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Vol 10, No 1, January/February 2002 67
Delayed-onset muscle soreness
(DOMS), or what is commonly
described as postexercise muscle
soreness, is the sensation of muscu-
lar discomfort and pain during
active contractions that occurs in a
delayed fashion after strenuous
exercise. Usually, the initial symp-
toms are most evident at the mus-
cle tendon junction and thereafter
spread throughout the entire mus-
cle. Skeletal muscle soreness and
injury are associated with intense
exercise. The soreness and accom-
panying muscle damage are even
more pronounced if the exercise
performed is new to the individual.
Thus, even individuals who are in
excellent athletic condition may ex-
perience muscle soreness and dam-
age when performing exercise to
which they are unaccustomed. The
relationship between the develop-
ment of DOMS and the loss of mus-
cle strength has yet to be explicitly
proven.
Symptoms
Sore muscles after exercise are usu-
ally described as stiff, tender, or
aching. The stiffness associated with
DOMS is not a function of antago-
nistic muscular action but is proba-
bly caused by edema occurring in
the perimuscular connective tissue.1
The symptoms of DOMS develop
during the first 24 to 48 hours, peak
between 24 and 72 hours, and disap-
pear within 5 to 7 days,2,3 usually
without intervention. Regardless of
the exact location of the palpable
region of soreness, passive stretch-
ing and renewed activity aggravate
the pain. Some controversy exists
regarding the relationship between
maximum voluntary force and
symptoms of soreness. Ebbeling
and Clarkson3suggested that there
is very little or no relationship be-
tween the development of soreness
and a decrease in muscle strength.
Newham et al4demonstrated return
of maximum quadriceps strength to
pre-exercise levels within 24 hours
after step exercise, while others have
reported that a period of >2 weeks is
necessary to recover maximum iso-
metric strength. In addition to ten-
derness with palpation, the examiner
also will find prolonged strength
loss, a reduced range of motion, and
elevated levels of serum creatine
kinase (CK).
Many studies have reported that
eccentric exercise results in a signifi-
cant increase in CK levels 24 to 48
hours after the exercise session5that
may peak between 3 to 6 days, de-
pending on the precise nature of the
exercise (Fig. 1, open circles). CK is
an intramuscular enzyme responsi-
ble for maintaining adequate adeno-
sine triphosphate levels during
muscle contraction. Its appearance
in the serum is interpreted as indi-
cating an increased permeability or
breakdown of the membrane sur-
Dr. Lieber is Professor of Orthopaedics and
Bioengineering, Veterans Affairs Medical
Center, and Department of Orthopaedics and
Bioengineering, University of California, San
Diego, Calif. Dr. Fridén is Professor of Hand
Surgery, Department of Hand Surgery,
Göteborg University, Göteborg, Sweden.
Reprint requests: Dr. Lieber, University of
California San Diego School of Medicine, 3350
La Jolla Village Drive, San Diego, CA 92161.
Copyright 2002 by the American Academy of
Orthopaedic Surgeons.
Abstract
Muscle pain after unaccustomed exercise is believed to result from repeti-
tive active lengthening of skeletal muscle. This “eccentric exercise” initi-
ates a sequence of events that includes muscle cytoskeletal breakdown,
inflammation, and remodeling such that subsequent exercise sessions result
in less injury and soreness. Recent studies of eccentric exercise using well-
defined animal models have identified the mechanical and cellular events
associated with the injury-repair process. In addition, neurophysiologic
studies have elucidated mechanisms of pain that operate in skeletal muscle.
Taken together, these studies improve our understanding of the muscle
injury process and will lead to rational therapeutic interventions to facili-
tate recovery.
J Am Acad Orthop Surg 2002;10:67-73
Morphologic and Mechanical Basis of
Delayed-Onset Muscle Soreness
Richard L. Lieber, PhD, and Jan Fridén, MD, PhD
rounding the muscle cell. Increased
CK levels resolve in 7 to 14 days. In
a similar delayed fashion, muscle
pain accompanying eccentric exer-
cise peaks 24 to 48 hours after the
exercise session but resolves more
rapidly compared with CK levels.
Interestingly, peak CK levels are not
strongly correlated with either the
timing of increased muscle pain or
the magnitude of tissue injury.
Another widely agreed-on find-
ing is that training prevents or at
least attenuates the magnitude of
muscle injury that occurs after
eccentric exercise (Fig. 1, solid cir-
cles). This training effect is pro-
duced only after eccentric training
of the specific muscle group being
tested. In other words, there is a
very high degree of specificity
regarding the protective effect of
exercise. General increased aerobic
fitness neither prevents nor attenu-
ates eccentric contraction-induced
muscle injury.
Skeletal Muscle Injury
Injury to muscle fibers can occur as
a result of direct trauma, disease, ap-
plication of myotoxic agents (such as
local anesthetics), inflammatory
processes, or intense exercise. The
association between the type of in-
jury and the nature of the pain that
accompanies it has been studied
using a number of experimental
models. Results from these studies
clarify the various mechanisms of
muscle fiber injury and factors that
influence the type and duration of
pain associated with it. The model
most commonly used to study
DOMS is the eccentric contraction
model.
Muscle Injury Resulting From
Eccentric Contractions
Among the variety of types of
muscle action are the eccentric, con-
centric, and isometric. During an
eccentric action, an activated muscle
is forced to elongate while produc-
ing tension. Its counterpart, concen-
tric action, produces tension during
muscle shortening. The intermedi-
ate, isometric contraction produces
tension while the muscle remains
essentially at a constant length. All
three actions are common compo-
nents of daily movement. The ten-
sion generated during eccentric
action is higher than that for either
of the other actions. Asmussen6es-
tablished that DOMS was primarily
associated with the eccentric com-
ponent of exercise. A muscle injury
model utilizing eccentric contrac-
tion, in which the muscle is actively
generating force during the length-
ening maneuver, has been imple-
mented in animals as well as hu-
mans.
Based on experimental studies of
skeletal muscles directly subjected
to eccentric exercise, investigators
believe that the very early events
causing muscle injury are mechani-
cal in nature.7,8 For example, during
cyclic eccentric exercise of the rabbit
tibialis anterior, significant mechan-
ical changes were observed in the
first 5 to 7 minutes of exercise. After
this period, histologic examination
revealed that a small fraction of
muscle fibers appeared to be larger,
more rounded, and more lightly
stained compared with surrounding
normal muscle fibers. Interestingly,
recent immunohistochemical stud-
ies have revealed structural disrup-
tion of the cytoskeleton within the
fibers at these very earlier time peri-
ods9that may provide further in-
sights into the damage mechanism.
Such pathologic changes also can be
seen following either sprint or dis-
tance running in humans and after
resistance training.10,11
Fiber Type-Specific Damage
Both animal and human studies
have provided evidence for selec-
tive damage of fast fiber types after
eccentric exercise.12,13 In human
studies, this damage was confined
Delayed-Onset Muscle Soreness
Journal of the American Academy of Orthopaedic Surgeons
68
Hours Days
Trained
Untrained
3300
2000
1000
500
200
100
60
Serum CK (IU/ml, Log Scale)
0 3.75 1235 7911
Figure 1 Time course of serum CK levels after a session of eccentric exercise in untrained
and trained young men. Note that the delayed and prolonged increase in CK levels in
untrained individuals is attenuated after training. (Reproduced with permission from
Lieber RL [ed]: Skeletal Muscle Structure and Function: Implications for Rehabilitation and
Sports Medicine. Baltimore, Md: Williams & Wilkins, 1992.)
to the type 2 muscle fibers in gener-
al (Table 1), but in animal studies,
damage has been further localized
to the type FG (often equated to
type 2B) fast fiber subtype. In one
study,12 231 “enlarged” rabbit tib-
ialis anterior fibers were observed
from six different muscles; all were
of the FG fiber type. Their average
size was about four times the nor-
mal muscle fiber area. For some
fibers observed in serial section, the
area and shape of the fiber changed
dramatically from one section to the
next12 (Fig. 2). Because FG fibers
are the most highly fatigable muscle
fibers, it has been speculated that
the high degree of fatigability of
these fibers may predispose them to
injury, but this has not been sup-
ported in detailed animal studies.14
At the ultrastructural level, the
most commonly reported morpho-
logic abnormality is the loss of the
regular orientation of Z bands with
the fibers. The most subtle form of
injury is the slight “wavy” appear-
ance of the Z band, while more
severe injury is manifest by com-
plete Z band or A band disruption
(Fig. 3). Despite the numerous re-
ports of this phenomenon, a mecha-
nistic explanation for selective Z
band damage is not available.
Inflammation After
Muscle Injury
Direct evidence of inflammatory
cells within skeletal muscle after ec-
centric exercise has been reported in
both animals and humans.5,15 The
early mechanical events are fol-
lowed by infiltration of circulating
monocytes that become macro-
phages after entering the tissue (Fig.
4). In a study of the rabbit tibialis
anterior,12 the time course of torque
generation in rabbit dorsiflexors
was measured after a single eccen-
tric exercise session; there was a mea-
surable progressive decline in force
that was delayed and occurred over
a 2- to 3-day period. The mecha-
nism for the progressive decline in
force was hypothesized by the au-
thors to be the infiltration of inflam-
matory cells and associated proteo-
lytic degradation of muscle tissue.
In this model, the progressive force
decline was about the same order of
magnitude as the force decline that
occurred as a result of the mechani-
cal injury itself. Cellular infiltration
was uniquely associated with the
eccentric exercise itself in that iso-
metrically exercised muscles were
devoid of infiltrating cells, and the
same force decrement was not ob-
served after isometric exercise of the
same duration. A similar scenario
has been proposed in human exer-
cise studies.16
Because the inflammatory pro-
cess itself can cause damage in ex-
cess of that caused by the exercise, it
is possible that prevention of in-
flammation would improve muscle
status following injury. Based on
this assumption, nonsteroidal anti-
inflammatory drugs (NSAIDs) are
commonly prescribed to provide
analgesia and to improve perfor-
mance. The specific objective effects
of the NSAIDs on muscle function
are, however, poorly understood,
and it is difficult to test muscle func-
tion in humans because the anal-
gesic effect of NSAIDs may itself
permit improved performance by
lessening or eliminating pain. The
anti-inflammatory medication flur-
biprofen was tested in the rabbit
muscle injury model described
above. Muscles were exercised with
a single eccentric exercise session,
after which the anti-inflammatory
medication was given for 7 days.17
Muscle contractile properties were
measured for the 28 days following
the exercise; interestingly, muscles
treated with the NSAID demon-
strated a significant short-term
improvement in contractile function
Richard L. Lieber, PhD, and Jan Fridén, MD, PhD
Vol 10, No 1, January/February 2002 69
Table 1
Characteristics of Human Skeletal Muscle Fiber Types
Type I Type IIA Type IIB
Other names Red, slow twitch (ST) White, fast twitch (FT)
Slow oxidative (SO) Fast oxidative glycolytic (FOG) Fast glycolytic (FG)
Speed of contraction Slow Fast Fast
Fatigability Fatigue-resistant Moderately fatigue-resistant Most fatigable
Aerobic capacity High Medium Low
Anaerobic capacity Low High High
Motor unit size Small Medium Large
Capillary density High Medium Low
(Adapted with permission from Garrett WE, Jr, Best TM: “Anatomy, Physiology, and Mechanics of Skeletal Muscle,” in Buckwalter JA,
Einhorn TA, Simon SR [eds]: Orthopaedic Basic Science: Biology and Biomechanics of the Musculoskeletal System, ed 2. American Academy of
Orthopaedic Surgeons, Rosemont, Ill: 2000, p. 692.)
but a subsequent loss in function
(Fig. 5). These data may have sig-
nificant implications for the use of
NSAIDs in pain treatment associated
with neuromuscular injury.
Skeletal Muscle Pain
Numerous studies have documented
the existence of pain after blunt trau-
ma, eccentric exercise, injection of
noxious agents, and peripheral nerve
disease in skeletal muscles. It is
clear, however, that muscle fiber
damage does not necessarily cause
pain. This statement is based on the
observation that muscle biopsies ob-
tained from patients with primary
muscle diseases such as Duchenne
muscular dystrophy reveal major
disruptions of the myofibrillar and
sarcotubular apparatus, yet the pa-
tients themselves remain pain free.
Thus, pain within muscle that occurs
after fiber injury probably results
from secondary events that occur
after the damage itself. Based on this
evidence and extrapolation of experi-
mental data obtained from muscles,
tendons, and joints, muscle pain is
thought to result from stimulation of
nociceptors within the muscle itself.
Skeletal Muscle Innervation
Muscles are supplied by a rich
and extensive network of receptors
that are innervated by small myelin-
ated (group III) and unmyelinated
(group IV) afferent nerve fibers.
These fibers conduct much more
slowly (Table 2) than do either the
α-motoneurons that project to the
muscle fibers (i.e., extrafusal muscle
fibers), the γ-motoneurons that pro-
ject to the muscle spindles (intra-
fusal muscle fibers), or even the Ia
afferents that feed back from muscle
spindles to the spinal cord.
Nociception in Skeletal Muscle
Although the bulk of the data on
the neurophysiology of pain has
been obtained from studies of cuta-
neous receptors, studies of muscle
and visceral pain are much more
clinically relevant. The extensive
studies by Mense et al18-20 provide a
wealth of understanding regarding
these nociceptive mechanisms in
muscle and viscera. They delineated
several important differences be-
tween muscle and visceral pain
compared with cutaneous pain.
First, cutaneous pain is localized
with great accuracy, and muscle
pain is difficult to localize. Second,
Delayed-Onset Muscle Soreness
Journal of the American Academy of Orthopaedic Surgeons
70
A B
Figure 3 Longitudinal electron micrographs of rabbit tibialis anterior muscle after 30 min of
eccentric contractions. A, Sample from normal muscle showing clean alignment of myofi-
brils across the field. B, Sample from muscle showing smearing of the Z band material
(small arrowheads) and extension of the Z bands into adjacent A bands (circled regions).
Figure 2 Cross-sectional light micrographs of rabbit tibialis anterior muscle under different
staining conditions. Enlarged fiber, shown with arrows, is of the FG fiber type. A, Hema-
toxylin-eosin. B, Myofibrillar adenosine triphosphate following preincubation at pH = 9.4.
C, Succinate dehydrogenase. D, α-Glycerophosphate dehydrogenase.
AB
CD
2 µm
while increasing the activation inten-
sity of cutaneous receptors does not
change the size of the receptive field,
increasing muscular pain intensity
results in referral to remote sites such
as other muscles, fascia, tendons,
joints, or ligaments. Third, muscle
pain is associated with symptoms
mediated through the autonomic
nervous system, such as decreased
blood pressure, nausea, and sweat-
ing, whereas cutaneous pain is not.
In contrast to results produced
from analogous studies of the skin,
repetitive electrical stimulation of
muscle afferents results only in
painful sensations. Increasing the in-
tensity does not modify the subjec-
tive nature of the pain and serves
only to elicit the description of a
“cramp” as well as a decreased ability
to localize the site of pain source.21
Additionally, the magnitude of re-
ferred pain is positively correlated to
the stimulation frequency of deep
nociceptive fibers.
Factors That Modulate
Nociception in Skeletal Muscle
The type III and IV nociceptors in
skeletal muscle have been studied
extensively in the cat hindlimb prep-
aration.18,19 The percentages of
motor and sensory nerves innervat-
ing the lateral gastrocnemius-soleus
muscles have been shown to be ap-
proximately 60% and 40%, respec-
tively. Of the sensory nerves, about
40% of them can be classified as
nociceptive, suggesting an overall
high sensibility within these mus-
cles (15% to 20% of the innervating
axons).
Experimental demonstration of
factors affecting nociception is ob-
tained by using single nociceptive
afferents from anesthetized cats
and experimentally perturbing the
system. For example, Mense and
Meyer18 measured the discharge
activity of these group III afferents
and saw almost no activity on light
touch with a painter’s brush (Fig. 6),
some activity on moderate touch,
and high activity with noxious touch
(pinching the muscle with forceps).
No activity was observed on pas-
sive stretch of the muscle within
the physiologic range (6 mm in this
case), but when the muscle was
stretched 9 or 12 mm, a moderate
level of activity was recorded. This
makes teleologic sense because
nociceptors are designed not only
Richard L. Lieber, PhD, and Jan Fridén, MD, PhD
Vol 10, No 1, January/February 2002 71
Figure 4 A, Cross-section of muscle fibers showing enlarged fiber (3) and two normal
fibers (1 and 2), and muscle spindle (ms). B, Longitudinal section of muscle along plane
shown in panel A(white dotted line) revealing the inflammatory process that leads to the
enlarged fiber type (3) and size variation observed (compare with Fig. 2). Enlarged fibers
thus represent “supercontracted” cells being digested by inflammatory cells close by.
(Reproduced with permission from Fridén J, Lieber RL: Segmental muscle fiber lesions
after repetitive eccentric contractions. Cell Tissue Res 1998;293:165-171.)
A B
2500
3000
2000
1500
1000
500
Day 3 Day 7 Day 28
Days after Exercise
TA Maximum Tension (g)
Untreated
Flurbiprofen
Figure 5 Maximum tetanic tension of tibialis anterior (TA) muscles from flurbiprofen-
treated versus untreated animals. The flurbiprofen-treated animals generated higher mus-
cle forces early in the treatment and lower muscle forces later in the treatment. (Adapted
with permission.17)
123
1
2
3
ms
25 µm
to signal tissue damage but also to
prevent it.
Inflammatory Factors
Other factors that caused in-
creased output from nociceptors
were injection of factors presumed
to be involved in the inflammatory
response, such as bradykinin ([BK]
cleaved from precursor plasma pro-
teins), 5-hydroxytryptamine (re-
leased from platelets after vascular
damage), and prostaglandins ([PGs]
a byproduct of the cyclooxygenase
pathway). All receptors studied
showed clear signs of BK-induced
sensitization characterized by a low-
ered threshold to local pressure
stimulation. Because BK is known
to release PGE2from cells, it can
actually potentiate its own action.
This finding has led to the idea that
compounds that block the effect of
PG synthesis (e.g., acetylsalicylic
acid [ASA]) might reduce or abolish
the stimulatory action of BK. This
was, in fact, the case. There was a
complete lack of effect of BK within
15 minutes of injection of ASA,
demonstrating the peripheral effect
of ASA in that connections with the
central nervous system were cut in
this preparation.
Ischemia
Ischemia for prolonged periods
(up to about 15 minutes) is not
painful and does not evoke sympa-
thetic reflexes. However, if a muscle
contracts under ischemic conditions,
pain rapidly develops. Most likely
BK is involved in this response be-
cause kinin is released from plasma
proteins during ischemia. Mense
and Stahnke19 demonstrated activa-
tion of group IV muscle receptors
during ischemic contractions. Mus-
cle contraction alone did not elicit
the response, but afferent activity in-
creased fourfold when the same con-
traction was performed while oc-
cluding the nutrient artery.
Reflex-Mediated Pain
Reports in some of the older clin-
ical literature suggest that increased
activity or excitability of the γ-motor
system causes the painful spasms
that sometimes appear in skeletal
muscle. Increased activity of the γ-
motor system would then lead to
increased discharge frequency in
muscle spindle afferent fibers that
would, in turn, lead to increased
activation of α-motoneurons. By
this mechanism, a vicious cycle
could result that would be strong
enough to lead to ischemic contrac-
tions and pain by any one of a num-
ber of the mechanisms described
above. Unfortunately, experimental
evidence supporting this concept is
lacking.20 The main finding of these
studies was that resting activity of
the γ-motoneurons was significantly
reduced by inflammation and that
the reflex excitability of the neurons
was likewise inhibited. These re-
sults demonstrated that nociceptive
muscle afferents actually inhibit
homonymous γ-motoneurons, which
may represent an advantage to the
muscle in that it could reduce po-
tentially damaging forces on it.
Summary
DOMS represents a time-varying
cascade of events that are uniquely
associated with eccentric training of
a skeletal muscle. Currently, there
is not an adequate explanation for
the relationship between muscle
damage observed and clinical symp-
toms of pain. Intramuscular pain,
similar to that observed after appli-
cation of inflammatory factors to
Delayed-Onset Muscle Soreness
Journal of the American Academy of Orthopaedic Surgeons
72
60 s
Thermosensitive unit (group IV)
Touch Mod.
p.
Nox.
p.
36 9 12 2 46
Stretch (mm) Contraction (kP)
Force 500
0
Counts (2s)−1
10
5
0
Impulses (2s)−1
Figure 6 Recording from intramuscular type III afferents with pressure of different levels
(left portion of panel) and with stretch above and beyond the physiological range (6 mm in
this case). (Reproduced with permission.18)
Table 2
Properties of Afferent Fibers in Peripheral Nerve
Axon Average
Fiber Group Myelinated Diameter (µm) Conduction (m/s)
I Yes 15 90-100
II Yes 10 40-50
III Yes 5 20-30
IV No <1 1
muscle, is likely to account for some
of the DOMS observed. In addition,
it is possible that reflex-mediated
pain also contributes to DOMS. In
the future, investigators will estab-
lish objective human models for
DOMS and perform more sophisti-
cated neurophysiologic analysis and
noninvasive imaging of the neuro-
muscular system to define the mech-
anism and prevention of DOMS
after athletic endeavors.
Richard L. Lieber, PhD, and Jan Fridén, MD, PhD
Vol 10, No 1, January/February 2002 73
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