Nerve muscle physiology1 /certified fixed orthodontic courses by Indian dental academy

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Nerve Muscle Physiology


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Sensation
Awareness of internal and
external events
Perception
Assigning meaning to a
sensation
Central Nervous System The brain and spinal cord
Peripheral Nervous System
All nervous system
structures outside the CNS; i.e. nerves
the cranial
nerves, ganglia and sensory receptors
Neuroglia
(neuro = nerve; glia = glue) Nonexcitable cells of neural tissue that support, protect, and
insulate neurons

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Neuron
Cell of the nervous system
specialized to generate and transmit nerve
impulses
Dendrite
(dendr = tree) branching
neuron process that serves as a receptive or input
region
Axon
(axo = axis) Neuron
process that conducts impulses

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Myelin Sheath
Fatty insulating sheath that
surrounds all but the smallest nerve fibers
Sensory Receptor
Dendritic end organs, or parts
of other cell types, specialized to respond to a stimulus
Resting Potential
The voltage difference which
exists across the membranes of all cells due to the unequal
distribution of ions between intracellular and extracellular
fluids
Graded Potential
A local change in membrane
potential that declines with distance and is not conducted
along the nerve fiber
Action Potential
A large transient depolarization
event, which includes a reversal of polarity that is
conducted along the nerve fiber

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Saltatory Conduction
Transmission of an action
potential along a myelinated nerve fiber in which the nerve
impulse appears to leap from node to node
Synapse
(synaps = a union) Functional
junction or point of close contact between two neurons or
between a neuron and an effector cell
Neurotransmitter
Chemical substance released by
neurons that may, upon binding to receptors or neurons or
effector cells, stimulate or inhibit those cells
Sensory Transduction
Conversion of stimulus energy
into a nerve impulse

 NEURONS:
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Are highly specialized
Are one of a few types of excitable cells (able to fire action
potentials) in the body
Conduct messages in the form of action potentials (nerve
impulses) from one part of the body to another
Are amitotic; they can not replace themselves; they do,
however, have extreme longevity
Have a high metabolic rate and can not survive for more
than a few minutes without oxygen

 Have

a cell body or soma and numerous thin
processes (extensions)
 Most cell bodies of neurons are located in the
CNS where they are protected by the cranium and
vertebral column
 Within cell bodies all standard organelles are
contained


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Dendrites are processes that receive information, they are
input regions of the neuron but they do not have the ability
to generate action potentials.
Axons
are processes that can generate and
conduct action potentials, they arise at an area associated
with neuron's soma called the axon hillock or spike
initiation zone (trigger zone); they may be very short or
very long depending on where they are conducting
information; can give off branches called axon collaterals;
finally they form synapses at their terminals.

MYELlNATED AND UNMYELINATED NERVE
FIBERS
The large fibers are myelinated, and the small ones are
unmyelinated.
The average nerve trunk contains about twice as many
unmyelinated fibers as myelinated fibers.
 The central core of the fiber is the axon, and the membrane
of the axon is the actual conductive membrane for
conducting the 'action potential. The axon is filled in its
center with axoplasm, which is a viscid intracellular fluid.
 Surrounding the axon is a myelin sheath that is often
thicker than the axon itself, and about once every 1 to 3
millimeters along the length of the axon the myelin sheath
is interrupted by a node of Ranvier.

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The myelin sheath is deposited around the axon by
Schwann cells
Saltatory conduction in myelinated fibers from
node to node -action potentials are conducted from
node to node
electrical current flows through the surrounding
extracellular fluids outside the myelin sheath as
well as through the axoplasm from node to node,
exciting successive nodes one after another.

Velocity of Conduction in Nerve Fibers

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The velocity of conduction in nerve fibers varies
from as little as 0.25 m/sec in very small
unmyelinated fibers to as high as 100 m/sec (the
length of a football field in 1 second) in very large
myelinated fibers.
The velocity increases approximately with the
fiber diameter in myelinated nerve fibers and
approximately with the square root of fiber
diameter in unmyelinated fibers.

BASIC PRINCIPLES OF ELECTRICITY
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All cells in the body have an unequal distribution of ions
(concentration gradient) and charged molecules (electrical
gradient) across their membranes.
all have a net negative balance inside relative to outside
(differences are always expressed as inside relative to
outside).
Because opposite charges attract, there is a driving force
which would lead to ions flow if not for the presence of the
membrane. This represents a potential energy, which is
called the potential difference or membrane potential, the
measure of this potential energy is called voltage and is
expressed in volts or millivolts.

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This membrane potential is present in all cells, including
neurons and muscle cells when they are at rest (are not
firing action potentials), and is called the resting
membrane potential, or resting potential. The size of
resting potential ranges from -20 to -200 millivolts in
different cells, in neurons it ranges from -50 to -100
millivolts and in muscles it averages about - 70 mV.
neurons and muscle cells are unique. Unlike all other
cells, they have the ability to actively change the potential
across their membranes in a rapid and reversible way. The
rapid reversal of membrane potential is referred to as an
action potential.

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Source of the potential difference is primarily due to:
1) Imbalance of Na+ and K+ across the membrane
2) Differences in the relative permeability of the
membrane to these two ions
Almost all membranes are more permeable to potassium
since there are a large number of K+ leak channels that are
always open
3) There are relatively few such channels for sodium
Na+/K+ pump- a carrier protein found in the membrane
transports 2 K+ ions into the cell and 3 Na+ ions out, with
the expenditure of one ATP

 1) Depolarization: membrane potential decreases
(becomes less negative)
2)
Hyperpolarization: membrane potential increases
(becomes more negative)


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Whether an action potential (AP) is generated or not
depends on the strength of depolarizing stimulus.
Stimuli can be:
1. Subthreshold
2. Threshold
3. Suprathreshold


Molecular Events Underlying the
Action Potential :

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The membrane of all excitable cells contains two
special gated channels. One is a Na + channel
and the other is a K + channel and both are
VOLTAGE GATED . At rest, virtually all of the
voltage-gated channels are closed, potassium and
sodium can only slowly move across the membrane,
through the passive "leak" channels
The first thing that occurs when a depolarizing
graded potential reaches the threshold is that the
voltage gated Na + channels begin to open
and Na + influx into the cell exceeds K + efflux
out of the cell

Two things happen next:
1) As the membrane depolarizes further and the cell
becomes positive inside and negative outside, the
flow of Na+ will decrease.
2)
Even more importantly, the voltage- gated Na+
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channels close
When the inactivation gates close, Na+ influx stops and
the repolarizing phase takes place.


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Next, the voltage gated K + channels are activated
at the time the action potential reaches its peak. At
this time, both concentration and electrical gradients
favour the movement of K+ out of the cell.
These channels are also inactivated with time but
not until after the efflux of K+ has returned the
membrane potential to, or below the resting level
(after hyperpolarization
/positive afterpotential ).


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All-or-none Phenomenon
Because the series of events becomes selfperpetuating once the membrane is depolarized past
threshold, and because all action potentials are of the
exact same size, it is said to be an all-or-none event.
If threshold is reached, you get an action potential
that is always the same. Therefore, both the
threshold and suprathreshold stimuli can generate
only one response - an action potential.


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As a result, the membrane cannot be excited to
generate another action potential at this site until the
ongoing event is over. This period during which the
membrane is completely unexcitable is the absolute
refractory period .
Once the membrane potential has returned to resting
conditions, another action potential can be
generated. However, before it happens there is a
short period during which the voltage gated K+
channels are still open producing hyperpolarization,
during which the membrane potential is further from
threshold and during which a larger than normal
stimulus is required to generate an action potential.
This is the relative refractory period .

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Synapses are the junctions between neurons and the
structures they innervate.
Electrical Synapses:
There are some specialized neurons, which are
connected by gap junctions, and through which ions
can flow and, hence, across which action potentials
can be directly propagated. these are relatively
uncommon in the nervous system they are extremely
important in the cardiac muscle tissue
Chemical Synapses:
Most neurons are separated from the object that they
innervate by a short gap. These gaps or junctions are
very narrow but the action potential cannot jump
across them. Instead, electrical activity is usually
transferred from the axon terminal to the next cell by
a chemical messenger - a neurotransmitter, such
transfer can occur in only one direction.

Neurotransmitters:
 At present there are over 100 chemical substances
believed to act as neurotransmitters in different parts
of the nervous system. Many neurons make more
than one transmitter and may release more than one
transmitter upon the arrival of a single action potential
at the axon terminal.
 The main neurotransmitters of the peripheral NS.
are:• Acetylcholine (Ach)
ACh is the primary neurotransmitter of the somatic NS
and the parasympathetic division of the ANS.
 • Norepinephrine (NE).
 NE is the primary neurotransmitter of the sympathetic
division of the ANS
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Skeletal muscle
 40% of adult body weight

 50% of child’s body weight
 Muscle contains:

75% water
 20% protein
 5% organic and inorganic compounds
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 Functions:

Movement
 Maintenance of posture
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Whole muscle
 Separate organ
 Encased in connective tissue – fascia
 Functions of fascia

Protect muscle fibers
 Attach muscle to bone
 Provide structure for network of nerves and
blood/lymph vessels
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Layers of fascia
 Epimysium

Surface of muscle
 Tapers at ends to form tendon
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 Perimysium
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Divides muscle fibers into bundles or fascicles

 Endomysium
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Surrounds single muscle fibers


PHYSIOLOGIC ANATOMY OF
SKELETAL MUSCLE
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skeletal muscles are made of numerous fibers
ranging from 10 to 80 micrometers in diameter.
Each of these fibers in turn is made up of
successively smaller subunits
In most muscles, the fibers extend the entire
length of the muscle; except for about 2 per cent
of the fibers,
each is innervated by only one nerve ending,
located near the middle of the fiber.

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Organization of
skeletal muscle,
from the gross to
the molecular
level..

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SARCOLEMMA. The sarcolemma is the cell.
Membrane of the muscle fiber.
It consists of a true cell membrane, called the
plasma membrane, and an outer coat made up of a
thin layer of polysaccharide material that contains
numerous thin collagen fibrils.
At the end of the muscle fiber sarcolemma fuses
with a tendon fiber, and the tendon fibers in turn
collect into bundles to form the muscle tendons
and thence insert into the bones.

Sarcoplasm – cytoplasm of muscle cell
 Sarcotubular system
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Sarcoplasmic reticulum
 Sarcotubules and transverse tubules
 Ca++ uptake, regulation, release and storage
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SARCOPLASM.
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The myofibrils are suspended inside the muscle
fiber in a matrix called sarcoplasm, which is
composed of usual intracellular constituents,
The fluid of the sarcoplasm contains large
quantities of potassium, magnesium, phosphate,
and protein enzymes.
There are tremendous numbers of mitochondria
that lie between and parallel to the myofibrils, it
indicates the great need for large amounts of
adenosine triphosphate (ATP) for the contracting
myofibrils..

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MYOFIBRILS;
ACTIN AND Troponin Tropomyosin(thin)
MYOSIN FILAMENTS.(thick)
Each muscle fiber contains several hundred to
several thousand myofibrils.
Each myofibril in turn has, lying side by side,
about 1500 myosin filaments and 3000 actin
filaments, which are large polymerized protein
molecules that are responsible for muscle
contraction.

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The thick filaments are myosin and the thin
filaments are actin.
myosin and actin filaments partially interdigitate
and thus cause the myofibrils to have alternate
light and dark bands.
The light bands contain only actin filaments and
are called I bands because they are isotropic to
polarized light.
The dark bands contain the myosin filaments as
well as the ends of the actin filaments where they
overlap the myosin and are called A bands because
they are anisotropic to polarized light..

 small projections from the sides of the

myosin filaments are cross-bridges. They
protrude from the surfaces of the myosin
filaments along the entire extent of the
filament except in the very center.
 Interaction between these cross- bridges
and the actin filaments causes contraction

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ends of the actin filaments are attached to Z disc.
From this disc, these filaments extend in both
directions to interdigitate with the myosin
filaments.
The Z disc is composed of filamentous proteins
different from the actin and myosin filaments
the entire muscle fiber has light and dark bands,
as do the-individual myofibrils. These bands give
skeletal and cardiac muscle their striated
appearance.

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The portion of a myofibril that lies between two
successive Z discs is called a sarcomere,
When the muscle' fiber is at its normal, fully
stretched resting length, the length of the
sarcomere is about 2 micrometers. At this length,
the actin filaments overlap the myosin filaments
and are just beginning to overlap one another.


Neuronal Control of Muscle
Contraction
 Movement requires contraction of many

fibers within a muscle & of many
muscles within the body – correctly
timed with one another & regulating the
strength of contraction
 Coordination generated within NS =
most muscle contract only when APs
arrive at Neuromuscular Junction

TRANSMISSION OF IMPULSES FROM
NERVES TO SKELETAL MUSCLE
FIBERS:NEUROMUSCULAR
JUNCTION

 The nerve ending makes a junction, called the

neuromuscular junction, with the muscle fiber
near the fiber's midpoint, and the action potential
in the fiber travels in both directions toward the
muscle fiber ends. With the exception of about 2
per cent of the muscle fibers, there is only one
such junction per muscle fiber.


PHYSIOLOGICAL ANATOMYOF THE
NEUROMUSCULAR JUNCTIONMOTOREND PLATE.


 The nerve fiber branches at its end to form a

complex of branching nerve terminals,
which invaginate into the muscle fiber but
lie outside the muscle fiber plasma
membrane. The entire structure is called the
motor end plate.


End Plate Potential And Excitation Of The
Skeletal Muscle Fiber
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sudden insurgence of sodium ions into the muscle
fiber when the acetylcholine channels open causes
the internal membrane potential in the local area
of the end plate to increase in the positive
direction as much as 50 to 75 millivolts, creating a
local potential called the end plate potential.
end plate potential created by the acetylcholine
stimulation is normally far greater than enough to
initiate an action potential in the muscle fiber.

Safety Factor For Transmission At The
Neuromuscular
Junction
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Each impulse that arrives at the
neuromuscular junction causes about three
times as much end plate potential as that
required to stimulate the muscle fiber
therefore the normal neuromuscular junction
is said to have a safety factor
repeated stimulation diminishes the number
of vesicles of acetylcholine released with
each impulse so much that impulse fails to
pass into the muscle fiber – FATIGUE

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A new action potential cannot occur in an
excitable fiber as long as the membrane is still
depolarized from the preceding action potential.
shortly after the action potential is initiated, the
sodium channels (or calcium channels, or both)
become inactivated, and any amount of excitatory
signal applied to these channels at this point will
not open the inactivation gates.
The only condition that will re-open them is for
the membrane potential to return to the original
resting membrane potential level.

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The period during which a second action potential
cannot be elicited, even with a strong stimulus, is
called the absolute refractory period. This period
for large myelinated nerve fibers is about
1/2500second..
After the absolute refractory period is a relative
refractory period, lasting about one quarter to one
half as long as the absolute period. During this
time, stronger than normal stimuli can excite the
fiber.

The cause of this relative refractoriness are:
(1) During this time, some of the sodium channels
still have not been reversed from their inactivation
state, and
(2) the potassium channels are usually wide open at
this time, causing greatly excess flow of positive
potassium ion charges to the outside of the fiber
opposing the stimulating signal
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Steps in muscle contraction
 Excitation

Action potential traverses nerve
 Neurotransmitter released into
neuromuscular junction - Ach
 Muscle fiber depolarization
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Sarcolemma to transverse tubules – Ca++
release from sarcoplasmic reticulum


 Coupling
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Ca++ binds to troponin-tropomyosin complex


 Contraction

Ca++ binding moves troponin-tropomyosin
complex
 Myosin heads attach to actin
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Crossbridge formation

Crossbridge cycling
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Moves the myosin heads along the actin and
shortens the sarcomere

 Relaxation

Ca++ removed from troponin-tropomyosin
complex
 Cross bridge detachment
 Ca++ pumped into SR – active transport
 Sarcomere lengthens
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Excitation-contraction coupling


GENERAL MECHANISM OF MUSCLE
CONTRACTION
The initiation and execution of muscle contraction
occurs in following sequential steps.
1. An action potential travels along a motor nerve to
its endings on muscle fibers.
2. At each ending, the nerve secretes a small amount
of the neurotransmitter substance acetylcholine.
3. The acetylcholine acts on a local area of the
muscle fiber membrane to open multiple
acetylcholine-gated channels through protein
molecules in the muscle fiber membrane.

4. Opening of the acetylcholine channels allows
large quantities of sodium ions to flow to the
interior of the muscle fiber membrane at the point
of the nerve terminal. This initiates an action
potential in the muscle fiber.
5. The action potential travels along the muscle fiber
membrane in the same way that action potentials
travel along nerve membranes.
6. The action potential depolarizes the muscle fiber
membrane and also travels deeply within the
muscle fiber Where it causes the sarcoplasmic
reticulum to release into the myofibrils large
quantities of calcium ions that have been stored
within the reticulum.

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7. The calcium ions initiate attractive forces
between the actin and myosin filaments, causing
them to slide together, which is the contractile
process.
8. After a fraction of a second, the calcium ions
are pumped back into the sarcoplasmic reticulum,
where they remain stored until a new muscle
action potential comes along; this removal of the
calcium ions from the myofibrils causes muscle
contraction to cease.

Sliding Filament Theory
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during contraction, thick
and thin filaments do not
change their length, but
slide past each other
(overlapping further) as
a
result,
individual
sarcomeres
shorten
,myofibrils shorten, the
entire cell shortens


Muscle contraction
 Types
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Isometric or static
Constant muscle length
 Increased tension
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Isotonic
Constant muscle tension
 Constant movement
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– Concentric - shortening
– Eccentric - lengthening

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It demonstrates that maximum contraction occurs
when there is maximum overlap between the actin
filaments and the cross-bridges of the myosin
filaments,
the greater the number of cross-bridges pulling the
actin filaments, the greater the strength of
contraction.
when the muscle is at its normal resting length,
which is at a sarcomere length of about 2
micrometers, it contracts with maximum force of
contraction.

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If the muscle is stretched to much greater than
normal length before contraction, a large amount
of resting tension develops in the muscle even
before contraction takes place; this tension results
from the elastic forces of the connective tissue,
blood vessels, nerves, and so forth.
the increase in tension during contraction, called
active tension, decreases as the muscle is stretched
much beyond its normal length

Relation of Velocity of Contraction to LOAD

A

muscle contracts extremely rapidly when
it contracts against no load-to a state of full
contraction in about 0.1 second for the
average muscle. When loads are applied,
the velocity of contraction becomes
progressively less as the load increases

ATP & Muscle Contraction
Muscle contraction is absolutely dependent on ATP
for 3 processes (Myosin ATPase breaks down ATP
as fiber contracts) :
1) hydrolysis of ATP energizes the myosin head which
begins the “power stroke” of the cross-bridge cycle
2) attachment of ATP to myosin facilitates the
dissociation of the actomyosin complex allows for
continues x-bridge cycling and further shortening
Each x-bridge cycle shortens the muscle 1% of its
resting length
3) Ca++ reuptake into the SR occurs through an ATP
dependent pump
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Sources of ATP for Muscle
Contraction


Summation
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contraction of individual muscle fibers is allor-none - any graded response must come
from the number of motor units stimulated at
any one time
summation = adding together of individual
muscle twitches to make a whole muscle
contraction - accomplished by increasing
number of motor units contracting at one time
(spatial summation) or by increasing
frequency of contraction of individual muscle
contractions (temporal summation)

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Summotion means the adding together of
individual twitch contractions to increase the
intensity of overall muscle contraction.
Summation occurs in two ways:
(1) by increasing the number of motor units
contracting simultaneously, which is called
multiple fiber summation,and
(2) by increasing the frequency of contraction,
which is called frequency summation and can lead
to tetanization.

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To the left are
displayed individual
twitch contractions
occurring one after
another at low
frequency of
stimulation. Then, as
the frequency
increases, there
comes a point when
each, new
contraction occurs
before the preceding
one is over. This is
called tetanization.


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CHANGES IN MUSCLE STRENGTH AT THE
ONSET OF CONTRACTION- THE
STAIRCASE EFFECT (TREPPE).
When a muscle begins to contract after a long
period of rest, its initial strength of contraction
may be as little as one half its strength 10 to 50
muscle twitches later. That is, the strength of
contraction increases to a plateau, a phenomenon
called the staircase effect or treppe.

 Reflects the amount of

Ca2+ available in
the sarcoplasm and more efficient
enzyme activity as the muscle liberates
heat - Principal behind warming-up
before physical activity


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Muscle fatigue –Prolonged strong contractions

leads to fatigue due to inability of contractile &
metabolic processes to supply adequately to maintain
the work load - nerve continues to function properly
passing AP onto the muscle fibers but contractions
become weaker due to lack of ATP


Hypertrophy - increase in muscle mass caused by

forceful muscular activity – increase power of muscle
contraction
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Atrophy - when a muscle is not used for a length of
time or is used for only weak contractions

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HYPERPLASIA OF MUSCLE FIBERS.
Under rare conditions of extreme muscle force
generation, the numbers of muscle fibers increase,
but by only a few percentage points, in addition to
the fiber hypertrophy process. This increase in
fiber numbers is called fiber hyperplasia.
it occurs by the mechanism of linear splitting of
previously enlarged fibers.

Effects of Muscle Denervation
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When a muscle loses its nerve supply, it no longer receives
the contractile signals that are required to maintain normal
muscle size.
atrophy begins almost immediately.
After about 2 months, degenerative changes also begin to
appear in the muscle fibers themselves.
If the nerve supply grows back to the muscle, full return of
function usually occurs in about 3 months, but from that
time onward, the capability of functional return becomes
less and less, with no return of function after 1 to 2 years.

Satellite Cells:
repair and regeneration

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Satellite cells play a critical role in repairing or
replacing myofibrils which have been
damaged
Proliferation and differentiation of satellite
cells -Migrate into cytoplasm (near point of
damage) - Fuse together to form myotubes
and align themselves within existing fiber, or
become a new fiber May play a role in
stretch induced muscle growth

Muscle Fiber Types


Contract or Relax? Effect of type of stimuli


Receptors in Muscle: Feedback
to CNS
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Muscle contains receptors that provide
sensory information regarding:
– Chemical changes (i.e., O2, CO2, H+):
chemoreceptors
– Tension development: Golgi Tendon
Organs (GTO’s)
– Muscle length: Muscle spindles
Information from these receptors provides
information about the energetic requirements
of exercising muscle and about movement
patterns

Muscle spindle – Detect dynamic and static
changes in muscle length– Stretch reflex
• Stretch on muscle causes reflex contraction

Golgi tendon organ (GTO) – Monitor
tension developed in muscle – Prevents
damage during excessive force generation
• Stimulation results in reflex relaxation of
muscle
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Muscle spindles respond
to muscle stretch Gamma
motor neurons are
coactivated during
contraction
– Causing contraction of
fibers within muscle spindle
– Deviations in consistency
signal excessive stretch


Golgi Tendon Organ

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Located in
tendon Monitor
muscle tension
Activation
causes inhibition
of alphamotor
neuron “Safety
mechanism”
against
excessive force
during
contraction

Role of spindles and GTO’s in muscle stretch
and spasm

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Reduced pliability of the myotendinous
regions(golgi receptors) of skeletal muscle
may increase risk of injury
– Effective stretching techniques are
designed to inhibit muscle spindles and to
activate GTO’s
Muscle cramps/spasms may be caused by
overactive spindles and underactive GTO’s in
fatigued skeletal muscle

 Myotactic reflex
 Clasp knife reflex


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