Musculoskeletal System

Muscles

Ligaments

Cartilage
Bones
Tendons
Provides form, support, stability, and movement to the body.

Ramachandran M. Basic Orthopaedic Sciences. 2007. Edward Arnold.UK

Miller MD. Review of Orthopaedics. 2008. 5 th ed.
Salter, RB. Musculoskeletal Disorders-General and Spesific, 3rd ed. 1999. Lippincott
Williams & Wilkins.

BASICS OF BONE

Functions of Bone
As a Structure
1. Provide the rigid framework
for the trunk and
extrimities to withstand
mechanical loads
2. To serve as levers for the
locomotor function of
skeletal muscles
3. To afford protection for
vulnerable viscera (skullbrain; spine-spinal cord;
thoracic cage heart &
lungs)

As an Organ
1. Contains
haematopoetic tissue
of the myeloid type
2. Reservoir or storage
for calcium,
phophorous,
magnesium, and
sodium.

Classification of Bone :
Long Short Flat Irregular
Bones vary in shape
and size
The unique shape of
each bone fulfills a
particular need
Bones are classified by
their shape as long,
short, flat, or
irregular bone
Bones differ in the
distribution of compact
and spongy osseous
tissues

Long Bones
Long bones have a
long shaft and two
distinct ends
Classification is
based on shape not
size
Compact bone on
exterior w/ spongy
inner bone marrow

Short Bones
Short bones are
roughly cubelike
Thin compact bone
layer surrounding
spongy bone mass
Short bones are
often carpal, tarsal
and sesamoid
bones

Flat Bones
Flat bones are thin,
flattened and
usually curved
Parallel layer of
compact bone with
spongy bone layer
between
Skull, sternum and
ribs are examples

Irregular Bones
Irregular bones
dont fit into the
previous categories
Complicated
shapes
Consist of spongy
bone with a thin
layer of compact
Examples are hip
bones & vertabrae

Bone Structure
Microscopic Level :
1.Woven bone
(Immature Bone) :
embryo newborn,
callus, metaphyseal
region
2.Lamellar Bone :
mature bone from
remodelling of
immature bone

As a Structure
1.Cortical Bone
(Compact Bone) : 80%
of the sekeleton,
composed by haversian
system or osteon.
2.Cancellous Bone
(Spongy or Trabecular
Bone) : Less dense and
undergoes remodelling
according to lines of
stress / Wolffs Law. More
elastic

Framework???

Histologic framework of Cortical Bone

Cellular Biology of Bone

(Morphology)
1. Osteoblasts : Form bone by generating the organic,
nonmineralized matrix. Derived from mesenchymal stem
cells
2. Osteocytes : Maintain bone. Make up 90% of the cells in
mature skeleton; former osteoblast that are surrounded by
newly formed matrix.
3. Osteoclasts : Resorb bone. Multinucleated, irregularly
shaped giant cells originate from hematopoietic cells in the
macrophage lineage (monocyte progenitors form giant
cells by fusion).
4. Osteoprogenitor Cells : Originate from mesenchymal
stem cells and become osteoblasts, cartilage, or fibrous
tissue. Line haversian canals, endosteum, and periosteum,
awaiting the stimulus to differentiate.

Bone
Matrix
Composed of organic components (40%) and inorganic components (60%).
Type of Matrix

Function

Composition

Types

Notes

Collagen

Provides tensile
strength

Primarily type I
collagen

90% of organic
matrix; Structure:
triple helix of one 2
and two 1 chains,
quarter-staggered to
produce a fibril

Proteoglycans

Partly rensponsible
for compressive
strength

Glycosaminoglycans
(GAG) protein
complexes

Inhibit
mineralization

Matrix proteins
(noncollagenase)

Promote
mineralization and
bone formation

Organic Matrix

Growth factors

Aid in bone cell

Osteocalcin (bone carboxyglutamic

acidcontaining
protein [bone Gla
protein])

Attracts osteoclasts;
direct regulation of
bone density; most
abundant
noncollagenous
matrix protein (1020% of total)

Osteonectin

Secreted by
platelets and
osteoblasts

Osteopontin

Cell-binding protein

TGF-

Present in small

Bone Matrix
Type of Matrix

Function

Composition

Types

Notes

Inrganic Matrix
Calcium
hydroxyapatite
[Ca10(PO4)6(OH)2]

Osteocalcium
phosphate
(brushite)

Provides
compressive
strength

Makes up most of
the inorganic
matrix; primary
mineralization in
collagen gaps
(holes and
pores),
secondary
mineralization on
periphery
Makes up the
remaining
inorganic matrix

Bone Remodelling
In General :
a.Wolffs Law : Bone remodels in response to stress
b.Pizoelectric Changes : in response to electric changes
c. Hueter-Volkmann Law : occurs in Basic multicellular units
(BMU). Remodelling (+) by mechanical factors logitudinally
. Cortical bone : Remodels by osteoclastic tunneling, ollowed
by layering of osteoblasts and successive deposition of
layers of lamellae until the tunnel size has narrowed to the
diameter of the osteonal central canal.
. Cancellous bone : Remodels by osteoclastic resorption
followed by osteoblasts laying down new bone.

Bone Remodelling
1.Bone resorbed by
osteoclastic activity
in the cortex and
cancellous
2.Osteoblasts form
new bone at the site
prior bone resorption
3.Osteoblasts become
incorporated into
bone as osteocytes.

Tissues Surrounding Bone

Periosteum :
Connective tissue
membrane that covers
bone. More highly
developed in children
because of its role in
the deposition of
cortical bone
Bone Marrow : Source
of progenitor cells;
controls the inner
diameter of bone.

Blood Supply
The skeletal system
receives 5-10% of the
cardiac output. Long
bones receive blood
from three sources
(systems):
1.Nutrient artery
system
2.MetaphysealPeriosteal vessels
Epiphyseal system
3.Periosteal system

Epi-Metaphyseal Vessels

Types of Bone Formation

Enchondral Bone
Formation /
Mineralization
Intramembranous
Ossification
Appositional
Ossification

1. Enchondral Ossification
Undifferentiated cells secrete the
cartilaginous matrix and
differentiate into chondrocytes. The
matrix mineralizes and is invaded by
vascular buds that bring
osteoprogenitor cells. Osteoclasts
resorb calcified cartilage, and
osteoblasts form bone.
Eg.
(1) embryonic long-bone
formation
(2) longitudinal growth (physis),
(3) fracture callus, and
(4) the bone formed with the use
of the demineralized bone matrix.

2. Intramembranous
Ossification
Occurs without a cartilage model.
Undifferentiated mesenchymal cells aggregate into
layers (or membranes).
These cells differentiate into osteoblasts and
deposit an organic matrix that mineralizes to form
bone.
Examples of intramembranous bone formation
include (1) embryonic flat bone formation
(pelvis, clavicle, vault of skull), (2) bone
formation during distraction osteogenesis,
and (3) blastema bone (occurs in young
children with amputations).

3. Appositional Ossification
Osteoblasts align themselves on the
existing bone surface and lay down
new bone.
Examples of appositional
ossification include (1) periosteal
bone enlargement (width) and
(2) the bone formation phase of
bone remodeling.

Type of Bone Formation

Epiphyseal Growth Plate

Ramachandran M. Basic Orthopaedic Sciences. 2007. Edward Arnold.UK

Miller MD. Review of Orthopaedics. 2008. 5 th ed.
Salter, RB. Musculoskeletal Disorders-General and Spesific, 3rd ed. 1999. Lippincott
Williams & Wilkins.

BONE METABOLISM

Normal Bone Metabolism

Serum calcium levels and bone mineral homeostasis are

related intimately and controlled by the synchronized
actions of Vitamin D3 metabolites, PTH (Parathyroid
Hormones), calcitonin, and other hormones.

Feedback mechanisms play an important role in

regulating plasma calcium and phoshate levels

Calcium

Bone serves as a reservoir for more than 99% of the bodys calcium.
Calcium is also important in muscle and nerve function, clotting mechanisms,
and many other areas.
Plasma calcium (<1% of total body calcium) is about equally free and bound
(usually to albumin). It is absorbed in the duodenum by active transport
(requiring adenosine triphosphate (ATP) and calcium-binding protein and
regulated by 1,25-(OH)2 vitamin D3) and by passive diffusion in the jejunum. The
kidney reabsorbs 98% of calcium (60% in the proximal tubule).
The primary homeostatic regulators of serum calcium are PTH and
1,25-(OH)2 vitamin D.
The dietary requirement of elemental calcium is approximately 600 mg/day
for children, about 1300 mg/day for adolescents and young adults (growth spurt
[ages 10-25 years]), and 750 mg/day for adult men and women (age 25-65
years). Pregnant women require 1500 mg/day, and lactating women require
2000 mg/day. Postmenopausal women and patients with a healing
long-bone fracture require 1500 mg/day.
Most people have a positive calcium balance during their first 3 decades of life
and a negative balance after the fourth decade. About 400 mg of calcium is
released from bone daily. Calcium may be excreted in stool.

Phosphate
In addition to being a key component of bone
mineral, phosphate is important in enzyme
systems and molecular interactions (metabolite
and buffer).
Approximately 85% of the bodys phosphate
stores are in bone. Plasma phosphate is mostly
unbound and is reabsorbed by the kidney
(proximal tubule).
Dietary intake of phosphate is usually adequate
(requirement is 1000-1500 mg/day). Phosphate
may be excreted in urine

Parathyroid Hormone (PTH)

An 84amino acid peptide synthesized in and
secreted from the chief cells of the (four)
parathyroid glands PTH helps regulate plasma
calcium.
It directly activates osteoblasts and modulates renal
phosphate filtration. Decreased calcium levels in the
extracellular fluid stimulate 2 receptors to release
PTH, which acts at the intestine, kidney, and bone.
PTH may affect bone loss in the elderly.
PTH-related protein and its receptor have
been implicated in metaphyseal dysplasia.

Vitamin D (active
metabolites)
Naturally occurring steroid activated by ultraviolet
irradiation from sunlight or utilized from dietary
intake.
It is hydroxylated to 25-(OH) vitamin D3 in the liver
and is hydroxylated a second time in the kidney.
Conversion to the 1,25-(OH)2 vitamin D3 form
activates the hormone, whereas conversion to the
24,25-(OH)2 vitamin D form inactivates it.
The active form works at the intestine, kidney, and
bone.
Phenytoin (Dilantin) causes impaired metabolism of
vitamin D.

Calcitonin
A 32amino acid peptide hormone produced by the
clear cells in the parafollicles of the thyroid gland;
has a limited role in calcium regulation.
Increased extracellular calcium levels cause secretion
of calcitonin, which is controlled by a 2 receptor.
Calcitonin inhibits osteoclastic bone resorption
(osteoclasts have calcitonin receptors;
decreases osteoclast number and activity) and
decreases serum calcium.
May also have a role in fracture healing and reducing
vertebral compression fractures in high-turnover
osteoporosis.

Other Hormones and Growth Factors

Estrogen : Prevents bone loss by inhibiting bone resorption (a
decrease in urinary pyridinoline cross-links is observed).
Corticosteroids : Increase bone loss (decrease gut absorption of calcium
by decreasing binding proteins; decrease bone formation [cancellous more
affected than cortical bone] by inhibiting collagen synthesis and osteoblast
productivity; they do not affect mineralization). Alternate-day therapy may
reduce the effects.
Thyroid hormones : Affect bone resorption more than bone formation,
leading to osteoporosis (large [thyroid-suppressive] doses of thyroxine can
lead to osteoporosis).
Growth hormone : Causes positive calcium balance by increasing gut
absorption of calcium more than it increases urinary excretion. Insulin and
somatomedins participate in this effect.
Insulin : Insulin type I diabetes; if poorly controlled, may lead to bone loss
Growth Factors : IL-1 and IL-6 and TNF-stimulate proliferation of
osteoclast precursors ; IGF activates osteoblasts and is produced by
osteoblasts; TGF activates osteoblasts, also stimulates osteoclasts (invitro)

Miller MD. Review of Orthopaedics. 2008. 5th ed. Saunders.

Elsevier Inc.
Einhorn TA, OKeefe RJ, Buckwalter JA. Orthopaedic Basic
Science. 2007. 3rd ed. Amer Academy of Orthopaedics
Surgeons.

BASICS OF JOINTS /
ARTICULAR CARTILAGE

Introduction
Articular cartilage, the resilient
load-bearing tissue that forms
the articulating surfaces of
diarthrodial joints, provides these
surfaces with the low friction,
lubrication, and wear
characteristics required for
repetitive gliding motion.
It also absorbs mechanical shock
and spreads the applied load
onto subchondral bone. In most
synovial joints, articular cartilage
provides these essential
biomechanical functions for 8
decades or more.
No synthetic material performs
this well as a joint surface.

How Many Types of Joint ?

Five distinct types of joints exist :
1.Syndesmosis : a joint in which the two bones are bound
together by fibrous tissue only (eg. Suture in skull bones)
2.Synchondrosis : the 2 bones are bound together by
cartilage. (eg. Epiphyseal plate, cartilaginous joints in base of
skull)
3.Synostosis : a joint at some stage has become obliterated
by bony union.
4.Symphysis : 2 oppositing surfaces are covered by hyaline
cartilage and joined by fibrocartilage and strong fibrous
tissue.
5.Synovial joint : 2 opposing surfaces are covered by hyaline
articular cartilage and joined peripherally by fibrous tissue
capsule and contains synovial fluid.

Articular Tissues
A
Cartilage
B
Synovium
C
Meniscus

Cartilage
Types :
1.Physeal cartilage / Growth
plate :
2.Fibrocartilage : at tendon insertion
into bone
3.Elastic cartilage : such as trachea
4.Fibroelastic cartilage : meniscus
5.Articular cartilage :

Articular Cartilage :
Composition
1. Water
2. Collagen
3. Proteoglycans
4. Chondrocytes
5. Matrix components

Articular Cartilage : Water

65-80% of wet weight
Shifts in and out of cartilage to allow
deformation of cartilage surface in response to
stress.
Water is not distributed homogeneously (65% in
deep zone, 80% at surface).
Water content increases (90%) in osteoarthritis.
Water is also responsible for nutrition and
lubrication. Increased water content leads to
increased permeability, decreased strength, and
decreased Youngs modulus (E).

Articular Cartilage :
Collagen
(10-20% of wet weight; >50% of dry weight)
Type II collagen accounts for approximately 95% of the total collagen content of
articular cartilage and provides a cartilaginous framework and tensile
strength. Type II collagen is very stable, with a half-life of
approximately 25 years.
Increased amounts of glycine, proline, hydroxyproline, and hydrogen bonding
are responsible for its unique characteristics.
Small amounts of types V, VI, IX, X, and XI collagen are present in the matrix of
articular cartilage.
Collagen type VI is a minor component of normal articular cartilage, but its
content increases significantly in early osteoarthritis.
Collagen type X is produced only by hypertrophic chondrocytes during
enchondral ossification (growth plate, fracture callus, HO formation,
calcifying cartilaginous tumors) and is associated with calcification of
cartilage; a genetic defect in type X collagen is responsible for
Schmids metaphyseal chondrodysplasia (affects the hypertrophic
physeal zone). Collagen type XI is an adhesive holding the collagen
lattice together.

Types of Collagen

Articular Cartilage :
Proteoglycan
(10-15% of wet weight)
Protein polysaccharides provide compressive strength.
Proteoglycans are produced by chondrocytes, are secreted into
the extracellular matrix, and are composed of subunits known as
glycosaminoglycans (GAGs, disaccharide polymers).
These GAGs include two subtypes of chondroitin sulfate
(the most prevalent GAG in cartilage) and keratin sulfate.
The concentration of chondroitin-4-sulfate decreases with
age, that of chondroitin-6-sulfate remains essentially
constant, and that of keratin sulfate increases with age.
Proteoglycans have a half-life of 3 months, provide structural
properties for the articular cartilage, provide elastic strength,
produce cartilages porous structure, and trap and hold water
(regulate and retain fluid in the matrix).

Articular Cartilage :
Chondrocytes

(5% of wet weight)

Active in protein synthesis, possess a double effusion
barrier; produce collagen, proteoglycans, and some
enzymes for cartilage metabolism, including the
metalloproteinases (breakdown cartilage matrix) and
tissue inhibitor of metalloproteinases; least active in
the calcified zone.
Deeper cartilage zones have chondrocytes with a
decreased rough endoplasmic reticulum (RER) and
increased intraplasmic filaments (degenerative
products). Chondroblasts, derived from undifferentiated
mesenchymal cells (stimulated by motion), are later
trapped in lacunae to become chondrocytes.

Articular Cartilage : Matrix

Adhesives (noncollagenous proteins,
such as fibronectin, chondronectin,
and anchorin CII)Involved in
interactions between chondrocytes
and fibrils. Fibronectin may be
associated with osteoarthritis.
LipidsUnknown function

Cartilage Layers

Synovium
The synovium mediates the
nutrient exchange between
blood and joint (synovial) fluid.
Synovial tissue is composed of
vascularized connective tissue
that lacks a basement
membrane.
Two cell types are present: type
A, important in phagocytosis,
and type B (fibroblast-like
cells), which produce synovial
fluid (broth). Other
undifferentiated cells have a
reparative role. A third type of
cell, type C, may exist as an
intermediate cell type.

Synovial Fluid
Consists of hyaluronic acid, lubricin (a lubricating glycoprotein),
proteinase, collagenases, and prostaglandins.
Synovial fluid is an ultrafiltrate (dialysate) of blood plasma added
to fluid produced by the synovial membrane; it contains no RBCs,
clotting factors, or hemoglobin.
It lubricates articular cartilage and provides nourishment
through diffusion. Synovial fluid exhibits non-Newtonian
flow characteristics (the viscosity coefficient is not a constant;
the fluid is not linearly viscous); its viscosity increases as the
shear rate decreases.
Lubricin is the key lubricating component.
Hyaluronan molecules in the knee become entangled and
behave like an elastic solid during high-strain activities (running,
jumping).
Analysis of synovial fluid in disease processes is important

Meniscus *knee*
Deepens the articular surface of a variety of synovial joints
(acromioclavicular, sternoclavicular, glenohumeral, hip,
knee), broadening the contact area and distributing the load,
such as that on the tibial plateau.
The meniscus is more elastic and less permeable than
articular cartilage.
The meniscus transmits 50% of the force across the
joint when the knee is extended and up to 90% in
deep flexion.
Three years after total meniscectomy of the knee,
20% of patients have significant arthritic lesions and
70% have x-ray changes; all experience arthrosis after
20 years. The severity of degenerative changes is
proportional to the amount of meniscus excised.

Meniscus

Miller MD. Review of Orthopaedics. 2008. 5th ed. Saunders.

Elsevier Inc.
Einhorn TA, OKeefe RJ, Buckwalter JA. Orthopaedic Basic
Science. 2007. 3rd ed. Amer Academy of Orthopaedics
Surgeons.

SKELETAL MUSCLES

Skeletal Muscle Architecture

Noncontractile Elemets :
1.Muscle Body :
2.Myotendineous junction :
weak link.
3.Sarcoplasmic reticulum :
stores Calcium
. Contractile Elements :
Derived from myoblasts ;
fascicles muscle fibers
myofibrils
sarcomeres.

Muscle Action
Nerve cell body delivers electrical signal to motor endplate
(junction between muscle and nerve) : nerve action potentials are
started with passage of sodium ions through voltage gated
channels
Ach (Acetylcholine) is released and diffuses across synaptic cleft to
bind to Ach receptor :
- myasthenia gravispatient has shortage of Ach receptors
- botoxblocks release of Ach from end plate
Ach binding triggers depolarization of sarcoplasmic reticulum
andrelease of calciuminto muscles cytoplasm
Calcium binds to troponin(on thin filaments) leading to a
configuration change of tropomycin (on thin filaments) and
exposure of actin filament
Exposed actin cross-bridges to myosin, and the ATP breakdown, the
two fibers contact past one another

Muscle Action

Types of Muscle Contraction

Types of Muscle Fiber

Energetic System
1.ATP-CP system (phosphagen system). Meets the metabolic
requirements for intense muscle activities that last up to 20 seconds,
such as sprinting a 100- to 200-meter dash. Converts stored
carbohydrates from within the muscle fiber itself to energy. Does
not use oxygen and does not produce lactate. Energy is
derived from the high-energy phosphate bonds during hydrolysis :
(ATP ADP + P + Energy) ; (ADP AMP + P + Energy)
2.Lactic anaerobic system (lactic acid metabolism)Meets the
metabolic requirements for intense muscle activities that last for 20120 seconds, such as a 400 meter sprint. Involves hydrolysis of
one glucose molecule to ultimately produce lactic acid plus energy,
converting two molecules of ADP to two molecules of ATP. : (glucose
lactic acid + Energy)
3.Aerobic systemWhen oxygen is available, the aerobic system
replenishes ATP through oxidative phosphorylation and the Krebs
cycle; uses glucose or fatty acids to produce ATP. Meets the
metabolic requirements for episodes of longer duration and
lower-intensity muscle activities.

Aerobic & Anaerobic System

Athletes & Training

The distribution of FT versus ST fibers is genetically
determined; however, specific training can selectively
improve these fibers.
Endurance athletes typically have a higher
percentage of ST fibers, whereas athletes
participating in strength-type sports (and sprinters)
have more FT fibers.
1. Endurance Training
2. Strength Training
3. Aerobic Training
4. Use of anabolic steroids
5. Sudden Death
6. Nutrition

Endurance Training
Training for endurance sports
consists of decreased tension and
increased repetitions, which induces
hypertrophy of the ST fibers and
increases the number of
mitochondria, capillary density, and
oxidative capacity, resulting in
increased resistance to fatigue.
This type of training also improves
blood lipid profiles.

Strength Training
Consists of increased tension and decreased repetitions, which increases the
number of myofibrils/fibers and induces hypertrophy (increased crosssectional area) of FT (type II) fibers.
Both types of training slow the lactate response to exercise. The cross-sectional
area of skeletal muscle reliably predicts the potential for contractile force.
Isokinetic exercises produce more strength gains than isometric
exercises.
Isotonic exercises produce a uniform strength increase throughout joint ROM.
Plyometric (bounding) exercises consist of a muscle stretch followed
immediately by a rapid contraction. The stretch stores elastic energy, which
increases the force of the concentric muscle contraction. Plyometrics is the
most efficient method of conditioning for improvement in power.
Closed-chain exercise refers to loading an extremity with the most distal
segment stabilized or not moving; this allows muscular co-contraction around a
joint, which minimizes joint shear (e.g., placing less stress on the ACL).
Oxygen consumption (VO 2) is an important consideration when training
athletes.

Aerobic Training
Aerobic conditioning (cardiorespiratory fitness) in a
healthy adult is recommended 3-5 days per week for 20-60
minutes per session (training at 60-90% of maximum heart
rate).
Long-distance runs increase aerobic capacity and endurance
but decrease flexibility and optimum explosive strength.
Aerobic conditioning has proved effective in lowering the
incidence of back injury in workers and in helping the elderly to
remain ambulatory.
In contrast to resistance exercise, aerobic exercise
increases stroke volume, which increases cardiac
output.
A significant decline in aerobic fitness (detraining) occurs
after just 2 weeks of no training.

Anabolic Steroids & Growth

Hormones
Anabolic (androgenic) steroids cause increased muscle strength,
increased body weight, testicular atrophy, irreversible deepening of the
female voice, reduction in testosterone and gonadotropic hormones,
growth retardation, oligospermia, azoospermia, gynecomastia,
hypertension, striae, cystic acne, alopecia (irreversible), liver tumors,
increased low-density lipoprotein (LDL), decreased high-density lipoprotein
(HDL), and abnormal liver isoenzyme lactate dehydrogenase (LDH).
Anabolic steroids do not increase aerobic power or capacity for muscular
exercise but have been shown to be more effective than corticosteroids for
long-term muscle strength recovery after contusion injury.
Athletes who use pure testosterone extract to enhance performance have
both anabolic and androgenic effects. The anabolic effects include muscle
development, increased muscle mass, and erythropoiesis.
Abuse of the growth hormone somatotropin among adults causes
selective hypertrophy of type I muscle fibers, which produces atrophy of
type II fibers and leads to muscle hypertrophy, with weakness and fatigue.

Sudden Death & Injury

Prevention

A syncopal episode in a young athlete

suggests a serious underlying cardiac
abnormality (and a risk of sudden death); a
timely medical evaluation is mandatory prior
to returning to athletics.
The most common cause of sudden death in
young athletes is hypertrophic obstructive
cardiomyopathy. While abdominal injuries in
athletes most commonly affect the kidney.
Wraparound polycarbonate glasses should be
worn to protect the eyes in racquet sports.

Nutrition
Weight reduction with fluid and food restriction) is associated with reduced
cardiac output, increased heart rate, smaller stroke volumes, lower oxygen
consumption, decreased renal blood flow, and electrolyte loss.
Carbohydrate loading involves increasing carbohydrates three days prior to
an event (marathon) and decreasing physical activity.
The best fluid replacement regimen for a competitive athlete is to consume
enough water to maintain prepractice weight and maintain a normal diet. Fluid,
carbohydrate, and electrolyte replacement is most effective when the osmolality
of the replacement fluid is <10% (glucose polymers minimize osmolality); fluid
absorption by the gut is enhanced by solutions of low osmolality.
Creatine supplements are used by some athletes to attempt to enhance
performance. The physiologic basis for this is that creatine is converted to
phosphocreatine, which acts as an energy reservoir for ATP in muscle. Recent
studies have shown that creatine supplementation can increase the
amount of work that is produced in the first few maximum-effort
anaerobic trials but does not increase peak force production.
Treatment of heat cramps includes passive stretching, cooling, and
fluid/electrolyte replacement.

MUSCLE INJURY

Muscle Injury
Muscle Strains
Most muscle strains
(the most common
sports injury) occur at
the myotendinous
junction in muscles
crossing two joints
(hamstring,
gastrocnemius) that
have increased type II
fibers Initially there is
inflammation and later
fibrosis.

Muscle Tears
Muscle tears occur most commonly
at the myotendinous junction,
often during a rapid (high-velocity)
eccentric contraction; eccentric
contractions develop the highest
forces observed in skeletal muscle.
Muscle tears typically heal with dense
scarring. Surgical repair of clean
lacerations in the mid-belly of skeletal
muscle usually results in minimal
regeneration of muscle fibers distally,
scar formation at the laceration, and
recovery of about one-half of muscle
strength.
Muscle activation (via stretching)
allows twice the energy absorption
prior to failure; bouncing types of
stretching are deleterious.

Muscle Injury
Mescle Soreness

Denervation

Delayed-onset muscle
soreness (DOMS) occurs 24-72
hours after intense exercise
and may result from eccentric
muscle contractions and be
associated with changes in the I
band of the sarcomere.
NSAIDs relieve DOMS in a
dose-dependent fashion, and
massage has varying effects;
other modalities (ice,
stretching, ultrasound,
electrical stimulation) have
not been shown to affect
DOMS.

Denervation causes muscle atrophy

and increased sensitivity to Ach
causing spontaneous fibrillations at
2-4 weeks after damage to the motor
axon.
Spasticity is related to increased
muscle reactivity to stretch.
Muscle strength gains during the first
10 days of rehabilitation are due to
improved neural firing patterns.
Later strength gains are due to
increases in ROM, muscle fiber size,
muscle repair, and tendon repair.
Trunk extensors are stronger than
trunk flexors.