ARTICLE
Damage to Skeletal Muscle from Eccentric
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Exercise
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Uwe Proske and Trevor J. Allen
Department of Physiology, Monash University, Melbourne, Victoria, Australia
PROSKE, U., and T.J. ALLEN. Damage to Skeletal Muscle from Eccentric Exercise. Exerc. Sport Sci. Rev., Vol. 33, No. 2,
pp. 98 –104, 2005. Evidence is provided for a mechanical event as the first step in the process leading to muscle damage after a series
of eccentric contractions. Aspects discussed include the decline in active tension, increase in passive tension, shift in length–tension
relation, soreness, swelling, and disturbed proprioception. Key Words: eccentric exercise, damage, pain, adaptation, sarcomere
INTRODUCTION
After prolonged concentric or isometric contractions of our
muscles we become fatigued, but this is short lived. Within
1–2 h we have usually recovered full function. However, after
a series of unaccustomed eccentric contractions we not only
become fatigued, but our muscles remain weak for days, and
they become stiff and sore the day after the exercise. The
reason for these additional effects is that eccentric contrac-
tions can lead to muscle damage. This review discusses a
number of aspects of the damage process and the conse-
quences for muscle properties. A summary of the sequence of
events is given in Figure 1.
THE INITIAL EVENT
Although it has been known for many years that eccentric
exercise leads to delayed-onset muscle soreness (DOMS), a
satisfactory mechanism for the initial event that leads to the
soreness has been put forward only relatively recently. For a
discussion, see Proske and Morgan (5). The basis for this
mechanism is the region of instability on the descending limb
of the sarcomere length–tension curve. Briefly, when the
myofibrils of a muscle fiber are stretched while contracting,
some sarcomeres resist the stretch more than others, perhaps
because their myofilament overlap is closer to their optimum
value or because the cross-sectional area of the myofibril is
Address for correspondence: Uwe Proske, Department of Physiology, PO Box 13F,
Monash University VIC 3800, Australia (E-mail: uwe.proske@med.monash.edu.au).
Accepted for publication: November 11, 2004.
0091-6331/3302/98 –104
Exercise and Sport Sciences Reviews
Copyright © 2005 by the American College of Sports Medicine
98
slightly greater at that point. As a consequence, weaker
sarcomeres take up most of the stretch. If this occurs on the
descending limb of the length–tension curve, these sarco-
meres get progressively weaker until there is no overlap
between the myofilaments. The rising passive tension in
elastic elements balances the tension in the remaining un-
stretched sarcomeres (5).
During a series of eccentric contractions, more and more
sarcomeres will become overstretched, beginning with the
weakest and including progressively stronger sarcomeres.
Each time the muscle relaxes, myofilaments in some over-
stretched sarcomeres may not reinterdigitate, and the sarco-
mere becomes disrupted. Overstretched, disrupted sarcomeres
lie scattered at random along the length of the myofibril.
Once one or more sarcomeres have become disrupted, the
damage may spread longitudinally to adjacent sarcomeres in
the myofibril and transversely to adjacent myofibrils. A point
will be reached at which the structural distortions produced
by the presence of overstretched sarcomeres lead to mem-
brane damage, including membranes of the sarcoplasmic re-
ticulum, transverse tubules, or the sarcolemma. This is ac-
companied by the uncontrolled movement of Ca2⫹ into the
sarcoplasm, triggering the next stage in the damage process
(Fig. 1).
This sequence of events provides a satisfactory explanation
for the initial event leading to damage to muscle fibers from
eccentric exercise. However, these ideas have not been uni-
versally accepted, and a major competing proposal is that the
initial event is not mechanical in origin. In the alternative
view, the damage is largely the result of excitation– contrac-
tion (E-C) uncoupling (8). The supporting evidence for this
hypothesis is based on intracellular Ca2⫹ measurements; one
could argue that an increase in Ca2⫹ is secondary to me-
chanical changes in the fiber (15). In addition, an E-C
coupling mechanism does not readily explain a shift in the
 Force remains depressed for up to a week after the eccentric
contractions, whereas recovery is complete within 1–2 h after
concentric contractions (Fig. 2). So, deficits in force mea-
sured at 2 h or later after the eccentric contractions are likely
to be only caused by the damage.
Second, eccentric contractions lead to a shift of the
length–tension relation of the muscle in the direction of
longer muscle lengths (see below). If this is not taken into
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account, and the measurement is made at the original length,

it will overestimate the fall in force. It has led to reports of
much greater falls in force from eccentric exercise than is
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really the case. For example, 50 eccentric contractions per-

formed across the optimum length of the medial gastrocne-
mius muscle of the anesthetized cat led tension to fall by 55%
of the control value. This was a measurement made at the
Figure 1. Steps in the damage process from eccentric exercise. Postu- original optimum length, determined from the muscle’s
lated series of events in muscle fibers damaged by a period of eccentric length–tension relation. When the length–tension relation
exercise. For details, see text. was remeasured after the eccentric contraction, optimum
length had shifted in the direction of longer muscle lengths
by 3.2 mm, representing 16% of the muscle’s working range.
length–tension relation of the muscle, a characteristic feature Tension measured at the new optimum length was now 39%
associated with damage from eccentric contractions (5). of control values. That is, not taking the length change into
An event supplementary to sarcomere disruption is the account overestimated the size of the force drop by 41%.
opening of stretch-activated cation channels as a result of Another effect attributed to eccentric contractions is that
membrane stresses produced by the mechanical changes (Fig. force at low stimulation rates is preferentially decreased com-
1). This leads to inward movement of Na⫹ and Ca2⫹ into the pared with force at high stimulation rates. This is sometimes
sarcoplasm (15).
To summarize, the sequence of events would begin with
disruption of sarcomeres. Structural distortions triggered by
the disruptions lead to membrane damage and interference
with E-C coupling. At the same time, the accompanying
stresses applied to membranous structures lead to opening of
cation channels. All of this produces an increase in sarco-
plasmic Ca2⫹ levels and the Ca2⫹ triggers proteolysis asso-
ciated with fiber breakdown and repair.
There have been repeated reports that the damage from
eccentric exercise can be reduced by muscle fatigue. Until
now, there has been no evidence in support of such views.
Experiments in our laboratory (4) have shown that eccentric
contractions applied to a muscle whose force output had been
reduced by 32% by a previous series of fatiguing concentric
contractions produced as much evidence of damage as from
the same contractions given to unfatigued muscle. The point
emphasizes that fatigue and damage are two quite separate
processes, and that neither force levels nor fatigue determines
the amount of damage from eccentric contractions (4). It is
a common misconception that high stresses during an active
stretch are responsible for eccentric damage.

THE FALL IN FORCE

A consequence of a series of eccentric contractions is a fall
in force, which is often measured isometrically. In consider-
ing the size of the fall, a number of factors must be taken into
account. First, if force is measured after a series of eccentric
contractions, it is likely that the force decline is caused by
both metabolic fatigue and damage. Fatigue effects can be
minimized by giving only a small number of eccentric con-
tractions (4) or by waiting for the fatigue effects to subside.
Figure 2. Force changes after concentric and eccentric exercise.
Changes in force measured as maximum voluntary contraction (MVC)
after a series of concentric contractions (dotted trace) and eccentric con-
tractions (continuous trace). Values are shown as means (⫾ SEM) for six
subjects. The preexercise value of MVC was assigned 100%, and has been
indicated by the dashed line. Further measurements were made immedi-
ately after the exercise, at 2 h and at 24 h. Asterisks indicate values
significantly different from controls. [Adapted from Walsh, L.D., C.W.
Hesse, D.L. Morgan, and U. Proske. Human forearm position sense after
fatigue of elbow flexor muscles. J. Physiol. 558:705–715, 2004.]

Volume 33 䡠 Number 2 䡠 April 2005 Eccentric Muscle Damage 99

 referred to as low-frequency fatigue. Such a decrease has been
used in the past to argue in support of E-C coupling as a major
determinant of eccentric damage. When the change in
length–tension relation is taken into account, low-frequency
depression is still present, but it is less by approximately 30%.
THE LENGTH–TENSION RELATION
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The length–tension relation is a fundamental property of
muscle. An important consequence of a series of eccentric
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contractions is a shift of the optimum length for peak active
tension in the direction of longer muscle lengths (Fig. 3).
This has now been shown in animals as well as in human
subjects (3).
The shift in the length–tension relation is a reliable and
useful measure of the amount of damage to the muscle pro-
duced by the eccentric contractions. Unlike the force drop, it
is independent of levels of fatigue (4). The size of the shift
correlates with the amount of damage after the eccentric
contractions (3). To explain the shift, it is proposed that after
the eccentric contractions, the disrupted sarcomeres lie scat-
Figure 3. Length dependence of damage from eccentric exercise. The
nerve supply to the medial gastrocnemius muscle of the anesthetized cat
was divided into three portions, each of which generated a similar amount
of tension. Length dependence of active tension of each portion was
measured before 50 eccentric contractions (open symbols, PRE) and af-
terwards (filled symbols, POST). A stretch of 6 mm at 50 mm·s⫺1 was
applied during each contraction. Length was expressed in millimeters
relative to the optimum length for peak active force for the whole muscle
(Lopt). Each curve plots the active tension generated at a number of dif-
ferent muscle lengths. The length corresponding to the peak active ten-
sion is indicated by an arrow. The length range covered by the active
stretches was from Lopt ⫺9 mm to Lopt ⫺3 mm (circles), Lopt ⫺6 mm to Lopt
(squares), and Lopt ⫹3 mm to Lopt ⫹9 mm (triangles). Eccentric contrac-
tions at the longer lengths led to larger falls in force and a greater shift in
optimum length (arrows). [Adapted from Whitehead, N.P., D.L. Morgan,
J.E. Gregory, and U. Proske. Rises in whole-muscle passive tension of
mammalian muscle after eccentric contractions at different muscle
lengths. J. Appl. Physiol. 95:1224 –1234, 2003.]
100 Exercise and Sport Sciences Reviews
tered at random along the myofibril. The presence of these
noncontracting sarcomeres in series with still functional sar-
comeres increases the series compliance of the fiber. This is
a nonlinear increase in compliance (i.e., it increases the fiber
rest length), but once the passive fiber is stretched, tension
rises more steeply than before, because there are effectively
fewer sarcomeres in series being stretched (12). The in-
creased series compliance leads to a shift of the muscle’s
optimum length for peak active force in the direction of
longer muscle lengths (3). There is no evidence of changes in
tendon properties accompanying the increase in compliance
in myofibrils.
PASSIVE TENSION
After a series of eccentric contractions, there is a rise in
whole-muscle passive tension. It was originally thought to be
the result of changes in the connective tissue matrix, and at
one stage it was believed to be associated with muscle swell-
ing. However, more recent studies on humans and animals
(12,13) have shown that it is specifically associated with
muscle damage and, like the shift in optimum length, and
unlike swelling, it is present immediately after the eccentric
contractions. This extra passive tension is present in the
absence of any recordable electrical activity and, is therefore
not nerve mediated (Fig. 4).
When a muscle is subjected to a series of eccentric con-
tractions, the degree of damage is determined by the length
at which the contractions are performed (Fig. 3). When the
active stretches extend onto the descending limb of the
length–tension curve (the region of sarcomere instability
(5)), some damage occurs, with the amount increasing with
length. In the anesthetized cat, 50 eccentric contractions,
given symmetrically about the optimum length, led to both a
shift in optimum length and a fall in active tension (12).
Accompanying changes in passive tension were measured by
recording tension during a slow stretch of the muscle over its
full physiological range. After the eccentric contractions,
passive tension was higher at most muscle lengths. However,
the increases were not uniform, and were greatest in the
region of the muscle’s optimum length (Fig. 4). At the
optimum length, passive tension had increased by 170%
above the preexercise level. A second observation made was
that over the period of 1 h after the eccentric contractions,
passive tension continued to increase until it was 210% of
control values. When the muscle was subjected to several
brief, rapid stretches, passive tension collapsed back to near
the postexercise value, and then over the next hour redevel-
oped with a similar time course. The approximate time con-
stant for redevelopment of passive tension was 10 min (12).
Our explanation for the rise in passive tension is that after
sarcomere disruption by the eccentric contractions, there is
the likelihood of membrane damage, perhaps at the level of
the t-tubules or sarcoplasmic reticulum. The consequent un-
controlled release of Ca2⫹ into the sarcoplasm activates the
contractile filaments to develop an injury contracture. Pre-
sumably, the contracture will be maintained as long as ATP
levels remain high. Sarcomeres within the region of injury
shorten, applying stresses to immediately adjacent areas,
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Figure 4. Changes in passive tension after a series of eccentric con-
tractions. Upper panel shows whole muscle passive tension for the medial
gastrocnemius muscle of the anesthetized cat, before (solid line) and after
(dotted line) 50 eccentric contractions, using 6-mm active stretches, ar-
ranged to lie symmetrically across the optimum length of the muscle.
Passive tension was measured using a slow stretch (1 mm·s⫺1) over the full
physiological range from Lopt ⫺12 mm to Lopt ⫹8 mm (Lopt, whole muscle
optimum length). Lower panel shows measurement of the change in
passive tension, above control values, at different muscle lengths. The
hatched bar at the bottom indicates the length range covered by the
eccentric contractions. [Adapted from Whitehead, N.P., D.L. Morgan, J.E.
Gregory, and U. Proske. Rises in whole-muscle passive tension of mam-
malian muscle after eccentric contractions at different muscle lengths.
J. Appl. Physiol. 95:1224 –1234, 2003.]
thereby spreading the contracture. This is a slow process, over
time leading to an increase in passive tension.
In other experiments we have shown that the number of
regions of disrupted, overstretched sarcomeres, as observed
under the electron microscope, become fewer with time after
a series of eccentric contractions (3). This observation sug-
gests that the sarcomere disruption process is sometimes
reversible, and that some sarcomeres are able to recover
normal realignment over time. If so, the series compliance of
the muscle should slowly decline after the eccentric contrac-
tions, which would contribute to the subsequent increase in
passive tension.
Volume 33 䡠 Number 2 䡠 April 2005
Why do rapid stretches reduce the passive tension? We
have considered two mechanisms. One possibility is that the
stretch may break up regions of contracture in damaged fibers
into a larger number of smaller areas, separated by empty
sarcolemmal tube. The presence of fiber segments that are
devoid of contractile material would reduce the level of
passive tension.
A second possibility is that rapid stretches applied to
damaged muscle fibers may lower passive tension by produc-
ing additional sarcomere disruption within the fiber. The
fiber segments in a state of contracture are likely to be stiffer
than adjacent, still functional sarcomeres. The stretch would
therefore be distributed nonuniformly and would disrupt
some of the normal sarcomeres. The resultant increase in
series compliance would lower passive tension. An observa-
tion consistent with such an interpretation is that after the
stretches the muscle had to be stretched further before pas-
sive tension began to rise (12).
Why does passive tension redevelop? Conceivably, regions
of contracture that are broken up by the stretches may
coalesce again, and so reduce the portions of the fiber devoid
of contractile material. In addition, series compliance would
be expected to fall again with time, and other parts of the
damaged fiber may enter a state of contracture.
Does the rise in passive tension have any functional im-
plications? It seems likely that the sensation of stiffness we
experience in our muscles after a period of eccentric exercise
is caused by the rise in passive tension. A common practice
among athletes is to carry out a series of warm-up stretches
before a competitive event. Should an individual carry some
damage from previous eccentric activity, such stretches are
likely to enhance flexibility by lowering passive tension
levels.
SORENESS AND SWELLING
A feature of eccentric exercise is that it leaves us stiff and
sore the next day. Stiffness has already been discussed. Al-
though there is general agreement about the origin of the
soreness and its mechanism, there are some interesting new
observations on this subject.
Once the damage process has reached the stage of ruptured
membranes and there is a rise in resting intracellular Ca2⫹,
this can trigger proteolysis and facilitate breakdown of the
damaged fibers. The accompanying inflammatory process (6)
involves invasion of the damaged areas by macrophages and
monocytes. Products of the inflammation, histamine, seroto-
nin, substance P, and prostaglandins act to sensitize muscle
nociceptors served by Gp III and Gp IV afferent fibers. The
inflammation is accompanied by edema, which is presumably
responsible for the muscle swelling. The onset of swelling
roughly parallels that for soreness, and is present at 24 h after
the exercise. Depending on the severity of the exercise,
swelling and soreness typically persist for another 3– 4 d.
Whereas the conventional view has sensitization of noci-
ceptors as a mechanism for the soreness, DOMS has a num-
ber of features that distinguish it from other kinds of muscle
soreness. It is not really soreness, but tenderness. There is
typically no chronic pain, and pain is experienced only
Eccentric Muscle Damage 101
 during mechanical stimulation— contracting, stretching, or
palpating the muscle. Pain from overt muscle injury or from
inflammatory muscle disease is typically chronic.
We have recently made an observation that contributes a
new point of view to discussions of the neural basis of DOMS
(9). When a mechanical probe is pushed into an unexercised
muscle sufficiently firmly, the subject experiences some dis-
comfort. If the probe is vibrated at 80 Hz, this relieves some
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If eccentric exercise damages the ordinary or extrafusal
muscle fibers, it seemed plausible that it might also damage
the intrafusal fibers of muscle spindles. In a second series of
animal experiments, the effects on muscle spindle responses
of a series of eccentric contractions were studied. Again, as
for tendon organs, the responses of spindles to stretch and to
fusimotor stimulation were normal after the eccentric
contractions.

of the discomfort, an example of the well-known phenome- If eccentric exercise does not damage muscle sense organs,
non, “rubbing it makes it feel better.” When the same thing what might be responsible for the disturbed proprioception?
is performed on an eccentrically exercised muscle with In experiments on the sense of force, subjects were asked to
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DOMS, the threshold for pain from mechanical stimulation generate a given level of force in elbow flexors of one arm and
is much lower than before, as expected, but now when the match it with their other arm (Fig. 5). Subjects are normally
probe is vibrated, pain is exacerbated, not reduced, by the quite good at such a task, achieving matching accuracy to
vibration. There has been a switch in the effect of muscle
vibration. Sensitized Gp IV afferents are unlikely to be able
to respond to high-frequency vibration because of their long
refractory period. Whether GpIII afferents can respond at
that frequency and, indeed, show some response at up to 120
Hz (9) remains uncertain. It is known, however, that 80 Hz
is the optimal frequency for stimulation of the primary end-
ings of muscle spindles. It raises the possibility that DOMS is,
in fact, an allodynia, in which changes in processing at the
level of the spinal cord allow mechanoreceptors, served by
large-diameter afferents, to access the pain pathway.

PROPRIOCEPTION

It is a common experience that after a period of intense

exercise, we feel unsteady on our legs and have difficulty in
performing finely skilled movements. Such anecdotal obser-
vations have led to the suggestion that exercise, particularly
eccentric exercise, can disturb proprioception. Consistent
with this suggestion, experiments in our laboratory have
shown that both the sense of force and the sense of position
in elbow flexor muscles of human subjects are disturbed after
a period of eccentric exercise (7,10).
It is currently believed that the sense of force may have
two components, one involving a peripherally derived signal
originating most probably from tendon organs, and a second
arising centrally as a sense of effort or of heaviness (2). The
sense of position is believed to be provided by afferent signals
coming from muscle spindles. Based on these propositions,
we considered the possibility that eccentric exercise not only
damaged the ordinary muscle fibers, but also disturbed the
function of muscle receptors. Any abnormal function might,
Figure 5. Matching forces after eccentric exercise. Upper panel shows
therefore, explain the disturbance to human proprioception. subjects with their arms strapped to paddles locked in the vertical position
In an animal experiment, responses of identified tendon by horizontal bars, the ends of which were attached to strain gauges. With
organs in the medial gastrocnemius muscle of the anesthe- elbow flexors of one arm, subjects generated 30% MVC under visual
tized cat were studied before and after a series of eccentric control, using a target level, and they matched this level with their other
arm without visual feedback. Lower panel shows force mismatches be-
contractions. The eccentric contractions produced extensive tween the two arms. Values before a period of eccentric exercise were
damage in the muscle, as indicated by the large decline in assigned a value of 0. Solid line, force mismatch, expressed in %MVC of
isometric force and the shift in optimum length. Taking into preexercise value, measured over 4 d after the exercise. Dashed line indi-
account that there was also an increase in passive tension cates the same measurements, but expressed in terms of the MVC deter-
after the eccentric contractions, it was found that the pop- mined on the day of measurement. This reduced, but did not abolish,
matching errors. [Adapted from Weerakkody, N.S., P. Percival, D.L. Mor-
ulation of tendon organs studied was able to faithfully mon- gan, J.E. Gregory, and U. Proske. Matching different levels of isometric
itor all of these changes, and there was no evidence of any torque in elbow flexor muscles after eccentric exercise. Exp. Brain Res.
abnormal function. 149:141–150, 2003.]

102 Exercise and Sport Sciences Reviews www.acsm-essr.org

 within a few percentage points. Elbow flexors of one arm
were then exercised eccentrically, and it was found that in a
subsequent matching trial subjects made large errors (Fig. 5).
The direction of the errors was consistent with subjects’
matching efforts, not forces. When the exercised arm acted as
the reference, achieving the reference level of force required
much more effort than before, because the muscle had been
fatigued and damaged by the eccentric exercise. It meant that
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in matching effort, the other unexercised arm generated
forces that were far higher that the reference level, yet
subjects believed that they were making an accurate match
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(10).
A similar series of experiments was performed on the sense
of position. One forearm was placed at a particular angle by
the experimenter. The blindfolded subject had to maintain
the unsupported arm at that angle, and then match its
perceived position with their other arm. Subjects were able to
match arm positions within 1–2° of accuracy. Then one arm
was exercised eccentrically, the damage indicators were mea-
sured, and the matching experiment was repeated. Here, too,
subjects made large and systematic errors. The findings led to
the conclusion that subjects use the effort required to hold
the arm at a particular angle against the force of gravity as a
positional cue. When arm muscles were damaged and fa-
tigued by the eccentric exercise, it meant that maintenance
of position by the exercised arm was associated with a much
larger effort, leading to matching errors (7).
The general conclusion from these experiments was that
with our arms in their normal working space, we rely on the
centrally derived sense of effort for information about posi-
tion and force levels. Proprioception is disturbed after intense
exercise because of a disturbance of the effort–force and
effort–position relationship.
THE REPEATED BOUT EFFECT
It is a common experience for us to feel stiff and sore the
day after having climbed down a mountain. That is because
leg muscles undergo eccentric contractions during downhill
walking. However, if we walk down the same mountain again
1 wk later, it leaves us much less sore afterwards. The muscles
have adapted to the first bout of exercise to provide them
with protection against further damage. This is the repeated
bout effect, which lasts for 3 wk or longer (1).
It has been proposed that the adaptation process after the
damage from the first bout of eccentric exercise involves
repair of the damaged fibers and incorporation of additional
sarcomeres in series. It is envisaged that the extra sarcomeres
are added without changing fiber length, so that sarcomere
length is now less for a given fiber length (5). As a conse-
quence, during a stretch across a given portion of the muscle’s
working range, the initial sarcomere length will be less, and
the stretch will be distributed across a larger number of
sarcomeres. The presence of the extra sarcomeres produces a
shift of the muscle’s length–tension relation in the direction
of longer lengths (1). It is therefore less likely for sarcomeres
to be stretched onto the descending limb of their length–
tension relation, which is the region of instability and dis-
ruption. Although it has been claimed that such a mecha-
Volume 33 䡠 Number 2 䡠 April 2005
nism would be too slow to account for the repeated bout
effect, animal experiments on muscle immobilization have
shown that additional sarcomeres can be incorporated in
fibers within 5 d (14).
The repeated-bout effect can provide the basis for a train-
ing program of eccentric exercise designed to provide pro-
tection against muscle damage. The aim would be to have a
program of increasing intensity that triggered the protective
adaptation without leaving the individual temporarily dis-
abled from stiffness and pain.
Consideration of the protection provided by a program of
eccentric training has acquired new significance in view of
the suggestion that eccentric damage under the conditions of
an elite sport can, at times, lead to a muscle strain injury (1).
Because the recurrence rates of such injuries are high, reha-
bilitation from a muscle strain should include a program of
mild eccentric exercise to provide protection against reinjury.
When a muscle group is subjected to a regular program of
concentric exercise in which the contracting muscle shortens
rather than being stretched, there is evidence that the muscle
adapts in the opposite direction, that is, it becomes more
vulnerable to damage from eccentric exercise (11). The sim-
plest interpretation is that for reasons of economy, and to
allow the muscle to generate tension at short lengths, fibers
lose some sarcomeres in series. That, in turn, shifts the
length–tension relation in the direction of shorter lengths,
making the muscle more susceptible to eccentric damage. It
is an important consideration for the design of training pro-
grams that aim to improve muscle speed and strength. Pro-
grams must be arranged so that they include a component of
eccentric activity to prevent an increase in vulnerability for
eccentric damage. We are left by all of this with the impres-
sion that muscle is a plastic tissue, adapting continuously and
specifically to the requirements of an activity to achieve peak
performance.
CONCLUSION
This review has focused on the view that a mechanical
event is the first step in the damage process after eccentric
exercise. The mechanism is based on the instability of the
descending limb of the sarcomere length–tension curve. Al-
ternative mechanisms based on E-C coupling dysfunction as
the initial event are not able to readily explain the shift in
optimum length that accompanies the muscle damage. It is
also intuitively less appealing to postulate that, for as yet
unexplained reasons, the point of weakness in the muscle is
somewhere within the E-C coupling machinery. Finally, a
mechanism based on sarcomere disruption is able to explain
the repeated-bout effect in terms of the incorporation of
additional sarcomeres in muscle fibers. So, eccentric exercise
leads to two shifts in the muscle’s length–tension relation.
An initial, damage-related shift is followed several days later
by an adaptation shift. With the secondary shift comes pro-
tection for the muscle against further damage.
It seems at first sight to be a design flaw that eccentric
contractions routinely cause damage at the level of sarco-
meres. However, such damage may well be the necessary
precursor for triggering the adaptation process that follows.
Eccentric Muscle Damage 103
 Presumably, a similar precursor event exists during adapta-
tion to shortening contractions. All of these changes take
place within the muscle itself. They emphasize the plasticity
of muscle as it adapts to changing conditions. It is likely that
there are also matching alterations in the neural control of
the muscle. A specific case in point is the change in central
excitability produced by the pain from DOMS (9). An ex-
citing area for future experiments will be to follow the
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changes within the central nervous system accompanying
different kinds of exercise.
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References
1. Brockett, C.L., D.L. Morgan, and U. Proske. Human hamstring muscles
adapt to eccentric exercise by changing optimum length. Med. Sci.
Sports Exerc. 33:783–790, 2001.
2. Gandevia, S.C. Kinaesthesia: roles for afferent signals and motor com-
mands. In: Handbook of Physiology, Section 12, Exercise: Regualtion and
Integration of Multiple Systems, edited by L.B. Rowell and J.T. Shepherd.
New York: Oxford University Press, 1996, pp 128 –172.
3. Jones, C., T. Allen, J. Talbot, D.L. Morgan, and U. Proske. Changes in
the mechanical properties of human and amphibian muscle after eccen-
tric exercise. Eur. J. Appl. Physiol. Occup. Physiol. 76:21–31, 1997.
4. Morgan, D.L., J.E. Gregory, and U. Proske. The influence of fatigue on
damage from eccentric contractions in the gastrocnemius muscle of the
cat. J. Physiol. 561:841– 850, 2004.
5. Proske, U., and D.L. Morgan. Muscle damage from eccentric exercise:
mechanism, mechanical signs, adaptation and clinical applications.
J. Physiol. 537:333–345, 2001.
104 Exercise and Sport Sciences Reviews
6. Smith, L.L. Acute inflammation: the underlying mechanism in delayed
onset muscle soreness? Med. Sci. Sports Exerc. 23:542–551, 1991.
7. Walsh, L.D., C.W. Hesse, D.L. Morgan, and U. Proske. Human forearm
position sense after fatigue of elbow flexor muscles. J. Physiol. 558:705–
715, 2004.
8. Warren, G.L., C.P. Ingalls, D.A. Lowe, and R.B. Armstrong. Excitation-
contraction uncoupling: Major role in contraction-induced muscle in-
jury. Exer. Sports Sci. Rev. 29:82– 87, 2001.
9. Weerakkody, N.S., P. Percival, M.W. Hickey, D.L. Morgan, J.E. Greg-
ory, B.J. Canny, and U. Proske. Effects of local pressure and vibration on
muscle pain from eccentric exercise and hypertonic saline. Pain 105:
425– 435, 2003.
10. Weerakkody, N.S., P. Percival, D.L. Morgan, J.E. Gregory, and U.
Proske. Matching different levels of isometric torque in elbow flexor
muscles after eccentric exercise. Exp. Brain Res. 149:141–150, 2003.
11. Whitehead, N.P., T.J. Allen, D.L. Morgan, and U. Proske. Damage to
human muscle from eccentric exercise after training with concentric
exercise. J. Physiol. 512:615– 620, 1998.
12. Whitehead, N.P., D.L. Morgan, J.E. Gregory, and U. Proske. Rises in
whole-muscle passive tension of mammalian muscle after eccentric
contractions at different muscle lengths. J. Appl. Physiol. 95:1224 –1234,
2003.
13. Whitehead, N.P., N.S. Weerakkody, J.E. Gregory, D.L. Morgan, and U.
Proske. Changes in passive tension of muscle in humans and animals
after eccentric exercise. J. Physiol. 533:593– 604, 2001.
14. Williams, P.E., and G. Goldspink. The effect of immobilisation on the
longitudinal growth of striated muscle fibres. J. Anatomy 116:45–55,
1973.
15. Yeung, E.W., and D.G. Allen. Stretch activated channels in stretch-
induced muscle damage: role in muscular dystrophy. Clin. Exp. Pharm.
Physiol. 31:551–556, 2004.
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