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Delayed Onset Muscle Soreness



Delayed onset muscle soreness (DOMS) is a familiar experience for the elite or 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, 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 administration. 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 demonstrated 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.
Sports Med 2003; 33 (2): 145-164
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
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.
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-
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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-
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
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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
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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
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... In R-AMSTAR, each domain's score ranges between 1 (minimum) and 4 (maximum), which means the total scores have a range of 11 (minimum) to 44 (maximum) (44). Therefore, the overall score can be translated into a quality grade, such as: A (high quality: 33-44), B (moderate quality: 23-32), C (low quality: [13][14][15][16][17][18][19][20][21][22] and D (very low quality: 11-12) (44). Following the recommendations that only ratings of 23/44 on the R-AMSTAR total score have at least moderate methodological quality, that was established as the criteria to include a systematic review in this overview (44). ...
... However, it seems that athletic massage and light exercise may be the most promising in International Journal of Exercise Science 874 reducing DOMS (16,18,23,69,93). Comparing with no intervention, SMR and massage were superior in reducing pressure-pain threshold, with no differences found between massage and SMR (1). ...
... Also, it was found that the constant rolling reduces arterial stiffness, increases arterial tissue perfusion, and improves vascular endothelial function (36,70,81). With this alterations, it is expected that a prosperous environment to enhance cellular waste products removal, decrease edema, and enhance tissue repair/healing will be created (16,74). Increased blood flow also hinders the margination of neutrophils and reduces prostaglandin production, subsequently decreasing inflammation (81,89). ...
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Introduction: Currently, the use of self-myofascial release (SMR) instruments is not uncommon in our society, especially in sports. The most common SMR instruments are foam rollers, roller massagers, and balls. Regardless of the instrument used, the main objectives are to enhance performance and recovery. Nevertheless, many studies point out that there is still a lack of robust scientific evidence documenting the exact mechanisms that explain its true effects, therefore some authors affirm that the reported benefits are anecdotal in nature. Objective: This overview aims to summarize, from systematic reviews, the effectiveness of SMR instruments on performance and recovery. Material and Methods: This study followed the PRISMA principles. Systematic reviews were found on the electronic databases according to an established P (healthy active individuals) I (SMR using instruments) C (other treatment, placebo, sham, or no treatment) O (performance and recovery) S (systematic reviews) search strategy. Additionally, methodological analysis was performed using R-AMSTAR. Results: Initially, it was found 15 systematic reviews. However, after methodological analysis, only 7 systematic reviews had sufficient quality to be included. From those, it was found that SMR using instruments is beneficial to enhancing short-term flexibility-related and recovery-related outcomes. Inconstant data was reported in muscular-related outcomes. Nevertheless, beyond pain during SMR, no major adverse effects were found. Different effects between time, pressure and other instrument characteristics were also found. Conclusion: SMR using instruments can be a safe intervention used in sports to enhance performance and recovery from previous training/competition or between matches.
... This central neuroplasticity accompanies the peripheral sensitization of nociceptive neurons [13,14]. The latter is due to inflammatory processes caused by ultrastructural muscle damage in the exercised muscles [15,16]. In detail, biopsy analysis of eccentric strained muscle tissue shows that there is a disruption of sarcomeres which leads to protein degradation and a local inflammatory response [2,17]. ...
... We found that responders showed significantly decreased PPTs (i.e., mechanical allodynia) in the exercised muscles. This is a result of peripheral sensitization of intramuscular nociceptors from algogenic substances released subsequent to muscle damage [15,16,62]. In addition, the inflammation that occurs in the region of damage may turn on silent nociceptive neurons that become activated in response to normally innocuous movement [63]; a mechanism that may explain MEP. ...
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Objective: To investigate the: (1) role of basic muscle pain sensitivity and psychological factors in the prediction of movement-evoked pain (MEP) following delayed onset muscle soreness (DOMS), and (2) association of MEP with changes in systemic muscle pain sensitivity following DOMS induction. Methods: Fifty-one participants were assigned to either eccentric resistance exercise or control groups. They completed questionnaires evaluating psychological distress and underwent muscle pain sensitivity evaluation by the pressure pain threshold (PPT) test at the exercised and remote muscles, before and 24 hours following the intervention. MEP intensity was determined in response to lifting a 3kg canister using a visual analogue scale (VAS). Results: The exercise group demonstrated MEP intensity of 5/10 on VAS and reduced PPTs at the main exercised muscle (p<0.001). A regression tree analyses revealed that the level of anxiety trait predicted a higher MEP intensity. A secondary analysis showed that 53% participants who were DOMS responders (MEP > mild intensity; ≥ 3/10 VAS) exhibited decreased PPTs in the exercised (p<0.001) and remote (p = 0.027) muscles following eccentric exercise. Characterization of DOMS responders revealed that, at baseline, they had lower PPTs in the exercised (p = 0.004) and remote (p = 0.001) muscles and reported higher psychological distress i.e., anxiety trait and depression symptoms (p<0.05), compared to non-responders. A regression analysis revealed that lower PPT or high levels of anxiety trait increased the probability to become a responder (p = 0.001). Conclusions: Susceptibility to MEP following DOMS is determined by muscle pain hypersensitivity and high levels of anxiety trait. MEP at the early stage of DOMS is linked with an increase in systemic muscle pain sensitivity suggestive of central mechanisms. This knowledge is valuable in translating science into clinical musculoskeletal pain management.
... The general consensus amongst researchers is that a single theory cannot explain the onset of DOMS. As a result, the model proposed for Cheung, et al. 26 , integrates aspects from other theories, which makes it easier to understand all the possible events that happen in this physiological process. The model works under the assumption that high tensile forces associated with lengthening exercise cause muscle and connective tissue damage in their structure. ...
... These events result in the accumulation of calcium and the activation of proteolytic enzymes that degrade the z-line of sarcomeres. It is proposed that in a few hours after, there is a significant elevation in circulating neutrophils and mast cells, starting with histamine and prostaglandin production that sensitizes type III and IV nerve endings to mechanical, chemical or thermal stimulation 1-4,8,22, 26 . ...
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Background: The study of functional impact of delayed onset muscle soreness has been limited to describe the decline on maximal isometric contraction, but muscular work and time to peak torque has not been examined yet. Purpose: To describe the changes induced by a session of lengthening contractions on muscle performance and delayed onset muscle soreness (DOMS). Methods: A quasi-experimental study was conducted in the Institutional laboratory; Twenty healthy men; mean age 21 SD 0.34 were recruited, all subjects performed 200 lengthening contractions of the quadriceps at 120º/s. Isometric and isokinetic peak torque, muscular work, time to peak torque, DOMS and creatine kinase activity were assessed at baseline, 48 h and 96 h post-exercise. The muscle performance was assessed with an isokinetic dynamometer and DOMS with a visual analog scale (VAS). Results: Relative to baseline, isometric and isokinetic peak torque and muscular work decreased in ~30% at 48 h post-exercise; delayed onset muscle soreness increased ~300%, which remained at 96 h post-exercise. Conclusions: These reflect that the decline in muscular performance is due to the changes in peak torque and muscular work, which has greater implications on muscle function. No changes were detected in time to peak torque. The alterations in muscular performance variables are accompanied by delayed onset muscle soreness which has also a negative impact on force production (29% of the drop on peak torque is explain by soreness intensity).
... Delayed-onset muscle soreness (DOMS) is a multi-factorial process associated with muscle pain or discomfort, which occurs after highintensity eccentric exercise (Cheung, Hume, & Maxwell, 2003;D. A. Connolly, Sayers, & McHugh, 2003). ...
... DOMS is also common when athletes are first introduced to certain types of activities regardless of the time of year (Cheung et al., 2003). ...
To quantify the effects of curcumin supplementation on exercise‐induced muscle damage, muscle soreness, inflammatory biomarkers, muscle strength, and joint flexibility via assessment of creatine kinase (CK), visual analogue scale (VAS) score, maximal voluntary contraction (MVC), and range of motion (ROM), respectively. Online databases, including PubMed, Google Scholar, and Scopus, were searched up to February 2021. RevMan® software (version 5.3) was used for assessing the risk of bias to assess the quality of studies. The mean differences (MD) and confidence intervals (95% CI) of CK activity (IU/L), VAS score, tumor necrosis factor (TNF‐α) (pg/ml), interleukin‐6 (IL‐6) (pg/ml), IL‐8 (pg/ml), MVC (nm) and ROM (degree) were pooled using a random‐ or fixed‐effect model. Between‐study heterogeneity was assessed using χ‐square or I2 statistic. Ten trials met the eligibility criteria and were included in the pooled analysis. Meta‐analysis showed that curcumin supplementation significantly reduced serum CK activity [WMD = −65.98 IU/L, 95% CI (−99.53 to −32.44)], muscle soreness [WMD = −0.56, 95% CI (−0.84 to −0.27)], and TNF‐α concentration [WMD = −0.22 pg/ml, 95% CI (−0.33 to −0.10)]. Also, curcumin supplementation elicited significant improvements in MVC [WMD = 3.10 nm, 95% CI (1.45–4.75)] and ROM [WMD = 6.49°, 95% CI (3.91–9.07)], although no significant changes in IL‐6 and IL‐8 levels were found. Dose–response analysis indicated that there is a significant non‐linear association between the daily dose and the final effect size regarding TNF‐α. Curcumin supplementation may improve some aspects of DOMS, including muscle damage, muscle soreness, inflammation, muscle strength, and joint flexibility. Further, well‐designed and high‐quality studies with larger sample sizes are needed to ascertain the long‐term effects and safety of curcumin supplementation.
... 7 It has been proposed that the short-term alleviation of pain during exercise is due to the breakup of adhesions in the sore muscles, an increased removal of noxious waste products via an increased blood flow, or an increased endorphin release. 21 Due to this theory, research has become focused on creating similar effects with passive modalities. Percussive therapy is a recent therapy that delivers gentle, rhythmic pulses to soft tissue with the use of a handheld device or therapeutic massager. ...
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Background Percussive therapy is hypothesized to speed recovery by delivering gentle, rhythmic pulses to soft tissue. However, patients often present with a differential soreness response after percussive therapy, which may lead to altered clinical outcomes. Purpose To compare the acute effects of percussion therapy on passive range of motion (ROM) and tissue-specific ultrasound measures (pennation angle [PA] and muscle thickness [MT]) between healthy individuals responding positively vs. negatively to percussive therapy performed on the dominant arm posterior rotator cuff. Study Design Cross-sectional laboratory study Methods Fifty-five healthy individuals were assessed on a subjective soreness scale before and after a five-minute percussive therapy session on the dominant arm posterior rotator cuff muscles. Participants with no change or a decrease in muscle soreness were assigned to the positive response group and participants who reported an increase in muscle soreness were assigned to the negative response group. Passive internal rotation (IR) and external rotation (ER) ROM and strength, and muscle architecture of the infraspinatus and teres minor were measured via ultrasound on the dominant shoulder. All dependent variables were collected before percussive therapy, and 20 minutes following percussive therapy. Results The positive response group had greater improvements than the negative response group in dominant arm IR ROM (2.3° positive vs. -1.3° negative, p=0.021) and IR strength (1.1 lbs vs. -1.2 lbs, p=0.011) after percussive therapy. No differences in ER strength or ROM were observed between groups. Regarding muscle architecture, the positive group had a lesser change in teres minor MT (0.00 mm vs. 0.11 mm, p=0.019) after percussive therapy. All other muscle architecture changes were not statistically different between groups. Conclusion Participants with a positive response to percussive therapy had increased dominant arm IR ROM and IR strength, and decreased teres minor MT, after percussive therapy compared to the negative response participants. Level of Evidence III
... Delayed onset muscle soreness (DOMS) is a well-known experience among gym goers. The sensations experienced can vary from slight muscle stiffness, which is no longer felt following the continuation of day-to-day movement, to severe, debilitating pain which renders one incapable of movement (Cheung et al. 2003). In sports contexts, DOMS has been realized as a major topic in the biomedical field. ...
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Delayed onset muscle soreness (DOMS) is a widely known phenomenon among gym goers. For many of them, experiencing DOMS the day after working out in the gym is often perceived as rewarding and something of which to brag and be proud. Although existing work within the biomedical field has undoubtedly shed light on coping with and managing DOMS, there remains little in-depth qualitative research on the gym goer's lived experience regarding this phenomenon. Following Becker's conceptual framework of using marihuana for pleasure, the paper will examine the way gym goers learn to attain pleasure and gratification in times of DOMS through a process of reframing and socialization. Ethnographic research was conducted for two years in two gyms, using a combination of participant observation and semi-structured interviews. Findings illustrate three coherent stages a novice gym goer experiences whilst becoming an experienced gym goer and enjoying DOMS: (1) learning the proper "working-out" technique required to experience positive effects; (2) recognizing the effects of DOMS and their connection with the work-out; and (3) enjoying the effects of DOMS caused by working out. Moreover, once gym goers manage to change the definition of negative sensations and interpret them as enjoyable, DOMS often becomes an indispensable experience which has to be religiously pursued. In this context, the audience in front of which the gym goers perform their DOMS serves as a "front region of behavior" for gaining social recognition by instrumentalizing their pain to strengthen and solidify their gym goer identity.
Background. Delayed onset of muscle soreness (DOMS) and its physiological consequences influenced an individual’s adherence to an exercise routine. Objective. This study aimed to evaluate the efficacy, safety, and tolerability of TurmXTRA® 60N (WDTE60N) on DOMS compared to placebo in recreationally active healthy subjects. Methods. This randomized, double-blind, placebo-controlled parallel-group study enrolled 30 healthy and recreationally active subjects (average age: 28.23 ± 4.20 years) and randomized them to receive WDTE60N (WDTE60N group; n = 15) or placebo (placebo group; n = 15). Study treatments were initiated 29 days before the eccentric exercise and were continued for 4 days after the exercise. The primary endpoint was the change in pain intensity measured by the visual analog scale (VAS) at the end of study treatment (at 96 hours after eccentric exercise) from baseline (measured immediately after exercise). Results. The VAS score indicated that subjects from the WDTE60N group reported significantly less pain after eccentric exercise compared to the placebo group (AUC0–96h: 286.8 ± 46.7 vs. 460 ± 40.5, respectively; p < 0.0001 ). Well-being status was assessed using the adapted version of the Hooper and MacKinnon questionnaire and was calculated as individual and cumulative scores of the domains (fatigue, mood, general muscle soreness, sleep quality, and stress) that demonstrated improvement in all domains and in overall well-being in the WDTE60N group compared to the placebo group ( p < 0.0001 ). Serum lactate dehydrogenase (LDH) was significantly lower in the WDTE60N group compared to the placebo group (AUC0–96h: 23623.7 ± 2532.0 vs. 26138.6 ± 3669.5, respectively; p = 0.0446 ). Conclusion. Intake of WDTE60N before and after eccentric exercise significantly reduced subjective perception of muscle soreness and serum LDH activity and increased the psychological well-being in recreationally active subjects.
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Unaccustomed or strenuous eccentric exercise is known to cause delayed-onset muscle soreness. A recent hypothesis postulated that mechano-energetic microinjury of the primary afferent sensory neuron terminals in the muscle spindles, namely a transient Piezo2 channelopathy, could be the critical cause of delayed-onset muscle soreness in the form of a bi-phasic non-contact injury mechanism. This theory includes that this microlesion could delay the medium-latency response of the stretch reflex. Our aim with this study was to investigate this hypothesis. According to our knowledge, no study has examined the effect of delayed-onset muscle soreness on the medium-latency response of the stretch reflex. Our findings demonstrated that a significant delay in the medium-latency stretch reflex could be observed right after a multi-stage fitness test in the quadriceps femoris muscles of Hungarian professional handball players who consequently experienced delayed-onset muscle soreness. The long-latency stretch reflex and most likely short-latency stretch reflex were unaffected by delayed-onset muscle soreness in our study, which is in line with earlier findings. We translate these findings as indicative of proprioceptive Type Ia terminal microdamage in the muscle spindle in line with the aforementioned new acute non-contact compression axonopathy theory of delayed-onset muscles soreness.
Background: The study of functional impact of delayed onset muscle soreness has been limited to describe the decline on maximal isometric contraction, but muscular work and time to peak torque has not been examined yet. Purpose: To describe the changes induced by a session of lengthening contractions on muscle performance and delayed onset muscle soreness (DOMS). Methods: A quasi-experimental study was conducted in the Institutional laboratory; Twenty healthy men; mean age 21 SD 0.34 were recruited, all subjects performed 200 lengthening contractions of the quadriceps at 120°/s. Isometric and isokinetic peak torque, muscular work, time to peak torque, DOMS and creatine kinase activity were assessed at baseline, 48 h and 96 h post-exercise. The muscle performance was assessed with an isokinetic dynamometer and DOMS with a visual analog scale (VAS). Results: Relative to baseline, isometric and isokinetic peak torque and muscular work decreased in ~30% at 48 h post-exercise; delayed onset muscle soreness increased ~300%, which remained at 96 h post-exercise. Conclusions: These reflect that the decline in muscular performance is due to the changes in peak torque and muscular work, which has greater implications on muscle function. No changes were detected in time to peak torque. The alterations in muscular performance variables are accompanied by delayed onset muscle soreness which has also a negative impact on force production (29% of the drop on peak torque is explain by soreness intensity).
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The effect of caffeine on mitigating exercise-induced muscle damage (EIMD) is still poorly understood, but it was hypothesized that caffeine could contribute to decreasing delayed onset muscle soreness, attenuating temporary loss of strength, and reducing circulating levels of blood markers of muscle damage. However, evidence is not conclusive and beneficial effects of caffeine ingestion on EIMD are not always observed. Factors, such as the type of exercise that induces muscle damage, supplementation protocol, and type of marker analyzed contribute to the differences between the studies. To expand knowledge on the role of caffeine supplementation in EIMD, this systematic review aimed to investigate the effect of caffeine supplementation on different markers of muscle damage. Fourteen studies were included, evaluating the effect of caffeine on indirect muscle damage markers, including blood markers (nine studies), pain perception (six studies), and MVC maximal voluntary contraction force (four studies). It was observed in four studies that repeated administration of caffeine between 24 and 72 h after muscle damage can attenuate the perception of pain in magnitudes ranging from 3.9% to 26%. The use of a single dose of caffeine pre-exercise (five studies) or post-exercise (one study) did not alter the circulating blood levels of creatine kinase (CK). Caffeine supplementation appears to attenuate pain perception, but this does not appear to be related to an attenuation of EIMD, per se. Furthermore, the effect of caffeine supplementation after muscle damage on strength recovery remains inconclusive due to the low number of studies found (four studies) and controversial results for both dynamic and isometric strength tests.
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This review is made of two parts ; each one is presented under the form of questions to which, by using only published scientific data, we try to give up-to-date answers and to highlight the limits of theories sometimes easily admitted concerning lactic acid effects. The first part of the review is mainly focused on the study of lactate synthesis and metabolism during and after exercise. This study would allow us to built our criticisms concerning : several a priori about lactate effects, about the concepts of « anaerobic lactic thresholds », and on the theories underlining these ones. The second part of the review is focused on possible consequences, but not proved, of lactate accumulation on the skeletal muscle function. How should we accept anymore to ear that lactic glycolysis has a poor energetic yield, or that lactate accumulation leads to cramps, fatigue, and other differed muscular pains ?
Perceived muscle soreness ratings, serum creatine kinase (CK) activity, and myoglobin levels were assessed in three groups of subjects following two 30-min exercise bouts of downhill running (-10 degrees slope). The two bouts were separated by 3, 6, and 9 wk for groups 1, 2, and 3, respectively. Criterion measures were obtained pre- and 6, 18, and 42 h postexercise. On bout 1 the three groups reported maximal soreness at 42 h postexercise. Also, relative increases in CK for groups 1, 2, and 3 were 340, 272, and 286%, respectively. Corresponding values for myoglobin were 432, 749, and 407%. When the same exercise was repeated, significantly less soreness was reported and smaller increases in CK and myoglobin were found for groups 1 and 2. For example, the percent CK increases on bout 2 for groups 1 and 2 were 63 and 62, respectively. Group 3 demonstrated no significant difference in soreness ratings, CK activities, or myoglobin levels between bouts 1 and 2. It was concluded that performance of a single exercise bout had a prophylactic effect on the generation of muscle soreness and serum protein responses that lasts up to 6 wk.
The purpose of this study was to determine the effects of ultrasound and phonophoresis using an anti-inflammatory–analgesic cream (trolamine salicylate) on delayed-onset muscle soreness (DOMS). Repeated eccentric contractions were used to induce DOMS in the elbow flexors of 40 college-aged women. Subjects were then assigned randomly to one of four groups: (1) group 1 (n=10) received sham ultrasound using placebo cream, (2) group 2 (n=10) received sham ultrasound using trolamine salicylate cream, (3) group 3 (n=10) received ultrasound using placebo cream, and (4) group 4 (n=10) received ultrasound using trolamine salicylate cream. Subjects were treated on 3 consecutive days. Muscle soreness and active elbow range of motion were assessed daily prior to each treatment. The subjects in group 3 experienced an increase in DOMS, whereas no increase in soreness was observed in the subjects in group 4. The authors concluded that ultrasound enhanced the development of DOMS but that this enhancement was offset by the anti-inflammatory–analgesic action of salicylate phonophoresis. These findings suggest that salicylate phonophoresis may be useful in clinical situations in which it is desirable to administer ultrasound without increasing inflammation.
Although delayed onset muscle soreness and increased serum creatine kinase activity (SCKA) following unaccustomed exercise is common in adults, little is known concerning these responses in children. The perception of muscle soreness and SCKA in children (n = 16) (M age = 10.4±.30 yr) was compared to a control group of adults (n = 15) (M age = 27.1±.87 yr) following a single bout of downhill running (30 min − 10% grade). Preexercise SCKA was not significantly different between the children (91.7±8.5 μmol•L−1•min−1) and the adults (77.1±5.9 μmol•L−1•min−1). The difference in SCKA (pre to 24 hours post) was significantly less (p<.01) for the children (68.6±16.2 μmol•L−1•min−1) than for the adults (188.7±36.8 μmol•L−1•min−1). When the groups were adjusted for weight differences, SCKA was not significantly different between the adults and the children. Regardless of age, males demonstrated a significantly greater increase in SCKA postexercise when compared to females. Soreness ratings (verbally anchored scale...
The efficacy of low-volt, microamperage stimulation (LVMAS) in the treatment of wounds and fractures has been demonstrated. Although these devices are also commonly used to treat musculoskeletal conditions, the efficacy of this practice has not been demonstrated. In this study, delayed onset muscle soreness (DOMS) served as a model for musculoskeletal injury to compare daily treatment with LVMAS and static stretching to a placebo treatment and static stretching. DOMS was induced in the elbow flexor muscle group in 16 subjects, who were evaluated for pain, elbow flexor muscle group strength, and elbow extension range of motion. These data were collected before the eccentric exercise bout, before and after treatment 24, 48, 72, and 96 hours following the exercise bout, and again 196 hours after the exercise bout. No significant differences were found between LVMAS and placebo treatments on any of the variables across the duration of the study, but the LVMAS did provide a transient analgesic effect 24 and 48 hours following the eccentric exercise.
HARRISON, B. C., D. ROBINSON, B. J. DAVISON, B. FOLEY, E. SEDA, and W. C. BYRNES. Treatment of exercise-induced muscle injury via hyperbaric oxygen therapy. Med. Sci. Sports Exerc., Vol. 33, No. 1, 2001, pp. 36–42. Purpose: This study examined the role of hyperbaric oxygen therapy (HBO) in the treatment of exercise-induced muscle injury. Methods: 21 college-aged male volunteers were assigned to three groups: control, immediate HBO (iHBO), and delayed HBO (dHBO). All subjects performed 6 sets (10 repetitions per set) of eccentric repetitions with a load equivalent to 120% of their concentric maximum. HBO treatments consisted of 100-min exposure to 2.5 ATA and 100% oxygen with intermittent breathing of ambient air (30 min at 100% O2, 5 min at 20.93% O2). HBO treatments began either 2 (iHBO) or 24 h (dHBO) postexercise and were administered daily through day 4 postexercise. Forearm flexor cross-sectional area (CSA) and T2 relaxation time via magnetic resonance imaging (MRI) were assessed at baseline, 2, 7, and 15 d postinjury. Isometric strength and rating of perceived soreness of the forearm flexors were assessed at baseline, 1, 2, 3, 4, 7, and 15 d postinjury. Serum creatine kinase (CK) was assessed on day 0 and on days 1, 2, 7, and 15 postinjury. Results: Mean baseline CSA values were: 2016.3, 1888.5, and 1972.2 mm2 for control, iHBO, and dHBO, respectively. All groups showed significant increases in CSA in response to injury (21% at 2 d, 18% at 7 d) (P < 0.0001), but there were no significant differences between groups (P = 0.438). Mean baseline T2 relaxation times were: 26.18, 26.28, and 27.43 msec for control, iHBO, and dHBO, respectively. Significant increases in T2 relaxation time were observed for all groups (64% at 2 d, 66% at 7 d, and 28% at 15 d) (P < 0.0001), but there were no significant differences between groups (P = 0.692). Isometric strength (P < 0.0001), serum CK levels (P = 0.0007), and rating of perceived soreness (P < 0.0001) also indicated significant muscle injury for all groups, but there were no differences between groups (P = 0.459, P = 0.943, and P = 0.448, respectively). Conclusion: These results suggest that hyperbaric oxygen therapy was not effective in the treatment of exercise-induced muscle injury as indicated by the markers evaluated.
The purpose of this study was to assess the effect of interferential current (IFC) on perceived pain and serum cortisol levels in subjects with delayed onset muscle soreness (DOMS). DOMS was induced in 10 subjects through repeated eccentric contractions of the elbow flexors. Forty-eight hours later subjects were evaluated. Starting at t = 0:00, blood samples were withdrawn from a superficial vein every 5 min for 65 min. At t = 0:05, subjects received IFC of 10 bps or IFC of 100 bps. Perceived pain levels were evaluated prior to catheter insertion and at t = 0:35, 0:50, and 0:65. Two mixed-model analyses of variance revealed a significant decrease in perceived pain scores across time for both treatment groups but no significant difference in serum cortisol for the two groups. It was concluded that IFC of high and low beat frequency is effective in controlling the pain of DOMS but does not elicit a generalized stress response as indexed by increasing serum cortisol levels.