’s Applied Sport Research. Canberra: Aus-
Exerc 1995; 27 (10): 1378-84 tralian Sports Commission, 1992: 77
53. Wessel J, Wan A. Effect of stretching on the intensity of 75. Friden J, Seger J, Ekblom B. Sublethal muscle fibre injuries
delayed-onset muscle soreness. Clin J Sports Med 1994; 4 (2): after high-tension anaerobic exercise. Eur J Appl Physiol
83-7 1988; 57: 360-8
54. Clarkson PM, Ebbeling C. Investigation of serum creatine kin- 76. Friden J, Kjorell U, Thornell LE. Delayed muscle soreness and
ase variability after muscle damaging exercise. Clin Sci 1988; cytoskeletal alterations: an immunocytological study in man.
75: 257-61 Int J Sports Med 1984; 5: 15-8
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
Delayed Onset Muscle Soreness 163
77. Friden J, Sjostrom M, Ekblom B. Myofibrillar damage follow- 97. Jones DA, Newham DJ, Clarkson PM. Skeletal muscle stiffness
ing intense eccentric exercise in man. Int J Sports Med 1983; 4: and pain following eccentric exercise of the elbow flexors.
170-6 Pain 1987; 30: 233-42
98. Eston RG, Finney S, Baker S, et al. Muscle tenderness and peak
78. Friden J, Sjostrom M, Ekblom B. A morphological study of
torque changes after downhill running following a prior bout
delayed onset muscle soreness. Experentia 1981; 37: 506-7
of isokinetic eccentric exercise. J Sports Sci (London) 1996; 14
79. Friden J, Lieber RL. Structural and mechanical basis of exercise (4): 291-9
induced muscle injury. Med Sci Sports Exerc 1992; 24 (5): 99. Nosaka K, Clarkson PM. Changes in indicators of inflammation
521-30 after eccentric exercise of the elbow. Med Sci Sports Exerc
80. Brown SJ, Child RB, Day SH, et al. Indices of skeletal muscle 1996; 28 (8): 953-61
damage and connective tissue breakdown following eccentric 100. Yates JW, Armbruster WJ. Concentric and eccentric strength
muscle contractions. Eur J Appl Physiol Occup Physiol 1997; loss and recovery following exercise induced muscle soreness
75 (4): 369-74 [abstract]. Int J Sports Med 1990; 11: 403
81. Armstrong R. Initial events in exercise-induced muscular injury. 101. Ebbeling CB, Clarkson PM. Exercise-induced muscle damage
Med Sci Sports Exerc 1990; 22 (4): 429-35 and adaptation. Sports Med 1989; 7 (4): 207-34
82. Clarkson PM, Byrnes WC, McCormick KM, et al. Muscle 102. Evans DT, Smith LL, Chenier TC, et al. Changes in peak
soreness and serum creatine kinase activity following isomet- torque, limb volume and delayed onset muscle soreness fol-
ric, eccentric and concentric exercise. Int J Sports Med 1986; lowing repetitive eccentric contractions. Int J Sports Med
7: 152-5 1990; 11: 403
83. Clarkson PM, Apple FS, Byrnes WC, et al. Creatine kinase 103. Orchard J, Marsden J, Lord S, et al. Pre-season hamstring
isoforms following isometic exercise. Muscle Nerve 1986; 10 muscle weakness associated with hamstring muscle injury in
(1): 41-4 Australian footballers. Am J Sports Med 1997; 25 (1): 81-5
84. Smith LL. Acute inflammation: the underlying mechanism in 104. Edgerton VR, Wolf SL, Levendowski DJ, et al. Theoretical
delayed onset muscle soreness? Med Sci Sports Exerc 1991; basis for patterning EMG amplitudes to assess muscle dys-
23 (5): 542-51 function. Med Sci Sports Exerc 1996; 28 (6): 744-51
85. Smith ME, Jackson CGR. Delayed onset muscle soreness 105. Miles MP, Ives JC, Vincent KR. Neuromuscular control follow-
(DOMS), serum creatine kinase (SCK) and creatine kinase- ing maximal eccentric exercise. Eur J Appl Physiol 1997; 76:
MB (%CK-MB) related to performance measurements in foot- 368-74
ball [abstract]. Med Sci Sport Exerc 1990; 22 Suppl. 2: S34
106. Zhou S, Carey MF, Snow RJ, et al. Effects of muscle fatigue
86. Rowlands AV, Eston RG, Tilzey C. Effect of stride length and temperature on electromechanical delay. Electromyogr
manipulation on symptoms of exercise-induced muscle dam- Clin Neurophysiol 1998; 38: 67-73
age and the repeated bout effect. J Sports Sci 2001; 19 (5):
333-40 107. Zhou S. Acute effect of repeated maximal isometric contraction
on electromechanical delay of knee extensor muscle. J Electro-
87. Weber MD, Servedio FJ, Woodall WR. The effects of three myogr Kinesiol 1996; 6: 117-1127
modalities on delayed onset muscle soreness. J Sports Phys
Ther 1994; 20 (5): 236-42 108. Boucher JP, Pepin A, Lefebvre R. Using the vastus medialis to
vastus lateralis IEMG ration as a neuromuscular imbalance
88. Harris C, Wilcox A, Smith G, et al. The effect of delayed onset index for the diagnosis of patello-femoral syndrome. Med Sci
muscle soreness (DOMS) on running kinematics. Med Sci Sport Exerc 1989; 24: 531-6
Sport Exerc 1990; 22 (2): S34
109. Brukner P, Khan K. Clinical sports medicine. Sydney: McGraw-
89. Vasudevan SV. Impairment, disability and functional capacity Hill Book Company Australia Pty Limited, 1993
assessment. In: Turk DC, Melzack RM, editors. Handbook of
pain assessment. New York: The Guilford Press, 1993: 100-1 110. Verducci FM. Interval cryotherapy decreases fatigue during
repeated weight lifting. J Athletic Train 2000; 35 (4): 422-6
90. Saxton JM, Clarkson PM, James R, et al. Neuromuscular
dysfunction following eccentric exercise. Med Sci Sports Ex- 111. Kokkinidis E, Tsamourtas A, Bruckenmeyer P, et al. The effect
erc 1995; 27 (8): 1185-93 of static stretching and cryotherapy on the recovery of delayed
muscle soreness. Exerc Soc J Sport Sci 1998; 19: 9
91. Hamill J, Freedson PS, Clarkson PN, et al. Muscle soreness
during running: biomechanical and physiological considera- 112. Gulick DT. Effects of various treatment techniques on the signs
tions. Int J Sport Biomech 1991; 7 (2): 125-37 and symptoms of delayed onset muscle soreness. Philadelphia
(PA): Temple University, 1995
92. Goff DA, Hamill J, Clarkson PM. Biomechanical and biochemi-
cal changes after downhill running [abstract]. Med Sci Sport 113. Denegar CR, Perrin DH. Effect of transcutaneous electrical
Exerc 1998; 30 Suppl. 5: S101 nerve stimulation, cold, and a combination treatment on pain,
decreased range of motion, and strength loss associated with
93. Gulick DT, Kimura IF, Sitler M, et al. Various treatment delayed onset muscle soreness. J Athletic Train 1992; 27 (3):
techniques on signs and symptoms of delayed onset muscle 200, 202, 204-6
soreness. J Athletic Train 1996; 31 (2): 145-52
114. Yackzan L, Adams C, Francis KT. The effects of ice massage on
94. Nosaka K, Clarkson PM. Variability in serum creatine kinase delayed muscle soreness. Am J Sports Med 1984; 12: 159-65
response after eccentric exercise of the elbow flexors. Int J
Sports Med (Stuttgart) 1996; 17 (2): 120-7 115. Braun B, Clarkson PM. Effect of cold treatment during eccentric
exercise [abstract]. Med Sci Sports Exerc 1989; 21 Suppl.: S32
95. Saxton JM, Donnelly AE. Light concentric exercise during
recovery from exercise-induced muscle damage. Int J Sports 116. Meussen R, Lievens I. The use of cryotherapy in sports injuries.
Med 1995; 16 (6): 347-51 Sports Med 1986; 3: 398-414
96. Howell JN, Chila AGA, Ford G, et al. An electromyographic 117. Magnusson SP, Simonsen EB, Aagaard P, et al. Viscoelastic
study of elbow motion during postexercise muscle soreness. J response to repeated static stretching in the human hamstring
Appl Physiol 1985; 58 (5): 1713-8 muscle. Scand J Med Sci Sports 1995; 5: 342-7
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
164 Cheung et al.
118. Smith LL, Brunetz MH, Chenier TC, et al. The effects of static 136. Kloth L. Electrotherapeutic alternative for the treatment of pain.
and ballistic stretching on delayed onset muscle soreness and In: Gersh M, editor. Electrotherapy in rehabilitation. Philadel-
creatine kinase. Res Q Exerc Sport 1993; 64 (1): 103-7 phia (PA): Davis, 1992: 197-217
119. Lin WH. The effects of massage, stretch and meloxicam on 137. Lambert MI, Marcus P, Burgess T, et al. Electro-membrane
delayed onset muscle soreness. Taoyuan: National College of microcurrent therapy reduces signs and symptoms of muscle
Physical Education and Sports, 1999 damage. Med Sci Sports Exerc 2002 Apr; 34 (4): 602-7
120. Lund H, Vestergaard-Poulsen P, Kanstrup IL, et al. The effect 138. Castro M. The complete homeopathy handbook. New York: St
of passive stretching on delayed onset muscle soreness, and Martin’s Press, 1991
other detrimental effects following eccentric exercise. Scand J
Med Sci Sports 1998; 8 (4): 216-21 139. Smith LL, Keating MN, Holbert D, et al. The effects of athletic
massage on delayed onset muscle soreness, creatine kinase and
121. Shellock FG, Prentice WE. Warming-up and stretching for neutrophil count: a preliminary report. J Orthop Sports Phys
improved physical performance and prevention of sports-relat-
ed injuries. Sports Med 1985; 2: 267-78 Ther 1994; 19 (2): 93-9
122. Hertel J. The role of nonsteroidal anti-inflammatory drugs in the 140. Hovind H, Nielsen ST. Effect of massage on blood flow in
treatment of acute soft tissue injuries. J Athletic Train 1997; 32 skeletal muscle. Scand J Rehabil Med 1974; 6: 74-7
(4): 350-8 141. Cafarelli E, Flint F. The role of massage in preparation for and
123. Kuipers H, Keizer HA, Verstappen FT, et al. Influence of a recovery from exercise. Sports Med 1992; 14: 1-9
prostaglandin-inhibiting drug on muscle soreness after eccen-
tric work. Int J Sports Med 1985; 6 (6): 336-9 142. Tiidus PM. Manual massage and recovery of muscle function
following exercise: a literature review. J Sports Phys Ther
124. Donnelly AE, McCormick K, Maughan RJ, et al. Effects of a 1997; 25 (2): 107-12
non-steroidal anti-inflammatory drug on delayed onset muscle
soreness and indices of damage. Br J Sports Med 1988; 22 (1): 143. Ernst E. Does post-exercise massage treatment reduce delayed
35-8 onset muscle soreness: a systematic review. Br J Sports Med
125. Adams SS, Bough RG, Cliffe EE, et al. Absorption, distribu- 1998; 32 (3): 212-4
tion, and toxicity of ibuprofen. Toxicol Appl Pharmacol 1989; 144. Kraemer WJ, Bush JA, Wickham R, et al. Continuous compres-
15: 1310-30 sion as an effective therapeutic intervention in treating eccen-
126. Hasson SM, Mundorf R, Barnes WS, et al. Effect of ultrasound tric-exercise-induced muscle soreness. J Sport Rehabil 2001;
on muscle soreness and performance. Med Sci Sports Exerc 10 (1): 11-23
1989; 21: S36
145. Harrison BC, Robinson D, Davison BJ, et al. Treatment of
127. Ciccone CD, Leggin BG, Callamaro JJ. Effects of ultrasound exercise-induced muscle injury via hyperbaric oxygen therapy.
and trolamine salicylate phonopheresis on delayed onset mus- Med Sci Sports Exerc 2001; 33 (1): 36-42
cle soreness. Phys Ther 1991; 71 (9): 666-78
146. Babul S. Hyperbaric oxygen therapy to enhance recovery from
128. Stay JC, Richard MD, Draper DO, et al. Pulsed ultrasound fails delayed onset muscle soreness [commentary]. Clin J Sport
to diminish delayed-onset muscle soreness symptoms. J Ath-
letic Train 1998; 33 (4): 341-6 Med 2000; 10 (4): 308
129. Allen JD, Mattacola CG, Perrin DH. Effect of microcurrent 147. Mekjavic IB, Exner JA, Tesch PA, et al. Hyperbaric oxygen
stimulation on delayed-onset muscle soreness: a double-blind therapy does not affect recovery from delayed onset muscle
comparison. J Athletic Train 1999; 34 (4): 334-7 soreness. Med Sci Sports Exerc 2000; 32 (3): 558-63
130. Butterfield DL, Draper DO, Richard MD, et al. The effects of 148. Staples JR, Clement DB, Taunton JE, et al. Effects of hyperbar-
high-volt pulsed current electrical stimulation on delayed- ic oxygen on a human model of injury. Am J Sports Med 1999;
onset muscle soreness. J Athletic Train 1997; 32 (1): 15-20 27 (5): 600-5
131. Denegar CR, Perrin DH, Rogol AS, et al. Influence of tran- 149. Carlsson CA, Pellettieri L. A clinical view on pain physiology.
scutaneous electrical nerve stimulation on pain, range of mo- Acta Chir Scand 1982; 148: 305-13
tion, and serum cortisol concentration in females experiencing
delayed onset muscle soreness. J Orthop Sports Phys Ther 150. Donnelly AE, Clarkson PM, Maughan RJ. Exercise-induced
1989; 11 (3): 100-3 muscle damage: effects of light exercise on damaged muscle.
132. Denegar CR, Yoho AP, Borowicz AJ, et al. The effects of low- Eur J Appl Physiol 1992; 64 (4): 350-3
volt, microamperage stimulation on delayed onset muscle 151. Hasson SM, Williams JH, Signorile JF. Fatigue-induced
soreness. J Sport Rehab 1992; 1 (2): 95-102 changes in myoelectric signal characteristics and perceived
133. Denegar CR, Huff CB. High and low frequency TENS in the exertion. Can J Sport Sci 1989; 14 (2): 99-102
treatment of induced musculoskeletal pain: a comparison
study. Athletic Train 1988; 23 (3): 235-7, 258
134. Schmitz RJ, Martin DE, Perrin DH, et al. Effect of interferential Correspondence and offprints: Patria A. Hume, School of
current on perceived pain and serum cortisol associated with Community Health and Sports Studies, Sport Performance
delayed onset muscle soreness. J Sport Rehabil 1997; 6: 30-7 Research Centre, Auckland University of Technology, Pri-
135. Baxter JD. Glucocortoid hormone action. In: Gill GN, editor. vate Bag 92019, Auckland, New Zealand.
Pharmacology of adrenal cortical hormones. Oxford: Per-
gamon Press Ltd., 1979: 93-103 E-mail: patria.hume@aut.ac.nz
Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)
