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The IOC Manual of Sports Injuries: An Illustrated Guide to the Management of Injuries in Physical Activity

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Exercise and physical activity are the most important determinants of health in de-veloping and transitioning countries, and sedentary living is the fourth independent risk factor for morbidity and mortality from noncommunicable disease. Regular physical activity reduces the risk of early death in general, and of cardiovascular disease, high blood pressure, type 2 diabetes, and even some types of cancer. Indeed, physical inactivity can present as great a risk to health as smoking, being overweight, high cholesterol, or high blood pressure. Furthermore, intense exercise is not neces-sarily more effective than other forms of exercise for prevention and treatment of chronic disease. Significant health benefits can be achieved through moderate physi-cal activity; as a matter of fact, standing as opposed to sitting will also incur health benefits. This holds true even at an advanced age. The least fit people are the ones who can derive the greatest health benefit from regular physical activity. Unfortunately, exercise and physical activity also have some unfortunate side effects. Injuries are a particular risk. Nevertheless, the net health effect is positive—the benefits of physical activity far exceed the problems caused by injuries.
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1 Types and Causes of Injuries
Roald Bahr1, Håkan Alfredson2, Markku Järvinen3, Tero Järvinen3, Karim Khan4,
Michael Kjær5, Gordon Matheson6, and Sverre Mæhlum7
1Norwegian School of Sport Sciences, Oslo, Norway
2University of Umeå, Sports Medicine Umeå Inc., Umeå, Sweden
3University of Tampere, Tampere, Finland
4Centre for Hip Health and Mobility, Vancouver, BC, Canada
5Bispebjerg Hospital, Copenhagen, Denmark
6Stanford University, Stanford, CA, USA
7Hjelp24 NIMI, Oslo, Norway
Exercise and physical activity are the most important determinants of health in de-
veloping and transitioning countries, and sedentary living is the fourth independent
risk factor for morbidity and mortality from noncommunicable disease. Regular
physical activity reduces the risk of early death in general, and of cardiovascular
disease, high blood pressure, type 2 diabetes, and even some types of cancer. Indeed,
physical inactivity can present as great a risk to health as smoking, being overweight,
high cholesterol, or high blood pressure. Furthermore, intense exercise is not neces-
sarily more effective than other forms of exercise for prevention and treatment of
chronic disease. Significant health benefits can be achieved through moderate physi-
cal activity; as a matter of fact, standing as opposed to sitting will also incur health
benefits. This holds true even at an advanced age. The least fit people are the ones
who can derive the greatest health benefit from regular physical activity.
Unfortunately, exercise and physical activity also have some unfortunate side effects.
Injuries are a particular risk. Nevertheless, the net health effect is positive—the
benefits of physical activity far exceed the problems caused by injuries.
Acute Injuries and Overuse Injuries
A sports injury may be defined as damage to the tissues of the body that occurs as a
result of sport or exercise. In this book, the term applies to any damage that results
from any form of physical activity. Physical activity can be defined as moving or
using the body, and it includes numerous forms of activity such as working, fitness
exercise, outdoor activity, playing, training, getting in shape, working out, and physi-
cal education.
Sport injuries can be divided into acute injuries and overuse injuries, depending on
the injury mechanism and onset of symptoms. In most cases, it is easy to classify an
injury as acute or overuse, but in some cases it may be difficult. Acute injuries occur
suddenly and have a clearly defined cause or onset. Overuse injuries occur gradu-
ally. However, an important concept with overuse injuries is that they exist along
a spectrum where the inciting events are below the threshold for clinical symp-
tomatology, but if not rectified, they eventually produce sufficient tissue damage to
result in clinical symptoms. This is important for physicians, therapists, and patients
The IOC Manual of Sports Injuries, First Edition. Edited by Roald Bahr.
©2012 International Olympic Committee. Published 2012 by John Wiley & Sons, Ltd.
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Figure 1.1 Hypothetical
overview of pain
and tissue injury in a
typical overuse injury.
(Reproduced with
permission from the
Norwegian Sports
Medicine Association.)
to understand, because it is not un-
common to “react” to “new” clinical
symptoms the same way one reacts
to acute injuries. Such a response
may ignore the underlying clinical
symptomatology and thus may inter-
fere with effective treatment. For ex-
ample, an athlete with a stress frac-
ture (a fatigue fracture) in the foot
will often state that the symptoms
originated during a specific run,
perhaps even from a specific step.
The injury may accordingly be mis-
classified as an acute injury. How-
ever, the actual cause of the stress
fracture is that the specific run was
a precipitating event on top of the
underlying spectrum of tissue dam-
age on the skeleton from overuse
over time. Therefore, these types of
injuries should be classified as over-
use injuries.
As shown in Figure 1.1, the pathological process is often under way for a period of
time before the athlete notices the symptoms. Repetitive low-grade forces that lead
to microtrauma in the tissues cause overuse injuries. In most cases, the tissue will
repair without demonstrable clinical symptoms. However, if this process continues,
the ability of the tissue to repair can be exceeded, resulting in a clinical overuse
injury with symptoms. It is vitally important that athletes as well as therapists and
physicians understand this concept so that correct treatment can be initiated.
The difference between acute injuries and overuse injuries can also be described in
biomechanical terms. Dynamic or static muscle action creates internal resistance
in the loaded structures (stress) that counteracts deformation (strain) of the tissue.
All tissue has a characteristic ability to tolerate deformation and stress, and injuries
occur when the tolerance level is exceeded. An acute injury occurs when loading is
sufficient to cause irreversible deformation of the tissue, whereas an overuse injury
occurs as a result of repeated overloading either in the loading itself or through
inadequate recovery time between loadings. Each incidence, alone, is not enough
to cause irreversible deformation, but the repeated actions can result in an injury
over time.
Acute injuries are most common in sports in which the speed is high and the risk of
falling is great (e.g., downhill skiing) and in team sports where there is much contact
between players (e.g., ice hockey and soccer). Overuse injuries make up the large por-
tion of injuries in aerobic sports that require long training sessions with a monotonous
routine (e.g., long-distance running, bicycling, or cross-country skiing). But a large num-
ber of overuse injuries also occur in technical sports, in which the same movement is
repeated numerous times (e.g., tennis, javelin throwing, weightlifting, and high jumping).
Why Do Injuries Occur?
The basic principle for training is that the body reacts to a specific physical training
load with specific predictable adaptation. Loading that exceeds what an athlete is
Pain threshold
Perceived moment of tissue injury
100%
Antecedent pain
Subclinical episodes
of failed
adaptation
Attempted return
to sport
Period of
overuse 20% permanent loss of function
Hypothetical point in time
when healing is sufficient
for sports activity
Total tissue damage
Time (weeks or months)
Pain level
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used to will cause the tissue that is
being trained to attempt to adapt to
the new loading. For example, train-
ing provides a stimulus that causes
the muscles to increase the pro-
duction of contractile proteins, the
muscle fibers become larger (and
more numerous), and the muscle
fibers specifically adapt to whether
the training requires primarily en-
durance or maximum strength. This
principle applies to all types of tis-
sue. The skeleton, tendons, liga-
ments, and cartilage adapt accord-
ingly. The tissue becomes stronger
and tolerates more (Figure 1.2).
However, if the training load ex-
ceeds the tissue’s ability to adapt,
injuries will occur. The risk of over-
use injuries increases when train-
ing load increases. This could result
from an increase in the duration of
individual training sessions or an increase in training intensity or the frequency of
training sessions. Often the duration, intensity, and frequency of training increase at
the same time, such as at a training camp or at the beginning of the season. There-
fore, it is common to say that overuse injuries are due to “too much, too often, too
quickly, and with too little rest,” which means that training load increases more
quickly than the tissue is able to adapt.
Various Types of Injuries
Sport injuries can be divided into soft-tissue injuries (cartilage injuries, muscle in-
juries, tendon injuries, and ligament injuries) and skeletal injuries (fractures). The
various types of tissue have distinctly different biomechanical properties and their
ability to adapt to training also varies. This chapter examines the characteristics of
the various types of tissue and the ways in which the skeleton, cartilage, muscles,
tendons, and ligaments can be injured.
Ligaments
Structure and Function
Ligaments consist of collagen tissue that connects one bone to another. Their pri-
mary function is passive stabilization of the joints. In addition, the ligaments serve
an important proprioceptive function.
Ligaments consist primarily of cells, collagen fibers, and proteoglycans. Fibroblasts
are the most important cell type, and their main function is to produce collagen (pri-
marily type I but several other types as well). The amount of proteoglycan is much
lower than the amount found in cartilage. While the collagen fibers in tendons are
organized in a parallel manner (in the longitudinal direction of the muscles), the
orientation of the fibers in ligaments can be parallel, oblique, or even spiral (e.g.,
the anterior cruciate ligament). The organization of fiber direction is specific to the
Immobilization Inactivity Normal activity Training
Biological properties
Figure 1.2 Adaption to
training. Immobilization
signicantly weakens
the biological properties
of the tissue, whereas
exercise improves
function. (Reproduced
with permission from
the Norwegian Sports
Medicine Association.)
TYPES AND CAUSES OF INJURIES
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function of each ligament. In addition, ligaments contain slightly more elastic fibers
than tendons.
Ligaments may insert directly or indirectly into the bone: directly with a transition
zone consisting of fibrocartilage first and mineralized fibrocartilage last (including
specialized collagen fibers that go down into the bone vertically), or indirectly by
growing into the surrounding periosteum.
Ligaments may be intra-articular (localized within a joint inside the joint capsule),
capsular (where the ligament projects as a thickening of the joint capsule), or extra-
capsular (localized outside the joint capsule). The cruciate ligaments are intra-artic-
ular ligaments. The anterior talofibular ligament is a capsular ligament, where it may
be difficult to distinguish between the ligament and the rest of the capsule, whereas
the calcaneofibular ligament is an extracapsular ligament. The type of ligament is
important for the healing potential after a total rupture. Following total rupture of
an intra-articular ligament, such as the anterior cruciate ligament, healing will not
take place, whereas the capsular ligaments have excellent healing potential. Blood
supply to ligaments also differs. Capsular ligaments have a good blood supply, just as
the surrounding joint capsule does, whereas the blood supply to intra-articular liga-
ments enters proximally or distally, typically resulting in a midzone of marginal vas-
cularization. The blood supply is important for the healing potential after an injury.
Ligaments contain a number of different nerve endings that supply the nervous sys-
tem with information about body position, movement, and pain. This information
is key in controlling the muscles that surround a joint such as the knee. Even if
the main function of ligaments is passive stabilization of the joint, much evidence
indicates that the proprioceptive
function of ligaments is more impor-
tant than previously thought. Liga-
ment injuries may reduce the ability
to register the position and move-
ments of the joint, even when the
injury does not result in significant
mechanical instability. This may in-
crease the risk of recurrent injuries.
Figure 1.3 shows how ligaments re-
act to stretching. At first, the wavy
pattern of the microscopic colla-
gen fibers straightens out and mini-
mal force is required to cause a
significant change in length. As force
increases further, the collagen fibers
will be stretched, and the relation-
ship between load and deformation
is linear. This means that the liga-
ment serves as an ideal spring in the
elastic zone, as long as the change in
length does not exceed about 4%. If a
force causes a change in length in ex-
cess of this, the collagen fibers will rupture—first single fibers and then all of the fibers
will fail (a total rupture). The strength and stiffness of a ligament depends on the longi-
tudinal and cross-sectional area. The greater the cross-sectional area, the stronger and
stiffer the ligament. A longer ligament is less stiff, but the maximum tensile strength
Elastic zone
2468
Plastic
deformation
Total
rupture
Load
Deformation (%)
Figure 1.3 Acute stress–
deformation curve for
ligaments. (© Medical
Illustrator Tommy Bolic,
Sweden.)
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does not change if the cross-sectioned
area is the same.
Adaption to Training
Connective tissue adapts slowly to in-
creased loading but weakens rapidly as
a result of immobilization (Figure 1.4).
The ligaments adapt to training by in-
creasing the cross-sectional area, as well
as by changing the material properties
so that they become stronger per unit
area. Normal everyday activity (without
specific training) is apparently sufficient
to maintain 80–90% of the ligament’s
mechanical properties. Systematic
training increases ligament strength by
10–20%. In contrast, the negative effect
of immobilization sets in quickly. After a
few weeks, strength is reduced to about
half. Systematic training causes strength
in the ligament substance to return after
several weeks, but the tensile strength in
the ligament–bone junction will remain at a reduced level for several months despite
systematic retraining.
Ligament Injuries
Unlike the tendons, where both acute and overuse injuries can occur, the ligaments
are typically injured because of acute trauma. The injury mechanism is sudden over-
loading, where the ligament is stretched with the joint in an extreme position. For
example, inversion trauma in the ankle may cause the lateral ligaments—primarily
the anterior talofibular ligament—to rupture.
Ruptures may occur in the midsubstance of the ligament or at the ligament–bone
junction (Figure 1.5). Sometimes avulsion fractures also occur, which means that
the ligament pulls a piece of the bone with it, usually with an eggshell shape. Sev-
eral factors determine the location of the rupture, including the age of the patient.
Children often sustain avulsion fractures, while midsubstance ruptures commonly
occur in adolescents and adults. The ligament–bone junction can be the weak point
in middle-aged patients, and avulsion fractures are most common in the elderly,
particularly if the skeleton is osteoporotic.
Overuse injuries in the ligaments are rare, and symptomatic inflammatory condi-
tions hardly ever occur. Nevertheless, overuse injuries may occur as the ligament is
gradually stretched out, probably because of repetitive microtrauma. One example
is the shoulder joint, where throwers (e.g., javelin throwers and baseball, handball,
and volleyball players) may stretch out their anterior ligaments. This may reduce
stability in the joint and predispose the athlete to pain because of entrapment of
the subacromial structures. However, one must be aware that the primary ligament
injury (stretching) is usually asymptomatic. The symptoms only appear if the insta-
bility causes muscular dysfunction and/or results in injury to other structures (e.g.,
the rotator cuff in the shoulder).
Figure 1.4 Schematic
representation of the
relationship between
training, immobilization,
and remobilization on the
structural and mechanical
properties of the
ligaments. (Reproduced
with permission from
the Norwegian Sports
Medicine Association.)
Remobilization
Immobilization
Recovery
(ligament
substance)
shtnoMskeeW
Recovery
(insertion site)
Training
Control
Structural/mechanical properties
Time
TYPES AND CAUSES OF INJURIES
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Internationally, ligament injuries are usually classified as mild (grade 1), moderate
(grade 2), or severe (grade 3). Mild injuries only cause structural damage on the
microscopic level, with slight local tenderness and no instability. Moderate injuries
cause a partial rupture with visible swelling and notable tenderness, but usually
with little to no change in stability. Severe injuries cause a complete rupture with
significant swelling and instability. Nevertheless, because the relationship between
the degree of structural damage, tenderness, and instability is highly variable, this
general classification of ligament injuries is very limited for clinical purposes. The
use of classification systems developed for the individual ligaments and joints, for
which specific tests have been developed, is recommended to grade the degree of the
injury. These types of tests and classification systems are described in the discussion
of the various regions of the body in Chapters 4–15.
An acute ligament rupture sets off a series of events—the inflammation process—
which can be divided into three stages: the inflammatory phase (phase 1), the
proliferative phase (phase 2), and the maturation phase (phase 3).
Total rupturePartial rupture
(a)(b)(c)
Figure 1.5 Various types
of ligament injuries. Total
and partial ruptures (a)
in the midsubstance,
(b) in the ligament–bone
junction, and (c) avulsion
fractures. (© Medical
Illustrator Tommy Bolic,
Sweden.)
The Inammation Process
Inflammation (“inflammare” [Lat.]; to set on fire, inflame) is a local tissue response in any vascularized
tissue subjected to loading, which results in cell damage. Inflammation consists of a characteristic chain
of vascular, chemical, and cellular events that may result in repair, regeneration, or formation of scar tis-
sue. The five cardinal signs of inflammation are rubor (redness), tumor (swelling), calor (heat, increased
temperature), dolor (pain), and functio laesa (loss of function). Among the cardinal signs, pain is generally
the most prominent in sport injuries, both as a symptom that the patient experiences subjectively and as a
finding, tenderness to palpation. However, it should be noted that painful conditions are not always related
to inflammation, as will be described later in the section on tendon injuries. Under normal conditions,
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erythrocytes, leukocytes, and plasma components are isolated intravascularly. An injury to the vascular
endothelium results in leakage of plasma components, erythrocytes, and leukocytes. The inflammation
process is activated by a series of different mediators that primarily result in increased vascular permeabil-
ity, activation of leukocytes, blood platelets, and the coagulation system (Figure 1.6). Vasoactive mediators
bind to specific receptors on endothelial cells and smooth muscle cells. This results in vasoconstriction
or dilatation. Neutrophils, granulocytes, monocytes, and lymphocytes are attracted to the injury site by
chemotactic factors that are released from the activated platelets and the injured cells. These cells release
a series of inflammation mediators. Key among these are growth factors, cytokines, chemokines, prosta-
glandins, and leukotrienes.
The Inammatory Phase (Phase 1)
The inflammatory phase begins with bleeding and the exudation of plasma. Activation of the coagulation
cascade causes clotting with a network of fibrin, fibronectin, and collagen blood cells. This network pro-
vides some initial strength to the clot. Blood platelets are activated and release a large number of growth
factors from their granules. These growth factors function as chemotactic factors recruiting inflammatory
cells to the site of the injury. Neutrophil granulocytes release a series of proteolytic enzymes that dissolve
the damaged extracellular matrix. Blood platelets and monocytes are recruited into the injured area, invade
the tissue and differentiate into macrophages that are actively engaged in the phagocytosis of cell debris
and release growth factors that attract pericytes, endothelial cells, and fibroblasts and stimulate cells to the
injured area. The inflammatory phase lasts a few days.
The Proliferative Phase (Phase 2)
The proliferative phase is characterized by the accumulation of large numbers of endothelial cells, macro-
phages, myofibroblasts, and fibroblasts to the site of the injury. Ingrowth of new capillaries (i.e., angiogen-
esis) begins at the edge of the injury site, and within a few days a rich capillary network supplying oxygen and
nutrients is established. The myofibroblasts and fibroblasts organize themselves perpendicular to the direc-
tion of capillary ingrowth and an immature granulation tissue is formed. These cells produce an extracellular
network that initially consists of fibronectin, type III collagen, and proteoglycans. After a week, the pro-
duction of type I collagen increases greatly. Some of the fibroblasts transdifferentiate into the contraction-
capable cells called myofibroblasts, which are responsible for the scar formation. At the same time, there is
continuous breakdown of the initial clot and the injured extracellular early loose connective tissue, and the
formation of mechanically stronger newly formed matrix. The macrophages accomplish this by “eating” the
superfluous cell components. In addition to that, most of the macrophages transform from inflammatory to
anti-inflammatory cells and direct the repair process by secreting growth factors needed for the repair. The
continuous deposition and removal of extracellular matrix (with the balance toward deposition) results in
remodeling of the injury and increased tensile strength. The proliferation stage lasts a few weeks.
Figure 1.6 Mediators of inammation.
(Reproduced with permission from the Norwegian
Sports Medicine Association.)
Injury
Chemotactic factors
Leukocyte activation
Arachidonic
acid
Proteases OxidantsCytokines
Activation of blood platelets
and the coagulation system
Vasoactive
mediators
Vascular permeability Thrombus formation
ProstaglandinesLeukotrienes
Cyclooxygenase
Lipoxygenase
TYPES AND CAUSES OF INJURIES
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The Maturation Phase (Phase 3)
The final tissue structure is established during the maturation and remodeling stage through continuous re-
modeling of the scar tissue. The numbers of macrophages and fibroblasts are significantly reduced and the
few remaining fibroblasts transform to myofibroblasts, and blood supply is finally established by removal
of the capillaries with lowered blood flow and most of the capillaries disappear. The granulation tissue is
converted (contracted) by myofibroblasts into a small scar. Thicker collagen fibers are formed in the direc-
tion of tension in the tissue from external load, and a network of lateral, cross-bridges providing mechani-
cal strength is established between them. Therefore, the form and function of the scar tissue depend on
the degree to which the tissue is subjected to loading during this stage. This stage may last several months,
which has important implications for return to sport.
Tendons
Structure and Function
Tendons consist of connective tissue that attaches muscle to bone. Their most im-
portant function is to transfer force from the muscles into the skeletal system, there-
by contributing to stabilizing the joints. Further, the elasticity of tendon allows for
short loading energy stored in the tendon to be released in, for example, jumping
activity. Apart from water, the main element in tendons is type I collagen, which
makes up 80–90% of the tendinous matrix content. To a large extent, the structure
of tendons resembles the structure of ligaments. The collagen is arranged in parallel
fibers and the tendons are constructed of increasingly large structures, the tropocol-
lagen, microfibrils, subfibrils, fibrils, and fascicles (Figure 1.7). The strict organiza-
tion into parallel bundles of various sizes is the main difference between tendons
and ligaments. The organization of the ligaments is more variable and dependent on
function.
Fascicles are surrounded by a loose connective tissue, endotenon, which makes it
easy for them to move in relation to each other. Endotenon also contains veins,
Fascicle with
endotendineum
Fibril
Tendon with epitendineum
Subfibril
Collagen fiber
Tropocollagen
Figure 1.7 The structure
of tendons (schematic).
(© Medical Illustrator
Tommy Bolic, Sweden.)
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nerve fibers, and lymph vessels. The surface of the tendon is surrounded by a white
synovial-like membrane, the epitenon, a loose connective tissue that also supports
blood vessels, lymphatics, and nerves. Some tendons are covered by a loose areolar
connective tissue, the paratenon, enveloping the tendon. The envelope of tendon is
dominated by type IV collagen and acts as an epithelium hindering the tendon to
adhere to surrounding tissues.
The muscle cell ends in a number of microscopic membranous infoldings that stick
out like small fingers into the myotendinous junction. The collagen fibers creep into
the folds that form between the fingers and attach to the basal membrane of the
muscle. At the other end, the tendons attach to bone via fibrocartilage and mineral-
ized fibrocartilage. Collagen fibers penetrate the mineralized fibrocartilage into the
subchondral bone, contributing to better attachment.
The relationship between stress and deformation of tendons is the same as for the liga-
ments (Figure 1.3). Initially, the collagen fibers are easily stretched from their normal
wavy appearance, in the elastic zone the tendon behaves like an ideal spring, whereas
ruptures occur in the deformation zones: first single fibers, then total ruptures.
Adaptation to Training
The tendons adjust to training in the same manner as the ligaments—by increasing
the tendon strength through collagen synthesis, cross-link formation and training im-
proved material properties of the tendinous tissue, and if trained sufficiently some
increase in tendon cross-sectional area can be seen. Acute exercise results in an in-
crease in collagen synthesis within and around the tendon tissue. Collagen synthesis
remains increased for 2–3 days, indicating that training every second or third day is
most likely a sufficient stimulus for tendon protein generation. In addition, the relative
load intensity required is less than in muscle, which means that also moderate exer-
cise, either concentric or eccentric, will result in elevated formation of new collagen
in tendon. Changes in physical activity levels, either increased training or detraining/
immobilization, quickly (within 1–3 weeks) alter mechanical properties, most likely
through increased or decreased cross-link formation, respectively. In contrast, chang-
es in collagen-rich fibril structures require several months to years to occur.
Tendon Injuries
Tendons can be injured in several different ways, both as acute injuries and as over-
use injuries. Because tendons are usually superficial, they can be severed by a pen-
etrating stab or a cut, such as one caused by the edge of a skate. Acute tendon
ruptures occur if force is generated in excess of the tendon’s ability to tolerate it.
These types of tendon ruptures usually occur in connection with eccentric force gen-
eration, such as in the Achilles tendon when pushing off at the start of a sprint run.
Tendon ruptures may be partial or total, and they usually occur in the midtendon
substance but may also occur in the bone–tendon junction or as avulsion fractures.
Acute tendon injuries are most common in athletes and recreational exercisers be-
tween 30 and 50 years of age in explosive sports, often without previous symptoms
or warning. Some studies reveal that structural and degenerative changes can be
seen in the tendon prior to exercise.
Tendons are the type of tissue that is most often affected by overuse injuries. Sev-
eral different terms are habitually used to describe these overuse injuries: tendinitis
(tendon inflammation), tenosynovitis (tendon sheath inflammation), tenoperiostitis
TYPES AND CAUSES OF INJURIES
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(inflammation of tendon insertions and origins), periostitis (periosteal inflamma-
tion), and bursitis/hemobursitis (bursal inflammation, possibly with bleeding). All
these terms describe the parts of the tendon or the surrounding tissue that is af-
fected, and all have the ending “itis,” indicating the pathophysiological condition of
inflammation.
Even though the concept of inflammation has been used traditionally, the pathogen-
esis for overuse injuries in tendons is uncertain. Although tendon loading does not
normally cause more than a 4% change in length (i.e., within the physiological elastic
zone), some sports require repetitive loading in excess of this (4–8% change in length),
which may cause collagen fibrils to rupture. Therefore, a potential explanation of what
is called tendinitis is that repetitive microtrauma causes injuries that are greater than
the fibroblasts are able to repair, resulting in inflammation. It is also possible that
cumulative microtrauma can affect collagen cross-bridges, other matrix proteins, or
microvascular elements in the tendon. Also, loading that extends the tendon less than
4% can lead to overuse symptoms, and it is likely caused by inadequate time to adapt
to each training load.
One problem with explaining tendon overuse as inflammation is that the histologi-
cal findings do not match those seen with inflammation—surgical specimens are
devoid of inflammatory cells. However, degenerative changes, changed fibril orga-
nization, reduced cell count, vascular ingrowth, and, occasionally, local necrosis
with or without calcification are seen. The concept of tendinosis was introduced
to describe these types of focal degenerative changes. Because the relationship be-
tween degenerative changes and symptoms is unclear, the terms “tendinosis” or
“tendinopathy” are now commonly used to describe chronic tendon pain. Table 1.1
provides an overview of old and new terminology for tendon disorders and injuries.
The new terminology emphasizes the need for the terminology to correspond to the
histological findings.
New Old Denition Histologic ndings
Paratenonitis Tenosynovitis
Tenovaginitis
Peritendinitis
An inammation of only the paratenon,
either lined by synovium or not
Inammatory cells in paratenon or peritendi-
nous areolar tissue
Paratenonitis with
tendinosis
Tendinitis Paratenon inammation associated
with intratendinous degeneration
Same as above, with loss of tendon col-
lagen, ber disorientation, scattered vascular
ingrowth, but no prominent intratendinous
inammation
Tendinosis Tendinitis Intratendinous degeneration due to
atrophy (aging, microtrauma, vascular
compromise, etc.)
Noninammatory intratendinous collagen de-
generation with ber disorientation, hypocellu-
larity, scattered vascular ingrowth, occasional
local necrosis, and/or calcication
Tendinitis Tendon strain or tear
(a) acute (less than 2
weeks)
(b) subacute (4–6 weeks)
(c) chronic (over 6
weeks)
Symptomatic degeneration of the
tendon with vascular disruption and
inammatory repair response
Three recognized subgroups. Each displays
variable histology from pure inammation with
hemorrhage and tear, to inammation super-
imposed upon preexisting degeneration, to
calcication and tendinosis changes in chronic
conditions. In chronic stage there may be:
interstial microinjury
central tendon necrosis
frank partial rupture
acute complete rupture
Table 1.1 Terminology for tendon disorders and tendon injuries.
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Bone
Structure and Function
The skeleton consists of bone, a special type of connective tissue that remodels continu-
ously as a response to a complex interplay between mechanical loading, systemic hor-
mones, and the calcium level in the blood. Bone may be classified as cortical (compact)
or trabecular (spongy), and the two types of bone have different functions and proper-
ties. The long bones consist primarily of cortical bone, whereas the vertebrae in the
spinal column consist of trabecular bone. Bone has many important functions, such as
protecting the underlying organs, serving as the body’s major calcium store, and provid-
ing the environment for hematopoiesis in marrow. However, in relation to injuries, the
skeleton’s most important function is as a lever in the locomotor apparatus.
Like other connective tissue, bone consists of cells, collagen fibers, and extracellu-
lar matrix. Bone cells develop from stem cells in the bone marrow, primarily as os-
teocytes, osteoblasts, or osteoclasts. The osteoblasts and osteoclasts are responsible
for remodeling bone. Located on bone surfaces, osteoblasts are bone-forming cells.
When an osteoblast has formed enough bone to be completely surrounded by a min-
eralized matrix, it is called an osteocyte. Osteoclasts are also found on the surface of
bone—their job is to absorb bone. Osteocytes communicate with each other and with
osteoblasts and osteoclasts on the surface
through channels in the extracellular ma-
trix, and this is an important signaling path
from mechanical loading to remodeling.
A recommended daily intake of minerals
(calcium and magnesium) and vitamin D is
necessary for optimum remodeling of bone.
The extracellular bone matrix consists of
both organic and inorganic components.
The inorganic component constitutes
more than half the bone mass and consists
primarily of calcium and phosphate as
crystals of hydroxyapatite. The inorganic
components contribute greatly to the char-
acteristic hardness and strength of bone.
Strength increases with increasing bone
mineral density, but skeletal architecture
is also very important. The main organic
component is collagen, which contributes
to bone’s elastic properties.
The skeletal surface is covered by a thick
layer of fibrous connective tissue, called
periosteum. Periosteum has a rich supply
of nerves and blood. For this reason, direct
trauma that causes bleeding in or under-
neath the periosteum can be very painful.
Periosteum is particularly well attached to bone in areas where muscles, tendons,
and ligaments attach to the skeleton. In these areas, collagen bundles (Sharpey’s
fibers) go down from the periosteum and into the underlying osseous tissue.
The longitudinal growth of the skeleton takes place in the growth zones (the physes)
(Figure 1.8). The growth zones are subject to injuries: 15% of all acute fractures
Growth zones
Apophysis
Metaphysis
Epiphysis
Diaphysis
Figure 1.8 Growth zones
in the tubular bones,
example from the tibia,
bula, and femur. The
physes are vulnerable to
injuries during the growth
spurt. (© Medical Illustrator
Tommy Bolic, Sweden.)
TYPES AND CAUSES OF INJURIES
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25 50 75
Bone mass
Age (years)
Figure 1.9 The
development of bone
mass as a function
of age and sex. The
dotted line shows the
potential development in
osteoporotic women after
menopause. (Reproduced
with permission from
the Norwegian Sports
Medicine Association.)
in children involve the physes. In addition, the apophyses are subject to overuse
injuries during the growth spurt. The combination of rapid development of muscle
strength and a large amount of training leads to physeal overuse injury (e.g., the
quadriceps muscle, as in Osgood–Schlatter disease, and the triceps surae muscle, as
in Sever disease insertions). Bone mass also increases during the growth period and
peaks when the athlete is in her third decade (Figure 1.9). After a period where bone
mineral remains stable at best, density decreases quite rapidly (1% per year or more)
in most women after menopause.
Bone has characteristic stress–deformation curves (Figure 1.10). Initially, in the
elastic zone, there is a linear relationship between load and deformation. If the load
increases into the plastic deformation zone, even small changes in force will cause
greater and greater deformation. Greater loading in the deformation zone results in
a complete fracture.
Adaptation to Training
When considering the effect of physical training on bone, it is important to consider
both the material property of bone (“bone mass”) as well as the geometric proper-
ties (bone shape and size). Bone is a structure (like a building or a bridge) and its
strength depends both on the material it is made of (bone mass in this case) and the
shape in which the material is arranged (geometry). That’s why there is an emphasis
on estimating the effect of physical training on bone strength—the load that a bone
can withstand before fracturing. Bone strength includes aspects of both bone mass
and bone geometry.
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Physical training increases bone mass (which can be measured as bone mineral
density using a DXA scanner) and bone geometry (measured using a peripheral CT
scanner). Training-related increases in bone strength are site specific to loaded bone.
Jumping will not improve upper limb bone strength, tennis increases strength of the
dominant arm only. Importantly, not all types of activity increase bone mass. Bone
responds to fast signals—rapid deformation—not to slow, gentle loads.
Athletes in power and jumping sports, such as weight lifters, gymnasts, volleyball
players, and squash players, have greater bone strength, all other things being equal
(e.g., size and sex), than other athletes. Normal weight runners are in the midrange
of athletes for bone strength; cyclists and swimmers have no higher bone mineral
density than control groups. This pattern emphasizes the need for impact loading to
promote bone strength.
With respect to the trajectory of change in bone strength over time, bone responds
maximally to physical activity during the growing years. In just two peripubertal
years (age 10–12 approximately in girls and 11–13 in boys), the individual can ac-
cumulate 25% of adult bone mass.
During the adult years (20s to 40s) intense training leads to preservation of bone
strength—bone mass is retained and structural (shape) changes occur to maintain
bone strength. In the postmenopausal years, strength training can largely prevent
the natural decline in bone strength that occurs in nonexercising women. Thus,
compared with women who do not exercise, older exercising women have a relative
net benefit in bone strength because they avoid the loss that is “physiological” in
their nonexercising counterparts.
Fractures
Fractures can be classified in various ways, but the most important difference is
between acute fractures and stress fractures. Acute fractures are caused by trauma
Load
Deformation
Plastic
deformation
Elastic
zone
Complete
fracture
Figure 1.10 Acute
stress–deformation curve
for bone. (Reproduced
with permission from
the Norwegian Sports
Medicine Association.)
TYPES AND CAUSES OF INJURIES
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that exceeds the tissues’ ability for tolerance, direct trauma (e.g., a kick to the leg),
or indirect trauma (e.g., twisting of the lower leg) (Figure 1.11).
Acute fractures can be broadly classified as transverse fractures, crushing fractures,
oblique fractures, and compression fractures, depending on the type of force that
caused the fracture, which usually contributes to giving them their characteristic ap-
pearance. Transverse fractures are generally caused by direct trauma to a small area,
commuted fractures are caused by greater direct trauma to a larger area, oblique or
spiral fractures are caused by indirect trauma with twisting (rotational, torsional) of
the bone, and compression fractures are caused by vertical compression of the bone
(e.g., by the femoral condyle being pressed down into the tibial plateau). Tearing of
the tendon or ligament insertion causes avulsion fractures. In addition, two special
types of fractures occur in children: (1) “greenstick fractures” (in which the bone is
“bent” like a soft twig) and (2) epiphyseal plate fractures (loosening of and possibly
a fracture through the growth zone).
Diagnostic signs of fractures are malalignment, abnormal movement, or shortening
of an extremity. Pain, swelling, and reduced range of motion (ROM) are usually also
present, but are less specific signs.
Figure 1.11 Torsional trauma like this can cause a fracture. (© Oslo Sports Trauma Research Center.)
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Unlike acute fractures, stress fractures do not necessarily have any specific triggering
trauma. In addition, there is a continuum of clinical reactions to loading. As men-
tioned in the preceding text, bone remodels continuously throughout life. Increased
loading results in microinjuries, circulatory injuries, and accelerated remodeling,
with increased osteoclast and osteoblast activity. At first, symptoms are absent de-
spite accelerated remodeling. Routine X-rays do not demonstrate any changes, al-
though magnetic resonance imaging (MRI) will demonstrate bone marrow edema,
and scintigraphy will demonstrate increased uptake of technetium. If excessive load-
ing continues, mild pain will set in a while after the training session begins, and
eventually earlier and earlier into the training session. This is different from pain
from soft tissues (such as the tendons), which typically occurs at the beginning of
training and usually decreases after warm-up. Continued training will increase the
intensity of pain, so that the pain will also be present after training and during other
activities such as regular walking. In these cases, both MRI and scintigraphy will
usually be positive, whereas plain X-rays often do not show any changes except a
subtle periosteal reaction. Positive X-rays will, of course, be seen if there is a com-
plete fracture. The development of stress fractures represents a physiological and
clinical continuum from normal remodeling via accelerated remodeling, stress reac-
tion, and stress fractures to complete fractures. Early diagnosis reduces treatment
time.
As with other loading injuries, a combination of factors contributes to stress. Key
among these are training errors (“too much, too often, and too quickly, and with too
little rest”), muscle fatigue (which presumably affects the shock-absorbing ability
of the foot when running), and malalignment in the lower extremities, surface, and
equipment (particularly footwear). If training is accurately documented, it will usu-
ally be seen that the athlete has made significant changes in training during recent
weeks. Menstrual and eating disorders can cause reductions in bone mineral density
and increase the risk of stress fractures.
Cartilage
Structure and Function
Cartilage consists of the ba-
sic elements in connective
tissue, cells, and extracellu-
lar matrix. There are three
types of cartilage—elastic,
hyaline, and fibrocartilage—
of which hyaline is the most
important. Hyaline cartilage
consists of several layers
characterized by a hori-
zontal organization of cells
in the extracellular matrix
in the surface layer and a
vertical organization in the
deeper layers (Figure 1.12).
The articular surface of most
joints is covered by hyaline cartilage that is 1–5 mm thick. Cells constitute less than
10% of the volume of the hyaline cartilage, the remainder consisting of macromolecules
Figure 1.12 Structure
of cartilage. (© Medical
Illustrator Tommy Bolic,
Sweden.)
Articular surface
Superficial
tangential
(10–20%)
Deep
(30%)
Calcified cartilage
Cancellous bone
Mid
(40–60%)
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(20%) and water (70%). The macromolecules are primarily collagen fibers and proteo-
glycan. Cartilage strength is mainly due to collagen—primarily type II, which is organized
like a network of long fibrils. The proteoglycans are woven into this network and have
two important properties: (1) they bind water and (2) they are negatively charged, so
that they repel each other. This causes the cartilage to naturally absorb water and swell
up. The amount of proteoglycan and water is greater in younger than in older athletes.
Hyaline cartilage does not have a nerve supply, blood supply, or lymph drainage. The
cartilage cells obtain oxygen and nutrients from the surrounding tissue and articular
fluid and dispose of waste matter through diffusion. When a joint is loaded so that the
cartilage surfaces are pressed against each other, the fluid is pumped out. The carti-
lage receives its nutrient supply through this process of cyclic loading and unloading.
Another key element of joint function is that the filmy synovial fluid between the two
hyaline cartilaginous surfaces makes friction very low, as low as wet ice on glass.
To understand the relationship between loading and deformation of hyaline car-
tilage, it is important to remember that the collagen fibers are organized as a net-
work—horizontally on the surface, more multidirectional in the middle section, and
more vertical in the deep layer. When loading begins, the fibers will be organized in
a wavy pattern (Figure 1.13). Eventually, the fibers will straighten out, and deforma-
tion increases linearly with the increase in load until tearing occurs—initially among
individual fibers and later among larger groups of fibers.
Fibrocartilage is strong and flexible; and it is located near joints, tendons, ligaments,
and in the intervertebral disks, where it forms a protective surface between the
tendons, ligaments, and bone. Therefore, fibrocartilage is primarily found in larger
joints, such as the hip, shoulder (glenoid lip), knee (menisci), and wrist (triangu-
lar fibrocartilage complex). In the knee, fibrocartilage contributes to improving the
articular congruence between the hyaline cartilaginous surfaces and to absorbing
shock, whereas in the hip, shoulder, and wrist it contributes to expanding the articu-
lar surface, as well, thereby increasing stability. Unlike hyaline cartilage, fibrocarti-
lage can have a blood and a nerve supply. For example, the nucleus fibrosis has a
Load
Change in length
Rupture
Linear area
Toe region
Figure 1.13 The stress–
deformation curve for
hyaline cartilage shows
the relationship between
loading and changes
in length. (Reproduced
with permission from
the Norwegian Sports
Medicine Association.)
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nerve supply in the outer superficial portion, whereas the menisci in the knees have
a blood supply in the inner capsular portion.
Adaptation to Training
Active loading of the articular cartilage causes the nutrients to diffuse in and outside of
the cartilage. Consequently, regular loading is necessary for normal cartilage function.
Cartilage adapts to activity (Figure 1.14). Immobilization, such as in a cast, reduces
function. It is also assumed that too much loading reduces biological properties.
Cartilage Injury
In acute injuries, hyaline cartilage can be destroyed through contusion, which causes
cracks, or when shearing forces in the joint cause vertical or horizontal rifts. Carti-
lage injuries occur often in connection with acute joint injuries. Patients with acutely
sprained ankles that result in lateral ligament injuries often have macroscopic car-
tilage injuries. Of patients who have an arthroscopic examination after having sus-
tained an acute knee ligament injury, full-thickness cartilage injuries are common.
Some patients have an isolated cartilage injury; others have osteochondral injuries
in which the underlying bone is also injured.
Articular cartilage injuries are classified on the basis of the size and depth of the le-
sion and the cause and accompanying pathology of the injury. The most important
is to distinguish between degenerative cartilaginous injuries (osteoarthrosis), where
changes are found at several places in the joint, and focal articular cartilage injuries,
where localized changes are found in one or two places in the joint. If the patient
has osteoarthrosis, hyaline cartilage degeneration, sclerosis of the underlying bone,
and the development of ossified cartilage in the outer edges of the joints (osteo-
phytes) occur. Large acute ligament injuries, such as anterior cruciate ligament inju-
ries, increase the risk of secondary osteoarthrosis later on. However, it is not known
whether this occurs because the acute injury starts the degenerative processes in
Biological properties
Activity level
Immobilization Physically active Hard training
Normal
Figure 1.14 Hypothetical
relationship between
physical loading and the
development of biological
properties in hyaline
cartilage. (Reproduced
with permission from
the Norwegian Sports
Medicine Association.)
TYPES AND CAUSES OF INJURIES
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the knee joint or because the loading pattern in the knee is changed as a result of
increased laxity. The cause of primary osteoarthrosis is still unknown, yet the pro-
cess may be due to increased loading of a normal joint or to cartilage failure despite
normal loading. Even without a recognized injury, it appears that the occurrence of
osteoarthrosis is more prevalent in former athletes than in the general public.
The ability of hyaline cartilage to repair is limited after injuries. This is attributed
to the lack of blood and nerve supply and the relative lack of cells in the carti-
laginous tissue. The inability to regenerate increases the risk that osteoarthrosis will
develop after a cartilage injury.
Fibrocartilage is also regularly injured in meniscal injuries and labrum injuries. In
most cases, these injuries are acute, but degenerative changes also occur. The blood
supply to fibrocartilage varies. In the meniscus of the knee, blood supply is good in
the capsular portions (“red meniscus”), where the possibilities for repair are good.
However, central portions (“white meniscus”) have a less good blood supply and
consequently poor potential to repair.
Muscle
Structure and Function
Muscles make up 40–45% of body mass. The structure of the musculature
(Figure 1.15) reflects its central function—to generate power. The muscle fibers
Muscle
Muscle fiber
with capillaries
Myofibril
Parallel with
tendinous
bridges
Fusiform Triangular Unipennate Multipennate
Figure 1.15 Schematic overview of the structure of musculature. (© Medical Illustrator Tommy Bolic, Sweden.)
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(muscle cells) are the muscles’ cen-
tral unit, and these can be organized
in several ways, such as unipennate,
multipennate, or fusiform patterns.
Pennate muscles are generally stron-
ger than fusiform muscles, because
several muscle fibers can work par-
allel to each other. However, be-
cause they contain shorter fibers,
the maximum contraction speed is
lower. The striated muscle cell is a
fiber with a diameter of 10–100 μm
and a length up to 20 cm. The pri-
mary elements in the muscle fibers
are myofibrils, which are composed
of protein filaments (mainly actin
and myosin). Capillaries surround
the muscle fibers, so that the ability
to supply the fibers with oxygen and
nutrients is very good.
The ability to generate force depends on the working conditions, as shown in
Figure 1.16. The generation of force without changes in the joint angle is called an
“isometric” or “static” muscle action (the length of the muscle is constant, but the
tension changes), whereas the muscle contraction where the length changes but ten-
sion remains constant is called “isotonic.” The generation of power while the muscle
is shortened is called “concentric” muscle contraction, whereas the term “eccentric”
is used when the muscle is extended while it offers resistance. For concentric muscle
action, maximal muscle force is reduced when the speed of contraction increases,
whereas in eccentric muscle activity, muscle force increases with increasing speed.
This means that the risk of muscle injuries is greater with eccentric than with con-
centric muscle action.
That working conditions play a decisive role in the generation of force
can be illustrated by comparing various types of jumps. Figure 1.17 shows
a notable difference between the generation of force against the surface
from a squat jump (a
strict concentric jump
from a 90º knee bend), a
countermovement jump (a
continuous eccentric–con-
centric movement), and
a drop jump (jumping af-
ter dropping down from a
height). The greater force
generated from a drop jump
significantly increases the
risk of acute strains, and the
risk of overuse injuries is
high in sports characterized
by this type of muscle ac-
tion. This is true not only of
the muscles but also of other
structures, such as tendons,
cartilage, and bone.
Velocity
cirtnecnoCcirtemosIcirtneccE
Force
Figure 1.16 The
relationship between force
and speed in different
types of muscular
exertion. (Reproduced
with permission from
the Norwegian Sports
Medicine Association.)
Countermovement
jump
1.0 s
1000 N
Drop jumpStanding jump
Figure 1.17 Force
generation in various
types of jumps.
(Reproduced with
permission from the
Norwegian Sports
Medicine Association.)
TYPES AND CAUSES OF INJURIES
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Adaptation to Training
Muscle is the tissue that shows the
greatest and most rapid response
to training. Muscle volume and
strength increase significantly after
a short period of specific strength
training (Figure 1.18). Two factors
contribute to increasing strength:
(1) the ability to recruit several mus-
cle fibers at the same time for the
contraction (neural factors) and (2)
muscle volume (muscular factors).
Muscle volume primarily increases
as a result of individual muscle fibers
increasing their cross-sectional area
(hypertrophy), and also by forming
new muscle cells (hyperplasia) from
stem cells (satellite cells) in the mus-
culature. Neural factors contribute
most to the initial strength increase,
whereas hypertrophy is primar-
ily responsible for the subsequent
strength increase.
The enhancement of endurance capacity of muscles, in turn, involves training-
induced increases in the oxidative capacity of the muscles (e.g., increased capil-
lary density and number of mitochondria). Both main types of training, endurance
(low-intensity, high volume) and strength (high-intensity, short duration) training,
are known to improve the energy status of working muscle, subsequently resulting
in the ability to maintain higher muscle force output for longer periods of time. Re-
cent experimental data demonstrate that strength training can also lead to enhanced
long-term (>30 min) and short-term (<15 min) endurance capacity in well-trained in-
dividuals and elite endurance athletes when high-volume, heavy-resistance strength
training protocols are applied. The enhancement in long-term endurance capacity
appears to involve training-induced increases in the proportion of type IIA muscle
fibers, as well as gains in maximal muscle strength and rapid force characteristics,
while also likely involving enhanced neuromuscular function.
Because strength increases after a few weeks but tendons, cartilage, and bone re-
quire months to adjust, there is a danger that overuse injuries will occur in these
structures in connection with the beginning of systematic strength and jump train-
ing. The patellar tendons and the Achilles tendons are examples of structures that
are especially vulnerable in adult athletes. This is particularly true when the patient
uses anabolic steroids, where there seems to be an increased risk for a total rupture
of muscle or tendons (e.g., of the quadriceps or the pectoralis major) is present. In
children and adolescents (e.g., Osgood–Schlatter disease and Sever disease), these
types of overuse problems usually affect apophyseal disks.
Muscle Injuries
Muscle injuries generally occur in two ways: (1) distension ruptures (pulled muscles,
i.e., strains) and (2) by direct trauma that results in contusion ruptures. Muscular
Weeks Months Years
Anabolic steroids
Strength
Neural adaptation
Hypertrophy
Strength increase
Time
Figure 1.18 Increase
in strength as a result
of systematic strength
training. (Reproduced
with permission from
the Norwegian Sports
Medicine Association.)
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lacerations also occur, although they are rare in sport. In addition, the musculature is
sometimes injured as a result of unusual and hard training, especially eccentric train-
ing. This may cause muscular soreness called delayed onset muscle soreness (DOMS).
Distension ruptures (strains) usually occur close to the myotendinous junction in
connection with maximum eccentric muscle action, such as in sprinters. The usual
locations are the hamstrings, adductor, and gastrocnemius muscles, but ruptures
may affect a large number of muscle groups. The athlete experiences immediate pain
from the muscle at the moment of impact, followed by tenderness and reduced con-
traction strength. The athlete can sometimes feel a bump in the muscle right away.
Eventually, this is replaced by swelling due to bleeding.
Contusion ruptures primarily occur in the quadriceps muscles, which are exposed
frontally and laterally on the thigh and, therefore, can easily be hit, for example,
by an opponent’s kneecap. The severity of contusion injuries varies from very mild
strain injury like DOMS to “real” strains, shearing type of muscle injuries, in which
myofibers and the associated connective tissue structures including blood vessels are
ruptured. Muscle injuries involving rupture of blood vessels cause internal bleeding
in the musculature. This is because the musculature is well vascularized and the
blood flow is usually high when the injury occurs. Therefore, a hematoma will oc-
cur almost instantly with this type of injury. Bleeding may be either intramuscular,
if there is no injury to the muscle fascia, or intermuscular, if the blood can escape
from the muscle compartments through an injured fascia (Figures 11.1 and 11.4). In
general, healing time is significantly longer with intramuscular bleeding than it is for
intermuscular bleeding.
What distinguishes the healing of injured skeletal muscle as well as the other soft tis-
sues from that of fractured bone is that the skeletal muscle heals by a repair process,
whereas the bone heals by a regenerative process. When most of the musculoskel-
etal tissues are being repaired, they will heal with a scar, which replaces the original
tissue, whereas when a bone regenerates, the healing tissue is identical to the tissue
that existed there before.
The healing of an injured skeletal muscle follows a fairly constant pattern irrespective
of the underlying cause (contusion, strain, or laceration). As described in the preced-
ing text for the soft-tissue injuries in general, three phases have been identified in
this process. These are (1) inflammatory (destruction), (2) proliferative (repair), and
(3) maturation (remodeling) phases.
In short, the natural course of muscle injury healing takes place as follows. After
the initial trauma, the ruptured myofibers contract and a hematoma fills the gap be-
tween the myofiber stumps. The injured ends of the myofibers undergo only local ne-
crosis, because the torn sarcolemma is rapidly resealed allowing the rest of the rup-
tured myofibers to survive. Activated platelets secrete growth factors that function
as chemoattractants for the inflammatory cells. Macrophages, having first invaded
the injury site from the torn blood vessels, remove the cell debris and secrete growth
factors that initiate angiogenesis, that is, blood supply to the injured area and also
activate the satellite cells, that is, the regenerative (reserve) stem cells of the muscle
tissue. The satellite cells reside between the sarcolemma and the basal lamina of the
myofibers and can survive even though the surrounding tissue undergoes necrosis.
There are two different populations of satellite cells, committed and stem satellite
cells, with very defined functions: committed satellite cells begin to differentiate into
myoblasts immediately after injury, whereas stem satellite cells begin to proliferate
first. After the round of proliferation, stem satellite cells contribute one daughter cell
TYPES AND CAUSES OF INJURIES
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to the formation of regenerating myoblasts, at the same time providing new satellite
cells by asymmetric cell division for future needs of regeneration. Thus, the regener-
ating myoblasts arise from both the committed and stem satellite cells then fuse to
form myotubes within a couple of days. The regenerating young myotubes grow in
length and size and, finally, mature into myofibers.
Simultaneously with the muscle fiber regeneration, the concomitant production of
a connective tissue scar by fibroblasts takes place between the regenerating muscle
fibers that try to pierce into connective tissue. Thus, the ends of the regenerating
myofibers do not usually reunite, but instead their ends attach to the extracellular
matrix of the interposed scar via adhesion molecules at the newly formed myotendi-
nous junctions. Thus, each ruptured myofiber remains divided into two independent
fibers bound together by the interposed (small) scar. Finally, the maturation of the
regenerated myofibers, retraction and reorganization of the scar tissue, and recovery
of the functional capacity of the muscle occur over time during the maturation phase
(Figure 1.19).
Tissue injury and bleeding result in an inflammatory reaction with the formation of
scar tissue. After this type of injury, there is little muscle tissue regeneration, so that
the injured muscle tissue is replaced by fibrous scar tissue without contractile prop-
erties. This contributes to the highly increased risk of recurrent injuries, for example,
hamstrings strains.
Occasionally, muscle hematomas lead to an unfortunate complication: myositis
ossificans (calcification or ossification of the injured tissue). The most common
(a)
(b)
(c)
Figure 1.19 In strains not
only the myobers rupture
but also their basal lamina
as well as mysial sheaths
and blood vessels
running in the endo- or
perimysium are torn (a).
The ruptured myobers
become necrotized only
over a short distance.
The injured part of the
ruptured myober inside
the remaining old basal
lamina is replaced by the
regenerating myober,
which then begins
to penetrate into the
connective tissue scar
between the stumps of
the ruptured myobers
(b). The maturation
of the regenerating
myobers includes
formation of a mature
contractile apparatus
and attachment of the
ends of the regenerated
myobers to the
intervening scar by newly
formed myotendinous
junctions (c). The
retraction of the scar pulls
the ends closer to each
other, but they appear to
stay separated by a thin
layer of connective tissue
to which the ends remain
attached by newly formed
myotendinous junctions.
(© Medical Illustrator
Tommy Bolic, Sweden.)
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23
location is on the thigh. After quadriceps contusion, it can affect as many as one of
five patients. Myositis ossificans is a nonneoplastic proliferation of bone and cartilage
within the skeletal muscle at the site of a previous single major trauma or repeated
injury or/and hematoma. Being a relatively rare complication of muscle injury, the
scientifically valid evidence regarding either the pathogenesis or the most optimal
treatment is virtually nonexisting. In sports, myositis ossificans is typically associ-
ated with prior sports-related muscle injury (i.e., re-injury to the same location), the
incidence being the highest in the high-contact sports in which the use of protective
devices is uncommon (e.g., rugby). The most common muscle involved is the quad-
riceps femoris, where even up to 20% of injuries could lead into myositis ossificans.
Increased susceptibility to myositis ossificans has also been described in individuals
with hemophilia or other bleeding disorder in conjunction with a soft-tissue injury.
Clinically, myositis ossificans should be suspected if pain and swelling are not clear-
ly subsiding 10–14 days after an injury to a skeletal muscle or if the healing does not
seem to progress normally despite the execution of a proper conservative treatment.
One should be particularly alert if the symptoms intensify weeks (or months) after
the trauma, especially if the site of injury becomes more indurated and the injured
extremity displays reduced joint ROM. Although it is sometimes possible to detect
the first signs of the ectopic bone in radiographs as early as 18–21 days after the
injury, the formation of ectopic bone usually lags behind the symptoms by weeks,
and thus, a definite radiographic diagnosis can only be made substantially later,
even months after the actual injury. It is important to be aware that the radiographic
appearance of the bone mass in the early stage can be confused with osteogenic sar-
coma. The conditions can be difficult to distinguish on histology as well.
Due to its rarity, the treatment principles of myositis ossificans are based more on
empirical experience than on clinical or experimental evidence than any other type of
muscle complaint. The proper first aid of muscle trauma (the prevention of formation
of a large hematoma) naturally creates the foundation for the treatment of this com-
plication. However, if the myositis ossificans still occurs despite the best prevention ef-
forts, there is little that can or should be done in the acute phase. Although indometh-
acin is quite commonly used in orthopedics in preventing heterotopic ossification, it
has not been validated for the prevention and/or treatment of myositis ossificans. The
surgical excision of the bone mass can be considered at later phases, if the symptoms
do not reside despite 12 months of watchful waiting. However, surgery should not be
performed until the ectopic bone has fully “matured,” which is 12–24 months after the
onset of the symptoms, as the excision of immature bone often results in recurrence.
Overall, the myositis ossificans could be considered to underscore the importance of
proper initial treatment of athletes with muscle injury. Despite the fact that a great
majority of muscle injuries heal virtually irrespective of the primary treatment, com-
promised healing of muscle injury (myositis ossificans) results in a delay in return to
sports that is highly comparable—and often even longer—than that associated with the
failed treatment of other sports-related major injuries.
Another complication of intramuscular hematomas is compartment syndrome.
Bleeding and intracellular and intercellular edema can cause such an increase in
pressure that circulation in a muscle compartment is compromised. This affects the
muscle primarily on the capillary level, rarely the large vessels. Thus, a good pulse
distal to the hematoma does not necessarily exclude the possibility of compartment
syndrome. The primary symptom is pain, eventually extreme pain, and the muscle
compartment is hard on palpation. Nerve function may be affected so that the pa-
tient feels paresthesia distally. If it is untreated, compartment syndrome may result
in necrosis of the muscles and major sequelae in the long term.
TYPES AND CAUSES OF INJURIES
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Muscle lacerations are rare in sport but may occur as a result of cuts from the edge
of a skate or a downhill ski. Transverse lacerations cut across the muscle fibers. The
wound muscle rupture is repaired as described in the preceding text for contusions
and strain, that is, with a fibrous scar tissue without contractile properties. This may
have consequences for muscle function.
Muscle stiffness (DOMS) is a troublesome but generally harmless symptom or the
mildest type of muscle injury that all active sports people will have experienced at
some point. DOMS is commonly a consequence of an overenthusiastic exercise of
untrained muscle, which is tolerated while engaged in that activity, but followed by
muscle soreness 1–3 days after the exercise. This phenomenon strikes especially if
the exercise includes eccentric work, that is, lengthening of contracted muscles like
in running downhill or squatting with weights. The symptoms of stiffness, soreness,
and tenderness with palpation develop during the first 1–2 days with a peak on
days 2 or 3, and they disappear usually with no treatment by days 5–7. The pain is
aggravated by passive stretch of the sore muscle and the strength of the muscle is de-
creased. This is usually associated with a rise in serum creatine kinase (CK), which
is usually modest but sometimes up to 20-fold. CK values peak around days 3–6 and
usually return to normal during the first week after the eccentric exercise. Inflam-
matory reaction has been reported in both experimental animals and in humans.
The pain in DOMS is mediated by nociceptors, which in DOMS are most likely
stimulated by factors (such as bradykinin, prostaglandins, and serotonin) released
from the inflammatory cells. Nonsteroidal anti-inflammatory drugs (NSAIDs) have
been used to reduce the pain, but the relatively mild inflammation does not actually
need any alleviation by treatment with NSAIDs. In humans, DOMS develops after
eccentric work excessive for the fitness level of the muscle. Even though DOMS is
associated with CK rise, which must indicate some degree of sarcolemmal damage
inducing leak of sarcoplasmic proteins, it has been demonstrated that in DOMS
usually no frank necrosis of myofibers ensues. The main structural finding has been
focal loss of the myofibrillar (sarcomeric) structures.
... Especially the supraspinatus tendon and the long biceps tendon as well as bursa subacromialis are compressed under the acromion. This causes inflammations such as tendinosis and bursitis which cause pain [8,[28][29][30][31][32]. The FITA study of 2002 stated that overuse injuries were located mainly in the shoulder (46.0%). ...
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