CLINICAL ORTHOPAEDICS AND RELATED RESEARCH

Number 403S, pp. S81–S89

© 2002 Lippincott Williams & Wilkins, Inc.

SESSION 2: ECCENTRIC MUSCLE

INJURY

Clinical Perspectives Regarding

Eccentric Muscle Injury
Donald T. Kirkendall, PhD; and William E. Garrett, Jr., MD, PhD

Muscle strain injuries occur to predictable mus-
cles at consistent locations during expected sport-
ing maneuvers when a muscle is stretched and
then activated, particularly during high intensity
bursts of activity. More than 30% of the injuries
seen in the clinician’s office are injuries to skeletal
muscle. The typical location of the injury is just
proximal to the distal muscle tendon junction re-
gardless of strain rate or architecture of the mus-
cle. After the injury, the muscle is weaker, con-
tinues to weaken, then recovers during the next
week. An inflammatory response is seen in the fol-
lowing 1 to 2 days. By the seventh day, fibrous tis-
sue replaces the inflammatory reaction and a scar
forms. When a muscle is stretched, its tension still
is reduced making the healing muscle more sus-
ceptible to a repeat injury. Viscoelastic properties
of muscle also can help explain how muscle can be
protected against strain injury. A 1
C increase
in muscle temperature (warm-up) increases the
muscle length to failure and a fatigued muscle is
more susceptible to strain injury. It probably is
From the Department of Orthopaedics, University of
North Carolina-Chapel Hill, Chapel Hill, NC.
Reprint requests to Donald T. Kirkendall, PhD, Dept of
Orthopaedics, CB# 7055, University of North Carolina,
Chapel Hill, NC 27599-7055.
DOI: 10.1097/01.blo.0000031989.92980.2b
impossible to prevent muscle strain injury; how-
ever, preventive measures can make muscle more
resistant to these stretch-induced injuries.
Common acute injuries to skeletal muscle such
as contusions, lacerations, strains, ischemia,
and complete ruptures can lead to significant
pain and disability with time lost to occupa-
tional and leisure activity participation. The
importance of strains, a stretch injury, is clear
to the occupational or sports medicine physi-
cian because stretch-induced injuries can ac-
count for as much as 30% of the typical sports
medicine practice.13,17
A muscle strain injury is characterized by a
disruption of the muscle-tendon unit6 leading
to localized pain and general weakness of the
muscle when activity is attempted. Improper
rest and rehabilitation of a minor strain of
skeletal muscle frequently precedes a far more
disabling injury that additionally increases the
time lost to work and athletics.
Despite the frequency of these injuries, the
understanding of the pathophysiology, treat-
ment, and recovery is limited especially when
one compares the understanding of damage to

S81

S82 Kirkendall and Garrett
ligament, tendon, and bone. The natural history,
self-limiting nature, and minimal surgical re-
quirements may have made stretch-induced
injuries of less interest to clinicians. The pur-
pose of the current review is to discuss stretch-
induced injuries, the mechanism of injury, lo-
cation of injury, treatment, and some pertinent
observations from the clinic.
Mechanism of Injury
To reproduce the injury in the laboratory, a ba-
sic understanding of how muscles are injured
in sport or occupational settings needs to be
appreciated. It is well-accepted that muscle
strain injuries occur when the muscle is acti-
vated while being stretched.13,18,28 In addition,
eccentric contraction of the muscle is a fre-
quent occurrence.9,17,28 Eccentric contraction
is an important factor contributing to the in-
jury because muscle forces can be higher dur-
ing lengthening23 that adds to the forces trans-
mitted to muscle by noncontractile connective
tissue.3 On the athletic field, muscle strain in-
juries are common in “speed athletes” such as
sprinters and participants in American foot-
ball, basketball, soccer, rugby, and others sports.
Certain muscles also are most susceptible to
injury than others as shall be shown.
Muscle injury constitutes a spectrum of
problems from the self-limiting delayed onset
muscle soreness2,4,11,21 to muscle strains to
complete disruptions or avulsions from bony at-
tachments. To study this, standard laboratory
techniques for muscle mechanics and electro-
physiology on hindlimb muscles in rabbits,
mainly, the tibialis anterior and the extensor
digitorum longus were used. A model was de-
veloped to produce a strain injury. The first
question was how strong a contraction was
needed to produce a strain injury and it was
found that activation alone failed to induce a
strain injury.5 To obtain an injury, stretch was
necessary. The forces needed to cause muscle
failure were several times the force normally
produced actively during a maximal isometric
contraction,7 suggesting that passive forces
must be considered. Therefore, intact muscle of
the hindlimb in rabbits, with intact neural and
Clinical Orthopaedics
and Related Research
vascular supply, could be passively stretched to
failure or activated during stretch.
Passive Stretch Injuries
Muscles stretched to fail do so at the proximal
or distal tendon. Factors that might influence
injury are the rate of strain (1, 10, and 100
cm/second), muscle architecture (pennation),
or mechanical properties of the muscle. Fail-
ure was independent of strain rate or architec-
ture and failed at the (most frequently distal)
muscle-tendon junction (Fig 1), leaving a
small variable amount of muscle tissue still at-
tached to the tendon.5 Therefore, the site of
stretched-induced injury was predictably near
the muscle-tendon junction, but most often
was not a complete avulsion because a small
variable amount of muscle remained connected
with the tendon. Another factor in muscle me-
chanics, muscle length, has no consistent effect
on muscle strain.
Active Stretch Injuries
Most clinicians would agree that strain injuries
occur during powerful eccentric contractions,
so a laboratory condition to mimic that seen
clinically was devised. Hindlimb muscles of
rabbits again were isolated and stretched to
Fig 1. The gross appearance of the tibialis ante-
rior muscle of the rabbit after controlled strain in-
jury is shown. A small hemorrhage is evident at
the distal tip of the injured muscle (arrow) at 24
hours. (Reprinted with permission from Garrett Jr
WE: Muscle strain injuries. Am J Sports Med
24(Suppl):S2–S8, 1996.)
Number 403S
October, 2002
failure. However, during stretch one of three
conditions of activation was applied: tetanic
stimulation, submaximal stimulation, or no
stimulation.15 The location of failure was pre-
dictable, the muscle-tendon junction, and the
total strain at failure were similar among the
three conditions. Interestingly, the force gen-
erated at failure only was 15% greater in the
activated muscles. However, the energy ab-
sorbed (the difference in strain energy between
passive and active conditions) was approxi-
mately 100% greater in the activated condition
(Fig 2), suggesting that passive elements of
muscle can absorb energy, but that their abil-
ity to absorb energy is enhanced greatly when
the muscle is activated.
This may suggest that muscles are able to
protect themselves and joint structures from in-
jury; the more energy that the muscle can ab-
sorb, the more resistant the muscle is to injury.
The passive and contractile elements of muscle
both contribute to the ability of the muscle to ab-
sorb energy. The passive elements (not depen-
dent on activation) include connective tissue and
the fibers. The contractile element of the muscle
also participates because activation of the mus-
cle increases the ability to absorb energy (Fig 2).
The increase in energy absorbed attribut-
Fig 2. The energy absorbed is shown as the area
under each length-tension deformation curve.
The lower curve is a passive preparation. The fig-
ure shows the relative differences in energy ab-
sorbed to failure in stimulated versus passive
muscle preparations. (Reprinted with permission
from Garrett Jr WE: Muscle strain injuries. Am J
Sports Med 24(Suppl):S2–S8, 1996.)
Eccentric Muscle Injury S83
able to contraction was approximately 100%.
Any condition that diminishes the ability of
the muscle to contract would reduce the abil-
ity of the muscle to absorb energy making the
muscle more susceptible to injury. Two vari-
ables that seem to be factors in muscle strain
injuries are fatigue and weakness.
Nondisruptive Injuries
So far, the discussion has been directed at in-
juries leading to a complete disruption of the
muscle-tendon unit. A change in linearity of
the force-displacement curve of a stretched,
inactivated muscle indicates a plastic defor-
mation has occurred, indicating alteration to
the material structure. Using this model, phys-
iologic, mechanical, and histologic character-
istics of muscle can be observed.
Although the model may cause a nondis-
ruptive injury, ultrastructural damage still oc-
curs. Histologic sections of these injuries show
damage near the muscle-tendon junction with
a variable amount of muscle tissue still at-
tached to the tendon with some hemorrhaging.
A pronounced inflammatory response is seen
shortly after the injury. By the seventh day, fi-
brous tissue starts to replace the inflammatory
reaction leading to scar tissue.15
This type of damage to the tissue would af-
fect the ability of the muscle to develop tension.
Immediately after injury the muscle is weaker,
developing only approximately 70% of the
normal tension. The weakness progresses and
within 24 hours, the muscle’s ability to develop
tension declines further to 50% of the con-
tralateral control muscle. With time, tension de-
velopment improves and by the seventh day,
the muscle can develop 90% of the tension pro-
duced by its contralateral control muscle.
In contrast, when muscle with a 7-day-old
nondisruptive injury is stretched and the ten-
sile strength is recorded, this tensile strength is
77% of the control muscle.16 This is well be-
low the 90% tension developed that was just
mentioned. As stretch is a factor in strains, this
loss of tensile strength may make the muscle
more susceptible to a second injury, a scenario
frequently seen by clinicians.

S84 Kirkendall and Garrett
The Visoelasticity of Skeletal Muscle
Important factors in preventing muscle strain in-
juries include flexibility, warm-up, and stretch-
ing before exercise. The beneficial adaptation
because of stretching frequently is attributed to
stretch reflex mechanisms. An additional fea-
ture of muscle, viscoelasticity, must be con-
sidered. Viscoelasticity should be observed by
hanging a weight on a muscle and observing its
new length, then watching the muscle slowly
continue to increase in length with time. For ten-
dons and ligaments, stretching the tissue to a
constant length leads to a gradual reduction in
tension with time called stress-relaxation. When
done cyclically, a gradual decrease in tension
occurs with each successive stretch.1
This gradual decrease in tension can be
seen experimentally. Hindlimb muscle from
rabbits was stretched from an initial force of
1.96 N to 78.4 N, held for 30 seconds then re-
turned to the initial force and repeated 10
times (Fig 3). The length necessary to reach
the predetermined tension increased 3.45%
during the 10 cycles and 80% of this change in
length occurring in the first four stretches.27
Fig 3. The percent increase in length of the exten-
sor digitorum longus when repeatedly stretched to
a constant tension is shown. (Reprinted with per-
mission from Garrett Jr WE: Muscle strain injuries.
Am J Sports Med 24(Suppl):S2–S8, 1996.)
Clinical Orthopaedics
and Related Research
Fig 4. Muscle tension of the extensor digitorum
longus when repeatedly stretched to the same
length (10% beyond resting length) is shown.
(Reprinted with permission from Garrett Jr
WE: Muscle strain injuries. Am J Sports Med
24(Suppl):S2–S8, 1996.)
Another way to look at the same feature is
to stretch the muscle to 10% above its resting
length and return it to its resting length and re-
peat 10 times (Fig 4). Tension is reduced by
approximately 17% during the 10 cycles with
most of the reduction occurring in the first four
cycles.25
It is obvious that repetitive stretching re-
duces the load on the muscle-tendon unit at any
given length in the absence of reflex effects or
other mediation by the central nervous system.
No differences were apparent for the two con-
ditions when repeated on innervated or dener-
vated muscle. These data clearly show a large
component of the changes in muscle caused
by stretching are a result of inherent muscle-
tendon viscoelasticity. Certainly, there are ad-
ditional reflex and central nervous system ef-
fects affecting muscle that is being stretched
especially during physiologic movements.
Clinical Applications
In the rabbit, muscle strain injuries occur at the
muscle-tendon junction. Is this the same finding
seen in the clinic? Acute hamstring strain in-
juries in 10 college athletes were evaluated clin-
ically and imaged with computed tomography
(CT) scans within 48 hours of the injury to de-
termine injury mechanism and location.8 All in-
juries occurred while sprinting or kicking a
Number 403S
October, 2002
soccer ball. The injury mostly was proximal
and lateral, typically to the biceps femoris. The
common mechanism involved ballistic hip flex-
ion and knee extension. By CT scanning, the in-
jured area appeared as a region of hypodensity
suggesting inflammation and edema, not local-
ized bleeding. To understand the anatomy at the
location of injury, cadaveric dissections were
done. In this sample, nine of 10 injuries seemed
to be to the long head of the biceps femoris, lo-
calized to the muscle tendon junction of the
common tendon of the hamstrings. The tenth pa-
tient (a soccer player) injured his semimembra-
neous while kicking overhead suggesting a dif-
ferent mechanism than that seen in the sprinters.
Additional imaging studies were done on 50
patients who had CT scans (n
27) or magnetic
resonance imaging (MRI) (n
23) to better ob-
serve the location of muscle strain injuries.22
Injuries were specific to the quadriceps, ham-
strings, adductors, and triceps surae groups. T2-
weighted images were better than T1-weighted
images for observing the edema, inflammation,
and possible hemorrhage. Computed tomogra-
phy scanning showed the expected areas of low
density. Quadriceps strains were to the rectus
femoris whereas adductor strains were to the ad-
ductor longus. Of the 17 hamstring strain in-
juries, 11 were to the biceps femoris, four were
to the semimembraneous, and two were to the
semitendinosus. All injuries to the triceps surae
group were at the distal muscle tendon junction
of the medial head of the gastrocnemius. The
effectiveness of CT scanning and MRI of
strain injuries was shown and particular mus-
cles susceptible to strain injuries were identi-
fied. The muscles were two-joint muscles (bi-
ceps femoris, rectus femoris, gastrocnemius), of
a complex architecture (adductor longus) and
occurred, as can be determined best by CT scan-
ning and MRI, at the muscle-tendon junction.
Clinically, there are curious, unexplained
muscle injuries, particularly a persistent intra-
substance strain of the rectus femoris. An un-
derstanding of the nature of the strain injury
was inconsistent with an understanding of the
anatomy of the rectus femoris. Dissection of the
rectus femoris muscle from cadavers shows a
Eccentric Muscle Injury S85
direct head originating from the anterior infe-
rior iliac spine and an indirect head originating
from the superior acetabular ridge.12 The ten-
don of the indirect head extended well into the
mass of the rectus femoris. Although prior lab-
oratory work showed that most strain injuries
occur superficially at the muscle tendon junc-
tion, clinical evidence pointed to a strain at the
muscle tendon junction of the deep, indirect
head giving the appearance of an intrasubstance
injury. These are different from the classically
seen injury near the distal tendon because of the
thigh asymmetry, chronic pain, and the devel-
opment of anterior thigh masses. Ten patients
with an incomplete intrasubstance strain of the
proximal, deep tendon of the rectus femoris
were evaluated with physical examination and
imaging studies. Patients presented anywhere
from 4 to 156 weeks after injury. Eight of the
10 injuries involved sprinting or kicking (two
patients could not recall the mechanism) and all
but one patient had pain when running. Imag-
ing studies detected the strain to be in the area
of the tendon of the indirect head of the rectus
femoris. Surgical exploration was done on two
patients leading to removal of the muscle in one
patient and the excision of a fibrotic mass in the
other patient. After surgery, both patients were
asymptomatic and returned to full activity. The
reason for chronic pain in these subjects was
unknown, but may be attributable to differential
activation of the superficial and deep portions
of the muscle.
Because so many strain injuries seem to be
dependent on the architecture of the muscle
and after clinical experience with anterior thigh
strains12 suggests a detailed study of the archi-
tecture of the rectus femoris seemed appropri-
ate to determine whether these persistent strains
were related to some curious architectural fea-
ture.10 The rectus femoris of fresh or embalmed
cadavers was dissected with the superficial and
deep tendons confirmed. The tendon of the
deep component extended nearly the muscle’s
entire length. It arose from the superior ac-
etabular ridge and traversed somewhat medi-
ally over the course of the muscle. It began
rounded, flattened out, and migrated laterally

S86 Kirkendall and Garrett
and was nearly vertical in the distal third of the
muscle (Fig 5). The pennation of the rectus
femoris was more complex than the typical
bipennate arrangement normally attributed to
the muscle. The proximal 1⁄3 seemed to be
unipennate whereas the distal 2⁄3 was bipennate.
The deep tendon and the bipennate arrangement
of the distal portion of the muscle created a
muscle within a muscle. Exploration of three
chronic strain injuries showed a pseudocyst
consisting of vascular, fibrotic loose connec-
tive tissue that surrounded the deep tendon.
Serous fluid collected between the connective
tissue and the tendon. This anatomic finding is
consistent with CT or MRI scans of vascular
fibrotic processes of the deep tendon of this in-
direct head.
Fig 5. The architecture of the indirect head of the
rectus femoris muscle is shown. (Reprinted with
permission from Garrett Jr WE: Muscle strain in-
juries. Am J Sports Med 24(Suppl):S2–S8, 1996.)
Clinical Orthopaedics
and Related Research
The most common hamstring strain seen in-
volves one muscle, usually the biceps femoris.
More extensive injuries involve more than one
muscle, typically at the common tendon of ori-
gin of the hamstrings. A unique mechanism of
severe hamstring strain injury involves water
skiers.20 Novice skiers assume a crouched posi-
tion before being pulled by the boat into a
standing position. If the skier extends the knees
too soon, the ski is forced down into the water.
Forward momentum of the boat pulls the skier
forward leading to excessive hip flexion while
the knees are extended. This powerful stretch
leads to a muscle-tendon junction injury or to a
more disabling injury involving avulsion from
the ischial tuberosity. Hamstring strains also
occurred in experienced skiers when falling
forward on a slalom ski. Twelve water skiers
with a history of skiing-induced hamstring in-
juries were followed up between .5 and 18
years after the injury. All patients knew they
had a significant injury when the accident oc-
curred. Complete or partial avulsion occurred at
the proximal tendon. The extent of the injury
was obvious on the physical examination, re-
vealing distal tendon retraction of the ham-
string muscles and obvious thigh asymmetry.
Conservative treatment leads to a poor progno-
sis whereas surgical repair is an alternative.
Seven of the 12 patients returned to prior sports
at a lower level and the rest of the patients, all
with complete disruptions, were hampered in
sports involving running or requiring agility.
Acute groin injuries also are common in ath-
letes, especially those who play soccer26 and ice
hockey. Frequently, the adductor longus is in-
jured during hip abduction. Direct and indirect
hernias also may occur. There is another ab-
normality in the lower abdominal wall muscu-
lature that causes a vague and poorly localized
groin pain. This pain happens during high in-
tensity, ballistic motions such as kicking or
sprinting. This injury most often is seen in very
high caliber athletes during intense training
and competition. This athletic pubalgia is as-
sociated with pain and muscle-tendon injury
in the inguinal area near the attachment of the
rectus abdominis to the pubis and in the adja-
Number 403S
October, 2002
cent internal oblique muscles, near the region
of abdominal wall weakness seen with direct
inguinal hernias. However, this pain may ex-
ist without any evidence of herniation. When
conservative measures fail, a herniorrhaphy
procedure reinforcing the abdominal wall mus-
culature can provide relief.
Prevention Strategies
Repetitive Stretch and Failure Properties
Viscoelastic properties contribute to changes
in muscle length and increased length can be
seen to decrease strain in a muscle. Therefore,
does stretching prevent muscle strains? To
study stretching, repeated stretch-release cy-
cles were studied with the rabbit model.24
First, the force to failure of the hindlimb mus-
cle was determined. The contralateral muscles
then were stretched cyclically to 50% or 70%
of the force to failure. Ten cycles to 50% of
failure force resulted in an increase in muscle
length at failure with no change in the force at
failure or energy absorbed. When muscles
were stretched to 70% of failure force, macro-
scopic evidence of failure was seen even be-
fore the 10 cycles were completed. Therefore,
cyclic stretching seems to be beneficial in that
stretching leading to forces in excess of 70%
may make the muscle more, rather than less,
likely for injury.
Warm-up
Viscoelasticity is known to be temperature de-
pendent and warm-up is considered to be pro-
tective against muscle strains. Hindlimb mus-
cle from the rabbit was held isometrically and
tetanically stimulated for 10 to 15 seconds
which resulted in a 1 C rise in muscle tem-
perature.19 Before failure, the muscle was able
to stretch more, and more force production
was capable. Although the changes might be
caused by temperature elevation, the effects of
stretch cannot be discounted despite the mus-
cle being held isometrically. A constant length
still must allow for some stretch of the muscle-
tendon unit as the fibers contract and elastic
components become stretched.
Eccentric Muscle Injury S87
Prior Injury
Clinically, physicians see a minor strain pre-
ceding a more major injury. This would sug-
gest that after a minor injury, the mechanical
characteristics of the muscle somehow are al-
tered, precipitating a more significant injury.
To determine the mechanical characteristics
of a muscle with a minor strain, the extensor
digitorum longus of rabbits had a nondisrup-
tive strain by stretching the muscle just short
of tissue rupture.27 Isometric and isotonic con-
tractile properties of the control muscle were
used for comparison. The muscle then was
stretched passively to failure at a rate of 10 cm
per minute. The peak tensile load and length at
that load were derived for use on the experi-
mental contralateral limb. The length change
to peak load (of the control limb) was dupli-
cated in the experimental muscle, just short of
a disruptive injury. The injured muscle then
was subjected to passive stretch to failure.
Histologic evaluation was done on the minor
injuries in a subset of rabbits. In the experi-
mental muscles, the peak load to rupture was
63% of control and the length at rupture was
79% of control. Isotonic shortening was re-
duced by 51% and 6% for 100 g and 1000 g
weights, respectively. The minor strain injury
caused incomplete disruptions along the mus-
cle tendon junction making a muscle more
susceptible to another injury when preceded
by a prior minor injury. Therefore, early return
to activity before complete healing is a risk for
more severe injury. In addition, aggressive re-
habilitation designed to return an athlete to
competition may be too stressful for the mus-
cle risking additional injury. Injection for lo-
cal pain relief while the muscle still is injured
also may not be appropriate because the lack
of inhibition from pain could result in exces-
sive stress on the muscle, also increasing the
risk of additional injury.
Fatigue
Clinical observation and the literature suggest
that muscle strain injuries occur late in training
sessions or competitive settings. This leads one
to conclude that fatigue must play some role in

S88 Kirkendall and Garrett
the risk of muscle injury. Mair et al14 fatigued
the extensor digitorum longus of rabbits to 25%
or 50% of the force of the contralateral control
by cycles of 5-second isometric tetanic con-
tractions followed by 1-second rest. The mus-
cle was activated while being pulled (at 1, 10,
or 50 cm/second) to failure. Similar data were
collected on the nonfatigued, contralateral con-
trol muscle. The force and length at failure and
the energy absorbed before failure were deter-
mined. There was a trend toward a reduction in
force for all strain rates tested. The rate of strain
did not influence force at failure. There was no
change in muscle length at any of the strain
rates and significantly less energy absorbed in
both fatigue conditions with the greatest loss
occurring in the most fatigued muscle. The re-
duction in absorbed energy was the greatest
when the muscle was pulled at 1 cm per second;
the slower the rate that the muscle is stretched,
the greater the energy that is absorbed. These
data indicate that muscles become damaged at
the same length regardless of fatigue. In con-
trast, fatigued muscle is unable to absorb en-
ergy before reaching the amount of stretch that
causes injuries. Proper conditioning to reduce
or to delay fatigue is seen as a part of a rationale
for prevention of muscle strain injury.
Treatment of Muscle Strain Injuries
The pain of a muscle strain may prompt physi-
cians to prescribe antiinflammatory medica-
tion in response to the inflammatory responses
known to occur after an injury. This treatment
largely is empirical. Before wide use of anti-
inflammatory drugs can be accepted, the ef-
fects of such medication on muscle recovery
need to be evaluated. Obremsky et al16 in-
duced a strain injury to the tibialis anterior of
rabbits (strain rate of 10 cm/minute) that sub-
sequently were administered piroxicam (16
mg/kg) within 6 hours plus 13 mg/kg every 6
hours. Contractile properties and histologic
features were determined at 1, 2, 4, or 7 days
after the injury. Data were compared with the
data from control animals that did not receive
medication. On Day 1, there was a signifi-
cantly greater force in the treated animals.
Clinical Orthopaedics
and Related Research
There was no difference between the treated
and untreated animals on Days 2, 4, or 7. The
treated animals had a delay in the histologic
repair process. These muscles showed delayed
inflammatory cell infiltration, necrosis, myo-
tube regeneration, and collagen deposition.
Based on these results, nonsteroidal antiin-
flammatory agents may be of some benefit for
the early treatment of pain control and func-
tional improvement. However, the delay in the
repair process seen histologically raised con-
cern regarding long-term treatment.
One of the most common injuries seen in the
office of the practicing physician is the muscle
strain. Until recently, few data were available
on the basic science of and clinical application
of this basic science to treatment and preven-
tion of muscle strains. Studies in the last 10 to
15 years represent action taken on the direction
of investigation into muscle strain injuries
from the laboratory and clinical fronts.
Findings from the laboratory indicate that
certain muscles are susceptible to strain injury
(muscles that cross multiple joints or have
complex architecture) and have a strain thresh-
old for passive and active injury. Strains are
the result of excessive stretch or stretch while
the muscle is being activated. When the mus-
cle tears, the damage is localized very near the
muscle tendon junction. After injury, the mus-
cle is weaker and at risk for additional injury.
The force output of the muscle recovers dur-
ing the following days while the muscle un-
dertakes a predictable progression toward tis-
sue healing.
Imaging has been used to document the site
of injury as the muscle-tendon junction. The
commonly injured muscles are the hamstrings,
the rectus femoris, the gastrocnemius and the
adductor longus although injuries inconsistent
with involvement of one muscle tendon junction
still proved to be at a tendinous origin within the
substance of the muscle. Some injuries have a
poor prognosis and may be helped with surgery
including injuries to the rectus femoris, the ham-
string origin, and the abdominal wall.
The risk of reinjury is increased with an in-
completely healed strain injury. Early use of
Number 403S
October, 2002
nonsteroidal antiinflammatory agents may be
helpful, but longer-term use may not be helpful.
Warm-up, temperature, and stretching may
be beneficial in reducing the risk of strain injury.
Many of the factors protecting muscle such
as strength, endurance, and flexibility also are
essential for maximum performance. Future
studies should clarify the repair and recovery
process emphasizing not only the recovery of
function, but also the susceptibility to reinjury
during the recovery phase.
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