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THE AMERICAN JOURNAL OF SPORTS MEDICINE, Vol. 24, No. 6
0 1996 American Orthopaedic Society for Sport8 Medicine
Muscle Strain Injuries
From the Division of Orthopaedic Surgery, Duke University Medical Center,
Common acute injuries to 8keletal muscle include contu-
sions, lacerationg, strains, igchemia, and complete rup-
tures. Any of these injuries can lead to significant pain and
disability causing time to be Iost to both occupational and
leisure activity participation. The importance of strains, or
stretch-induced injuries, is Clear to the clinician in the
occupational or sports medicine practices when one
considers that stretch-induced injuries can account for up to
30% of the typical sport8 medicine practice. 13
There are a variety of noncontact or indirect injuries
that can affect muscle function. Examples include
delayed onset muscle soreness, partial strain injury, and
a com-plete rupture of the muscle. These injuries
represent a continuum of injuries that have one thing in
common: eccentric exercise, when the muscle develops
tension while lengthening. 17.28 In comparison with
concentric contractions, eccentric contractions generate
high forca with fewer active motor units. 23
In delayed onset muscle soreness, eccentric loading,
es-pecially during unaccustomed exercise, results in
micro-scopic damage to the contractile element of muscle
center-ing on what appearg to be random disruptions of
the Z•lines.4 Reversible pain, weakness, and limited range
of motion are the hallmarks of delayed onset muscle sore-
ness. Pain usually peaks 1 to 2 days after exercise2 and
weakness and limited range of motion can persist for over
a week.i1•21 Of particular interest iB the rapid adaptation
of muscle as demonstrated by successive bouts of the un-
accustomed exercise producing progressively less per.
ceived soreness and less tissue damage. 2
A muscle strain injury is characterized by a disruption
of the muscle-tendon unit.5 Localized pain and general
weakne88 of the muscle are seen when activity is at-
tempted. In contrast to the protective aspect8 of delayed
onset muscle soreness, improper rest and rehabilitation
of a minor strain of skeletal muscle frequently precedes a
far more disabling injury, which further increases the
time Iost to work and athletics.
Although muscle strain injuries are 80 freâuently seen,
our understanding of the pathophysiolow, treatment, and
• Address correspondence and reprint requests to William E. Garrett.
Jr.. MD. Box 3435, Duke Universtty Medcal Center, Durham. NC 27710.
William E. Garrett, Jr.: MD, PhD
Durham, North Carolina
recovery of thege injuries is limited, especially when one
compares them to our understanding of damage to liga-
ment, tendon, and bone. We seem to know the least
about that which we see the most. Perhaps the natural
hi8tory, the self-limiting nature, and minimal surgical
require-ments have made these stretch-induced injuries
of less interest to clinicians. The purpose of thi8 brief
review is to discuss 8tretch-induced injuries: the
mechanism of injury, location of injury, treatment, and
some pertinent observa-tions from the clinic.
INJURY MECHANISMS
To reproduce the injury for study in the laboratory, one
needs a basic understanding of how muscles are injured
in sport or occupational settings.
Most cliniciang would
agree that muscle strain injuries
occur when the muscle
is either stretched passively or activated during
stretch.
18'28 Also, eccentric contraction of the muscle
ig a frequent occurrence.9•
Eccentric contraction is an
important factor because muscle forces can be higher dur-
ing lengthening23; this adds to the forces by the paseive,
connective tissue element.3 On the athletic field, muscle
strain injuries occur to "speed athletes" such as sprintere
and participants in such sports ag American football, bas-
ketball, soccer, and mgby. Further, certain mugcles geem
to be more susceptible to injury than otherg, as Will be
shown in this discussion.
My colleagues and I conducted a laboratory 8tudy of
standard techniques in the examination of muscle me-chanics
and electrophysiology of rabbit hindlimb muscles, most often
the tibialis anterior and the extensor digitorum longus
muscles. It was necessary to develop a model for the
reproducible production of an injuw. The initial find-ing was
that activation alone failed to result in either a partial or
complete strain injury.6 To obtain an injury, stretch was
necessary. The forces needed to cause muscle failure were
several times the force normally produced during active
maximal isometric contraction,7 suggesting that passive
forces must be congidered. Therefore, a model of muscle
injury was defined. Intact muscle of the rabbit hindlimb, with
neural and vascular eupply intact, could be stretched to
failure or activated during Btretch.
vol. 24, No. 6, 1996
Injury Resulting From Passive Stretch
Muscles were 8tretched to failure from the proximal or
distal tendon. Of interest is the effect of rate of strain (1, 10,
and 100 cm/sec) and muscle architecture (pennation) or
mechanical properties of the muscle. Regardless of the
strain rate or architecture, the muscle failed at the (most
frequently distal) muscle-tendon junction (Fig. 1), leaving a
small, variable amount of muscle tissue Still attached to
the tendon.6 Thus, the site of stretch-induced injury was
predictably near the muscle-tendon junction, but most
often it was not an avulsion because a variable and small
amount of muscle remained in continuity with the tendon.
Another variable of interest in passive strain is the
influence that muscle length might have on strain. While
mugcle length hag significant importance on a variety of
biomechanical properties, there is a Wide variability of
strain based on the length of the muscle.
Injury Resulting From Active Stretch
Most clinicians would agree that 8train injuries occur during
powerful eccentric contractions; thus, a laboratory condition
to mimic that which is seen clinically was de-vised. Rabbit
hindlimb muscles were isolated as previ-ously described
and 8tretched to failure; however, one of three conditions of
activation—tetanic stimulation, sub-maximal stimulation,
and no stimulation—were applied during stretch. 16 At
failure, the location was, as usual, the muscle-tendon
junction and the total strain at
was
I
Figure 1. Gross appearance of the tibialis anterior muscle of
the rabbit after controlled strain injury. A small hemorrhage is
evident at the distal tip of the injured (left) muscle at 24 hours.
Muscle Strain Injuries
similar among the three conditions. Of interest was that
the force generated at failure was only 15% greater in the
activated muscles; however, the energy absorbed (the
dif• ference in strain energy between passive and active
con-ditions) was about 100% greater in the activated
condition (Fig. 2). This suggests that passive element8 of
muscle have the ability to absorb energy, but this ability
is greatly enhanced when the muscle is activated, which
may also suggest that muscles are able to protect
themselves and joint structures from injury. The more
enerw that the muscle can absorb, the more resistant the
muscle is to injury. Both the passive and contractile
elements of mus-cle contribute to the ability of the
muscle to absorb enero'. The passive elements, which
do not depend on activation, include connective tisgue
and the fibers themselves. The contractile element of the
muscle also participates be-cause activation of the
muscle increases the ability to absorb energy (Fig. 2).
The increase in energy absorbed because of
contraction was previously noted to be about 100%. Any
condition that diminishes the ability of the muscle to
contract also re-duces the ability of the muscle to absorb
enero', making the muscle more susceptible to injury.
Two variables that are commonly cited in muscle strain
injuries are fatigue and weakness.
Injuries That Are Nondisruptive
The preceding discussion was directed at injuries that
resulted in 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 the rabbit hindlimb model, physiologic, mechanical, and
histologic characteristics of muscle can be observed.
Although the model may result in a nondisruptive in-jury,
ultrastructural damage occurs. Histologic section of these
injuries show damage near the muscle-tendon junc-
Stlmulated
Muscle
Force
pae•lw
Length
Figure 2. Energy absorbed is shown as the area under
each length-tension deformation curve. The figure shows
the rel• ative differences in energy absorbed to failure in
stimulated versus passive muscle preparations.
 S4 Garrett

American Journal of Sport8 Medicine

tion with a variable amount of muscle tissue Still attached to 5

the tendon; some hemorrhaging occurs. A pronounced
inflammatory response is seen 1 to 2 days after the injury.
By the 7th day, fibrous tissue begins to replace the inflam-
matory reaction, leading to scar tissue.
4
Such damage to the tissuc 8hould affect the ability of EDL
the muscle to develop tension. Immediately after the in-
jury, the mugcle is able to develop 70% of the norrnal 3 N:IC
amount of tension. Within 24 hours, the muscle'8 ability to
develop tension further declines to 50% of the contralat-
eral control muscle. ñereafter, tension production im-
proved and, by the 7th day, the muscle was able to 1

develop 90% of the tension produce) by it8 contralateral 1

control mugcle.
In contrast, when muscle with a 7-day-old nondisrup-
tive injury was stretched and the tensile strength re-
corded, the tensile strength was only 77% of the control
muscle. Thi8 is well below the 90% of tension developed
o'
that wag just mentioned. As strains are partly caused by
stretch, this logs of tensile strength may make the
muscle morc susceptible to a gecond injury, a scenario
frequently seen by clinicians. Figure 3. Percent increase in length of the extensor
digito. rum longus muscle (EDL) when repeatedly
Viscoelasticity of Skeletal Muscle lengthened to a constant tension.

Important factors in preventing muscle 8train injuries

include flexibility, warmup, and preexercise 8tretching. The
beneficial adaptation caused by stretching has most
frequently been ascribed to stretch-reflex mechanisms. An
additional feature of muscle, viscoelasticity, needs to be
considered. Viscoelasticity can be visualized if one imag-
ines hanging a weight on a muscle and observing its new
length, and then watching the muscle 810wly continue to
increase in length with time. When doing this experiment
with tendons and ligamenta, stretch the tiseue to a con-Stant
length and notice that the tension gradually de-creases with
time. This is referred to as stress-relaxation. Perform thi8
cyclically and a gradual decrease in tension occurs with
each succe88ive stretch.l
A series of studies was designed to determine if similar
features are prevalent in the muscle•tendon unit. Rabbit
hindlimb muscle was 8tretched from an initial force of 1.96
N to 78.4 N, held for 30 seconds, and then returned to the
initial force. This cycle was repeated 10 times (Fig. 3). The
length necessary to reach the predetermined tension in-
creased 3.45% over the 10 cycles, with 80% of thi8 change
in length occurring in the firet four 8tretches.24
Another way to look at the same featurc is to 8tretch
the muecle to 10% above ita resting length and return it
to itg resting length. This cycle was repeated 10 times
(Fig. 4). Tension was reduced by nearly 17% over the 10
cycles, with the bulk of the reduction again occurring in
the first four cycles. 27
What 8hould be obvious is that repetitive 8tretching
reduces the load on the muscle-tendon unit at any given
length. Of particular interest is the absence of reflex ef-fect8
or other mediation by the central nervous system. These
experimente were repeated for innervated and de-nervated
muscle and no differences were apparent for the two
conditions. These data clearly show a large component
100
60
2
40
20
1 2 5 6 8
Figure 4. Muscle tension of the extensor digitorum longus
muscle when repeatedly stretched to the same length
(10% beyond resting length).
of the changes in muscle caused by stretching are a
result of inherent muscle•tendon viscoelasticity with
neural in-fluence. There are additional reflex and central
nervous 8YBtem actions affecting muscle that is being
stretched, especially during physiological movementa.
CLINICAL APPLICATIONS
It iB important to take the findings of laboratory-baged
project8 and apply them to the clinic getting. In the rabbit, it
wag demonstrated that muscle gtrain injuries occur at the
muscle-tendon junction. Would thi8 be the game find-ing in
athletes seen in the clinic? We evaluated acute hamgtring
8train injuries in 10 college athletes within 48 hours of the
injury.8 All athletes were examined clinically and imaged
with CT to determine the mechanism and
vol. 24, No. 6, 1996
location of their injuries. All injuries occurred while either
sprinting or kicking a soccer ball. The injuries were pri-
marily proximal and lateral, typically in the biceps femo-ris
muscle. The common injury mechanigm involved bal-listic
hip flexion and knee extension. fie injured area appeared as
a region of hypodensity by CT scanning, sug-gesting
inflammation and edema, but there was no local-ized
bleeding. To better understand the location of injury,
cadaveric disgections were performed. It appeared that the
long head of the biceps femorig muscle was the most
frequently injured muscle in our sample (9 of 10 athletes).
The injury was localized to the muscle•tendon junction of the
common tendon of the hamstrings. The 10th patient (soccer
player) injured his semimembranosus muscle while kicking
overhead, suggesting a different mechanism than that seen
in the sprinters.
Further imaging studieg were performed on a larger
sample of athletes injured with a variety of mechanigms.
22 Fifty patients underwent CT (N = 27) and magnetic reg.
onance imaging (MRI) (N = 23) to detect muscle 8train
injuries. Injuries were localized to the quadriceps, ham-
string, adductors, and triceps surae muscle groups. The
T2.weighted images were better than Tl-weighted imageg for
visualizing the edema, inflammation, and possible
hemorrhage of muscle strain injuries. The CT scanning
showed the expected areas of low density. Quadriceps
strains were isolated to the rectus femoris muscle. Adduc-
tor strains were confined to the adductor longus muscle. Of
the 17 hamstring strain injuries, 11 were to the bíceps
femori8 muscle, 4 to the semimembranosus muscle, and 2 to
the semitendinosus muscle. All injuries to the triceps surae
group were at the distal muscle-tendon junction of the
medial head of the gastrocnemius muscle.
The effectiveness of both CT and MRI in imaging strain
injuries was demonstrated. Importantly, the particular
muscles susceptible to strain injuries were identified. The
muscles were, predictably, two-joint muscles (biceps fem-
oris, rectus femoriB, gastrocnemius) or th08C of a
complex architecture (adductor longus muscle) and
occurred, as can best be determined by CT and MRI
imaging, at the muscle•tendon junction.
In the clinic, physicians encounter curious, unexplained
muscle injuries such as the persistent strain of the rectus
femoris muscle. We needed to determine, therefore, if our
understanding of the nature of the strain injury was con-
sistent with our understanding of the anatomy of the
rectug femoris muecle. 12 Cadaveric disgection of the
rectus femoris muscle shows a direct head that originates
at the anterior inferior iliac spine and an indirect head
originat-ing from the superior acetabular ridge. The tendon
of the indirect head can extend well into the mase of the
rectug femoris muscle. While prior laboratory work demon-
8trated that most strain injuries occur superficially at the
muscle•tendon junction, clinical evidence pointed to a
strain at the muscle-tendon junction of the deep, indirect
head of the rectug femoris muscle. These are quite differ-
ent from the typically seen injury near the distal tendon
because asymmetry, chronic pain, and anterior thigh
maeses are evident.
Muscle Strain Injuries
We evaluated with physical examination and imaging
studiee 10 patient8 who had an incomplete
intrasubstance strain of the proximal, deep tendon of the
rectug femoris muscle. Patient8 were seen from 4 to 156
weeks postin-jury. Eight of the 10 injuries involved
sprinting or kicking (2 athletes could not recall the
mechanism of injury); all but 1 athlete had pain when
running. Imaging studies detected the strain to be in the
area of the tendon of the indirect head of the rectus
femoris muscle. Surgical explo• ration was performed in
two patient8, with removal of the muscle in one patient
and the exci8ion of a fibrotic mass in the other. Both
patient8 were asymptomatic and returned to full activity.
The reason for chronic pain in these ath-letes was
unknown, but it may be caused by differential activation
of the superficial and deep portiong of the muscle.
Because so many strain injuries seem to depend on the
architecture of the muscle, and after our experiences
noted in Hughes et al.,12 a detailed study of the architec-
ture of the rectus femoris muscle seemed appropriate to
detennine if these persi8tent strains were related to some
curioue architectural feature.10 The rectus femorig
muscle of fresh or embalmed cadavers was dissected.
The super-ficial and deep tendons were confirmed. The
tendon of the deep component penetrated nearly the
entire length of the muscle. It arose from the superior
acetabular ridge and was somewhat medial throughout it8
course through the muscle. The tendon began rounded,
then flattened out, and migrated laterally and wag nearly
vertical in the distal third of the mugcle (Fig. 5). The
pennation of the rectus femoris muscle was more
complex than the simple bipennate arrangement normally
ascribed to the muscle. The proximal third appeared to be
unipennate while the distal two-third8 wag
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 connective tissue
that surrounded the deep tendon. A serous fluid was
collected between the connective tissue and the tendon.
Thie anatomic finding i8 consistent with CT or MRI
images of vascular fibrotic processes of the deep tendon
of the indirect head of the muscle.
A common hamgtring strain
clinically encoun.
tered typically involves one muscle, usually the bicepe
femori8. More extensive injuries involve more than one
muscle, typically at the common tendon of origin of the
hamstring. A unique mechaniem of severe hametring
strain injury involves water 8kier8.20 rme novice skier
assumeg a crouched position before being pulled by the
boat into a standing position. If the skier extende the
knees too soon, the ski is forced down into the water.
Forward momentum of the boat pu118 the skier fomvard,
leading to excessive hip flexion while the knees are ex-
tended. Thie powerful 8tretch leads to either a muscle•
tendon junction
or to a more disabling injury in-
volving avulsion of the tendinoug origin from the ischial
tuberosity. Hamgtring strains algo occur in experienced
skiers secondary to a separate mechanism of falling for-
ward on a single shalom 8ki.
S-6 Garrett
-1 Indirect Head
-J Direct Head
Muscle
O Posterior Fascia
Figure 5. Architecture of the indirect head of the rectus
fem-oris muscle.
We studied 12 water 8kiers with a history of skiing-
induced hamgtring injuries between 0.5 and 18 yearg after
injury.20 All patients realized that they had a significant
injury when the injury occurred. Complete or partial avul-
sion had occurred at the proximal tendon. The extent of
the injury was obvious on physical examination by the
distal tendon retraction of the hamstring muscles and
visible agymmetry. Conservative management of thi8 in-
jury leads to poor prognosis but surgical repair is an
alternative. Seven of the 12 patients in our 8tudy returned
to prior sport8 at a lower level; the Other 5 patients, all
with complete tendon disruptions, were hampered in
sport8 involving running or requiring agility.
Acute groin injuries are also common in sports, espe-
cially in the game of soccer.26 The adductor longus
muscle is commonly injured during hip abduction. Direct
and indirect hernias may algo occur. In addition, there is
an abnormality in the lower abdominal wall musculature
causing a vague and poorly localized pain in the groin.
This pain is noted during high-intensity, ballistic motions
American Journal of Sport8 Medicine
such as kicking a soccer ball or sprinting. It is most com-
mon in high-caliber athletes doing intense training and
competition. The "athletic pubalgia" iB associated with
pain and muscle-tendon injury in the inguinal area near
the attachment of the rectus abdominus muscle to the
pubis, and in the adjacent internal oblique muscles near
the region of abdominal wall weakness noted with direct
inguinal hernias. This pain may exist, however, without
any evidence of herniation. When conservative measures
fail, a herniorrhaphy procedure reinforcing the abdominal
wall musculature can provide excellent relief.
These clinical investigations should be interpreted in
light of basic science studies. Imaging studies and direct
observation demonstrated muscle disruption near the
muscle-tendon junction in common muscle injuries. Dis-
ruption did not occur in the midsubstance of the muscle
fibers. The muscle-tendon unit could also be injured
within the tendon or at the tendon-bone junction. Eccen-
tric activation was the common mechanism of injury, as
the basic science studies suggested.
PREVENTION STRATEGIES
Repetitive Stretch and Failure Properties
The prior work cited suggests that viscoelastic properties
of muscle contribute greatly to changes in muscle length,
and increased length can decrease strain in a muscle. A
more practical question relates to the use of stretching, a
commonly used method to prevent muscle strains. To
study stretching, we used the rabbit model to examine
repeated stretch-release cycle8.25 First, the force to
failure of the hindlimb muscle was determined, then the
con-tralateral muscles were cyclically stretched to 50% or
700/0 of the force to failure. Ten cycles to 50% of failure
force resulted in an increase in muscle stretch at failure
with no change in the force at failure or energy absorbed.
When muscles were cyclically stretched to 70% of failure
force, there was macroscopic evidence of failure even
before the 10 cycles were completed. Thus, cyclic
stretching appears to be beneficial and stretching that
leads to forces in excess of 70% may make the muscle
more, rather than less, likely for injury.
Warmup
Viscoelasticity is known to be temperature-dependent
and warmup is considered to protect against muscle
8traing. We attempted to mimic warmup that was caused
by prior activity as opposed to extemal heating.19 Rabbit
hindlimb muscle was held isometrically and tetanically
stimulated for 10 to 15 seconds, which resulted in a 10C
rise in muscle temperature. The muscle was able to
stretch more before failure and was capable of more
force production. While the changes may be due to
temperature elevation, the effects of stretch cannot be
discounted in spite of the muscle being held
isometrically. A constant length Still must allow for some
8tretch of the mugcle•tendon unit as the fiberg contract
and elastic components become 8tretched.
vol. 24, No. 6, 1996
PRIOR INJURY
There appearg to be n risk of reinjury to a previously
strained muscle. Clinically, patients with a major muscle
strain usually describe a prior minor injury. This would
suggest that, after a minor injury, the mechanical charac-
teristics of the muscle are somehow altered. Such an al•
teration might precipitate a more major injury. To deter-
mine the mechanical characteristics of a muscle with a
minor strain, we studied the extensor digitorum muscle of
rabbits by creating a nondisruptive gtrain by stretching
the muscle just short of tissue rupture.24 Isometric and
isotonic contrnctile properties of the control muscle were
used for comparison. Finally, the muscle was passively
8trctched to failure at a rate of 10 crWmin. The peak
tensilc load and length at that load were derived for use
on the experimental contralateral limb. The length change
to peak load (of the control limb) was duplicated in the ex-
perimental muscle, just short of a disruptive injury. The
injured muscle was then subjected to passive stretch to
failure. Histologic evaluation was performed on the minor
injuries in a subset of rabbit8. In the experimental mus-
cles, the peak load to rupture was 63% of control and the
Icngth at rupture was 790/0 of control. Isotonic shortening
was reduced by 51% and 6% for 100 and 1000 g weights,
respectively. The minor 8train injury caused incomplete
disruptions along the muscle-tendon junction. Thug, a
prior minor injury makes the muscle more gusceptible to
another injury.
This guggests that early retum to activity before com-
plete healing entai)8 a risk for further, more major injuty.
In addition, aggressive rehabilitation designed to return
an athlete to competition may be t.oo stressful for the
muscle, risking further injury. Further, injection for local
pain relief while the muscle is Still injured may not be
appropriate because the lack of inhibition from pain
could result in excessive stress on the muscle, also
increasing the risk of further injury.
FATIGUE
Clinical observation and findings in the literature suggest
that muscle strain injuries occur late in either training
sessions or competitive settings. This leads one to the
conclude that fatigue must play some role in the ri8k of
muscle injury. Mair et al.14 fatigued the extensor digito-rum
longus muscle of rabbits to 25% or 50% of the force of the
contralateral control by cycles of 5-second isometric tetanic
contractions followed by 1 second of rest. The mus-cle was
activated while being pulled (at 1, 10, or 50 cm/sec) to failure.
Similar data were collected on the unfatigued contralateral
control muscle. The force and length at fail-ure were
determined, as was the energy absorbed before failure. There
was a trend toward reduction in force for all groups (8train
rates) tested. The rate of strain did not influence force at
failure. There was no change in muscle length at any of the
strain ratee. There was significantly less enerw absorbed in
both fatigue conditions, with the greatest lose occurring in
the most fatigued muscle. The
Muscle Strain Injuries
reduction in absorbed energy was the greatest when the
muscle was pulled at 1 crn/sec.
The 810wer the rato that the muscle is stretched, the
greater the energy that is absorbed. Muscleg absorb en-ergy
while controlling and regulating limb movcment. These data
indicate that muscles become damaged at the game length,
regardles8 of fatigue. In contrast, fatigued muscle is unable
to absorb enero' before reaching the amount of stretch that
causes injuries. Proper condi-tioning to reduce or delay
fatigue is seen as a part of a rationale for the prevention of
muscle strain injury.
Treatment of Muscle Strain Injuries
The pain of a muscle strain in a patient may prompt
physicians to prescribe antiinflammatory medication in
response to the inflammatory responses known to occur
after an injury. This treatment is largely empirical. Bcfore
Wide use of antiinflammatory medication can be accepted,
the effects of such medication on muscle recovering from an
injury need to be evaluated. Obremsky et ai.16 caused a
strain injury of the tibiali8 anterior muscle in 5() rabbit8
(strain rate of 10 cWmin) that were subsequently admin-
istered piroxicam (16 mgkg) within 6 hours, plus 13 mg/kg
every 6 hours. Forty rabbit8 served as controls and received
no medication. Contractile properties and histol-ogy were
determined at 1, 2, 4, or 7 days after the injury. On Day 1,
there was a significantly greater force in the treated animale.
There was no difference between the treated and untreated
animals on Days 2, 4, or 7. The treated animals showed a
delay in the histologic repair process. The muscles in the
treated anima18 showed de-layed inflammatory cell
infiltration, necrosi8, myotube re-generation, and collagen
deposition. Based on these re-sult8, nonsteroidal
antiinflammatory agents may be of some benefit for the early
treatment of pain control and functional improvement.
However, there was some con-cern regarding long-term
treatment because of the delay in the repair process seen
histologically.
SUMMARY
One of the most common injuries seen in the office of the
practicing physician is the muscle strain. Until recently,
little data were available on the basic science and
clinical application of this basic science for the
treatment and prevention of muscle 8trains. Studies in
the last 10 year8 represent action taken on the direction
of investigation into muscle strain injuries from the
laboratory and clinical fronts.
Pindings from the laboratory indicate that certain mus-
cles are susceptible to strain injury (muscles that croes
multiple jointg or have complex architecture). These mus-
cles have a strain threshold for both passive and active
injury. Strain injury is not the result of mugcle contraction
alone, rather, strains are the result of excessive 8tretch or
stretch while the muscle is being activated. When the
muscle tears, the damage is localized very near the mus-cle-
tendon junction. After injury, the muscle is weaker and at
risk for further injury. The force output of the
S-8 Garrett American Journal of Sports Medicine

muscle returns over the following days as the muscle 2. Clancson PM. Newham DJ: Associatms beueen musde soreness,
dam• and fatigue. Adv Exp Med Biol 384:457-469, 1995
3. Elttman H: Biomechancs of muscle. J 1966
undertakes a predictable progression toward tissue Bmeunt Surg 48A:363 —377,
4. Fiden J. Lieber R': Structuml and mechanml basis o'exercise -induced
healing.
Current imaging studies have been used clinically to musde nury. Med Sci spotÉ Exem 24:521-530, 1992
document the Bite of injury to the muscle•tendon 5. Garrett WE Jr: Muscle strain injuries: Clinical aM basic aspects.
junction. The commonly injured muscles have been spotE Exerc 22:436-443, 1990 Sd
described and include the hamstring, the rectus femori8, 6. Garrett WE Jr. Almekjnders L, Seaber AV: Biomecrunbs of muscle toare
gastrocnemius, and adductor longus muscleg. Injuries
and stretchiongmeinjuries,biomechanicalTransOfthmfailure RespropertiesSoc9:of384, 1984
inconsistent with involvement of a single muscle-tendon
junction proved to be at tendinous origins rather than 7. Garren WE Jr. Nikolaou PK, Ribbeck BM. et a': TM enect 01 muscJe
within the muscle belly. Important information has also musde
been provided re-garding injuries with poor prognosis, under passive extension. Am J Sputs Med 16: 7—12, 1988
which are poten-tially repairable gurgically, including hamsfring musde strairs.
injuries to the rectus femori8 muscle, the hamstring 8. Garrett WE Jr. Rich FR. Nikolaou Pt<. et al: Computed tomography of
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New data can algo be applied to the field with respect tecture. Am J Spott Med Z: 493-499. 1995
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12. Hughes C. Hassünan CT IV, Best TM. et a': l'Eonvlete, intrasubstance
injury to the muscle. Fortunately, many of the factors
protecting mus-cle, such as 8trength, endurance, and strah injuries o' the rectus femois. Am J A.%d 23:500—506. 1995
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of function, but aleo the
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ACKNOWLEDGMENTS 16. Obromsiv WT. Seaber AV. Ribbed« BM, et a':
logica: assessment ot a controlJed muscie strain injury treatedandwithhistopiroxi•-cam AmJ

fris research agenda could not have been conducted with- 17. Peterson L, RenstromMedZP:.•558Spons-561,Injuries:1994Thelr
out the able agsi8tance of and Treatnent.
the following colleagues: Chicago. Yearbook PuN8hers. 1986
Louie Almekinders, Frank Bassett, Tom Best, James 18. Radin EL Simon SR. Rose R". et al: br the
Dalton, Rich Gli880n, Carl Hasselman, Chad Hughes,
OümaedÊ SUf9"'. New York, John Wiley, 1979
John Iahnes, Scott Mair, Pantelis Nikolaou, Tom Noonan,
Wil-liam Obremsky, Ross Rich, Marc Safron, Peter 19. Safran MR. Gantt WE Jr. Suber AV. et al: The role of wamup in
Sallay, Tony Seaber, Kevin Speer, and Dean Taylor. I musaNar iNu" pmenthn. Am J Abd 16: 123—129. 1988
also ac-knowledge the asai8tance of Don Kirkendall in 20. Sanay Pl, FñedtDM' n, et a'; Hamstring injuries among
the prep-aration of this manuscript. water skiers. FuMional outcome and prwenbon. Am J
24:
130-136. 1996
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