nerve muscle physiology1 / orthodontic courses by indian dental academy

8/12/2019 Nerve Muscle Physiology1 / orthodontic courses by Indian dental academy

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Nerve Muscle Physiology

INDIAN DENTAL ACADEMY

Leader in continuing dental education

www.indiandentalacademy.com



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Sensation Awareness of internal andexternal events

Perception Assigning meaning to asensation

Central Nervous System The brain and spinal cord

Peripheral Nervous System All nervous systemstructures outside the CNS; i.e. nerves the cranialnerves, ganglia and sensory receptors

Neuroglia (neuro = nerve; glia = glue) Non-excitable cells of neural tissue that support, protect, andinsulate 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 thatsurrounds all but the smallest nerve fibers

Sensory Receptor Dendritic end organs, or partsof 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 unequaldistribution of ions between intracellular and extracellularfluids

Graded Potential A local change in membrane

potential that declines with distance and is not conductedalong the nerve fiber

Action Potential A large transient depolarizationevent, which includes a reversal of polarity that isconducted along the nerve fiber



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Saltatory Conduction Transmission of an actionpotential along a myelinated nerve fiber in which the nerveimpulse appears to leap from node to node

Synapse (synaps = a union) Functionaljunction or point of close contact between two neurons orbetween a neuron and an effector cell

Neurotransmitter Chemical substance released byneurons 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



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NEURONS: Are highly specialized

Are one of a few types of excitable cells (able to fire actionpotentials) in the body

Conduct messages in the form of action potentials (nerveimpulses) 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



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Have a cell body or soma and numerous thin

processes (extensions)

Most cell bodies of neurons are located in theCNS 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 conductinginformation; can give off branches called axon collaterals;

finally they form synapses at their terminals.



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MYELlNATED AND UNMYELINATED NERVE

FIBERS

The large fibers are myelinated, and the small ones areunmyelinated.

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 membraneof the axon is the actual conductive membraneforconducting 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 3millimeters along the length of the axon the myelin sheathis 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 fromnode to node -action potentials are conducted from

node to node

electrical current flows through the surrounding

extracellular fluids outside the myelin sheath aswell as through the axoplasm from node to node,

exciting successive nodes one after another.



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Velocity of Conduction in Nerve Fibers

The velocity of conduction in nerve fibers varies

from as little as 0.25 m/sec in very smallunmyelinated fibers to as high as 100 m/sec (thelength of a football field in 1 second) in very largemyelinated fibers.

The velocity increases approximately with thefiber diameter in myelinated nerve fibers andapproximately with the square root of fiberdiameter in unmyelinated fibers.



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BASIC PRINCIPLES OF ELECTRICITY

All cells in the body have an unequal distribution of ions(concentration gradient) and charged molecules (electricalgradient) across their membranes.

all have a net negative balance inside relative to outside

(differences are always expressed as inside relative tooutside).

Because opposite charges attract, there is a driving forcewhich would lead to ions flow if not for the presence of themembrane. This represents a potential energy, which iscalled the potential difference or membrane potential, themeasure of this potential energy is called voltage and isexpressed in volts or millivolts.



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This membrane potential is present in all cells, includingneurons and muscle cells when they are at rest (are notfiring action potentials), and is called the resting membrane

potential, or resting potential. The size of resting potentialranges from -20 to -200 millivolts in different cells, inneurons it ranges from -50 to -100 millivolts and inmuscles it averages about - 70 mV.

neurons and muscle cells are unique. Unlike all other

cells, they have the ability to actively change the potentialacross their membranes in a rapid and reversible way. Therapid reversal of membrane potential is referred to as anaction 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 potassiumsince there are a large number of K+leak channels that arealways 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



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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 notdepends on the strength of depolarizing stimulus.Stimuli can be:

1. Subthreshold

2. Threshold

3. Suprathreshold



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The membrane of all excitable cells contains twospecial gated channels. One is a Na+channel andthe other is a K+channel and both are

VOLTAGE GATED. At rest, virtually all of thevoltage-gated channels are closed, potassium andsodium 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 thevoltage gated Na+channels begin to open andNa+influx into the cell exceeds K+efflux out ofthe cell

Molecular Events Underlying theAction Potential:



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Two things happen next:

1) As the membrane depolarizes further and the cellbecomes positive inside and negative outside, theflow of Na+will decrease.

2) Even more importantly, the voltage- gated Na+

channels close

When the inactivation gates close, Na+

influx stops andthe repolarizing phase takes place.



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Next, the voltage gated K+channelsare activatedat the time the action potential reaches its peak. Atthis time, both concentration and electrical gradients

favour the movement of K+out of the cell.

These channels are also inactivated with time butnot until after the efflux of K+ has returned themembrane 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 self-perpetuating once the membrane is depolarized pastthreshold, and because all action potentials are of theexact same size, it is said to be an all-or-none event.

If threshold is reached, you get an action potentialthat is always the same. Therefore, both the

threshold and suprathreshold stimuli can generateonly one response - an action potential.



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As a result, the membrane cannot be excited togenerate another action potential at this site until theongoing event is over. This period during which themembrane is completely unexcitable is the absolute

refractory period. Once the membrane potential has returned to

resting conditions, another action potential can begenerated. However, before it happens there is ashort period during which the voltage gated K+

channels are still open producing hyperpolarization,during which the membrane potential is further fromthreshold and during which a larger than normalstimulus is required to generate an action potential.

This is the relative refractory period.www.indiandentalacademy.com


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Synapses are the junctions between neurons and thestructures they innervate.

Electrical Synapses:

There are some specialized neurons, which areconnected by gap junctions, and through which ionscan flow and, hence, across which action potentialscan be directly propagated. these are relatively

uncommon in the nervous system they are extremelyimportant in the cardiac muscle tissue

Chemical Synapses:

Most neurons are separated from the object that theyinnervate by a short gap. These gaps or junctions are

very narrow but the action potential cannot jumpacross them. Instead, electrical activity is usuallytransferred from the axon terminal to the next cell bya chemical messenger - a neurotransmitter, suchtransfer can occur in only one direction.



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Neurotransmitters:

At present there are over 100 chemical substancesbelieved to act as neurotransmitters in different partsof the nervous system. Many neurons make morethan one transmitter and may release more than one

transmitter upon the arrival of a single actionpotential 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 thesympathetic division of the ANS



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Skeletal muscle

40% of adult body weight

50% of childs body weight

Muscle contains: 75% water

20% protein

5% organic and inorganic compounds Functions:

Movement

Maintenance of posturewww.indiandentalacademy.com


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Whole muscle

Separate organ

Encased in connective tissuefascia

Functions of fascia

Protect muscle fibers

Attach muscle to bone

Provide structure for network of nervesand blood/lymph vessels



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Layers of fascia

Epimysium Surface of muscle

Tapers at ends to form tendon

Perimysium Divides muscle fibers into bundles or fascicles

Endomysium

Surrounds single muscle fibers



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PHYSIOLOGIC ANATOMY OF

SKELETAL MUSCLE

skeletal muscles are made of numerous fibersranging from 10 to 80 micrometers in diameter.

Each of these fibers in turn is made up ofsuccessively smaller subunits

In most muscles, the fibers extend the entirelength 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 athin layer of polysaccharide material that containsnumerous thin collagen fibrils.

At the end of the muscle fiber sarcolemma fuses

with a tendon fiber, and the tendon fibers in turncollect into bundles to form the muscle tendonsand thence insert into the bones.



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Sarcoplasmcytoplasm of muscle cell

Sarcotubular system

Sarcoplasmic reticulum Sarcotubules and transverse tubules

Ca++uptake, regulation, release and storage



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SARCOPLASM.

The myofibrils are suspended inside the musclefiber in a matrix calledsarcoplasm, which iscomposed of usual intracellular constituents,

The fluid of the sarcoplasm contains largequantities of potassium, magnesium, phosphate,and protein enzymes.

There are tremendous numbers of mitochondria

that lie between and parallel to the myofibrils, itindicates the great need for large amounts ofadenosine triphosphate (ATP) for the contractingmyofibrils..



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MYOFIBRILS;

ACTIN AND Troponin Tropomyosin(thin)

MYOSIN FILAMENTS.(thick)

Each muscle fiber contains several hundred toseveral thousand myofibrils.

Each myofibril in turn has, lying side by side,

about 1500 myosin filaments and 3000 actinfilaments, which are large polymerized proteinmolecules that are responsible for musclecontraction.



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The thick filaments are myosin and the thinfilaments are actin.

myosin and actin filaments partially interdigitateand thus cause the myofibrils to have alternatelight and dark bands.

The light bands contain only actin filaments andare called I bandsbecause they are isotropic to

polarized light.

The dark bands contain the myosin filaments aswell as the ends of the actin filaments where theyoverlap the myosin and are calledA bandsbecausethey are anisotropic to polarized light..



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small projections from the sides of the

myosin filaments are cross-bridges. They

protrude from the surfaces of the myosinfilaments along the entire extent of the

filament except in the very center.

Interaction between these cross- bridgesand 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 bothdirections 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 giveskeletal and cardiac muscle their striatedappearance.



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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, fullystretched 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.



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Neuronal Control of MuscleContraction

Movement requires contraction of manyfibers within a muscle & of many

muscles within the bodycorrectlytimed with one another & regulating thestrength of contraction

Coordination generated within NS =most muscle contract only when APsarrive at Neuromuscular Junction



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The nerve ending makes a junction, called theneuromuscular junction, with the muscle fiber

near the fiber's midpoint, and the action potentialin 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.

TRANSMISSION OF IMPULSES FROM

NERVES TO SKELETAL MUSCLE

FIBERS:NEUROMUSCULAR

JUNCTION



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PHYSIOLOGICAL ANATOMYOF THE

NEUROMUSCULAR JUNCTION-

MOTOREND PLATE.



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The nerve fiber branches at its end to form a

complex of branching nerve terminals,

which invaginate into the muscle fiber butlie outside the muscle fiber plasma

membrane. The entire structure is called the

motor end plate.



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End Plate Potential And Excitation Of The

Skeletal Muscle Fiber

sudden insurgence of sodium ions into the muscle

fiber when the acetylcholine channels open causes

the internal membrane potential in the local areaof the end plate to increase in the positive

direction as much as 50 to 75 millivolts, creating a

local potentialcalled the end plate potential.

end plate potential created by the acetylcholinestimulation is normally far greater than enough to

initiate an action potential in the muscle fiber.


Safety Factor For Transmission At The


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Safety Factor For Transmission At The

Neuromuscular

Junction

Each impulse that arrives at theneuromuscular junction causes about threetimes as much end plate potential as that

required to stimulate the muscle fibertherefore the normal neuromuscular junctionis said to have a safety factor

repeated stimulation diminishes the number

of vesicles of acetylcholine released with eachimpulse so much that impulse fails to passinto the muscle fiberFATIGUE



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A new action potential cannot occur in anexcitable fiber as long as the membrane is stilldepolarized from the preceding action potential.

shortly after the action potential is initiated, thesodium channels (or calcium channels, or both)

become inactivated, and any amount of excitatorysignal applied to these channels at this point will

not open the inactivation gates.

The only condition that will re-open them is forthe membrane potential to return to the originalresting membrane potential level.



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The period during which a second action potentialcannot be elicited, even with a strong stimulus, iscalled the absolute refractory period. This period

for large myelinated nerve fibers is about1/2500second..

After the absolute refractory period is a relativerefractory period, lasting about one quarter to one

half as long as the absolute period. During thistime, stronger than normal stimuli can excite thefiber.



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The cause of this relative refractoriness are:

(1) During this time, some of the sodium channels

still have not been reversed from their inactivationstate, 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 fiberopposing the stimulating signal



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Steps in muscle contraction

Excitation

Action potential traverses nerve

Neurotransmitter released intoneuromuscular junction - Ach

Muscle fiber depolarization

Sarcolemma to transverse tubulesCa

++

release from sarcoplasmic reticulum



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Coupling

Ca++binds to troponin-tropomyosin

complex



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Contraction

Ca++binding moves troponin-tropomyosin

complex Myosin heads attach to actin

Crossbridge formation

Crossbridge cycling Moves the myosin heads along the actin and

shortens the sarcomere



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Relaxation

Ca++removed from troponin-tropomyosin

complex Cross bridge detachment

Ca++pumped into SRactive transport

Sarcomere lengthens



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Excitation-contraction coupling



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GENERAL MECHANISM OF MUSCLE

CONTRACTION

The initiation and execution of muscle contractionoccurs in following sequential steps.

1. An action potential travels along a motor nerve toits endings on muscle fibers.

2. At each ending, the nerve secretes a small amountof the neurotransmitter substance acetylcholine.

3. The acetylcholine acts on a local area of themuscle fiber membrane to open multipleacetylcholine-gated channels through proteinmolecules in the muscle fiber membrane.



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4. Opening of the acetylcholine channels allowslarge quantities of sodium ions to flow to the

interior of the muscle fiber membrane at the pointof 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 potentialstravel along nerve membranes.

6. The action potential depolarizes the muscle fibermembrane and also travels deeply within the

muscle fiber Where it causes the sarcoplasmicreticulum to release into the myofibrils largequantities of calcium ions that have been storedwithin the reticulum.



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7. The calcium ions initiate attractive forcesbetween the actin and myosin filaments, causingthem 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 thecalcium ions from the myofibrils causes musclecontraction to cease.



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Sliding Filament Theory

during contraction, thickand thin filaments do notchange their length, butslide past each other

(overlapping further) asa result, individualsarcomeres shorten,myofibrils shorten, theentire cell shortens



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Muscle contraction Types

Isometric or static

Constant muscle length

Increased tension

Isotonic

Constant muscle tension

Constant movement

Concentric - shortening

Eccentric - lengthening



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It demonstrates that maximum contraction occurswhen there is maximum overlap between the actinfilaments and the cross-bridges of the myosin

filaments, the greater the number of cross-bridges pulling the

actin filaments, the greater the strength ofcontraction.

when the muscle is at its normal resting length,which is at a sarcomere length of about 2micrometers, it contracts with maximum force ofcontraction.



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If the muscle is stretched to much greater than

normal length before contraction, a large amount

of resting tensiondevelops 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, calledactive tension, decreases as the muscle is stretched

much beyond its normal length



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Relation of Velocity of Contraction to LOAD

A muscle contracts extremely rapidly when

it contracts against no load-to a state of fullcontraction in about 0.1 second for the

average muscle. When loads are applied,

the velocity of contraction becomesprogressively less as the load increases



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ATP & Muscle Contraction

Muscle contraction is absolutely dependent on ATPfor 3 processes (Myosin ATPase breaks down ATPas fiber contracts) :

1) hydrolysis of ATP energizes the myosin head which

begins the power stroke of the cross-bridge cycle2) attachment of ATP to myosin facilitates the

dissociation of the actomyosin complex allows forcontinues x-bridge cycling and further shorteningEach x-bridge cycle shortens the muscle 1% of itsresting length

3) Ca++ reuptake into the SR occurs through an ATPdependent pump


Sources of ATP for Muscle


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Sources of ATP for Muscle

Contraction



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Summation

contraction of individual muscle fibers is all-or-none - any graded response must comefrom the number of motor units stimulated at

any one time summation = adding together of individual

muscle twitches to make a whole musclecontraction - accomplished by increasing

number of motor units contracting at onetime (spatial summation) or by increasingfrequency of contraction of individual musclecontractions (temporal summation)



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Summotion means the adding together ofindividual twitch contractions to increase theintensity of overall muscle contraction.Summation occurs in two ways:

(1) by increasing the number of motor unitscontracting simultaneously, which is calledmultiple fiber summation,and

(2) by increasing the frequency of contraction,which is calledfrequency summation and can leadto tetanization.



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To the left aredisplayed individualtwitch contractionsoccurring one afteranother at lowfrequency ofstimulation. Then, as

the frequencyincreases, therecomes a point wheneach, newcontraction occurs

before the preceding

one is over. This iscalled 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 ofcontraction increases to a plateau, a phenomenon

called thestaircase effect or treppe.



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Reflects the amount of Ca2+ availablein the sarcoplasm and more efficient

enzyme activity as the muscle liberatesheat - Principal behind warming-upbefore physical activity



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Muscle fatigueProlonged strong contractionsleads to fatigue due to inability of contractile &metabolic processes to supply adequately to maintainthe work load - nerve continues to function properly

passing AP onto the muscle fibers but contractionsbecome weaker due to lack of ATP

Hypertrophy - increase in muscle mass caused byforceful muscular activityincrease power of muscle

contractionAtrophy - 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 calledfiber hyperplasia.

it occurs by the mechanism of linear splitting ofpreviously enlarged fibers.



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Effects of Muscle Denervation

When a muscle loses its nerve supply, it no longer receivesthe contractile signals that are required to maintain normal

muscle size. atrophy begins almost immediately.

After about 2 months, degenerative changes also begin toappear in the muscle fibers themselves.

If the nerve supply grows back to the muscle, full return offunction usually occurs in about 3 months, but from thattime onward, the capability of functional return becomes

less and less, with no return of function after 1 to 2 years.


Satellite Cells:


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Satellite Cells:

repair and regeneration

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, orbecome a new fiber May play a role in

stretch induced muscle growth


Muscle Fiber Types


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Muscle Fiber Types



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Contract or Relax? Effect of type of stimuli



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Receptors in Muscle: Feedback


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p

to CNS

Muscle contains receptors that providesensory information regarding:

Chemical changes (i.e., O2, CO2, H+):chemoreceptors

Tension development: Golgi TendonOrgans (GTOs)

Muscle length: Muscle spindles

Information from these receptors providesinformation about the energetic requirementsof exercising muscle and about movementpatterns



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Muscle spindleDetect dynamic and static

changes in muscle lengthStretch reflex

Stretch on muscle causes reflex contraction Golgi tendon organ (GTO)Monitor tension

developed in musclePrevents damage

during excessive force generation

Stimulation results in reflex relaxation ofmuscle



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Muscle spindles respond tomuscle stretch Gamma

motor neurons are

coactivated duringcontraction

Causing contraction of

fibers within muscle spindle

Deviations in consistency

signal excessive stretch



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Golgi Tendon Organ

Located in

tendon Monitor

muscle tension

Activation

causes inhibition

of alphamotor

neuron Safety

mechanism

against

excessive force

during

contraction


Role of spindles and GTOs in muscle stretch


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p

and spasm

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 GTOs

Muscle cramps/spasms may be caused byoveractive spindles and underactive GTOs in

fatigued skeletal muscle



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Myotactic reflex

Clasp knife reflex



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