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Muscle strain injuries

Article  in  Current Opinion in Rheumatology · April 2000

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Muscle strain injuries
Tero A.H. Järvinen,*† Minna Kääriäinen,*† Markku Järvinen, MD, PhD,*††
and Hannu Kalimo‡
Muscle injuries–lacerations, contusions or strains–are by far
the most common injuries in sports. After first aid following the
RICE principle (Rest, Ice, Compression and Elevation), therapy
must be tailored according to the severity of the injury and
based on the knowledge gained from experimental studies on
regeneration of injured muscle. Most muscle injuries can be
treated conservatively with excellent recovery, but complete
ruptures with complete loss of function should be managed
surgically. Immediately after the injury, a short period of immo-
bilization is needed to accelerate formation of the scar
between the stumps of the ruptured myofibers, to which the
stumps adhere. The optimal length of immobilization depends
on the grade of the injury, and should not be longer than
needed for the scar to bear the pulling forces without rerup-
ture. Early mobilization is required to invigorate adhesion,
orientation of the regenerating muscle fibers, revascularization
and resorption of the connective tissue scar. Another impor-
tant aim of early mobilization, especially in clinical sports medi-
cine, is to minimize inactivity-induced atrophy as well as loss of
strength and extensibility, which are rapidly appearing adverse
sequelae of prolonged immobilization. Curr Opin Rheumatol 2000,
12:155–161 © 2000 Lippincott Williams & Wilkins, Inc.
*Section of Orthopaedics, Department of Surgery, Tampere University Hospital,
Tampere, Finland; †Medical School and Institute of Medical Technology,
University of Tampere, Tampere, Finland; ‡Department of Pathology, Turku
University Hospital and University of Turku, Turku, Finland
Correspondence to Prof. Markku Järvinen, MD, PhD, Department of Surgery,
Tampere University Hospital, P.O. Box 2000, FIN-33520 Tampere, Finland;
e-mail: markku.jarvinen@uta.fi
Current Opinion in Rheumatology 2000, 12:155–161
Abbreviations
ECM extracellular matrix
MTJ myotendinous junction
NMJ neuromuscular junction
NSAIDs nonsteroidal anti-inflammatory drugs
ISSN 1040–8711 © 2000 Lippincott Williams & Wilkins, Inc.
Muscle strain injury
Muscle injuries are the most common injury in sports,
their incidence varying from 10 to 55% of all injuries
sustained in sport events [1,2]. The majority of muscle
injuries (more than 90%) are caused either by contu-
sion or by excessive strain of the muscle. Distraction
strain occurs in a muscle on which an excessive pulling
force is applied, resulting in overstretching. Strain
injuries are especially common in sports that require
sprinting or jumping [1,3]. These injuries are often
located near the myotendinous junction (MTJ) of the
superficial muscles working across two joints, such as
the rectus femoris, semitendinosus, and gastrocnemius
muscles [1].
Diagnosis of muscle injuries
Clinical examination begins with inspection and careful
palpation of the involved muscles. The function of the
injured muscles should also be tested both with and
without resistance. Diagnosis is simple when a history of
strain is accompanied by objective evidence of swelling.
Small hematomas and those deep within the muscle are
more difficult to diagnose clinically. Their dimensions
can be determined by ultrasonography, computed
tomography, or magnetic resonance imaging [4]. Based
on the current knowledge, ultrasonography can be
recommended as the method of choice for the diagnosis
of the muscle injury [4,5]. If there is a clear discrepancy
between the physician’s subjective and clinical findings
and the ultrasonography, the use of magnetic resonance
imaging should be considered, especially in the groin
area as well as in injuries close to the MTJ [6].
Clinical classification of muscle strains
The clinical manifestation of a muscle strain depends on
the severity of the injury and on the nature of the
hematoma. Muscle strains are classified in three cate-
gories according to their severity: (1) Mild (first degree)
strain: a tear of a few muscle fibers; minor swelling and
discomfort with no or only minimal loss of strength and
restriction of the movements; (2) Moderate (second
degree) strain: a greater damage of muscle with a clear
loss of strength; (3) Severe (third degree) strain: a tear
extending across the whole muscle belly, resulting in a
total loss of muscle function.
Muscle strain often results in a large hematoma, because
the intramuscular blood vessels are torn. In the injured
155
156 Nonarticular rheumatism, sports-related injuries, and related conditions
muscle, two different types of hematomas can be identi-
fied: (1) Intramuscular: Intact muscle fascia limits the
size of the hematoma. In this case, the extravasation of
blood increases the intramuscular pressure, which
compresses and finally limits the size of hematoma.
Clinical findings are pain and loss of function; (2)
Intermuscular hematomas develop if the muscle fascia is
ruptured and the extravasated blood spreads into the
intermuscular spaces without a significant increase in
the pressure within the muscle. The patient may not
experience major pain as long as pressure in the injured
area does not increase.
The pathobiology of the muscle injury
The damage caused by the strain of the skeletal muscle
is classified as a shearing injury (Figs. 1, 2). In shearing
injury, not only the myofibers but also the mysial
sheaths are torn [7]. The repair process of the shearing
injury can be divided into three phases: (1) the destruc-
tion phase, which is characterized by hematoma forma-
tion, myofiber necrosis, and inflammatory cell reaction:
(2) the repair phase, consisting of phagocytosis of the
necrotized tissue, regeneration of the myofibers, produc-
tion of connective tissue scar, and capillary ingrowth; (3)
the remodeling phase, which consists of maturation of
the regenerated myofibers, contraction and reorganiza-
tion of the scar tissue, and restoration of the functional
capacity of the repaired muscle (Fig. 2) [7]. Repair and
remodeling often occur simultaneously.
Figure 1. A schematic picture of the healing skeletal muscle
The ruptured myofibers contract and the gap between the stumps (central zone,
cz) becomes at first filled by a hematoma. Myofibers are necrotized within their
basal lamina over a distance of about 1–2 mm, within which segment complete
regeneration usually occurs (regeneration zone, rz). Beyond that only reactive
changes are observed in the survival zone (sz).
Each myofiber is innervated at a single point of neuromuscular junction (NMJ,
black dots). Because myofibers are usually ruptured on either side of the row of
NMJs in adjacent fibers, the adjunctional stumps of fibers 1 and 3–5 on the right
“ad” side remain innervated, whereas their abjunctional stumps on the left “ab”
side become denervated. Even the adjunctional stump of fiber 2 has become
denervated because its NMJ is located in the rz. Reinnervation of the abjunc-
tional stumps occurs via penetration of new axon sprouts through the scar of cz
and formation of the new NMJs (here shown as one sprout and NMJ [white dot]).
Fiber 2 becomes reinnervated when regeneration in the adjunctional rz takes
place.
Figure 2. A schematic presentation of a shearing injury of
skeletal muscle
Day 2: The necrotized part of the transected myofibers is being removed by
macrophages. Connective tissue formation by fibroblasts has begun in the
central zone. Day 3: Satellite cells have become activated into myoblasts within
the basal lamina cylinders in the regeneration zone. Day 5: Myoblasts in the
regeneration zone have fused into myotubes. The connective tissue in the central
zone has become denser. Day 7: The regenerating muscle cells extend out of
the old basal lamina cylinders into the central zone and begin to pierce through
the scar. Day 14: The scar of the central zone has further condensed and the
regenerating myofibers have nearly crossed the gap of the central zone. Day 21:
The scar is formed between the interlacing myofibers with little intervening
connective tissue.
Destruction phase
Rupture of muscle after the strain
The site of rupture of an otherwise healthy muscle
occurs close to its distal MTJ after the strain [1,8]. The
ruptured myofibers contract and a gap is formed
between the stumps. Because skeletal muscle is richly
vascularized, hemorrhage from the torn vessels is
inescapable and the gap becomes filled with a
hematoma, later replaced by scar tissue (Figs. 1,2). The
contraction status of the muscle significantly modifies
the extent of injury, because the capacity of the muscle-
tendon unit to resist stretching is directly related to the
tension of the muscle: in contracted muscle nearly twice
as great a force as in relaxed muscle is needed to cause
rupture [1,8]. Besides, in contracted muscle the rupture
is more superficial than in relaxed muscle. In the latter,
the rupture is usually adjacent to the underlying bone,
because the pressure is transmitted to the deeper
muscle layers, where the muscle is then compressed
against the bone surface [1,8].
Necrosis of myofibers
In shearing injuries the mechanical force tears the entire
myofiber (Fig. 1), damaging the myofiber plasma
membrane and leaving sarcoplasm open at the ends of
the stumps. Because myofibers are very long, string-like
cells, the necrosis initiated at this site extends all along
the whole length of the ruptured myofiber, unless the
spread of necrosis is stopped within some hours after the
injury by a “fire door,” ie, by condensation of cytoskele-

tal material to form the so-called contraction band,
which can limit the necrosis to a local process of about
1.5–2 mm in length (regeneration zone) (Fig. 1) [7].
Inflammation
The blood vessels are also torn in shearing injuries; thus,
blood-borne inflammatory cells gain immediate access
to the injury site [9] (Fig. 2). Later, substances released
from the necrotized parts of myofibers serve as chemoat-
tractants for further extravasation of inflammatory cells
[9]. Macrophages and fibroblasts within the injured
myofibers are also activated and provide additional
chemotactic signals (eg, growth factors) to circulating
inflammatory cells [9,10]. In the acute phase, polymor-
phonuclear leukocytes predominate but are soon
followed by monocytes, which are transformed into
macrophages actively engaged in proteolysis and phago-
cytosis of the necrotic material (Fig. 2) [9,11].
Remarkably, the basal lamina surrounding the necro-
tized part of the injured myofiber is resistant to the
attack of macrophages; it remains intact and serves as a
scaffold inside which the viable satellite cells begin the
formation of new myofibers [11].
An additional complication of muscle injuries is the
damage of the intramuscular nerve branches, which leaves
the whole muscle or parts of it denervated (Fig. 1) [7,12].
Repair and remodeling phase
The healing of muscle strain consists of two simultane-
ous processes: (1) regeneration of the damaged
myofibers and nerves, and (2) formation of a connective
tissue scar. These two processes are at the same time
supportive but also competitive with each other [7,13].
Regeneration of myofibers
Although myofibers are considered to be irreversibly
postmitotic, the marked regenerative capacity of skele-
tal muscle has been guaranteed already during fetal
development by the setting aside of undifferentiated
reserve cells called satellite cells, which lie underneath
the basal lamina of each individual myofiber (Fig. 3).
There are two different populations of satellite cells in
skeletal muscle [14]. One population, called committed
satellite cells, is ready to begin differentiation to
myoblasts immediately after the injury, whereas the
other population, stem satellite cells, undergoes cell
division(s) before differentiation. By proliferation the
latter population at the same time replenishes the
reserve of satellite cells for future episodes of regenera-
tion [14]. Thus, satellite cells proliferate within the
preserved basal lamina of the regeneration zone, differ-
entiate to myoblasts, and thereafter fuse with each other
into multinucleated myotubes. They also fuse with
surviving parts of the injured myofiber. Finally, the
regenerating parts of myofibers acquire their mature
Muscle strain injuries Järvinen et al. 157
Figure 3. A schematic presentation of fetal development and
regeneration of myofibers via the activation of satellite cells
Satellite cells (A2-B2-C-D or A3-B3-C-D) have been set aside underneath the
basal lamina during fetal development (A2 and a3), to be used in growth and
repair. After injury, committed satellite cells (csc) immediately begin differentia-
tion into myoblasts (mb) without prior cell division (B2), whereas the stem satel-
lite cells (ssc) first divide and thereafter one of the daughter cells differentiates
into a myoblast (B3) and the other one replenishes the pool of stem satellite
cells (B4). Myoblasts fuse into myotubes (mt), which then grow and mature into
myofibers, the sarcoplasm of which becomes filled with contractile filamentous
proteins organized in myofibrils and with myonucei located subsarcolemmally.
mpc, myogenic precursor cell.
form with cross-striated bundles of myofilaments and
peripherally located myonuclei [11].
After regenerating myofibers have filled the old basal
lamina (Fig. 2), they extend out of the opening of the
basal lamina to the connective tissue scar. The emerging
muscle cells form multiple branches, tips of which have
the structure of a growth cone [15]. These try to pierce
through the scar, but after having extended only a rela-
tively short distance from the opening of the basal
lamina, the tips begin to adhere to the connective tissue
by forming mini-MTJs. It is known that the intervening
scar progressively diminishes in size, and thus the
stumps are brought closer to each other.
Myofiber regeneration continues to the myotube phase
without nerve supply, after which atrophy follows, if
reinnervation is not accomplished (Fig. 1) [12]. If the
axons rupture (neurogenic denervation), the reinnerva-
tion requires growth of new axons distal to the rupture.
On the other hand, because myofibers are innervated at
a single neuromuscular junction (NMJ), rupture usually
creates an adjunctional stump with preserved contact
with the NMJ, and an abjunctional stump which has
become “myogenically” denervated. Reinnervation of
the abjunctional myofiber stumps requires sprouting of
the healthy axons, their penetration across the scar
tissue, and the formation of new NMJs on the dener-
vated myofiber stump (Fig. 1) [12].
158 Nonarticular rheumatism, sports-related injuries, and related conditions
Formation of the connective tissue scar
The gap between the ruptured muscle fibers is filled by
a hematoma. Within the first day the hematoma is
invaded by inflammatory cells, including phagocytes,
which begin disposal of the blood clot [9,15]. Blood-
derived fibrin and fibronectin cross-link to form a
primary matrix, which acts as a scaffold and anchorage
site for the invading fibroblasts and gives the initial
strength to the scar to withstand the forces applied on it
(Fig. 2). Fibroblasts begin to synthesize proteins as well
as proteoglycans of the extracellular matrix (ECM)
[16–19]. Fibronectin is expressed among the first ECM
proteins, followed by type III collagen. The production
of type I collagen is activated later and remains elevated
for several weeks [16–19].
From the time of injury until days 10–12, the scar is the
weakest point of the injured muscle [20•], but thereafter
the rupture occurs within myofibers next to the newly
formed mini-MTJs [26]. Subsequently, increase in the
tensile strength of the scar takes place simultaneously
with the production of type I collagen [17,20]. The
mechanical stability of the collagen, in turn, is based on
the formation of intermolecular cross-links [21]. After
maturation of the scar, rupture usually occurs within the
regenerating myofibers near the proximal/distal attach-
ment line to the scar (ie, next to the newly formed mini-
MTJs). However, the scar and the muscle do not reach
normal strength until weeks after the injury, indicating
that a long time is needed until the strength of the
muscle is completely restored [13,20,22].
Connective tissue transmits contraction forces across the
gap, allowing the use of the injured limb before the
repair process is completed. However, proliferation of
fibroblasts can rapidly lead to an excessive formation of
scar tissue, creating a mechanical barrier that restricts
and delays regeneration of muscle and nerve fibers
across the injury gap [13,22]. An attempt should be
made to prevent this by limiting the size of the
hematoma by adequate immediate treatment of the
injured muscle (see below).
Vascularization of the injured muscle
The key step in the regeneration of injured muscle
tissue is the vascularization of the injured area [7,23–25].
The restoration of vascular supply is a prerequisite for
the regeneration of injured muscle [23]. The new capil-
laries sprout from surviving trunks of blood vessels and
pierce toward the center of injured area [23], providing
adequate oxygen supply in the regenerating area [24].
Young myotubes have only a few mitochondria and a
moderate aerobic metabolism, but strongly increased
activity of anaerobic metabolism [25]. However, aerobic
metabolism is the major energy pathway during the final
regeneration of multinucleated myofibers [25]. Therefore,
the regeneration of muscle fibers does not progress from
the myotube stage unless capillary ingrowth provides
enough oxygen for aerobic metabolism [23,25].
Adhesion of myofibers to the extracellular matrix
In normal skeletal muscle, the ends of each fiber are
attached to either a tendon or a fascia by specialized
MTJs, constructed to withstand considerable loads. The
binding of the myofibers (in essence of the sarcoplasmic
contractile myofilaments) to the ECM is mediated by
two main chains of molecules: (1) an integrin, and (2) a
dystrophin-associated chain [7,26,27••].
When myofibers are breached, the upregulation of inte-
grin-associated molecules appears to be the “first aid” in
reestablishing adhesion between myofibers and ECM.
Integrin-associated molecules are incorporated in the
plasma membrane along the sides of the breached
fibers, which reinforces lateral adhesion to surrounding
endomysium at the early phase, when the tips of the
stumps are still growing into the scar tissue [27••].
Later, and most important, mini-MTJs are formed at the
tips of regenerating stumps with clustering of integrin-
associated and dystrophin-associated molecules at these
new mini-MTJs [7,27••]. At the same time, dystrophin-
associated molecules become responsible for lateral
adhesion in the regeneration zone. Thus, strong termi-
nal adhesions employing exactly the same adhesion
molecules as normal MTJs are established at the ends of
the stumps [27••]. Thus the single (preinjury) tendon-
myofiber-tendon unit becomes replaced by two units of
tendon-muscle-mini-MTJ units separated by the scar;
whether myofibers will ever be able to fuse across the
scar is not known.
Effects of immobilization and remobilization
on the healing process
Current opinion is that early mobilization is the method
of choice in the treatment of muscle ruptures [2]. Early
mobilization induces more rapid and intensive capillary
ingrowth to injured area, as well as better muscle fiber
regeneration and orientation than other forms of
therapy [2,13,23]. More important, the functional prop-
erties of injured muscle return sooner to the normal
level [22].
Mobilization started immediately after the injury often
causes reruptures at the original injury site. However,
reruptures can be avoided by immobilizing the injured
muscle immediately after the injury [13,17,21,22].
Immobilization allows the newly formed granulation
tissue to reach sufficient tensile strength to withstand
the forces created by contracting muscle [17,22].
Although short immobilization is beneficial in the
early phase of muscle regeneration, long immobiliza-

tion causes significant atrophy of healthy myofibers
and has a tendency to reduce the tensile strength
[13,17,22]. Therefore, the immobilization period
should be kept as short as possible, ie, only the first
few days immediately after the injury [2]. Active mobi-
lization started right after the first few days provides
ideal conditions for regeneration and the best final
outcome [2,13,17,22].
Deciding upon the right time to start active remobiliza-
tion after the muscle strain can be difficult for the physi-
cian. This decision can, however, be based on two
simple and inexpensive measures: the ability to stretch
the injured muscle as much as the healthy contralateral
muscle, and the pain-free use of injured muscle in basic
movements. When this critical point is reached, the
patient should be encouraged to start active, progressive
mobilization [2,6].
Treatment of muscle injuries
Immediate treatment
The immediate treatment for muscle strain is known as
the RICE principle: Rest, Ice (cold), Compression, and
Elevation. These four procedures have the same objec-
tive: to minimize bleeding from ruptured blood vessels to
rupture site. This will prevent the formation of a large
hematoma, which has a direct impact on the size of scar
tissue at the end of the regeneration. A small hematoma
and the limitation of interstitial edema accumulation on
the rupture site also shorten the ischemic period in the
granulation tissue, which in turn accelerates regeneration.
After the initial treatment during the first few days, the
contractile status of the injured muscle should be re-
examined. If it has not improved from the original
postinjury level, the possibility of large intramuscular
hematoma or total rupture of the muscle should be
suspected. Measurement of intramuscular pressure,
puncture and aspiration of the injured area (if fluctua-
tion is present), ultrasonography or magnetic resonance
imaging examination, and sometimes even surgical
intervention may be necessary.
Compression
A compression bandage reduces the size of an intramus-
cular hematoma [28]. Compression should be applied
immediately after the muscle injury (in the field), even in
cases when injury is just suspected (diagnosis can await
the immediate care!). Together with the compression,
cold should be applied to the injured area (ice packs),
and should last for 15 to 20 minutes and be repeated at
intervals of 30 to 60 minutes. Experimentally, early
cryotherapy has beneficial effects: it is followed by a
significantly smaller hematoma between ruptured
myofiber stumps, less inflammation, and somewhat
accelerated regeneration [29].
Muscle strain injuries Järvinen et al. 159
Elevation of the injured extremity decreases blood flow
to the injury site and increases venous return, thus further
limiting the size of the hematoma. The rest period
provides an adequate immobilization period and should
last 1 to 5 days, depending on the severity of injury. Use
of crutches is recommended in severe injuries, as well as
when injuries are located at sites (like the groin area)
where immobilization can not be otherwise attained [6].
Nonsteroidal anti-inflammatory drugs
Nonsteroidal anti-inflammatory drugs (NSAIDs) should
be a part of early treatment and should be started imme-
diately after the injury [30–34•]. Short-term use of
NSAIDs in the early phase of healing decreases the
inflammatory cell reaction [31], and has no adverse effects
on tensile or contractile properties of injured muscle
[31,33]. Although the use of NSAIDs in the treatment of
muscle injuries can be recommended [30–34•], glucocor-
ticoids lead to a delayed elimination of hematoma and
necrotic tissue as well as retarded muscle regeneration.
Therefore, their use is contraindicated [31,35•].
Therapeutic ultrasound
Therapeutic ultrasound is widely recommended and
used in the treatment of muscle strains, although no
clinical evidence exists on its effectiveness.
Experimental studies are not encouraging: although
therapeutic ultrasound promotes the proliferation phase
of myoregeneration, it does not have a significant effect
on the final outcome [36•].
Hyperbaric oxygen
Experimentally, adequate restitution of the blood
supply to the injured area is the first sign of the regener-
ation and the requirement for restoration of injured
muscle [23–25]. Indeed, it was recently presented in
rabbits that hyperbaric oxygen therapy during the early
phase of the repair substantially improves the final
outcome [37••]. Clinical studies to prove the efficacy of
hyperbaric oxygen therapy in the treatment of soft
tissue injuries in sports are still lacking, but this therapy
is a fascinating possible option to speed up muscle
regeneration [37••,40].
Operative treatment
Surgical treatment of muscle injuries should be reserved
for the most serious injuries, because in most cases conser-
vative treatment results in a good outcome. Surgical treat-
ment is indicated only in cases of (1) large intramuscular
hematomas, (2) third-degree strains or tears of muscles
with few or no agonist muscles, and (3) second-degree
strains, if more than half of the muscle belly is torn [6,38].
Experimental studies suggest that in the most severe
cases, the operative treatment may be of benefit
[32••,38], especially when the gap (diastasis) between
160 Nonarticular rheumatism, sports-related injuries, and related conditions
the stumps is long. By surgically bringing the stumps
closer to each other, the surgeon improves circum-
stances [20•,32••,38]. Surgery can eliminate the devel-
opment of extensive scar tissue within the muscle tissue
and facilitate the reinnervation of the myogenically
denervated stumps (see above) [32••].
Treatment after 3 to 5 days
After the primary treatment, 3 to 5 days after the injury,
lesser partial ruptures and intramuscular hematomas
should be supported with elastic bandage and early
mobilization of the injured muscle carefully started in
the following order:
1. First, isometric training without load, and later
with increasing load within the limits of pain.
2. Cautious and controlled isotonic training with and
without load. Isokinetic dynamic training with
minimal load can also be started early (requires
special equipment).
3. Local heat or contrast treatment (ie, alternating
cold and heat) may be of value, accompanied with
careful passive and active stretching of the affected
muscle within the limits of pain.
A carefully structured rehabilitation program accelerates
recovery. All physical rehabilitation activities should
start with warming-up of the injured muscle, which
reduces muscle viscoelasticity and relaxes muscles
neurally. Stimulated (warm) muscles absorb more energy
during physical exercise than unstimulated muscles and,
thus, the risk of reruptures is reduced [1,39]. The other
purpose of the stretching is to distend the scar tissue
while it is still plastic. Painless elongation can be gradu-
ally achieved by stretching at first for 10 to 15 seconds,
with gradual prolongation up to 1 minute. It is important
that the patient always warm up before stretching. This
will minimize the risk of reruptures [1,39].
References and recommended reading
Papers of particular interest, published within the annual period of review,
have been highlighted as:
• Of special interest
•• Of outstanding interest
1 Garrett WE: Muscle strain injuries. Am J Sports Med 1996, 24:S2–S8.
2 Järvinen M, Lehto MUK: The effect of early mobilization and immobilization
on the healing process following muscle injuries. Sports Med 1993,
15:78–89.
3 Crisco JJ, Jokl P, Heinen GT, Connell MD, Panjabi MM: A muscle contu-
sion injury model: biomechanics, physiology, and histology. Am J Sports
Med 1994, 22:702–710.
4 Thorsson O, Lilja B, Nilsson P, Westlin N: Comparing ultrasonography,
magnetic resonance imaging and scintigraphy in evaluating an experimentally
induced muscular hematoma. Scand J Med Sci Sports 1993, 3:110–116.
5 Thorsson O, Lilja B, Nilsson P, Westlin N: Ultrasound examination of soft
tissue injury of the lower limb in athletes. Am J Sports Med 1993,
20:601–603.
6 Kujala U.M, Orava S, Järvinen M: Hamstring injuries: Current trends in treat-
ment and prevention. Sports Med 1997, 23:397–404.
7 Kalimo H, Rantanen J, Järvinen M: Muscle injuries in sports. Bailliere’s Clin
Orthop 1997 (special issue), 2:1–24.
8 Garrett WE Jr, Safran MR, Seaber AV, Glisson RR, Ribbeck BM:
Biomechanical comparison of stimulated and nonstimulated skeletal
muscle pulled to failure. Am J Sports Med 1987, 15:448–454.
9 Tidball JG: Inflammatory cell response to acute muscle injury. Med Sci
Sports Exercise 1995, 27:1022–1032.
10 Cantini M, Carraro U: Macrophage-released factor stimulates selectively
myogenic cells in primary muscle cultures. J Neuropath Exp Neurology
1995, 54:121–128.
11 Hurme T, Kalimo H: Activation of myogenic precursor cells after muscle
injury. Med Sci Sports Exercise 1992, 24:197–205.
12 Rantanen J, Ranne J, Hurme T, Kalimo H: Denervated segments of injured
skeletal muscle fibres are reinnervated by newly formed neuromuscular
junctions. J Neuropath Exp Neurol 1995, 54:188–194.
13 Järvinen M: Healing of a crush injury in rat striated muscle. 2. A histological
study of the effect of early mobilization and immobilization on the repair
processes. Acta Pathologica Microbiologica Scand 1975, 83A:269–282.
14 Rantanen J, Ranne J, Hurme T, Kalimo H: Satellite cell proliferation and
expression of myogenin and desmin in regenerating skeletal muscle:
evidence for two different populations of satellite cells. Lab Invest 1995,
72:341–347.
15 Hurme T, Kalimo H, Lehto M, Järvinen M: Healing of skeletal muscle injury.
An ultrastructural and immunohistochemical study. Med Sci Sports
Exercise 1991, 23:801–810.
16 Hurme T, Kalimo H, Sandberg M, Lehto M, Vuorio E: Localization of type I
and III collagen and fobronectin production in injured gastrocnemius
muscle. Lab Invest 1991, 64:76–84.
17 Lehto M, Duance VC, Restall D: Collagen and fibronectin in a healing
skeletal muscle injury: an immunohistochemical study of the effects of
physical activity on the repair of injured gastrocnemius muscle in the rat. J
Bone Joint Surg 1985, 67B:820–828.
18 Lehto M, Järvinen M: Collagen and glycosaminoglycan synthesis of injured
gastrocnemius muscle in rat. Eur Surg Res 1985, 17:179–185.
19 Lehto M, Järvinen M, Nelimarkka O: Scar formation after skeletal muscle
injury: A histological and autoradiographical study in rats. Arch Orthop
Trauma Surg 1986, 104:366–370.
20 Kääriäinen M, Kääriäinen J, Järvinen TLN, Sievänen H, Kalimo H, Järvinen
• M: Correlation between biomechanical and structural changes during the
regeneration of skeletal muscle after laceration injury. J Orthop Res 1998,
16:197–206.
Comparison of biomechanics and morphology in injured skeletal muscle.
21 Lehto M, Sims TJ, Bailey AJ: Skeletal muscle injury: molecular changes in
the collagen during healing. Res Exp Med 1985, 185:95–106.
22 Järvinen M: Healing of a crush injury in rat striated muscle. 4. Effect of early
mobilization and immobilization on the tensile properties of gastrocnemius
muscle. Acta Chirurgica Scand 1976, 142:47–56.
23 Järvinen M: Healing of a crush injury in rat striated muscle. 3. A microangio-
graphical study of the effect of early mobilization and immobilization on
capillary ingrowth. Acta Pathologica Microbiologica Scand 1976,
84A:85–94.
24 Józsa L, Reffy A, Demel Z, Szilagyi I: Alterations of oxygen and carbon
dioxide tensions in crush-injured calf muscles of rat. Zeitschrift
Experimentelle Chirurgie 1980, 13:91–94.
25 Järvinen M, Sorvari T: A histochemical study of the effect of mobilization
and immobilization on the metabolism of healing muscle injury. In Sports
Medicine. Edited by Landry F, Orban WAR. Miami: Symposia Specialists,
1978:177–181.
26 Hurme T, Kalimo H: Adhesion in skeletal muscle regeneration. Muscle
Nerve 1992, 15:482–489.
27 Kääriäinen M, Kääriäinen J, Järvinen TLN, Nissinen L, Heino J, Järvinen M,
•• Kalimo H: Integrin and dystrophin associated adhesion protein complexes
have complementary functions during regeneration of shearing-type muscle
injury. Neuromusc Dis 1999, in press.
Description of the adhesion of injured muscle fibers to the scar.

28 Thorsson O, Hemdal B, Lilja B, Westlin N: The effect of external pressure
on intramuscular blood flow at rest and after running. Med Sci Sports
Exercise 1987, 19:469–473.
29 Hurme T, Rantanen J, Kalimo H: Effects of early cryotherapy in experimental
skeletal muscle injury. Scand J Med Sci Sports 1993, 3:46–51.
30 Almekinders LC: Anti-inflammatory treatment of muscular injuries in sports.
Sports Med 1993, 15:139–145.
31 Järvinen M, Lehto M, Sorvari T, Mikola A: Effect of some anti-inflammatory
agents on the healing of ruptured muscle: an experimental study in rats. J
Sports Traumatol 1992, 14:19–28.
32 Menetrey J, Kasemkijwattana C, Fu FH, Moreland MS, Huard J: Suturing
•• versus immobilization of a muscle laceration: a morphological and func-
tional study in a mouse model. Am J Sports Med 1999, 27:222–229.
Excellent study on the operative treatment of muscle injury.
33 Obremsky WT, Seaber AV, Ribbeck BM, Garrett WE Jr: Biochemical and
histological assessment of a controlled muscle strain injury treated with
piroxicam. Am J Sports Med 1994, 22:558–561.
34 Thorsson O, Rantanen J, Hurme T, Kalimo H: Effects of nonsteroidal anti-
• inflammatory medication on satellite cell proliferation during muscle
contraction. Am J Sports Med 1998, 26:172–176.
NSAIDs in the early phase of the muscle regeneration.
View publication stats
Muscle strain injuries Järvinen et al. 161
35 Beiner JM, Jokl P, Cholewicki J, Panjabi MM: The effects of anabolic
• steroids and corticosteroids on healing of muscle contusion injury. Am J
Sports Med 1999, 27:2–9.
Description of the effects of anabolic steroids and corticosteroids in the injured
skeletal muscle.
36 Rantanen J, Thorsson O, Wollmer P, Hurme T, Kalimo H: Effects of thera-
• peutic ultrasound on the regeneration of skeletal muscle myofibers after
experimental muscle injury. Am J Sports Med 1999, 27:54–59.
A study on the therapeutic ultrasound in the treatment of skeletal muscle injury.
37 Best TM, Loitz-Ramage B, Corr DT, Vanderby R Jr: Hyperbaric oxygen in
•• the treatment of acute muscle stretch injuries: results in an animal model.
Am J Sports Med 1998, 26:367–372.
A study of hyperbaric oxygen therapy.
38 Almekinders LC: Results of surgical repair versus splinting of experimen-
tally transected muscle. J Orthopaedic Trauma 1991, 5:173–176.
39 Noonan TJ, Best TM, Seaber AV, Garrett Jr WE: Thermal effects on skele-
tal muscle behavior. Am J Sports Med 1993, 21:517–522.
40 Research Committee on the AOSSM: Hyperbaric oxygen therapy in sports
•• [editorial]. Am J Sports Med 1998, 26:489–490.
Current opinion on hyperbaric oxygen therapy in sports medicine.