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Presents:
The Anatomy of Exercise
Educator:
Willem Stegeman, DPT, MTC, CEAS
Jorit Wijnmaalen, DPT, MBA, MTC, CEAS
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Why do we need to know and understand the
anatomy of muscle?
•This will allow the clinician to specify their exercise program
geared towards the function of the muscle. Different muscles
have different functions and these functions are in part defined by
the anatomy of the muscle.
•There are approximately 639 skeletal muscles in the human
body. There are different types of muscles, each with their
distinct anatomy.
•Understanding the anatomy of the muscle will also help the
clinician understand how different (intrinsic and extrinsic)
factors can impact muscles and exercising.
•We are looked upon as the experts when it comes to exercise
therapy. Understanding the anatomy of muscles is an important
part of being an exercise expert.
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Program Objectives:
•Reviewing muscular anatomy and physiology
•This will include a review of tissue healing
•Discuss how extrinsic factors such as medication,
progression, exercise objectives etc. may affect the exercise
therapy program
•Discuss how intrinsic factors including disease processes
age, vital signs etc. may affect muscles and exercise
programs.
•Discuss the basics of exercise therapy
•Discuss common exercise principles
•Open chain vs. closed chain
•Eccentricisometricconcentric
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A few rules:
•We are in a hospital and should be aware of
any codes that might be called.
•Bathrooms are right outside of this room
•We will break for lunch are around noon
•Please turn off all cell phones.
•I would like to make this lecture as interactive
as possible. Please feel free to ask questions,
share your experiences, opinions etc. with the
rest of the group.
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About the educators:
•Background
•Education
•Work experience
•Hobbies
About
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• 4 educators
– Dr Brian Healy
– Johan Sloots
– Dr. Willem Stegeman
– Dr Jorit Wijnmaalen
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About
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More courses:
• Orthopedic Joint Replacement course: 10.5 CE
• Comprehensive Management of back &
neck pain: 10 CEU
• Joint Replacement, online: 7 CEU
 Thoracic Outlet Syndrome: 6 CEU, Online
 HIV/Medical Errors/Abuse: 4 CEU
 The anatomy of exercise: 7.5 CEU
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Muscular anatomy and physiology
Muscle Types:
Smooth muscles
Cardiac muscles
Skeletal muscles
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Smooth muscles
•These muscles are very important in physiological
regulation.
•Help to regulate the flow of blood.
•Help control BP
•They control the movement of food through the digestive
system.
•Control of the uterus during labor
•Contraction of a smooth muscle cell is generated by a sliding
mechanism of the myofilaments.
•Contraction is involuntary and may be initiated by
•Nerve impulse
•Hormones (i.e. cardiac function)
•Mechanical change to the muscle
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Smooth Muscles
•Crucial difference with skeletal
muscles: nervous control is
absolutely required for skeletal
muscles, smooth muscles can, to a
degree, work with out nervous
stimulation!
•Lastly, these muscles are not
striated (the myofilaments are
arranged into light and dark bands
as in striated muscles).
Striations are formed by alternating segments of thick and thin
protein filaments, which are anchored by segments called T-lines
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Cardiac Muscles
This muscle may look like a
skeletal muscles (especially
the contraction of it since
they are striated as well)
but it acts much like
smooth muscle (it does not
require nervous system
input to function)
• The attachment site
between cells is called an
intercalated disc, which is
present only in cardiac
muscle cells and allows
forces to be transmitted
from one cell to the next.
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Skeletal Muscles:
•Striated (banded) type. This distinctive banding pattern of
striated muscle is an effect that comes from the alignment of
sarcomeres in register across the myofibrils
•Skeletal muscles are under voluntary control; no skeletal
muscle works without “orders” from the nervous system
•Skeletal muscles have elongated muscle cells (fibers) with
multiple nuclei lying along the periphery of the cell. The
sarcoplasm of each cell is contained by a sacrolemma (plasma
membrane) and an external lamina.
•Each muscle contains many myofibrils and each myofibril
contains thin actine and thick myosin myofilaments.
•These muscles normally make up the largest portion of a
person's lean body mass
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Skeletal Muscles
•These are the muscles that are responsible for all voluntary
movements (movements controlled by the central nervous
system and which typically are directed at some sort of
interaction with the environment)
•These muscles only contract in response to instructions
from the central nervous system (few exceptions)
Shivering is a response to the cold. Human have a stable body
temperature - the average temperature of the human body is
36.9[degrees]C (98.6[degrees]F). In order to remain healthy
humans must keep their body temperature within the narrow
range of 36[degrees].-38[degrees]C. The hypothalamus,
which acts as a thermostat. It responds if the skin cools down
and as nerve endings signal danger. in cold conditions, the
skin's thermal receptors send messages to the hypothalamus,
which directs blood away from the skin to minimize heat
exchange with the air.
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•As the skin cools, shivering sets in with the muscles contracting
and releasing in bursts, to exert some "muscle exercise" in order
to increase heat production and warm the body
•Shivering is an early warning sign of cold stress and a signal to
get out of the cold or put on extra clothing.
•Shivering usually starts in the head and neck, then spreads
down through the back and to the muscles in the lower body
Some muscles shiver more efficiently than others - such as the
mouth muscles that make the "teeth chatter."
•With more body cooling, shivering becomes more violent, with
maximum shivering at a cooling to 34[degrees]-35[degrees]C.
Moderate hypothermia (core body cooling) sets in around
33[degrees]-30[degrees]C with cessation of shivering as people
lose core heat.
•Below 30[degrees]C, hypothermia becomes severe and lifethreatening.
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•A drop in core body temperature of only 2[degrees]C can
produce confusion, light-headedness, stumbling and slowed
movements. With increasing cooling of the core temperature,
severe hypothermia sets in with coma and eventually death.
•When shivering stops, it is a danger signal.
•But if the sense of cold is impaired or if the shivering response
is less efficient, people are at increased risk of hypothermia and
cold injuries, such as frostbite.
•Some people have a reduced ability to respond to cold, for
example the elderly, who cannot shiver as readily as younger
people.
•They may therefore not respond to cold and are especially prone
to hypothermia. Not recognizing the early symptoms of
hypothermia, the sluggish behavior can be taken for slowed
reflexes or signs of other disorders and not receive proper
medical attention.
•Babies younger than a year old also cannot shiver.
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Skeletal Muscles
•In short, these skeletal muscles have the following
functions:
•provide joints with the forces necessary to produce
movement
•to control movement
•to stabilize and protect joints when loads are applied to
them.
•Skeletal muscles are a striated type of muscle with a rich
blood supply, extensive afferent and efferent innervation and
an extremely high metabolic capacity.
•Skeletal muscles have a tremendous adaptive capacity that
allows then to hypertrophy, atrophy, increase in physiological
length, decrease in physiological length and change
metabolic capacities.
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Skeletal Muscles
Out of the three muscle types discussed, the skeletal
muscle are the muscles that we will be most concerned
within this course.
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Muscular anatomy and physiology
Let’s review!
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The Anatomy review of a skeletal muscle
•Each muscle cell is surrounded by a basal lamina and
connective tissue.
•They are bound to each other and to surrounding tissues by
connective tissue to form a gross "muscle". Skeletal muscle
fibers are NOT joined by cell junctions.
•The endomysium consists of the basal lamina and thin
connective tissue that surrounds individual muscle cells.
•The perimysium consists of sheets of connective tissue
which separate the fibers into groups known as fascicles.
•The epimysium surrounds the groups of fasicles that
comprise the “muscle”.
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Quick anatomic review of a skeletal muscle
•Connective tissue transmits the mechanical force of muscle.
•Tendons connect muscle to bone. The myotendinous junction
occurs at the end of the muscle cell where the terminal actin
filaments connect to the plasma membrane
•Skeletal muscle fibers are multi-nucleate cells that arise by
fusion of mono-nucleate myoblasts.
•The many nuclei are located at the periphery of the cell.
•Mono-nucleate satellite cells, associate with the muscle fiber
and reside within the muscle basal lamina. They promote
limited regeneration of muscle in the adult.
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The Yellow line is
corresponding to
the tendon. How
do we classify this
Connective tissue?
Dense Regular. The
yellow arrows are
pointing the nuclei
of the fibroblasts
making the
collagen.
The blue line is
showing where the
Striated Muscle is
beginning
The muscle-tendon junction
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Innervation of a Skeletal Muscle
•Skeletal muscle is innervated and highly vascularized, due to
its high energy requirements. It is penetrated of blood vessels
into the epimysium with branches into the peri- and
endomysium.
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Innervation of a Skeletal Muscle
•Motor end plates (neuromuscular junctions) are
specialized sites at which a nerve contacts a muscle cell.
•The terminal branches of motor axons lie in the surface of
the muscle cell, where the plasma membrane is highly
folded.
•Muscle action begins at the motor end plate (or
neuromuscular junction), which is analogous to a synapse
•Acetylcholine(ACh) binds to receptors localized in the
muscle membrane at the motor end plate, resulting in local
depolarization at the end plate.
•When this depolarization exceeds the threshold, it will
result in an action potential
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Neuromuscular Junction or
Motor End Plate
axon of Motor (Efferent)
Neuron
White arrow - Skeletal
Muscle Fiber
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Innervation of a Skeletal Muscle
•Additional proprioceptor endings (Golgi tendon organs) are
located at the point where muscle fibers attach to tendon
•These Golgi tendon organs (GTO) respond to tension (force)
exerted by the muscle; activity in these axons inhibits muscle
contraction (they are for instance stretched when a joint is
swollen).
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Nerve Conduction
•Both nerve cells and muscle cells are excitable
•Their cell membrane can produce electrochemical
impulses and conduct them along the membrane.
•In muscle cells, this electric phenomenon is also associated
with the contraction of the cell
•The origin of the membrane voltage is the same in nerve
cells as in muscle cells. In both cell types, the membrane
generates an impulse as a consequence of excitation.
•The long nerve fiber, the axon, transfers the signal from
the cell body to another nerve or to a muscle cell
•The axon may be covered with an insulating layer called
the myelin sheath, which is formed by Schwann cells
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Nerve Conduction
•This myelin sheath is not continuous but divided into sections,
separated at regular intervals by the nodes of Ranvier
•The junction between an axon and the next cell with which it
communicates is called the synapse.
•Information proceeds from the cell body uni-directionally over
the synapse, first along the axon and then across the synapse to
the next nerve or muscle cell (think about peripheral leasion)
•The part of the synapse that is on the side of the axon is called
the pre-synaptic terminal
•The part on the side of the adjacent cell is called the
postsynaptic terminal. Between these terminals, there exists a
gap.
•A chemical neurotransmitter, released from the pre-synaptic
cell, is responsible for the impulse to transfer across the synapse.
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Nerve Conduction
•This transmitter, when released, activates the postsynaptic
terminal. The synapse between a motor nerve and the muscle it
innervates is called the neuromuscular junction
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Nerve Conduction
•If a nerve cell is stimulated, the trans-membrane voltage
necessarily changes. The stimulation may be
•excitatory (i.e., depolarizing; characterized by a decrease
in the normally negative resting voltage) or
•inhibitory (i.e., hyperpolarizing, characterized by an
increase in the magnitude of the membrane voltage).
•After stimulation the membrane voltage returns to its original
resting value
•If the excitatory stimulus is strong enough, the trans-membrane
potential reaches the threshold, and the membrane produces a
characteristic electric impulse, the nerve impulse.
•Remember the Na+/K+ pump?
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Nerve Conduction
Many factors may affect nerve conductivity but discussion of
those factors would be outside the scope of this lecture.
•Temperature
•Properties of the membrane
•Sodium levels
•Calcium levels
•Age
•Anatomical changes because of disease (ALS)
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Nerve Conduction
•A myelinated axon (surrounded by the myelin sheath) can
produce a nerve impulse only at the nodes of Ranvier
•In these axons the nerve impulse propagates from one node to
another
•The myelin sheath increases the conduction velocity
•The conduction velocity of the myelinated axon is directly
proportional to the diameter of the axon
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Nerve Conduction
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Types of Skeletal muscles
Not all skeletal muscle is the same.
•Some cells are thicker than others
•Some shorten faster
•Some produce more tension
•Some fatigue more rapidly
Looking at these different features, there appear to be three
major types of skeletal muscles:
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Types of Skeletal muscles
• Slow Twitch
• Fast Fatigue Resistant
• Fast Twitch Fatigable
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Slow Twitch
•These muscles produce the least amount of
force. They actually produce less than half the
force produced by fast twitch fatigue resistant
fibers and are most resistant to fatigue.
•Slow twitch muscles use oxygen for power and
have a predominance of aerobic enzymes.
•Slow twitch muscles are red, because they
contain lots of blood vessels.
•These muscle fibers are "hit", or engorged with
nitrogen-rich blood, during higher rep training,
specifically in sets of 12 to 20 reps.
• Slow twitch muscles are used for holding
posture
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Fast Twitch (Type II)
•Fast Twitch fibers use anaerobic metabolism to create
fuel and so they are much better at generating short
bursts of strength or speed than slow muscles.
•These types of muscles are best trained during sets of 25 repetitions.
•They fatigue more quickly.
•Fast twitch fibers generally produce the same amount
of force per contraction as slow muscles, but they get
their name because they are able to fire more rapidly.
•Having more fast twitch fibers can be an asset to a
sprinter since she needs to quickly generate a lot of
force (genetically determined, 50/50 on average; some
research suggests that some fibers might be able to
convert).
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Two Types:
Type IIa Fibers / Fast Fatigue Resistant
•These fast twitch muscle fibers are also known as
intermediate fast-twitch fibers.
•They can use both aerobic and anaerobic metabolism
almost equally to create energy.
•In this way, they are a combination of Type I and Type II
muscle fibers.
•Produce forces greater than slow twitch fibers but less than
fast twitch fatigable fiber.
•These fibers are more resistant to fatigue than fast
fatigable but less fatigue resistant than slow twitch fibers.
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Type IIb Fibers
•These fast twitch fibers use anaerobic metabolism to
create energy and are the "classic" fast twitch muscle fibers
that excel at producing quick, powerful bursts of speed.
•This muscle fiber has the highest rate of contraction
(rapid firing) of all the muscle fiber types, but it also has a
much faster rate of fatigue and can't last as long before it
needs rest.
•Produce the greatest amount of force
•Are least resistant to fatigue
•Force produced is typically 2-3 times greater than fast
twitch fatigue resistant fibers
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Skeletal
Muscle
Types
Slow
Twitch
Fibers
Fast
Fatigue
Resistant
Other
name
Red, Slow
oxidative
Type I
White, fast
oxydative,
glycolytic
Type IIA
Twitch Twitch Fatigue Oxydative Fiber
Motor Capillary Mitotime tension rate
capacity diameter unit size density chondria
Slow
Low
High
Small
Small
High
Many
Fast
Interme Interme
diate diate High
Large
Large
High
Many
High
Large
Large
Low
Few
Fast
Twitch White, fast,
Fatiguable Type IIB Fast
Slow
Fast
Low
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Conclusion
•So the lesson here is quite simple. As we are exercising our
patients, we must keep in mind the main objective of our
exercise program.
•In order to recruit the largest possible number of muscle
fibers of both types during the exercise program, we must
vary the repetition ranges .
•Keeping in mind that on average, there is a 50/50 split of
these fibers so…
•Any therapist, who puts a patient on an exercise program
that doesn't include a variation of repetition ranges might
significantly limit the success of the exercise program.
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Skeletal Muscle Fiber Arrangement
•It is important to realize that there are different alignments of
muscle fibers in the various skeletal muscles.
•These different fiber arrangements will have an effect on the
length, mechanical properties and the number of muscle fibers
of a muscle.
•Muscle fibers can be arranged in parallel or at angles to the
tendon.
•Parallel fibered muscles are muscle composed of parallel aligned
fibers. These muscles have long muscle fibers that can produce a
large excursion on the tendon.
•Fusiform
•Triangular
•Spiral
•Pinnated fibers muscles are muscles composed of angled fibers
•Unipinnate
•Bipinnate
•Multipinnate
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Parallel
Fusiform
Unipennate
Triangular
Spiral
Bipennate
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Structure & Function of a Skeletal muscle
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•The cell comprises a series of striped
or striated, thread-like myofibrils.
•Within each myofibril there are
protein filaments that are anchored by
dark Z line.
•The fiber is one long continuous
thread-like structure.
•The smallest cross section of skeletal
muscle is called a sarcomere which is
the functional unit within the cell. It
extends from one Z line to the next
attached Z line. The individual
sarcomere has alternating thick myosin
and thin actin protein filaments.
•Myosin forms the center or middle of
eache M line. Thinner actin filaments
form a zig zag pattern along the anchor
points or Z line.
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Muscle Contraction
Upon stimulation by an action potential, skeletal muscles
perform a coordinated contraction by shortening each
sarcomere.
The best proposed model for understanding contraction is
the sliding filament model of muscle contraction.
•Actin and myosin fibers overlap in a contractile motion
towards each other.
•ATP binds to the cross bridges between myosin heads and
actin filaments. The release of energy powers the
swiveling of the myosin head
•Myosin filaments have club-shaped heads that project
toward the actin filaments.
•Larger structures along the myosin filament called myosin
heads are used to provide attachment points on binding
sites for the actin filaments.
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Muscle Contraction (cont.)
•The myosin heads move in a coordinated style, they swivel
toward the center of the sarcomere, detach and then reattach to
the nearest active site of the actin filament.
•This is called a rachet type drive system.
•This process consumes large amounts of adenosine
triphosphate (ATP).
•Calcium ions are required for each cycle of the sarcomere.
•Calcium is released from the sarcoplasmic reticulum into the
sarcomere when a muscle is stimulated to contract. This
calcium uncovers the actin binding sites.
•When the muscle no longer needs to contract, the calcium ions
are pumped from the sarcomere and back into storage in
the sarcoplasmic reticulum
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Images from Purves et al., Life: The Science of Biology, 4th Edition, by Sinauer Associates
(www.sinauer.com) and WH Freeman (www.whfreeman.com)
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Muscle contraction (cont.)
•ATP is the main source of energy for all muscle contraction.
•There are several chemical reactions that take place to produce
ATP.
•When a muscle is used, a chemical reaction breaks down ATP
to produce energy:
ATP + Actin + Myosin
Energy
Actomyosin + Phosphate + ADP +
•This is the chemical reaction that produces energy, however,
there is only enough ATP stored in the muscle cell for two or
three slow twitch contractions, or one burst of power from a
fast twitch contraction. More ATP must be created.
•There are three enzyme systems that can create more ATP.
The enzyme system that is used depends on whether the type of
muscle is fast twitch or slow twitch, and whether the muscle is
used for strength, burst power, or endurance.
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Muscle Contraction (Cont.)
The Strength Enzyme System
•When muscle strength is required, ATP is created quickly
from the following chemical reaction.
•The enzyme creatine kinase mediates ATP production from
the high energy molecule creatine phosphate by an anaerobic
reaction:
•CP + ADP
ATP + Creatine
•The CP (Creatine Phosphate) is depleted in just a few
seconds. This is the reason your maximum power can be
maintained for only a few seconds. To continue producing
high strength power, the speed enzyme system kicks in.
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Muscle Contraction (Cont.)
The Burst Power Enzyme System
•The enzymes required for this reaction are depleted in less
than two minutes.
•This reaction is called Anaerobic Glycolysis because it uses
glucose without oxygen.
•Glucose
2ATP + 2 Lactate
•To continue muscle usage requires the aerobic system to
kick in.
•The aerobic system uses oxygen and sugar for fuel.
•The ability to perform well after about two minutes of
maximum exertion depends on the aerobic conditioning of
the body.
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Muscle Contraction (Cont.)
The Endurance Enzyme System
This system consists of three processes:
1. Carbohydrate Metabolism: Carbohydrates metabolize most
efficiently and are therefore used first
2. Fat Metabolism: If no carbohydrates are available, the body
metabolizes fat.
3. Amino Acid Protein Metabolism: If no fat is available, the
body metabolizes Amino Acids.
The body stores glucose and fatty acids for these reactions. In
addition, the cardiovascular system provides a continuous
supply of oxygen.
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Muscle Contraction (Cont.)
•Cardiac muscle is adapted to be highly resistant to fatigue: it
has a large number of mitochondria, enabling continuous aerobic
respiration.
•The heart is so tuned to aerobic metabolism that it is unable to
pump sufficiently in ischaemic conditions. (It has no back up
system).
•At basal metabolic rates, about 1% of energy is derived from
anaerobic metabolism. This can increase to 10% under
moderately hypoxic conditions, but, under more severe hypoxic
conditions, not enough energy can be liberated by lactate
production to sustain ventricular contractions.
•Under basal aerobic conditions, 60% of energy comes from
fat (free fatty acids and triglycerides), 35% from carbohydrates,
and 5% from amino acids. However, these proportions vary
widely according to nutritional state. For example, during
starvation, lactate can be recycled by the heart
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Muscle Contraction (Cont.)
•Glycogen is stored in the muscles and liver in sufficient
quantities for about two hours of strenuous exercise.
•This timeframe can be extended by aerobic physical
conditioning and high carbohydrate diet.
•After the glycogen stores are used up, the body obtains its
energy from fatty acid metabolism and amino acid protein
metabolism.
•These reactions are not efficient, which consequently causes
your strength and endurance to drop drastically (hitting a brick
wall or man with the hammer).
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EXERCISING AND BUILDING MUSCLES
•Muscles change and develop with regular exercise but the
effects differ, depending on whether you engage in strength,
speed, or endurance training.
•Strength and burst training causes the muscle fibers to enlarge.
•Individual muscle fibers increase in diameter as a result of an
increase in intracellular protein fibrils.
•Endurance training causes more blood vessel formation than
does speed or strength training, which produces an increased
capacity for aerobic metabolism within the muscle cell.
•This change is seen after a few weeks of training and is
maximized in about three months. The aerobic enzymes that
metabolize carbohydrates, fats, and proteins, double.
•It is important to develop your strength and speed systems, but
if you want to continue past about two minutes of high intensity
workouts, you need to have your aerobic systems developed
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Motor Units within a muscle
•A motor unit is defined as all of the muscle fibers supplied by a
single motoneuron, and therefore, by a single axon and its branches
•Skeletal muscles are organized into hundreds of motor units,
each of which involves a motor neuron, attached by a series of thin
finger-like structures called axon terminals.
•These attach to and control discrete bundles of muscle fibers. A
coordinated and fine tuned response to a specific circumstance will
involve controlling the precise number of motor units used.
•While individual muscle units contract as a unit, the entire muscle
can contract on a predetermined basis due to the structure of the
motor unit.
•Motor unit coordination, balance, and control frequently come
under the direction of the cerebellum of the brain. This allows for
complex muscular coordination with little conscious effort, such as
when one drives a car without thinking about the process.
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Motor Units within a muscle
•Muscles responsible for fine coordination have small motor
units.
•Muscles responsible for gross movements have large motor
units.
•The smaller motor units are more excitable than the larger
ones, and are stimulated first when a weak signal is sent by
the CNS to contract a muscle
•As the strength of the signal increases, more motor units are
excited in addition to larger ones, with the largest motor units
having as much as 50 times the contractile strength as the
smaller ones
• As more and larger motor units are activated, the force of
muscle contraction becomes progressively stronger. This
concept is know as “the size principle”.
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Motor Units within a muscle: Conclusion
•At low exercise intensities, like walking or slow running, slow
twitch fibers are selectively utilized because they have the lowest
threshold for recruitment.
•If suddenly the pace is increased to a sprint, the larger fast units
will be recruited.
•In general, as the intensity of exercise increases in any muscle,
the contribution of the fast fibers will increase.
•For the muscle, intensity translates to force per contraction and
contraction frequency/minute.
•Motor unit recruitment is regulated by required force. In the
unfatigued muscle, a sufficient number of motor units will be
recruited to supply the desired force (wave contraction).
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Motor Units within a muscle: Conclusion
•Initially desired force may be accomplished with little or no
involvement of fast motor units. However, as slow units
become fatigued and fail to produce force, fast units will be
recruited as the brain attempts to maintain desired force
production by recruiting more motor units.
•Consequently, the same force production in fatigued muscle
will require a greater number of motor units.
•This additional recruitment brings in fast, fatigable motor
units.
•As a result, fatigue will be accelerated toward the end of long
or severe bouts due to the increased lactate produced by the
late recruitment of fast units. (Again, the man with the
hammer)
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Contraction Strength
•For skeletal muscles, the force exerted by the muscle is
controlled by varying the frequency at which action potentials
are sent to muscle fibers.
•Action potentials do not arrive at muscles synchronously,
and during a contraction some fraction of the fibers in the
muscle will be firing at any given time.
•Typically when a human is exerting a muscle as hard as they
are consciously able, roughly one-third of the fibers in that
muscle will be firing at once, but various physiological and
psychological factors (including Golgi tendon organs and
Renshaw cells) can affect that.
•This 'low' level of contraction is a protective mechanism to
prevent avulsion of the tendon - the force generated by a 95%
contraction of all fibers is sufficient to damage the body.
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Contraction Strength
•The repetitive firing of a motor unit creates a train of impulses
known as the motor unit action potential train (MUAPT).
•To sustain muscle contraction, the motor units must be
repeatedly activated . As the firing rates of motor units active in
a contraction increase, the twitches associated with each firing
will eventually fuse to yield large forces
•The firing rates of earlier recruited motor units are greater
than those of later recruited motor units at any given force value
•The control to the muscle is not designed to generate constantforce contractions.
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Maximal Voluntary Contraction (MVC)
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Contraction Strength
• So concluding, the strength of a muscular contraction can be
influenced 2 factors:
1. By increasing the number and size of contractile units
simultaneously, called multiple fiber summation.
2. By increasing the frequency at which action potentials
are sent to muscle fibers, called frequency summation.
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Types of Muscle Contraction
1. Concentric muscle contraction
2. Eccentric muscle contraction
3. Isometric muscle contraction
4. Isotonic muscle contraction
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Concentric muscle contraction
• Muscle contraction in which the muscles shorten while
generating force. The insertion and origin of the muscle are
moving toward eachother.
• During a concentric contraction muscle fibers slide across
each other pulling the Z-lines together
• During a concentric contraction, a muscle is stimulated to
contract according to the sliding filament mechanism.
• This occurs throughout the length of the muscle, generating
force at the musculo-tendinous junction, causing the muscle
to shorten and changing the angle of the joint.
• In relation to the elbow, a concentric contraction of the
biceps would cause the arm to bend at the elbow.
• A concentric contraction of the triceps would change the
angle of the joint in the opposite direction, straightening the
arm.
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Eccentric Muscle Contraction
•During an eccentric contraction, the muscle elongates while
under tension. The origin and the insertion of the muscle are
moving away from eachother.
•The muscle acts to decelerate the joint at the end of a
movement or otherwise control the repositioning of a load.
•This can occur involuntarily (when attempting to move a
weight too heavy for the muscle to lift) or voluntarily (when the
muscle is 'smoothing out' a movement).
•Over the short-term, strength training involving both
eccentric and concentric contractions appear to increase
muscular strength more than training with concentric
contractions alone.
•During an eccentric contraction of the biceps muscle, the elbow
starts the movement while bent and then straightens as the hand
moves away from the shoulder. During an eccentric contraction
of the triceps muscle, the elbow starts the movement straight and
then bends as the hand moves towards the shoulder.
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Eccentric Muscle Contraction
•Muscles are approximately 10% stronger during eccentric
contractions than during concentric contractions
•Eccentric contractions are being researched for their ability to
speed rehab of weak or injured tendons. Achilles tendinitis has
been shown to benefit from high load eccentric contractions.
•During virtually any routine movement, eccentric contractions
assist in keeping motions smooth.
•Muscles undergoing heavy eccentric loading suffer greater
damage when overloaded (such as during muscle building or
strength training exercise) as compared to concentric loading.
•During an eccentric contraction, the filaments slide past each
other the opposite way, though the actual movement of the myosin
heads during an eccentric contraction is not known.
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Eccentric Muscle Contraction
•Exercise featuring a heavy eccentric load can actually result
in greater muscular damage and delayed onset muscle
soreness one to two days after training.
•Exercise that incorporates both eccentric and concentric
muscular contractions (i.e. involving a strong contraction and a
controlled lowering of the weight) can produce greater gains in
strength than concentric contractions alone.
•While unaccustomed heavy eccentric contractions can easily
lead to overtraining, moderate training may confer protection
against injury.
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Isometric Muscle Contraction.
•An isometric contraction of a muscle generates force without
changing length.
•An example can be found in the muscles of the hand and
forearm grip an object; the joints of the hand do not move but
muscles generate sufficient force to prevent the object from
being dropped.
• Isometrics are done in static positions, rather than being
dynamic through a range of motion.
•The joint and muscle are either worked against an immovable
force (overcoming isometric) or are held in a static position
while opposed by resistance (yielding isometric).
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Isotonic Muscle Concentration
Isotonic contractions occur when tension in the muscle
remains constant despite a change in muscle length. This
can occur only when a muscle's maximal force of
contraction exceeds the total load on the muscle.
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A: Concentric/eccentric
B: Isometric
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Other Types of Muscle Contraction
•Spasm
•Hypnic jerk
•Dystonia
•Myoclonus
•Cramp
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Spasm
•is a sudden, involuntary contraction of a muscle, a group of
muscles
•usually harmless and ceases after a few minutes
•In very severe cases, the spasm can induce muscular
contractions that are more forceful than the sufferer could
generate under normal circumstances. This can lead to torn
tendons and ligaments.
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Hypnic jerk
•A hypnic or hypnagogic jerk is an involuntary muscle twitch
(commonly known as a myoclonic twitch) which occurs
during the transition into hypnagogia.
•It is often described as an electric shock or falling
sensation, and can cause movement of the body in bed.
•Hypnic jerks are experienced by most people, especially
when exhausted or sleeping uncomfortably
•Hypnic jerks may be felt once or twice per night
•This normally happens to subjects who have deprived
themselves of sleep for longer than 24 hours, or to those who
have recently awakened after insufficient sleep
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Dystonia
•Dystonia is a neurological movement disorder in which
sustained muscle contractions cause twisting and repetitive
movements or abnormal postures.
•The disorder may be inherited or caused by other factors such
as birth-related or other physical trauma, infection, poisoning
(eg. lead poisoning) or reaction to drugs.
Torticollis
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Myoclonus
•Myoclonus is a brief, involuntary twitching of a muscle or a
group of muscles.
•The myoclonic twitches or jerks are usually caused by sudden
muscle contractions; they also can result from brief lapses of
contraction.
•Contractions are called positive myoclonus; relaxations are
called negative myoclonus.
•The most common time for people to encounter them is while
falling asleep (hypnic jerk).
•Myoclonic jerks can also be a sign of a number of neurological
disorders.
•Hiccups are also a kind of myoclonic jerk specifically affecting
the diaphragm.
•Myoclonic jerks may occur alone or in sequence, in a pattern or
without pattern. They may occur infrequently or many times each
minute. Most often, myoclonus is one of several signs in a wide
variety of nervous system disorders such as multiple sclerosis,
Parkinson's disease, Alzheimer's disease, and Creutzfeldt-Jakob
disease (CJD) and some forms of epilepsy.
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Cramp
•Cramps are sometimes called Charley horses, are unpleasant,
often painful, sensations caused by contraction or over
shortening of muscles.
•Cramps can be caused by cold, overexertion or low calcium
level in blood (especially for adolescents where they need
calcium for both blood and bone maturing).
•Illness or poisoning can also cause cramps, particularly in the
stomach, which is referred to as colic if it fits particular
characteristics
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Cramp: Causes.
•Hyperflexion
•Inadequate oxygenation
•Exposure to large changes in temperature
•Dehydration
•Low blood salt
•Low blood calcium
Muscle cramps may also be a symptom/complication of
pregnancy, kidney disease, thyroid disease, hypokalemia or
hypocalcemia (as conditions), restless legs syndrome,
varicose veins[1], and multiple sclerosis.[2]
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Electrolyte disturbance may cause cramping and tetany of
muscles, particularly hypokalaemia (a low level of potassium)
and hypocalcaemia (a low level of calcium).
This disturbance arises as the body loses large amounts of
interstitial fluid through sweat. This interstitial fluid is
composed mostly of water and table salt (NaCl).
The loss of osmotically active particles outside muscle
cells(NaCl) leads to a disturbance of the osmotic balance and
swelling of muscle cells as these contain more osmotically
active particles.
This causes the calcium pump between the muscle lumen
and sarcoplasmic reticulum to short circuit and the calcium
ions remain bound to the troponin and the muscle
contraction is continued.
This may occur when the lactic acid is high in the cells.
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Practical
•Isometric
•Eccentric
•Concentric
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Muscle Functions
Muscle tissue has four main properties:
•Excitability or the ability to respond to stimuli
•Contractibility or the ability to contract
•Extensibility or the ability of a muscle to be stretched
without tearing
•Elasticity or the ability to return to its normal shape
Through contraction, the muscular system performs three
important functions:
•Motion - walking, running etc.
•Heat production - maintain normal body temperature
•Maintenance of posture - standing, sitting etc.
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Muscle Functions
•Muscles have two states
•Relaxed
•Contracted.
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Motion: Understanding Muscle Levers
There are different types of levers dependent upon the position
of fulcrum, effort and resistive force.
•First Class lever: Muscle force and resistive force is on
different sides of the fulcrum e.g. the head resting on the
vertebral column. As the head is raised, the facial portion of
the skull is the resistance, the fulcrum is between the atlas and
occipital bone, and the effort is the contraction of the muscles
of the back.
•Second Class lever: Muscle force and resistive force act on
the same side of the fulcrum, with the muscle force acting
through the level longer than that through which the resistive
force acts - e.g. raising the body up onto the toes. The body is
the resistance, the ball of the foot is the fulcrum, and the effort
is the contraction of the calf muscle.
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Third Class lever:
•Muscle force and resistive force act on the same side of the
fulcrum, with the muscle force acting through the lever shorter
than that through which the resistive force acts - e.g. adduction
of the thigh. The weight of the thigh is the resistance, the hip
joint is the fulcrum, and the contraction of the adductor muscle
is the effort.
•Most of the limbs of the human body are articulated by third
class levers.
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Motion: Understanding Muscle levers
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Muscle Function: Heat production
•Muscle contractions produce heat and as much as 70% of
body heat is produced by energy produced in muscle
tissue.
•Blood is an essential element in temperature control during
exercise, taking heat from the body core and working
muscles and redirecting it to the skin when the body is
overheating.
•When the internal heat of the body reaches too low a level
thermo-receptors in the skin relay a message to the
hypothalamus in the brain. In response to this signal, the
skeletal muscles contract and relax in an involuntary manner
(shivering) increasing muscle activity to generate heat.
•In turn, muscles are also responsive to exterior heat - cold air
increases muscle tone, and hot conditions have a relaxing
effect on muscles.
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Maintenance of posture
•As well as enabling movement, muscles also maintain
posture and body position.
•Sensory receptors in the muscles monitor the tension and
length of the muscles and provide the nervous system with
crucial information about the position of the body parts,
therefore enabling posture to be maintained.
•Muscles are never completely at rest, nor do they actually
have to shorten in length when they contract.
•The tension or tone produced as a result of these
contractions between various opposing groups of muscle
helps us remain in a static position, even when we are
asleep.
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Break!
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Connective Tissue
Connective tissue is a form of fibrous tissue.
It is one of the four types of tissue in traditional
classifications (the others being epithelial, muscle and
nervous tissue.
Understanding the microscopic and macroscopic
structure of connective tissue along with the
biomechanical characteristics is important as a
foundation for every therapist using exercise therapy to
improve a patients function.
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Knowledge of tissue histology and biomechanics
will improve a therapists’ understanding of the
influence of implications of trauma, immobilization
and remobilization of this tissue.
Connective tissue accounts for 16% of a persons
bodyweight, and stores 23% of a body’s total water
content.
•Collagen is the main protein of connective tissue, making
up about 25% of the total protein content.
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Blood, cartilage and bone are usually considered connective
tissue, but, because they differ so substantially from the other
tissues in this class, the phrase "connective tissue proper" is
commonly used to exclude those three.
Connective tissue proper includes the following five types:
•loose connective (organ walls and it fills space)
•dense connective (Collagen type I, tendons, liggs)
•Elastic (can be stretched 1.5 x original length), skin, lungs,
arteries, veins etc.
•Reticular: The fibers form a soft skeleton to support the
lymphoid organs (lymph nodes, red bone marrow, and spleen).
•Adipose
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Components of connective structures:
•Water
•Type I collagen fibers
•Ground substance
•Elastin fibers
•Fibroblasts
The fibers and ground substance, which exist outside the
cells, are collectively called the extra-cellular matrix.
Function:
Separates and protects cells,
bearing weight, tension
offering defense.
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Defense
•Connective tissue contains cells and metabolites important
in immune function, such as inflammation, and in tissue
repair after injury.
Nutrition and transport of molecules
•Blood vessels, which are also considered a connective
tissue, transport substances throughout the body.
•Components in connective tissue regulate movement of
nutrients between cells.
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•In ordinary connective tissue the majority of the cells are
fibroblast. These are involved in the production of fibrous
elements and the non- fibrous ground substance.
•They are particularly active during wound repair, migrating
along strands of fibrin by amoeboid movements and
distributing themselves through the healing area to start repair.
•Fibroblast activity is influenced by various factors as partial
pressure of Oxygen (V.A.C. ), steroid hormone levels and
nutrition.
•Macrophages, mast cells, plasma cells and pigment cells are
the other cell types characteristic of connective tissue.
Lymphocytes and leukocytes are more variable but may
increase considerably in pathological conditions.
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Connective tissue forms the following:
•base of the skin
•muscle sheaths
•nerve sheaths
•tendons
•ligaments
•joint capsules
•fascia
•periosteum
•blood vessel walls
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•bed and framework of the internal organs
•bone
•adipose tissue
•cartilage
•intervertebral discs
•aponeuroses
•lens capsules
•kidney glomeruli
•granulation tissue
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Traditional classification of connective tissue
structures:
Loose connective tissue
•Areolar (space filling)
•Adipose
•Reticular
Dense Connective tissue
•Regular
•Irregular (for support of organs etc.)
•Elastic
Cartilage
•Hyaline
•Fibrocartilage
•Elastic
Other
•Bone
•Blood
•Lymphatics
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• Unlike other connective tissues, cartilage
does not contain blood vessels.
• The chondrocytes are fed by diffusion,
helped by the pumping action generated by
compression of the articular cartilage or
flexion of the elastic cartilage.
• Thus, compared to other connective
tissues, cartilage grows and repairs more
slowly.
• The same is true for the intervertebral disk,
which is made out of fibrocartilage)
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Except for cartilage, connective tissue is
innervated (has a nerve supply).
Vascularity (blood supply) in tendons and
ligaments is sparse, whereas cartilage is
avascular (has no blood supply).
FIBERS
•Collagen
•Elastic
•Reticular fibers
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Fiber types
Collagenous fibers:
Collagen is the main protein of connective tissue making up abou
25% to 35% of the whole-body protein content.
•Tough bundles of collagen called collagen fibers are a major
component of the extracellular matrix that supports most tissues
and gives cells structure from the outside, but collagen is also
found inside certain cells.
•Collagen has great tensile strength, and is the main component
of fascia, cartilage, ligaments, tendons, bone and skin.
•Along with soft keratin, it is responsible for skin strength and
elasticity, and its degradation leads to wrinkles that accompany
aging. It strengthens blood vessels and plays a role in tissue
development.
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Degradation of collagen?
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Elastic fibers:
Elastic fibers (or yellow fibers) are bundles of proteins
(elastin) found in extracellular matrix of connective tissue and
produced by fibrobasts and smooth muscle cells in arteries.
These fibers can stretch up to 1.5 times their length, and snap
back to their original length when relaxed (if not stretched
past their physiological length)..
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Reticular fibers:
•Reticular fibers or reticulin is a histological term used to
describe a type of fiber in connective tissue composed of
type III collagen.
•Reticular fibers crosslink to form a fine meshwork
(reticulum).
•This network acts as a supporting mesh in soft tissues
such as liver, bone marrow, and the tissues and organs of
the lymphatic system.
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Collagen Fibers, types:
Collagen One - skin, tendon, vascular, ligamenture,
organs, meniscus, annulus, bone (main component of
bone) Great circulation with great tensile strength
Collagen Two - cartilage (main component of cartilage),
nucleus pulposus. Poor Circulation, compression
tension strength
Collagen Three - reticulate (main component of reticular
fibers), skin, blood vessels, granulation tissue, commonly
found alongside type I.
Collagen Four - forms bases of cell basement membrane
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Characteristics of collagen based structures
Tensile strength
Extensibility
Type I - found principally in structures
exposed to tension
Mostly found in skin, tendon, ligament, capsule,
annulus, muscle, menisci and bone
Type II - found principally in structures
exposed to pressure
Mostly found in nucleus pulposus and articular
cartilage
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Bone
Components: minerals, water, type I collagen,
proteoglycans
Mineral gives the bone its hardness and ability to
withstand compression loads. Tolerance of tensile
loads is due to both mineral and matrix components
combined.
Determinants of the mechanical properties of bone:
•Size and density of bone
•Mechanical properties of the bone substance
•Geometrical characteristics of the bone specimen
•Loading mode applied (compression, tension, etc)
•Rate of loading
•Frequency of loading
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Cortical bone:
•Very high ultimate strength
in compression and tension
•High stiffness
•Compression strength
15000PSI
•Tension strength 12000PSI
•Shear strength 4000PSI
•Stiffness and ultimate load
increase with increasing
speed of
loading
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Trabecular bone
•Moderate to low ultimate
strength
•Moderate to low stiffness
Strength – lower than for
cortical bone, but depends
on porosity
•Stiffness and ultimate
load increase with
increasing
speed of loading
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Cortical bone (a.k.a. compact bone) 5-30% porous
External shell of all bones, also forms diaphysis
(shaft of the bone). Lamellar build up.
Trabecular bone 30-90% porous. Also named
cancellous or spongy bone. Fills the ends of long
bones and is inside of flat and irregular bones (e.g.
vertebrae).
Bone is 65% mineral, 30% collagen, 5%
proteoglycan by dry weight. Fresh bone is 25%
water by weight
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Shoulder Arthritis
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Non WB. Guess which site…
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Tendons, ligaments and joint capsules
The density and regularity of these structures are
determined by the strength required and the
uniformity of direction of loads they are exposed to.
Components: water, type I collagen, ground
substance, elastin fibers, fibroblasts
Dense regular: tendons, ligaments
Dense irregular: capsule, fascia
Determinants of the mechanical properties of these
types of connective tissue:
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Tendons, ligaments and joint capsules
Size and density of the structures
Properties of the collagen and elastic fibers
contained in the structure
Proportion of collagen and elastic fibers in the
structure
Orientation of fibers in the tissue
Genetics
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Dense regular
connective tissue
Dense irregular
connective tissue
r
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Mechanical properties of tendons, ligaments
and joint capsules
•Tensile strength up to 12000 PSI
•Fail at strains as low as 9% with structures
with little or no elastic fiber content
(extremity tendons), and at strains of up to
70% for structures with a high elastic fiber
content (ligamentum flavum)
•Ultimate load increase with increasing speed
of loading, stiffness does not increase
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Clinical notes
Aging affects connective tissues in that there is a
general loss of collagen. They do however acquire an
increased number of cross links with age, resulting in
greater tensile strength.
During pregnancy the hormone relaxin is released
during the last trimester causing a general loss of
stiffness and strength in connective tissue.
NSAID’s can cause increased tensile strength in
connective tissues (increase of collagen content and
proportion of non-soluble collagen).
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Clinical notes
Connective tissue structures are subject to fatigue type
failures from exposure to loads that are too large, too
numerous or too frequent (overuse or repetitive strain
injuries)
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Cartilage:
Components of cartilage structure: (in
descending order of relative amounts)
•Water
•Type II collagen (mostly in ligaments and
tendons) = compressive cartilage
•Type I collagen ( mostly in fibro cartilage)
•Elastin (mostly in elastic cartilage)
•Proteoglycans
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•Articular cartilage is 60-87% water, 10-30% type
II collagen, and 3-10% proteoglycans by weight.
•About 30% of the water is bound within the matrix
with the remainder being in cells or free to move in
the interstices.
•Proteoglycans compression results in release of
synovial fluid, decreased compression leads to
absorption of synovium (sponge effect)
•Synovial fluid: lubrication of joints, adhesion of
joint surfaces (glass plates) and nutrition for
cartilage (which is aneural, avascular and
alymphatic)
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Sensory receptors
Type:
location:
Fired by:
Type I
postural
capsule
oscillations
Type II
dynamic
capsule
oscillations
Type III
sustained
inhibitive
capsule/
stretch or
ligament
pressure
Type IV nociceptive
inflammation
most tissues injury and
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Sensory Receptors
Type 1 receptors (Merkel’s disk receptors):
Present in the superficial layers of the fibrous
joint capsule. They respond to stretch and
pressure within the capsule (inhibitive) and are
slow-adapting receptors with a low threshold.
They signal joint position and movement.
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Type 2 receptors: (Ruffini endings)
Present in the deep layers of the fibrous
capsule. They respond to rapid movement,
pressure change and vibration but adapt
quickly. They have a low threshold and are
inactive when the joint is at rest.
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Sensory Receptors
Type 3 receptors are present in
ligaments. (Pacini)
These receptors inform the central
nervous system of ligamentous
tension, so preventing excessive
stresses. The threshold is high and
they adapt slowly. They are not
active in rest.
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Sensory Receptors
Type 4 : Free unencapsulated terminals, also called
nocisensors
These sensors ramify within the fibrous capsule,
adjacent fatpads and around bloodvessels. They are
thought to signal excessive joint movements and
also to signal pain; they have a high threshold and
are slow-adapting. The synovial membrane is
relatively sensitive to pain due to the absence of
these nerve endings.
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•All these receptors influence muscle tone via
the spinal reflex arcs which are formed by the
same nerves that supply the muscles acting on
the joint.
•Parts of the joint capsule supplied by a given
nerve correspond with the antagonist muscles.
•Tension given on this part of the capsule
produces reflex contraction of these muscles and
prevents overstretching of the capsule.
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•In consequence, all receptors have an important
function in stabilizing and protecting the joint.
•After rupture of joint capsule and ligament,
perception is considerably disturbed due to
disruption of afferent information. For example a
sprained ankle shows loss of control off
locomotion. Even months after repair of
ligamentous and capsular tissues has taken place,
perception might still be distorted.
•Increased likelihood to re-injury in the acute
healing phase.
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Neural Arch supplying
agonist and antagonist
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If you stretch in the elastic only, you won’t achieve anything. In
fact, studies suggest that this actually may shorten the muscle
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Effects of immobilization on connective tissue
Before we discuss theses effects, let’s discuss the three stages
of tissue healing
•Inflammation
•Cell proliferation
•Remodeling
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Effects of immobilization on connective tissue
Inflammation
During the initial inflammatory stage, which lasts 35days,
prostaglandins initiate multiple tasks:
•stimulate the immune system
•build up platelets around the lesion
•attract white blood cells that protect against
infection
•clean up the damaged tissue.
Specialized cells called fibroblasts produce disorganized
fibrous (scar) tissue.
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Mechanical trauma to soft connective tissue leads to a
generalized inflammatory reaction.
This reaction has several mostly functional effects that
prompt the subject to restrict activities while it
initiates the reparative process (e.g. pain)
Stages of inflammation
•Vasoconstriction stage of the arterioles. This
decreases the blood flow to reduce bleeding.
followed by vasodilatation and increased capillary
permeability. This phase usually starts within 5 –
10 min and may last up to 1 – 3 days.
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Stages of inflammation (Continued)
Exudation stage: Starts within a few hours. Physical signs:
local warmth, swelling and pain. During this phase
plasma, cells and protein flow into the damaged area. This
dilutes potential noxious substances and products of cell
destruction. . The cellular part of the exudate consist of
multiple cells influencing phagocytosis. Another important
product of plasma is fibrinogen which forms extensive
networks for the fibroblast which migrates along strands
of fibrin by amoebic movements and distribute themselves
through the healing area.
In the presence of an inflammatory reaction there is a
significant stimulus for abnormal production of non
neoplastic fibrous tissue which can interfere with
granulation and repair.
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Stages of inflammation (Continued)
•Granulation phase (within 48 hours to 6 weeks) vascular
infiltration and fibroblast proliferation. Fibroblast and
capillaries grow along the fibrin network. This usually
starts within 48 hours and by day 5 after the injury the
amount of collagen formed is significant and it increases
for up to 6 weeks. Normally the initial arrangement of
these fibers is disorganized. Capillaries at the edge of the
injured tissue infiltrate via forming arches capable of
maintaining circulation. This ensures supply of oxygen
and nutrition into a relatively anoxic region and at the
same time enables removal of metabolic waste products.
These regenerating capillaries are still very fragile and
therefore stay within the support of the newly synthesized
collagen.
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Stages of inflammation (Continued)
•Repair (begins at the end of the third week and
may continue for 1 to 3 years) At the end of the
third week maturation begin. From this time
vascularization decreases and many of the new
vessels atrophy and disappear as the
bloodsupply becomes appropriately adjusted to
the needs of the tissue. Also the amount form
and strength of scar collagen tissue changes.
Tension by gentle movements in functional
directions reorients the collagen and breaks
weak, unnecessary intermolecular cross links
that may have formed.
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Stages of inflammation (Continued)
Mechanical stress thus has its greatest influence
on the remodeling process at this time. Nonfunctional collagen is while this is taking place
removed by phagocytosis. Tensile strength in the
functional directions slowly increases due to the
continuing process of crosslinking and the
formation of bundles oriented with their
longitudinal axis in the direction of the greatest
stress. Remodeling may be due to
•Turn over of collagen
•Fiber linkage
•Increased intermolecular bondage.
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Self perpetuating inflammation.
The reaction of tissues to harmful stimuli frequently
is an excessive prolongation of the normal response.
Excessive edema formation, muscle spasms and other
defense mechanisms can, when not managed
appropriately may lead to chronic disability by
impeding movement that is crucial in the early stages
of the lesion.
Cyriax described the chronic inflammation of soft
tissues as a self perpetuating inflammation.
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Such may be a result from a trauma though can
continue long after the cause had ceased.
This is particularly prone to happening after minor
injury to a tendon or a ligament.
Cyriax describes the cause as lack of movement during
the period of tissue repair causing adhesive scar
formation. He suggests local steroid infiltration to
interrupt the inflammatory process. An even better
result may be reached by deep transverse friction
massages to get rid of the chaotically formed scar tissue
eventually followed by manipulation.
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The Cell proliferation phase.
During the second phase, the cell proliferation
phase, which lasts 4-6 weeks, cells proliferate to
replace the damaged cells and scar tissue becomes
organized.
Physical activity eliminates unnecessary scar
tissue that has inadvertently adhered to
neighboring tissue(!!)
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The Remodeling Phase.
During the remodeling stage, lasting about six
months or more, the repaired tissue remodels itself.
Interestingly forensic anthropologists and
archeologists observe changes in bone structure, for
example, to determine the types of work a person
performed based on the fact that remodeling is an
automatic process accompanying use.
During the third stage of healing this process can
restore damaged tissue so it is stronger than it was
before the injury. If remodeling doesn’t occur, it
leads to weakened tissue prone to reinjury.
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So keeping these characteristics in mind, consider
the following:
•Injuries are an opportunity to become stronger.
•When the three stages proceed normally, tissue
becomes stronger and less prone to injury. This
principle is used by performance athletes.
•Likewise, pain is rare if the damage heals quickly
and thoroughly, without abnormal adhesions.
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The effect of immobilization has been well
documented and studied:
•Loss of GAG (Glycosaminoglycans) in connective
tissues.
•Increase in crosslink formation in connective tissues.
•Poor orientation of newly deposited collagen fibers.
•Fatty fibrous infiltration of edematous areas.
•Pannus formation inside of joints. Ulcerated cartilage
found in immobilized non traumatic dog knees after 6
weeks of immobilization via casting and exostosis with
deep ulceration after 8 weeks.
•General atrophy of all tissue types.
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Effects of immobilization
•A study by Noyes et al. (1974) using the ACL in monkeys,
that did not have a trauma or surgery, showed that after 8
weeks of immobilization using a lower limb cast, there was
significant loss of ligament tensile strength which took 9
months to recover from. The predominant mode of failure in
these experiments was ligament failure as opposed to
avulsion fracture failure.
•Another important study is that of Amiel et al from 1985
done on rabbits. This showed a decrease in collagen mass of
a the MCL of a rabbit by 30% and sign. decrease in tensile
strength.
•Tipton et al. reported similar findings in decreased number
and size of collagen bundles when examining ACL’s in dogs
through a light microscope.
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Effects of immobilization
Gerber et al published a study in Sweiz Z Sportmed. in
1980, that claims they found 20% loss of maximum
muscle-strength after 2 weeks of immobilization in a
plaster cast.
•They also found slow muscle fibers more susceptible
to immobilization atrophy and felt this was due to their
greater dependence on oxidative metabolism.
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Effects of immobilization
Erickson et al described findings of laxity, destruction of
ligament insertion sites and failure at a lower load after
3 months of immobilization, in Medicine science and
Sports in 1976.
•Appell described significant disturbances in
neuromuscular coordination of muscle groups after
immobilization in Sports Med. in 1990.
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Benefits of Flexibility and Range of motion.
A decrease in musculoskeletal flexibility has been
associated with both the aethiology as well as the
consequences of musculoskeletal injuries (Nicholas
1970, Glick 1980).
•Furthermore it has been documented that
flexibility training, effectively increases range of
motion in human subjects ( de Vries1962,
Henrickson et al 1984)
•However it is crucial that health professionals prior
to prescribing flexibility training evaluate a subject
and keep in mind the established guidelines for
flexibility of joints and muscles ( Janda 1983,
Kendall & Mc Greary 1983).
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Benefits of Flexibility and Range of motion.
When range of motion testing reveals values that exceed
the normal flexibility training might be considered
contra- indicated. Instead stability-training, posture
training and strengthening should be considered.
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Effects of mobilization on tissue healing and
repair.
With this basic biological knowledge there is now
rationale for the use of early controlled
mobilization of patients with ligament trauma.
•The use of a limited motion cast with adjustable
double-action hinge for the knee joint is now
accepted in clinical practice and enhances more
rapid repair and remodeling as well as preserving
quadriceps strength and bulk.
•Now patients are usually mobilized early in a
limited motion cast for a minimum of 3 weeks with
range of motion from 20-60degrees.
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Effects of mobilization on tissue healing and
repair.
•Analysis of transverse session cuts through the ACL’s
of the exercised rats showed a 29% increase in fibrils
with a significant increase in fibril diameter. In the
exercised PCL the amount of collagen found per
microgram of DNA was almost double that of the
control group, suggesting that the PCL was more loaded
with this exercise regimen than the ACL.
•Similar structural observations have been made for
collagen fibers of exercised mice flexor tendons
(Michna 1984)
Amiel et al (1987) have shown that maximal collagen
deposition and turn over occurs during the first 3-6
weeks post injury in the rabbit.
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Effects of mobilization on tissue healing and
repair.
•Frank et al (1991) have further shown that collagen
remodeling of the repairing rabbit MCL appears to
be encouraged by early immobilization but after 3
weeks of collagen alignment and remodeling
appears to be favored by mobilization.
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Effects of mobilization on tissue healing and repair.
•The benefits of early mobilization in most of the soft
tissue lesions already was advocated by Hippocrates
more than 2400 years ago.
•He described the increase in circulation, aiding nutrition
and eliminating cartilage damage.
•Numerous studies since have found significantly
improvement in strength of ligaments, tendons and
capsule with exercise training.
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Effects of mobilization on tissue healing and repair.
•Oakes did a study in 1988 where 5 rats were placed on a
progressive 4 week exercise program of alternate days of
swimming and treadmill running. At the conclusion the
rats were running 60-80 min on a 10% incline and on
alternate days swimming for 60 min with 3% body
weight attached to their tails. Five caged rats of similar
age and bodyweight were controls.
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Definitions:
Flexibility: The range of motion that is available in a joint or
group of joints that is influenced by muscles, tendons and
bones ( Anderson & Burke 1991)
•Flexibility has also been described as the degree to which
muscle length permits movement over that which it has an
influence (Toppenburg and Bullock 1986)
•Flexibility in the musculotendinous unit is directly related
to tension in that musculotendinous unit.
•There are two components to tension.
•An active component which lies in the reflex activity of
the muscle
• a passive component which lies in the viscous and
elastic properties of the connective tissue.
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Benefits of flexibility training
•Decreased risk for injury: Musculotendinous units that
posses greater flexibility are less likely to be
overstretched. Flexible joints can withstand greater
amount of stress before injury occurs.
•Decreased muscle soreness: Stretching has been
advocated as a method to decrease muscle soreness.
•Improved athletic performance: It has been suggested (
Broms 1984) that reduced ROM can reduce
workefficiency. Musculotendinous unit flexibility is
needed to move a limb through its ROM.
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Benefits of flexibility training
•Also stretching will reduce stiffness and enhance
“rebound performance”. Mechanical work is absorbed by
the series elastic component of the musculotendinous unit
during eccentric contraction and is stored as potential
energy. This energy is then available for use during the
subsequent concentric contraction.( Bosco & Komi 1979)
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Benefits of flexibility training
Muscle relaxation (De Vries 1962)
•Avoidance of skeletal dysfunction, which was defined
by Mc Kenzie as the syndrome that is the result of
prolonged incorrect biomechanical usage of the joints.
•Prevention of scar tissue formation in the
musculotendinous units shortened position (Reilly 1992)
•Prevention of imbalance at the joints, which is the result
of one muculotendinous unit at a joint being either
significantly weaker or significantly less flexible than the
other musculotendinous units at that joint (Kendall and
Mc Greary).
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Benefits of flexibility training
Flexibility training is essential to restore loss of range of
motion in soft tissue following injury or surgery. There are
multiple factors responsible for loss of ROM in soft tissue
following injury or surgery:
•Increased fibrosis in the scar. Scarformation is
normally self-limiting though is frequently excessive in
wounds.
•Woundcontraction, inward movement of woundedges
by myofibroblast as part of the repair process.
•Immobilization or prolonged usage in limited ROM.
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Benefits of flexibility training (continued)
•Nerve root tension
•Decreased tissue temperature
•Increased age
•Obesity
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•If not adequately managed this could lead to contractures,
pain, dysfunction and even disability.
•Loss of ROM is one of the main reasons for failed
orthopedic surgeries including Total Knee Arthroplasties,
Rotator Cuff repairs and even post arthroscopic shoulder
decompression and athroscopic menisectomies and
frequently can simply be prevented by
adequate Rehabilitation.
•It is also the number one reason for frustration by
orthopedic surgeons upon follow up visits and loss
of referrals.
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Physiology of stretching:
•Stretching implies that a force applied to the tissue
elongates the tissue.
•Elongation is being accomplished by a combination of
neural effects and plastic/ elastic effects of the tissue.
•A force that is applied to a tissue and held will decrease
activity of the stretch reflex , with decrease in neural
excitability.
•The non contractile element within the musculotendinous
unit, fascial sheats, connective tissue, is mainly responsible
for the plastic elongation of the unit..
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Methods of stretching
PNF:
a) Contract-relax; a therapist stretches a muscle to the
point where a limitation in ROM is felt. The therapist holds
the muscle in this or a sub maximum position and lets the
patient actively contract against the resistance of the
therapist. The muscle is then relaxed and moved passively
to the new lengthened position.
The rationale behind this is that increased stress through
contraction of the musculotendinous unit will result in
autogenic inhibition in the musculotendinous unit. The
Golgi Tendon Organ activity will decrease tension and
cause relaxation by resetting the musculotendinous unit
length.
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Methods of stretching
PNF:
b)Contract-relax agonist- contract; with this form of
stretching the muscle is stretched as with the contractrelax. However in addition to this the therapist facilitates
contraction of the antagonist, to obtain reciprocal inhibition
of the unit being stretched.
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Ballistic stretching:
•During Ballistic stretching the limb is moved to the end of
its ROM where the stretch sensation is felt, either by the
clinician or the subjects themselves. Once this stretched
position is achieved, repetitive bouncing or jerking
movements are added.
•Use of ballistic stretching appears to increase risk of
injury due to sudden increases in musculotendinous unit
ROM. It’s effectivity in research has also been questioned
by Voss 1985, Matthews 1993, who felt that lengthening of
the musculotendinous unit can not be achieved without
relaxation of the stretch reflex.
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Static stretching:
The most common method of stretching that is used by
athletes, coaches and therapist is the static stretch. Static
stretching is characterized by the limb being moved slowly
and gently to the end of its available ROM, in order to
obtain a stretch sensation in the tissues.
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•To ensure optimal effectiveness of flexibility training it
is essential that the stretches are being executed in a
proper position, with the right amount of force and that
the subject warms up before stretching.
•A study by Gerson from 1955 showed significantly
greater increase in ROM of the m. triceps surea after
static stretching when continuous ultrasound application
for 7 min was added.
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•Williford et al studied the effect of active warm up prior
to stretching.In this study the flexibility of the shoulder
hamstrings trunk and ankles were measured. The subjects
were divided into 2 groups. Group 1 performed a stretch
that was held for 30 sec. followed by another stretch of 30
sec. The second group was instructed to jog lightly but
progressively for 5min. and than perform the same
stretching routine. Results indicated that the stretching
only group gained 11% in ROM. The group that did a
warm up prior to stretching however gained 25%.
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•Voss researched the effect of position on the efficacy
of stretch procedures. He felt that increased ROM in a
musculoskeletal unit cannot be achieved when the unit
is contracting. In this study normal subjects underwent
3 types of stretching procedures to the Hamstrings.1.
Standing and stretching 2.standing but stretching a non
weight-bearing hamstring muscle 3.lying supine and
stretching a non weight bearing hamstring muscle. The
ROM was measured after 3 repetitions of 30 sec. hold.
The standing and weight bearing group gained 4deg.
the standing and NWB group gained 5 deg. The group
that stretched in supine gained an avg. of 10 deg.
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Conclusion and practical guidelines:
•Injury or surgery can result in decreased joint ROM /
flexibility, mainly due to fibrosis and wound
contraction.
•Flexibility training is an important component of
rehabilitation in order to minimize the loss of ROM.
•Flexibility training should begin in the first week
following injury or surgery to prevent decrease in ROM.
•Static stretching is the most commonly used form of
stretching. It is Safe and effective.
•PNF is more effective than static stretching but it
requires some training to master the technique and in
some instances an assistant.
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Conclusion and practical guidelines:
•Ballistic stretching may be effective but it has been
postulated to increase the risk of injury
•Two to three static stretch sessions should be performed
per day for maximum benefit.
•An optimum static stretch session should consist of 3
stretches lasting 30 sec each.
•A warm-up has additive effect if it precedes a static
stretch session.
•A static stretch should be performed in a NWB position
with the muscle relaxed for max. gain in ROM.
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Common Medications and their effect on Exercise
•Aspirin: Watch the side effects. Do not take with NSAID’s (will negate
the blood thinning effect)
•Muscle relaxors
•Flexeril: Look at half life
•Skelaxin
•Sinemet/dopamine (increases heart function with low BP)
•Stimulates beta 1 receptors in heart, causing more complete and
forceful contractions
•Cardiac function controlling medication
•BP controlling medication
•HR controlling medication
•Kidney function controlling medication
•Pulmonary function controlling medication
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The importance of a thorough evaluation
•The concept is very simple here; without a complete and
detailed evaluation, you cannot develop an appropriate
exercise program.
•This evaluation is ongoing and does not stop after the “
initial evaluation” (there is a reason for that name…)
•Understanding the true dysfunction and understanding why
that dysfunction exists will put the clinician in the position to
address the dysfunction effectively and permanently.
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Different types of exercises with different objectives
•Objectives/Goals of exercise:
•Strength
•Muscular Atrophy
•Coordination
•Firing Patterns
•Endurance
•ROM
•PROM vs. AROM
•Endfeel?
•PROM of the Joint
•Muscle length (Muscle energy)
•Muscle tone
•Decrease of muscle tone
•Increase of muscle tone
•Pain control
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Components of an effective Exercise Program:
•Starts with a thorough and complete evaluation (evaluate the
complete chain.
•Have clear outcome objectives.
•What are you looking to exercise
•Why are you exercising that
•What outcome do you expect
•Depends on patient/age/function/other intrinsic and
extrinsic factors
•Measure and document these objectives ongoing
•Don’t over exercise. Exercise to improve function not too
complete a number of reps.
•When you feel or see the correct movement, continue to the
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Components of an effective Exercise program:
•Get the buy-in from the patient
•Detailed documentation
•Quality of the movement
•Speed
•Cues given/needed
•Strength
•Shaky/Tremorous
•Coordination
•Sensation
•Intensity
•Activity it is related to improve
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Progression/Regression of exercise
•Establish base point or midline
•Method of observation
•Points of contact: Progress from larger base of
support to smaller base of support
•Open chain vs. Closed chain
•# of repetitions or sets
•Speed of the reps
•Alignment/change angles
•Cues: tactile& Verbal
•Level of resistance
•Point of reference
•eccentric Isometric  concentric
•Stabilize vs. destabilize
•Weightshifting/weightbearing
•Sequence: Instruct correct
movementrepeatchallenge add
complexityput into a functional activity
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Exercise Therapy
We will now discuss and practice several patient scenarios.
We’ll present several patients with different conditions and
develop an appropriate and effective exercise strategy for
them.
These patients will fall into the following categories:
•Neurological conditions
•Orthopedic conditions
•Surgical
•Non-surgical
•Geriatrics
•Sports injuries
•Spine conditions
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Neurological conditions
Includes conditions such as
•CVA
•ALS
•MS
•Parkinson’s
•Muscular Dystrophy
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CVA
•Inhibition
•Assess movements occurring and compare it to
normal. Then only allow for normal movements to
occur
•Facilitation
•Facilitate normal movement and keep a close eye
on the result of your facilitation
•Three focus areas:
•Postural control
•Transitional movement
•Function in Postures
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CVA
Framework for normal movement:
•Trunk mobility and control
•Midline orientation
•Movement of the base of support (weight shift)
•Head control
•Limb function
Treatment sequence:
•Ask for the movement
•Facilitate the movement where needed
•Take the patient through the movement
•Stretch/mobilize/increase ROM
•Repeat/challenge/add complexity/put into function
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CVA
Guidelines for facilitation utilizing physical cues
•Know the movement
•Determine your points of contact
•Determine the direction of your pressure
•Determine how much pressure: Initial
contact/additional pressure
•Facilitate in functional activities/provide a purpose
where appropriate
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CVA
Activity training
•Activities selected are preferable related to the
environment the patient is currently living in or returning
to.
•Pt’s interest. What does the patient want to work on?
•Activities selected must provide the opportunity to
demonstrate the component being tested.
•Pt’s level of function to the activity. Find the right
activity (it needs to be a bit of a challenge but you do not
want to discourage the patient. Also try higher level
activity to help improve lower level activity)
•When assessing the performance, break down the
activity observed into movements etc. that can then be
separately addressed or that can be addressed more
successfully in a different activity,
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CVA
•Find the impairment limiting the activity
•Write a comprehensive management plan/treatment plan
that addresses both the impairments and the activities
that are restricted or limited.
PRACTICAL
•Midline training in sitting
•Sit to stand to chair (and chair to chair)
•Stepping forward from standing
•Arm function in sitting (with hand and with use of
walker) going into standing
•Midline in standing using corner principle (also for
amputees)
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CVA: Do’s and don’ts when working on the flaccid arm.
Do’s
•Get the attention of the patient
•Wear a face that tells the patient he/she can do it
•Scapula/humerus have to move in all directions
•Align before you move
•Ask the patient to push straight down
•Only use this to initiate movement, don’t repeat this if the patient is
doing it incorrectly
•Pay attention to the slightest movement, focus on this! You're
programming the brain!
•When you feel the correct movement, continue with the correct
sequence, go to the next level.
•If you see no movement, alternate this with the stool/walker exercise.
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CVA: Do’s and don’ts when working on the flaccid arm.
Don’ts
•Ignore normal alignment
•Provide too much resistance
•Let go too suddenly
•Wait too long
•Move fast
•Let them push forward
•Let the weight go over the fingers
•Flex the wrist
•Let elbow pop out (rotation of the shoulder)
•Repeat for no reason if the patient is doing it, move to the next level
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ALS
A-myo-trophic means “No muscle nourishment." When a muscle has no
nourishment, it "atrophies" or wastes away. "Lateral" identifies the areas in a person's
spinal cord where portions of the nerve cells that signal and control the muscles are
located.
As motor neurons degenerate, they can no longer send impulses to the muscle fibers
that normally result in muscle movement.
ALS
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In short, the supply of motor neurons that control a
particular muscle has degenerated, and these cannot be
regenerated by exercise or anything else
•In the early stages of ALS exercise may be helpful in reducing
stress and preventing muscle atrophy.
•In the later stages exercise may help to avoid some of the
discomfort that accompanies muscle weakness and tightness.
•Keep in mind that exercise should never create discomfort.
•Particularly in the earlier stages of ALS, many people have
found both physiological and psychological boosts from various
types of exercise. Along with helping to combat stress,
providing a brief escape and being a welcome way to relax,
proper exercise is important for preventing atrophy of muscles
from disuse — a key to remaining mobile for as long as possible
— and, as long as the pt is able to exercise comfortably, for
keeping their cardiovascular system strong.
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ALS
•The key to gaining these benefits is finding the most
appropriate exercise for your patient.
•While the medical literature has firmly established the
importance of exercise for people without serious medical
conditions, very little research has been done on the subject of
exercise and its role in ALS.
•In fact, it isn’t known whether exercises are beneficial for
increasing muscle strength for people with ALS.
•As the disease advances, the patient will continue to benefit
from doing range-of-motion and stretching exercises.
•It is important to realize that exercise will not strengthen
muscles that have been weakened by ALS
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ALS
So, in review the purpose of exercise for people
with ALS include:
•to maintain or improve the flexibility of muscles not
affected by ALS;
•to maintain the flexibility of muscles that have been
affected;
•to maintain the flexibility of joints in the neck, trunk and
limbs.
•Please keep in mind: It is important that all exercise be
performed in moderation. Fatigue will only increase your
patient’s weakness and rob them of energy that they need
for theirr daily routines and activities.
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Multiple Sclerosis
•Multiple sclerosis is an
autoimmune condition in
which the immune system
attacks the central nervous
system (CNS), leading to
demyelination.
•Disease onset usually
occurs in young adults, is
more common in women,
and has a prevalence that
ranges between 2 and 150
per 100,000 depending on
the country or specific
population
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Multiple Sclerosis
•MS affects the areas of the brain and spinal cord known as
the white matter.
•Different types with different progressions
•White matter cells carry signals between the grey matter
areas, where the processing is done, and the rest of the body
•When the myelin is lost, the neurons can no longer
effectively conduct their electrical signals. The name multiple
sclerosis refers to the scars (scleroses - better known as
plaques or lesions) in the white matter
•Although much is known about the mechanisms involved in
the disease process, the cause remains elusive: the most
widely-held theory being that the condition results from
attacks to the nervous system by the body's own immune
system.
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Multiple Sclerosis
•This disease does not have a cure, but several therapies have
proven helpful
•Treatments attempt to return function after an attack, prevent
new attacks, and prevent disability and also reduce the
inflammatory damage effects of active leasions.
•The prognosis, or expected course of the disease, depends on
the subtype of the disease, the individual patient's disease
characteristics, the initial symptoms, and the degree of
disability the person experiences as time advances.
•Life expectancy of patients, however, is nearly the same as
that of the unaffected population, and in some cases a nearnormal life is possible.
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Multiple Scleroris
T1-weighted MRI scans (post-contrast) of same brain slice at
monthly intervals. Bright spots indicate active lesions.
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Multiple Sclerosis: Relapses
•Multiple sclerosis relapses are often unpredictable and can
occur without warning with no obvious inciting factors.
•Some attacks, however, are preceded by common triggers. In
general, relapses occur more frequently during spring and
summer than during autumn and winter.
•Infections, such as the common cold, influenza, and
gastroenteritis, increase the risk for a relapse.
•Emotional and physical stress may also trigger an attack, as can
severe illness of any kind
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Multiple Sclerosis: Treatment
•During symptomatic attacks administration of high doses of
intravenous corticosteroids has become a routine treatment
routine.
Stops the attack and limits the damage
Does not affect the long term prognosis
-May cause osteoporosis
-Effect is typically short term
•When the initial disease course is the relapsing-remitting
subtype, the average time until such equipment is needed is
twenty years
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MS
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MS
Recent research suggests that multiple sclerosis is triggered when the immune system goes
awry and attacks the protein sheath of nerve cells. This led scientists to test beta interferon, a
substance which inhibits certain white blood cells, to treat the disease. Studies showed beta
interferon can reduce the number and severity of multiple sclerosis attacks and brain
abnormalities in patients. It was recently approved for widespread use by patients with one form
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MS
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MS
•Most studies have shown that persons with MS will not respond
to an acute bout of exercise, as would the average, age- and
gender-matched, non-disabled, adult without MS.
•Furthermore, variability in the type and magnitude of
symptoms seen with this disease often results in a wide range of
responses to acute exercise.
•In spite of the variability, one common effect of acute exercise
in individuals with MS is an overwhelming sense of fatigue
during the recovery period following exercise.
•Some research has shown that in the presence of an upper
motor neuron lesion, antagonist muscles are also activated
during concentric contraction of an agonist.
•Maximal muscle force during sustained dynamic exercise has
also been shown consistently lower for persons with MS
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MS
•A supervised program of aerobic exercise for as little as 15
weeks can improve aerobic fitness level (i.e., VO2max) in some
persons with MS.
•Improvement in aerobic fitness has been reported as to be as
little as 22% and as great as 48% . Less dramatic changes are
often seen in more severely impaired persons (+7%).
•This raises an important issue regarding the development of
realistic expectations based upon the baseline impairment level
of the individual.
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MS
When evaluating fitness in the person with MS, it is important to
consider special needs related to the specific symptoms
experienced by the client:
Flexibility:
•Because many MS patients experience lower extremity
spasticity, flexibility may be restricted in the hip, knee and ankle
joints.
•Hip flexor, hamstring, and gastroc-soleus tightness is
particularly problematic and should be evaluated in the sitting
position (e.g., Sit-and-Reach Test).
•Use of this test will serve to eliminate any problem with
balance during testing. Lateral trunk flexibility should also be
evaluated from a sitting position or, if standing, the clinician
may place his/her hands on the client's waist to prevent loss of
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MS
Balance:
•To truly appreciate how balance deficits might affect the MS
patient's ability to perform exercise safely, balance should be
evaluated under both static and dynamic conditions.
•A fairly short and easy battery of tests can be found using the
Berg Balance Scale. This test is valid for neurological conditions
such as MS and takes approximately 15 minutes to administer.
• The results of this test will provide a better understanding of
the client's ability to exercise safely using standard equipment.
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MS
Aerobic Fitness:
•As previously noted, many persons with MS experience
problems with balance.
•In addition, foot drop associated with dorsiflexor weakness can
be present prior to exercise or it may be easily initiated shortly
after the onset of weight bearing exercise.
•Therefore, for safety purposes, aerobic fitness is best evaluated
using a bicycle ergometer. Even so, this mode of exercise testing
can also present challenges. Ankle clonus (i.e., spasmodic
alternation of contraction and relaxation of muscles), and
sensory abnormalities (e.g., numbness, tingling, and deficits in
joint proprioception) can make it difficult for the client to keep
their feet on the pedals. The use of standard toe clips and Velcrosecured heel straps can reduce or eliminate this problem.
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Parkinson’s
•Parkinson's disease is a
degenerative disorder of the
central nervous system that often
impairs the sufferer's motor skills and
speech, as well as other functions
•It is characterized by muscle rigidity,
tremor, a slowing of physical
movement (bradykinesia) and, in
extreme cases, a loss of physical
movement (akinesia).
•The primary symptoms are the results of decreased stimulation of the
motor cortex by the basal ganglia, normally caused by the insufficient
formation and action of dopamine, which is produced in the
dopaminergic neurons of the brain.
•Secondary symptoms may include high level cognitive dysfunction
and subtle language problems. PD is both chronic and progressive
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Parkinson’s Pathology
Dopaminergic pathways of the human brain in normal condition
(left) and Parkinson's disease (right). Red Arrows indicate
suppression of the target, blue arrows indicate stimulation of
target structure
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Parkinson’s Pathology
•The direct pathway facilitates movement and the indirect
pathway inhibits movement, thus the loss of these cells
leads to a hypokinetic movement disorder.
•The lack of dopamine results in increased inhibition of
the ventral anterior nucleus of the thalamus, which sends
excitatory projections to the motor cortex, thus leading to
hypokinesia.
•Latest research on pathogenesis of disease has shown that
the death of dopaminergic neurons by alpha-synuclein is due
to a defect in the machinery that transports proteins
between two major cellular organelles — the endoplasmic
reticulum (ER) and the Golgi apparatus.
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Parkinson’s Pathology
•The symptoms of Parkinson's disease result from the loss of
pigmented dopamine-secreting (dopaminergic) cells in the
pars compacta region of the substantia nigra (literally "black
substance").
•These neurons project to the striatum and their loss leads to
alterations in the activity of the neural circuits within the
basal ganglia that regulate movement, in essence an
inhibition of the direct pathway and excitation of the indirect
pathway.
•Most people with Parkinson's disease are described as
having idiopathic Parkinson's
•Someone who has Parkinson's disease is more likely to have
relatives that also have Parkinson's disease. However, this
does not mean that the disorder has been passed on
genetically
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Parkinson’s Treatment
Parkinson's disease is a chronic disorder that requires broadbased management including patient and family education,
support group services, general wellness maintenance, physical
therapy, exercise, and nutrition
At present, there is no cure for PD, but medications or surgery
can provide relief from the symptoms
•The most widely used form of treatment is L-dopa in various
forms. L-dopa is transformed into dopamine in the
dopaminergic neurons.
•However, only 1-5% of L-DOPA enters the dopaminergic
neurons. The remaining L-DOPA is often metabolized to
dopamine elsewhere, causing a wide variety of side effects. Due
to feedback inhibition L-dopa eventually becomes
counterproductive
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Parkinson’s Treatment
•MAO-B inhibitors. Selegiline and rasagiline reduce the
symptoms by inhibiting Monoamine Oxidase-B (MAO-B)
inhibitors, inhibit the breakdown of dopamine secreted by the
dopaminergic neurons. This might result in side effects such as
insomnia.
•Sinemet: A form of Levodopa. Levodopa is used as a prodrug
to increase dopamine levels for the treatment of Parkinson's
disease, since it is able to cross the blood-brain barrier, whereas
dopamine itself cannot.
•Once levodopa has entered the central nervous system (CNS), it
is metabolized to dopamine.
•Half life is 45-90 minutes. (The biological half-life of a
substance is the time it takes for a substance (drug)to lose half of
its pharmacologic activity).
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Parkinson’s
•Because Parkinson's disease affects the ability to move, exercise
helps to keep muscles strong and improve flexibility and
mobility.
•Exercise will not stop Parkinson’s disease from progressing;
but, it will improve the patient’s balance and it can prevent joint
stiffening.
•Evidence suggests that regular exercise can improve some of the
typical Parkinson’s symptoms, including tremor, rigidity,
slowness and impaired movement and therefore enhance the
quality of life.
•See handout for sample exercise program
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Orthopedic conditions
•Surgical
•Total Hip Replacement
•Total Knee Replacement
•Total shoulder replacement
•Rotator Cuff repair
•Non-surgical
•Joint sprains/strains
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Geriatrics
Most of your geriatric patients will require a different exercise
approach because of age related changes to their exercise
physiology. In addition, many of these patients will suffer from
conditions that may affect their exercise tolerance including
(Eighty-four percent of individuals aged 65 and over have at least one
chronic illness):
CHF
HTN
Hyperlipidemia
DM
PVD
Alzheimer’s
As we know, these diseases bring other symptoms (cognitive
impairment, falls, incontinence, low body mass index,
dizziness, vision impairment, hearing impairment) and
dependency in activities of daily living (bathing, dressing,
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Congestive Heart Failure
•Left-sided heart failure causes fluid to back up and accumulate in the
lungs. This leads to the patient symptoms of shortness of breath,
inability to sleep on only one pillow, waking up in the middle of the
night gasping for breath, inability to exercise without shortness of
breath, inability to catch your breath while at rest, and for severe cases
coughing and gurgling with frothy sputum.
•Right-sided heart failure causes the blood entering the heart from the
body to back up in the veins causing swelling of the legs, feet , and
stomach. Usually, because the chambers of the heart are interconnected
and work off a pressure system, congestive heart failure is a
combination of left and right sided heart failure
•Scientific evidence has demonstrated significant
improvement in cardiopulmonary function, functional status,
and psychosocial status of individuals with heart failure
•It also has been documented that patients with CHF have
abnormal hemodynamic responses to exercise making it
difficult for physical therapists to develop exercise programs for
these individuals.
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Exercise objectives for patients with CHF.
•Beta Blockers
•ACE inhibitors
•Diuretics
•increase exercise tolerance
•decrease dyspnea and fatigue
•reduce the risk of arrhythmias
•Improve the quality of life
•Initial stress testing is important to create a baseline
•Patients may need to begin aerobic exercise with interval
training and progress slowly.
•Strength exercise is also useful.
•Exercise used along with the customarily prescribed CHF
medications improves symptoms more than either modality
alone.
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Things to consider:
•The heart's impaired pumping efficiency results in decreased
blood flow to the muscles
•Pulmonary congestion interferes with alveolar gas
transport, causing dyspnea and reducing the oxygen
available for delivery to the muscles
•Hormonally, CHF is associated with elevated levels of
catecholamines, which increases vascular resistance and
further reduce muscle oxygenation
•Muscle atrophy often occurs early in the disease probably as
a result of decreased activity and reduced blood flow.
•There is an increased proportion of type 2 (fast-twitch)
muscle fibers, which produce more lactate at lower
workloads and thus fatigue more easily than type 1 fibers
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Other benefits of exercises for CHF patients
•Studies documenting the benefits of exercise for CHF
patients are fewer than those demonstrating its benefits for
coronary artery disease patients
•Increased Exercise tolerance,-defined as time to
exhaustion at sub-maximal intensity—increases in the range
of 26% to 37%. Individuals report less fatigue, more energy,
and more endurance after training programs. This effect
doubles when the patient is also taking ACE inhibitors.
•Quality of life. Research (3,5-9) has also shown that
exercise can produce significant and lasting changes in
patients' quality of life. One investigator (5) found that 50%
of patients returned to work after exercise training. Three
years after the study, 92% were still physically active, 31%
were asymptomatic during activity, and 46% reported
minimal impairment in daily life
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Other benefits of exercises for CHF patients
•Functional improvements. Improvements in walking
speed became apparent by the fourth week of the trial and
rose to a mean of 18% over baseline by the end of the trial.
Peak oxygen uptake, resting heart rate, peak power output,
and ventilatory threshold also improved significantly, while
fatigue decreased significantly. Patients in a control group
showed virtually no changes in these variables
•Cellular changes. A number of investigators have observed
a reversal of the decline in mitochondria and peripheral
oxidative capacity associated with CHF. For example, in a 6month study of patients who exercised 40 minutes daily,
volume density of cytochrome c oxidase-positive
mitochondria increased by 41%, and the change was
significantly associated with oxygen uptake at the ventilatory
threshold and with peak oxygen uptake.
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Exercise protocol for CHF
•Although most studies have used aerobic programs in which
patients aimed at achieving 50% to 75% of maximum heart rate
with exercise, less demanding protocols are beneficial as well.
In one controlled trial, 27 patients who had mild, chronic CHF
were randomly assigned to 8 weeks of low-intensity aerobic
training (performed at 40% of peak oxygen uptake, 3 times per
week) or no training. Significant increases in peak oxygen
uptake, volume density of mitochondria, lactic acidosis
threshold, and peak workload occurred in the training group but
not in controls.
•Another trial (7) tested the effects of graded resistance
training on CHF patients. By using a protocol that works one
muscle group at a time, researchers hoped to achieve positive
results while putting less demand on the cardiovascular system,
relative to other methods of strength training. After 90 days, the
patients' scores on a multidimensional quality-of-life survey
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•In addition to its positive impact on the disease itself, regular
exercise is beneficial for a host of other medical and nonmedical problems to which CHF patients are prone.
•Seventy percent of CHF cases are related to coronary heart
disease and hypertension, and exercise has a documented
value for both.
•Exercise also improves lipid profiles and reduces the risk of
diabetes.
•Most CHF patients are over 65, and exercise has been shown
to help prevent and ameliorate osteoporosis and the decreased
mobility of aging.
•Research has shown that the greatest aerobic gains occur
when CHF patients exercise at 60% to 80% of their
maximum heart rate. (symptom free max HR)
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•To calculate a safe, maximally effective target heart rate for the
patient's exercise prescription, subtract the resting heart rate from
the maximum heart rate on the test, multiply by 0.6 to 0.8, and add
back the resting pulse.
•A gradual approach. Long warm-ups are important to promote
vasodilatation before the demands of exertion. A protocol of at least
10 minutes of stretching, slow walking, or other exercise can
increase blood flow to muscles without raising the pulse above 40%
to 50% of maximum heart rate
•Ideally, patients should exercise—walk or ride a stationary
bicycle—at their prescribed heart rate for 20 to 40 minutes three to
five times a week.
•Patients should generally start interval training with 2 to 4 minutes
of exercise followed by a minute of rest, until they can do 10 to 15
minutes of exercise. They should then work up to 5 minutes of
exercise followed by 2 minutes of rest for a total of 20 to 40
minutes of exercise per session. Patients should progress gradually
until they can sustain continuous exercise for the entire session.
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•Strength training. While aerobic training is the cornerstone
of the exercise program, exercises to strengthen ventilatory
muscles of the diaphragm and abdomen have been shown to
reduce dyspnea, improve quality of life, and boost exercise
tolerance
•Resistance training using dumbbells and ankle weights or
strength training machines can be added to redress the muscle
fatigue that often limits activity in CHF.
•Using low weight and high repetitions prevents straining and
breath holding, which place greater demands on the heart.
•The focus should be on the major muscles of the upper and
lower body and torso. One to two sets with 12 to 15
repetitions per set provides an adequate training stimulus.
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Cautions for patients.
•Patients must be taught the signs of decompensation—
angina, worsening breathlessness, weight gain, or leg
swelling—and counseled to discontinue exercise and seek
medical attention if they occur.
•Exacerbations are common in CHF and are usually unrelated
to exercise, but patients should refrain from activity until the
condition has been controlled
•Patients—especially those with impaired renal function—
should avoid excessive water consumption. Sodium
restriction (a maximum of 2 g per day) is usually part of the
strategy to minimize edema.
•Given the considerable benefits of exercise, its limited risks,
and its compatibility with other modes of treatment, a
systematic training program should be part of the management
of CHF for almost all patients.
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Hypertension
•Having high blood pressure and not getting enough
exercise are closely related
•Regular physical activity makes your heart stronger. A
stronger heart can pump more blood with less effort. If your
heart can work less to pump, the force on your arteries
decreases, lowering your blood pressure.
•Becoming more active can lower the systolic blood
pressure — the top number in a blood pressure reading —
by an average of 5 to 10 millimeters of mercury (mm Hg).
•That's as good as some blood pressure medications. For
some people, getting some exercise is enough to reduce the
need for blood pressure medication.
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Hypertension
•It takes about one to three months for regular exercise to
have an impact on blood pressure.
•These benefits last only as long as you continue to exercise
•Flexibility and strengthening exercises such as lifting
weights are an important part of an overall fitness plan, but it
takes aerobic activity to control high blood pressure.
•Any physical activity that increases heart and breathing
rates is considered aerobic. Mowing the lawn, raking
leaves or scrubbing the floor counts — as long as it takes
effort.
•Other common forms of aerobic activity include climbing
stairs, walking, jogging, bicycling and swimming.
•Aim for at least 30 minutes of aerobic activity most days of
the week.
•Taking the stairs instead of the elevator or taking a walk
during your lunch break.
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Hyperlipidemia
•The term hyperlipidemia means high lipid levels.
•Lipid is the scientific term for fats in the blood. At proper
levels, lipids perform important functions in the body, but
can cause health problems if they are present in excess.
•Typically associated with high cholesterol and high
triglyceride levels.
•High lipid levels can speed up a process called
atherosclerosis, or hardening of the arteries. Plaque is made
of lipids and other materials circulating in your blood. As
more plaque builds up, your arteries can narrow and stiffen.
•Atherosclerosis increases your risk of heart disease, stroke,
and other vascular diseases.
• Fortunately, you may be able to reduce high lipid levels
and, therefore, prevent or slow the progression of
atherosclerosis.
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Hyperlipidemia
•Exercise makes is an important component of the management
of hyperlipidemia.
•Physician often will recommend an exercise program, such as
walking briskly for 20 to 30 minutes most days of the week.
•Exercise can help lose or maintain weight, relieve stress, raise
HDL, and lower triglycerides and LDL.
•Make sure to talk with your physician before starting any
exercise program and gradually increase how long and how
often you exercise.
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Diabetes Mellitus
•Exercise can help control weight and lower blood sugar
levels. It also lowers the risk of heart disease, a condition
that is common in people who have diabetes.
•Exercise can also help you feel better about yourself and
increase your overall health.
•Focus should be on aerobic exercises
•Exercise changes the way the body reacts to insulin.
•Regular exercise makes the body more sensitive to
insulin, and the blood sugar level may get too low
(called hypoglycemia) after exercising. Symptoms
include: feel a change in your heartbeat, suddenly sweat
more, feel shaky or anxious, or feel hungry.
•Shoes and footcare are very important because of
peripheral neuropathy that might be present.
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So before you exercise a patient with DM, you
should do the following:
•Get a complete medical history.
•Check patient’s blood sugar level before and after exercising.
•Have the patient check their feet for blisters or sores before
and after exercising.
•Make sure the patient wears the proper shoes and socks.
•Make sure the patient drinks plenty of fluid before, during
and after exercising.
•Warm up before exercising and cool down afterward.
•Have a snack handy in case your blood sugar level drops too
low.
•Know when your patient is taking insulin (and how often,
how much)
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PVD
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Peripheral Vascular Disease (PVD)
Pathophysiology of PVD
•Atherosclerosis is the initiating event which limits oxygen
delivery to skeletal muscle during exercise.
•This leads to skeletal muscle ischemia, which leads in turn to
muscle dysfunction.
•Finally, continuance of this process leads to muscle injury
manifested by denervation, mitochondrial DNA injury, abnormal
oxidative metabolism, and muscle atrophy.
•Exercise therapy is the cornerstone of treatment for PVD
but must be done in a rigorous fashion.
•It is important to objectively assess the severity of claudication
using a treadmill exercise test. Patients are instructed to exercise
until moderate claudication occurs and then rest.
•Exercise followed by rest cycles should be repeated in 30- to
40-minute sessions 3 to 4 times weekly.
•Exercise is not recommended for people with severe rest pain.
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Peripheral Vascular Disease
•Randomized trials of exercise for patients with intermittent
claudication have shown significant increases in exercise
duration and quality of life.
•Patients assigned to an exercise program were able to increase
their exercise time until developing pain by 180%, compared
with a 40% increase for patients receiving usual care.This
translates into an extra 2 blocks of walking time.
•Other studies have suggested that patients who exercise in a
supervised program do better than those who exercise
unsupervised.
•The best predictors of a response to exercise therapy are: 1)
program involves walking exercise rather than biking or
swimming; 2) patients push to moderate pain; 3) sessions
continue for longer than 6 months; and 4) sessions are
supervised.
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Alzheimer’s
•Moderate exercise helps many people with Alzheimer's
disease feel better — both physically and emotionally.
•As little as 20 minutes of walking three times a week can
boost mood, decrease risk of falls, reduce wandering and
delay nursing home placement in people with Alzheimer's.
•Research has shown that exercising reduces the tendency
of an Alzheimer patient to become depressed (typically,
70% becomes depressed)
•In a sample of people with Alzheimer's, a moderate
exercise program totaling at least 60 minutes a week for
three months reduced rates of depression.
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Improving sleep
•Sleep disturbances are common in people with Alzheimer's
disease. Some become agitated at bedtime, wander at night or
sleep fitfully. Caregivers become exhausted when they can
obtain only a few hours of sleep at a time, night after night.
•Regular physical activity is a natural sleep-enhancer. A daily
walk or exercise class can help a person with Alzheimer's
sleep more soundly at night.
Fall Prevention
•Moderate exercise improves strength and coordination, which
can reduce the risk of falls and injury.
Reduce wandering
•Studies have shown that giving an Alzheimer patient
functional activities as an exercise, reduces wandering. Tie the
exercises to an activity, such as walking the dog, getting the
mail, sweeping, folding the laundry and other things and make
it a daily routine for the patient.
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Case Discussions
CASE 1
85 year old male.
Condition: Day 1 s.p Right THA ( non cemented 50% WB)
Factors to consider: Has been confused, is aneamic.
Lives alone in a mobile home
Function to be restored: Walking.
How would you start this patient day one and progress him.
With what frequency would you treat. And are there other
factors you would consider.
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Spine Disorders
•Spinal Stenosis vs. Claudication
•How do we differentiate?
•How do we exercise?
•Pelvic tilts vs. aerobic exercise
•Lumbar instability: Iliopsoas
•Poor posture, forward head posture.
•Cervical neck exam and basic exercises/stretching
•S/P surgery:
•Laminectomy (new endoscopic approach)
•ACD
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Case Discussions
CASE 1
85 year old male.
Condition: Day 1 s.p Right THA ( non cemented 50% WB)
Factors to consider: Has been confused, is aneamic.
Lives alone in a mobile home
Function to be restored: Walking.
How would you start this patient day one and progress him.
With what frequency would you treat. And are there other
factors you would consider.
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Case 2
85 year old male
Condition: Day 3 s.p. Right THA
Factors to consider: Feels great wants to get up is 50% WB
Is scheduled to go to SNF tomorrow.
How would you treat this patient today.
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Case 3
85 year old male. Day 8 s.p. R THA. Has been in SNF for 4
days. Desperately wants to go home. He hates old people,
appears depressed, did not eat all day yesterday. Patient lives in
a mobile home. Reportedly can’t wash his face due to receiving
IV- Fluids.
How would you treat this patient today ? How would you
progress?
What are your goals for today?
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Case 4
85 year old male. 12 days s.p. right THA (50% WB)
Patient came home last night from SNF. Both sons carried
him up 3 steps into his mobile home. You walk into his home
and find him in his favorite spot. A 20 year old couch with
broken springs in the bottom. He is thrilled to be home.
How would you treat this patient today? Where would you
start and how would you progress
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Case 5
85 year old male, 4 weeks s.p. right THA. Lives in mobile
home. Reports he saw his dr. today who wanted him to get
rid of the walker and start walking with a quad cane. How
would you treat this patient today? And how would you
progress?
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Case 6
85 year old male 6 weeks s.p right THA( FWB) Presents to
you in outpatient clinic.
Wants to get back to playing golf. His mobile home sit on
the 18th hole. Problem is he can’t stand the pain in his groin
when walking. He has been having to use his walker a lot.
You notice the pt walks in an abducted gait pattern with
grossly 30 deg. abduction throughout stance phase.
How would you treat this patient today?
Name 3 dysfunctions that could contribute to this gait
pattern.
How would you progress?
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Case 7
Your patient is a 17 year old female volleyball player
who is 3 days s.p. ACL-repair of the R knee. She
presents with extensive swelling in her complete R leg.
Severe pain in R thigh and knee. Wearing a ROM brace
set at 0-90deg.
The orders are for therex, gt training FWB as per
protocol.
What would you do today?
How would you progress?
What are your 2 priority short term goals, and how do
you intent to meet them?
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Case 8
Your patient is a 17 year old high school student who
presents 3 days after repair of a torn ACL and a repaired
torn medial meniscus. Before the surgery she was
immobilized for 4 weeks with a brace locked in 30 deg
flexion. Today she is wearing a ROM-brace set at 0-90deg.
and she is avoiding WB on her Sx.-leg. She complains to
you about extreme pain 10/10 on VAS. She has been unable
to sleep. Appears pale
The prescription requests therex as per protocol (no rom
resticktions) and gt-training 50%WB.
How would you preceed? how would you progress? What
are your first 3 priorities?
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Case 9
Your patient is a 60 year old male. Dx. Torn Rotator cuff R
shoulder. He reports he tore his RTC while stepping on the
back of a garbage truck while working. He presents 5 days
post open RTC repair wearing an immobilizer. Which he
states he has to wear for 6 weeks. The pain is rated 9/10
with inability to get comfortable. I take “catnaps” all day
and night. Pt. has been unable to take of his immobilizer.
The prescription for PT. Requests PROM/ AAROM with
weight of arm supported. No erot. ext. beyond neutral.
How would you start treating this patient and how would
you progress.
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Case 10
Your patient is the same sanitation worker but he is
8weeks sp RTC repair and cleared to start weight and
resistive training.
How would you start this phase? And how would you
progress?
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Questions or suggestions?
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References:
http://www.stolaf.edu/people/giannini/biological%20anamations.html
http://science.nhmccd.edu/biol/ap1int.htm
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