chapte 3 muscle

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Chapter 3

Muscle Physiology
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Objectives

After studying this chapter, you should be able to:

Differentiate the major classes of muscle in the body.

Describe the molecular and electrical makeup of muscle cell

excitationcontraction coupling.

Define thin and thick filaments and how they slide to createcontraction.
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Objectives contd Differentiate the role(s) for Ca2+ in skeletal, cardiac,

and smooth muscle contraction.

Distinguish the functional differences between redand white muscle.

Identify the general concepts involved in the slidingfilament model for skeletal muscle contraction.

Be familiar with the roles played by ATP


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Outline Skeletal Muscle Structure

Neuromuscular Junction

Motor Unit Structure of Muscle Fiber

How Fiber Contracts

Characteristics of Contractions

Metabolism of Skeletal Muscle

Types of Skeletal Muscle

Neural Control

Cardiac & Smooth Muscle


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Skeletal Muscle Tissue Skeletal muscles are organs

Vary in shape and size

A skeletal muscle is composed of cells Each cell is as long as the muscle

Small muscle: 100 micrometers long; 10 micrometersin diameter

Large muscle: 35 centimeters long; 100 micrometersin diameter

Skeletal Muscle cells are called MUSCLE FIBERS


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10-6

Composition of Skeletal Muscle Each skeletal muscle is composed of

fascicles.

bundles of muscle fibers

Muscle fibers contain myofibrils.

composed ofmyofilaments


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Muscle Classification Functionally

1. Voluntarily

2. Involuntarily

Structurally

1. Striated

2. Smooth

Combined

1. Visceral

2. Cardiac

3. Skeletal


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TYPES OF MUSCLE

LOCATION MICROSCOPIC

APPEARANCE

RELATIONSHIP

WITH THE

NERVOUS

SYSTEM

SPEED OFCONTRATION

SKELETAL HEAVYILYSTRIATED VOLUNTARY SLOW TO FASTCONTRACTIONS

VISCERAL NONSTRIATED

(SMOOTH)

INVOLUNTARY VERY SLOW

CONTRACTIONS

CARDIAC LIGHTLYSTRIATED

AUTORHYTHMIC SLOWCONTRACTIONS


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3 Types of Muscle Tissue Skeletal muscle

Attaches to bone, skin or fascia

Striated with light & dark bands

Nuclei multiple and peripherally located

Voluntary control of contraction & relaxation


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3 Types of Muscle Tissue Cardiac muscle (Heart),

Striated in appearance

Involuntary control Single nucleus centrally located

Autorhythmic because of built in pacemaker


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3 Types of Muscle Tissue Smooth muscle

Nonstriated in appearance

Involuntary

Single nucleus centrally located

In walls of hollow organs -- blood vessels, GI

eye, glands, skin


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GENERAL FUNCTIONS1. Skeletal muscle

Movement and heat production.

2. Smooth muscle

Propulsion of food and urine.

3. Cardiac muscle

pumping blood to the lungs and body.


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Muscular System Functions Body movement

Maintenance of posture

Respiration

Production of body heat

Communication

Constriction of organs and vessels Heart beat


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Properties of Muscle

Contractility

Ability of a muscle to shorten with force

Excitability Capacity of muscle to respond to a stimulus

Extensibility

Muscle can be stretched to its normal resting lengthand beyond to a limited degree

Elasticity

Ability of muscle to recoil to original resting length

after stretched


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Skeletal Muscle -- Connective

Tissue

Connective tissue components of the muscle include

Epimysium = surrounds the whole muscle perimysium = surrounds bundles (fascicles) of

10-100 muscle cells.

Fascicles: Composed of columns of muscle fibers. Endomysium = separates individual muscle cells

All these connective tissue layers extend beyond themuscle belly to form the tendon


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Structure of Skeletal Muscle


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Muscle Fiber or Myofibers

Are cells(number is fixed). Muscle cells are long, cylindrical & multinucleated

Sarcolemma = muscle cell membrane

Sarcoplasm filled with tiny threads called myofibrils &

myoglobin (red-colored, oxygen-binding protein)


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Muscle fiber


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Transverse Tubules

T (transverse) tubules are invaginations of the Sarcolemmainto the center of the cell filled with extracellular fluid

carry muscle action potentials down into cell

Mitochondria lie in rows throughout the cell near the muscle proteins that use ATP during contraction


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Myofibrils & Myofilaments

Muscle fibers are filled with threads called myofibrilsseparated by SR (sarcoplasmic reticulum)

Myofilaments (thick & thin filaments) are the contractileproteins of muscle


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Sarcoplasmic Reticulum (SR)

System of tubular sacs similar to smooth ER in nonmuscle cells. Parallel to the myofibrils

Stores Ca+2 in a relaxed muscle

Action potential releases Ca++ from the vesicles

Release of Ca+2 triggers muscle contraction


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Internal organization:


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Striations:


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Structure of Muscle Fiber


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Structure of Muscle Fiber

Each fiber is packed with myofibrils

Myofibrils are 1 in diameter and extend length of fiber

Packed with myofilaments Myofilaments are composed ofthickand thin filaments that

give rise to bands which underlie striations


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Filaments: Thick

Myosin

Thin

Actin

They interdigitate partially

Myosin has cross bridges

They interact with actin; leads tocontraction

Actin is anchored to z disk or line

Z disk or line passes across the

myofibrils


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Thick filament

composed of structural protein, myosin.

Head (cross bridge) possesses actin binding site andATPase activity.

Thin filament

Has tropomyosin & troponin Tropomyosin

Prevents coupling with myosin by masking activesite

Troponin is a regulatory protein bound to

tropomyosin


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Troponin Three-polypeptide complex

Tn I: inhibitory subunit Tn T: helps position tropomyosin

on actin

Tn C: binds to Ca2+


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Actin filament Troponin is embedded in

actin at regular intervals

It has high affinity for Ca++

Ca++ causes conformationalchange

Ca++ Tugs and pushestropomyosin deeper into thegroove

Unmasks active site

Unmasking triggersinteraction with myosin

St t f M fib il


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A bandis dark, containsthick filaments (mostly

myosin)

Light area at center of A

band is H band

= area where actin

and myosin dont

overlap

I bandis light, contains

thin filaments (mostly

actin)

At center of I band is

Z line/disc where

actins attach

Structure of Myofibril


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M linesare structural proteins that anchor myosin during

contraction

Titin is elastic protein attaching myosin to Z disc thatcontributes to elastic recoil of muscle


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SARCOMERE

A is the functional contractile unit of Skeletalmuscle.

It consists of three types of proteins

1. Contractile proteins

2. Regulatory proteins

3. Structural proteins Contractile proteins generate Force during contraction.

The Two contractile proteins areActin and myosin.


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Regulatory proteins help to switch the contraction process

on and off.

The two regulatory proteins are Tropomyosin and

Troponin.

Structural proteins contribute to the alignment, stability,

elasticity, and extensibility of myofibrils. There are a number of structural proteins including

Titin,

Connectin, and

Myomesin.


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MYOSIN


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MYOSIN


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ACTIN, TROPOMYSOIN,

TROPONIN


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SARCOMERE


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SARCOMERE


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Contractile subunit of a muscle fiber

From Z to Z

Sarcomere


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Organization of the sarcomere

Thick filaments = myosin filaments

Composed of the protein myosin

Has ATP-ase enzymes


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Organization of the sarcomere, contThin filaments = actin filaments

Composed of the protein actin


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Myosin filaments have heads (extensions,or cross bridges)

Myosin andactin overlap


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At rest, there is a bare [H] zone thatlacks actin filaments


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Organization of myofilaments


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Organization of myofilaments


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Mechanisms of Contraction

Muscle contraction:

Occurs because ofsliding of thinfilaments over andbetween thickfilaments towardscenter.

Shortening thedistance from Zdisc to Z disc.

Sliding Filament Theory Of


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Sliding Filament Theory OfContraction

Actin myofilaments sliding over myosin toshorten sarcomeres

Actin and myosin do not change length Shortening sarcomeres responsible for skeletal

muscle contraction

During relaxation, sarcomeres lengthen


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Sliding Filament Theory contd

Sliding of filaments is produced by the actionsof cross bridges.

Cross bridges are part of the myosin proteins thatextend out toward actin.

Form arms that terminate in heads.

Each myosin head contains an ATP-binding site.

The myosin head functions as a myosin ATPase.


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Sliding Filament Theory(continued)


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Sliding filament model II:


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Sarcomere Shortening


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Contraction Myosin binding site splits ATP to ADP and Pi.

ADP and Pi remain bound to myosin until myosin

heads attach to actin. Pi is released, causing the power stroke to occur.

Power stroke pulls actin toward the center of the Aband.

ADP is released, when myosin binds to a fresh ATP atthe end of the power stroke.


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Contraction (continued)

Release of ADP upon binding to anotherATP, causes the cross bridge bond to break.

Cross bridges detach, ready to bind again. Synchronous action:

Only 50% of the cross bridges are attached atany given time.


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Contraction (continued)

C B id


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Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Cross Bridges

Are formed by heads of myosin molecules that extend toward and

interact with actinSliding of filaments is produced by actions of cross bridges

Each myosin head contains an ATP-binding site which functions as

an ATPase

12-24

C B id


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Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Cross Bridges continued

Myosin cant bind to actin unless it is cocked by ATP

After binding, myosin undergoes conformational change (power

stroke) which exerts force on actin

After power stroke myosin detaches

12-25


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Regulation of Contraction

Regulation of cross bridge attachment toactin due to: Tropomyosin:.

Lies within grove between double row of G-actin.

Troponin: Attached to tropomyosin.

Serves as a switch for muscle contraction and

relaxation. In relaxed muscle:

Tropomyosin blocks binding sites on actin.


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Excitation-Contraction Coupling

Mechanism where anaction potential causesmuscle fiber

contraction Involves

Sarcolemma

Transverse or T tubules

Terminal cisternae Sarcoplasmic reticulum

Ca2+

Troponin


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Sequence of contraction

Excitation: Step 1

Action potential (AP) travels tonerve ending

ACh release at the NMJ Activation of Nicotinic receptors by

ACh

Na channels are opened

AP is generated in the muscle fiber

Depolarization of Sarcolemma

AP transmitted down T-tubule

Sarcoplasmic reticulum releasesCa++


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Sequence of Contraction

Contraction: Step II Ca++ binds to troponin C

Active actin site isexposed

Myosin heads bind toactin

Myosin heads rotate

Myosin heads disengage Cycle repeats (Ca++ and

ATP needed)


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Energy Production Action potential reaches muscle fibers Myosin head (MH) combines with ATP

MHs ATPase activated ATP is cleaved by ATPase MH + ATP ADP+ Pi + Energy


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Relaxation Step III

APs must cease for the muscle to relax.

ACh-esterase degrades ACh.

Ca2+ release channels close.

Ca2+ pumped back into SR through Ca2+-ATPase pumps.

Actin sites are covered by troponin.

Choline recycled to make more ACh.

Steps of Muscle Contraction

Sliding Filament Model of Contraction
http://steps%20of%20muscle%20contraction%20-%20youtube.flv/http://steps%20of%20muscle%20contraction%20-%20youtube.flv/


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Sliding Filament Model of Contraction

Regulatory Role of Tropomyosin and Troponin


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Regulatory Role of Tropomyosin and Troponin

PiADP

G-actin moves

Cytosolic Ca2+

Tropomyosin shifts,exposing binding

site on G-actin

TN

Power stroke

Initiation of contraction

Ca2+ levels increase

in cytosol.

Ca2+ binds totroponin.

Troponin-Ca2+

complex pullstropomyosinaway from G-actinbinding site.

Myosin bindsto actin andcompletes powerstroke.

Actin filamentmoves.

(b)

1

2

3

4

5

1

2

3

4

5


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Motor Unit

When somatic neuron is activated, all the muscle fibers itinnervates contract with all or none contractions.

Innervation ratio: Ratio of motor neuron: muscle fibers.

Fine neural control over the strength occurswhen many small motor units are involved.

Recruitment: Larger and larger motor units are activated to

produce greater strength.


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Motor Unit (continued)

Each somatic neurontogether with all themuscle fibers it

innervates. Each muscle fiber

receives a singleaxon terminal from a

somatic neuron. Each axon can have

collateral branches toinnervate an equal #

of fibers.

Motor Unit


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Motor Unit Motor unit - One motor neuron and the muscle fibers it innervates

Number of muscle fibers varies among different motor units

Number of muscle fibers per motor unit and number of motor units

per muscle vary widely

Muscles that produce precise, delicate movements contain fewer fibers per

motor unit

Muscles performing powerful, coarsely controlled movement have larger

number of fibers per motor unit


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Region where the motor neuron stimulates the musclefiber

The neuromuscular junction is formed by :

1. End of motor neuron axon (axon terminal) Terminals have small membranous sacs (synaptic vesicles)

that contain the neurotransmitter acetylcholine(ACh)

2. The motor end plate of a muscle

A specific part of the sarcolemma that contains AChreceptors

Though exceedingly close, axonal ends and musclefibers are always separated by a space called thesynaptic cleft



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Function of Neuromuscular Junction


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Pharmacology of the NMJ

Botulinum toxin blocks release of neurotransmitter at theNMJ so muscle contraction can not occur

bacteria found in improperly canned food

death occurs from paralysis of the diaphragm

Curare (plant poison from poison arrows)

causes muscle paralysis by blocking the ACh receptors

used to relax muscle during surgery Neostigmine (anticholinesterase agent)

blocks removal of ACh from receptors so strengthensweak muscle contractions of myasthenia gravis

also an antidote for curare after surgery is finished

PATHOPHYSIOLOGY OF


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PATHOPHYSIOLOGY OFMUSCLES


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MUSCULAR DYSTROPHY

DEGENERATION OF MUSCLE TISSUE

MAY BE INHERITED

BODY DOES NOT PRODUCE THE

PROTEIN DYSTROPHIN

MUSCLE CELL MEMBRANE DISTORTED


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Disease characterized by a shortage ofACh receptors

Autoimmune disease Body destroys its own Ach receptors

Interferes with neuromuscular junctionevents

Drooping eyelids, difficulty swallowing &talking, generalized weakness


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MYASTHENIA GRAVIS

Receptors on muscle membrane foracetylcholine are destroyed

Normal receptor

Defective receptors

Muscle Twitch


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A muscle twitch is the response of

the muscle fibers of a motor unit to a

single action potential of its motorneuron. (A single contraction-

relaxation cycle)

The fibers contract quickly and

then relax. Three Phases:

Latent Periodthe first few ms after

stimulation when excitation-

contraction is occurring

Period of Contractioncrossbridges are active and the muscle

shortens .

Period of RelaxationCa2+ is

pumped back into SR and muscle

tension decreases to baseline level

Factors Affecting Force of Muscle Contraction


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Number of motor units recruited, recruitment also helps provide smooth

muscle action rather than jerky movements

The relative size of the muscle fibersthe bulkier the muscle fiber(greater cross-sectional area), the greater its strength

Asynchronous recruitment of motor units -while some motor units are

active others are inactive - this pattern of firing provides a brief rest for

the inactive units preventing fatigue Degree of muscle stretch


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Muscle Contractions of Different Force-Force Summation

Summation

means the adding together of individual twitch contractions toincrease 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 fibersummation, and

2. By increasing the frequency of contraction, which iscalled frequency summationand can lead to tetanization.


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Multiple Fiber Summation

When the central nervous system sends a weak signal tocontract a muscle, the smaller motor units of the muscle arestimulated.

As the strength of the signal increases, larger and largermotor units begin to be excited.

This is called the size principle.

It allows the gradations of muscle force.

Important feature of multiple fiber summation

Asynchronous recruitment of motor units -while somemotor units are active others are inactive - this pattern offiring provides a brief rest for the inactive units preventing

fatigue and provides smooth contraction


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Frequency Summation andTetanization


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Individual twitch contractions occurring one after another atlow frequency of stimulation.

As the frequency increases, new contraction occurs before the

preceding one is over. As a result, the second contraction is added partially to the

first, so that the total strength of contraction risesprogressively with increasing frequency.

At the highest frequency the successive contractions fusetogether, and the whole muscle contraction becomes smoothand continuous, as shown in the figure.

This is called tetanization


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Twitch, Summation, and Tetanus

Incomplete tetanus:

Stimulator delivers an increasing frequency of electrical shocks.

Relaxation period shortens between twitches.

Strength of contraction increases.

Complete tetanus: Fusion frequency of stimulation.

No visible relaxation between twitches.

Smooth sustained contraction.

Treppe:- Staircase effect. A phenomenon in w/c the strength of contraction increases to a

plateau. Due to increase in intracellular Ca2+.

Represents warm-up.


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Twitch, Summation, and Tetanus (continued)

Types of Muscle Contractions


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Types of Muscle Contractions

Isometric: No change in length but tensionincreases

Postural muscles of body

Isotonic: Change in length but tension constant

Concentric: Overcomes opposing resistance andmuscle shortens

Eccentric: Tension maintained but muscle lengthens

Muscle tone: Constant tension by muscles forlong periods of time


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Isotonic and Isometric Contraction


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Isotonic and Isometric Contraction

Isotonic contractions = a load is moved

concentric contraction = a muscle shortens to produce force andmovement

eccentric contractions = a muscle lengthens while maintaining force andmovement

Isometric contraction = no movement occurs

tension is generated without muscle shortening

maintaining posture & supports objects in a fixed position

Isometric Contractions


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In isometric contractions, increasing muscle tension (force) ismeasured

No change in overall muscle length

L th T i R l ti hi


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Length-Tension Relationship

Strength of muscle contractioninfluenced by: Frequency of stimulation.

Thickness of each muscle fiber. Initial length of muscle fiber.

Ideal resting length: Length which can generate maximum force.

Overlap too small: Few cross bridges can attach.

No overlap: No cross bridges can attach to actin.


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Energy Sources

ATP provides immediate energy for musclecontractions from 3 sources

Creatine phosphate

During resting conditions stores energy to synthesize ATP

Anaerobic respiration

Occurs in absence of oxygen and results in breakdown ofglucose to yieldATP and lactic acid

Aerobic respiration Requires oxygen and breaks down glucose to produceATP,

carbon dioxide and water

More efficient than anaerobic


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Metabolism of Skeletal Muscles

Oxygen debt: Oxygen that was withdrawn from hemoglobin and

myoglobin during exercise.

Extra 02 required for metabolism tissue warmedduring exercise.

02 needed for metabolism of lactic acid producedduring anaerobic respiration.

When person stops exercising, rate of oxygenuptake does not immediately return to pre-exercise levels. Returns slowly.

M t b li f Sk l t l M l


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Metabolism of Skeletal Muscles (continued)

Phosphocreatine (creatine phosphate): Rapid source of renewal of ATP.

ADP combines with creatine phosphate.

[Phosphocreatine] is 3 times [ATP]. Ready source of high-energy phosphate.


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Slow- and Fast-Twitch Fibers

Skeletal muscle fibers can be divided on basisof contraction speed:

Slow-twitch (type I fibers).

Fast-twitch (type II fibers).

Differences due to different myosin ATPaseisoenzymes that are slow or fast.


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Slow- and Fast-Twitch Fibers(continued)

Slow-twitch orhigh-oxidative(type I fibers):

High oxidativecapacity for aerobicrespiration.

Resistant to fatigue.

Contract moreslowly,

smaller in diameter

Have rich capillary

supply. Numerous

mitochondria andaerobic enzymes.

High [myoglobin]. Red fibers.

Sl d h b


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Slow- and Fast-Twitch Fibers

Fast-twitch or low-oxidative (type IIX fibers): White fibers.

Adapted to respire anaerobically.

Have large stores of glycogen.

Have few capillaries.

high activity of myosin ATPase,

Have few mitochondria. Extraocular muscles that position the eye.

Sprint activity (basket ball, weight lifting, field hockey).


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Intermediate (type II A) fibers: Great aerobic ability.

Resistant to fatigue.

Distribution offast-twitch and slow twitch vary genetically

Most muscles have both but varies for eachmuscle

Effects of exercise Hypertrophies: Increases in muscle size

Atrophies: Decreases in muscle size


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Red Vs White meat

Red muscle fibers have more mitochondria than white

Red has more enzymes for oxidative energy metabolism

Red contract slowly, but sustain contraction for long time

Bursts of action potentials are 10-20/sec

Red found in antigravity muscles (leg muscles)

White rely on anaerobic metabolism

White can contract rapidly (30-60/sec) and powerfully butwill fatigue rapidly

White muscles are involved in escape reflexes (jumping)

Alpha motor units in white are bigger, larger diameter,

fast conducting axons

Characteristics of Muscle Fiber Types


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Characteristics of Muscle Fiber Types


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Muscle Fatigue

Decreased capacity to work and reducedefficiency of performance

Types:

Psychological

Depends on emotional state of individual

Muscular

Results fromATP depletion

Synaptic

Occurs in neuromuscular junction due to lack ofacetylcholine


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Inability to contract after prolonged activity

central fatigue is feeling of tiredness and a desire tostop (protective mechanism)

depletion of creatine phosphate decline of Ca+2 within the sarcoplasm

Factors that contribute to muscle fatigue

Interruption of blood flow through a contracting muscle

Insufficient oxygen or glycogen

Buildup of lactic acid and ADP

Insufficient release of acetylcholine from motor neurons

OXYGEN DEBT


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OXYGEN DEBT

For a muscle to return to its resting stateLactic acid must be removed

O2 reserves must be replenished

ATP reserves must be replenished

Creatine phosphate must be replenished

The amount of oxygen required for theseprocesses is termed the oxygen debtRepresents the difference between the

amount of O2 needed for aerobic muscleactivity and the amount of O2 actually used

All non-aerobic sources of ATP contribute to

debt


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Muscle Tone

Involuntary contraction of a small number ofmotor units.

Results from a low rate of nerve impulsescoming from the spinal cord

keeps muscles firm even though relaxed

does not produce movement

Essential for maintaining posture (head upright) Important in maintaining blood pressure

tone of smooth muscles in walls of blood vessels


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Atrophy and Hypertrophy

Atrophy

wasting away of muscles

caused by disuse (disuse atrophy) or severing of the

nerve supply (denervation atrophy) the transition to connective tissue can not be reversed

Hypertrophy

increase in the diameter of muscle fibers

resulting from very forceful, repetitive muscular activityand an increase in myofibrils, SR & mitochondria.

Hyperplasia of Muscle Fibers.

Increase number of muscle fibers


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This increase in fiber number is

called fiber hyperplasia. When it does occur, themechanism

is linear splitting of previously enlarged fibers.

Rigo Mo tis


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Rigor Mortis

Rigor mortis is a state of muscular rigidity that begins3-4 hours after death and lasts about 24 hours

After death, Ca+2 ions leak out of the SR and allowmyosin heads to bind to actin.

Since ATP synthesis has ceased, cross bridges cannotdetach from actin until proteolytic enzymes begin todigest the decomposing cells.

Ph i l f S th M l


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Physiology of Smooth Muscle

Contraction starts slowly & lasts longer

no transverse tubules & very little SR

Ca+2 must flows in from outside

Calmodulin replaces troponin

Ca+2 binds to calmodulin turning on an enzyme(myosin light chain kinase) that phosphorylates themyosin head so that contraction can occur

enzyme works slowly, slowing contraction

Two Types of Smooth Muscle


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yp

Visceral (single-unit)

In the walls of hollowviscera & small BV

Autorhythmic

Gap junctions cause fibersto contract in unison

Multiunit

Individual fibers with own

motor neuron ending Found in large arteries,

large airways, iris & ciliarybody

Multi vs. Single-Unit Muscle


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Multi vs. Single Unit Muscle

Properties of Single-Unit Smooth Muscle


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Copyright 2008 Pearson Education, Inc., publishing as Benjamin Cummings.

Properties of Single Unit Smooth Muscle

Gap junctions

Pacemaker cellswith spontaneousdepolarizations

Innervation to fewcells

Tone = level of

contraction withoutstimulation

Increases/decreasesin tension

Graded Contractions

No recruitment

Vary intracellularcalcium

Stretch Reflex

Relaxation inresponse tosudden

or prolongedstretch

Smooth Muscle


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Smooth Muscle

Does not containsarcomeres.

Contains > contentof actin than myosin

(ratio of 16:1). Myosin filaments

attached at ends ofthe cell to dense

bodies. Contains gap

junctions.


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Properties of Smooth Muscle

One nucleus

Tropomyosin

No troponin

Dense bodies analogous to Z line

Slow myosin ATPase

Myosin has light chains

Little sarcoplasmic reticulum


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Smooth Muscle Contraction

Depends on rise in free intracellular Ca2+.

Ca2+ binds with calmodulin.

Ca2+ calmodulin complex joins with and activatesmyosin light chain kinase.

Myosin heads are phosphorylated.

Myosin heads binds with actin.

Relaxation occurs when Ca2+ concentrationdecreases.



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p g

Ca2+

Ca2+ Ca2+ Calmodulin

Phosphorylatedmyosin lightchain

Unphosphorylatedmyosin lightchain

Endoplasmicreticulum

No myosinATPase activity

No crossbridgeactivity

Myosin ATPaseactive

Crossbridgecycling

ContractionSmooth muscle cell

MLCK

Ca-calmodulin


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Spontaneous Depolarizations


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p p


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Smooth Muscle Tone

Ca+2 moves slowly out of the cell

delaying relaxation and providing for state ofcontinued partial contraction

sustained long-term

Useful for maintaining blood pressure or a

steady pressure on the contents of GI tract


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Regulation of Contraction

Regulation of contraction due to

nerve signals from autonomic nervous system

changes in local conditions (pH, O2, CO2,temperature & ionic concentrations)

hormones (epinephrine -- relaxes muscle inairways & some blood vessels)

Cardiac muscle has properties of


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Cardiac muscle has properties ofskeletal and smooth muscle.

It is found in the walls of the heart.

It is highly organized and striated. These are

similarities to skeletal muscle tissue.

It can generate action potentials whichspread throughout the walls of the heart.

This is similar to single-unit smooth muscle.

Cardiac Muscle


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Cardiac Muscle

Contain actin and

myosin arranged insarcomeres.

Contract via sliding-filament mechanism.

Adjacent myocardialcells joined by gapjunctions. APs spread through

cardiac muscle through

gap junctions. Behaves as one

unit.

All cells contribute tocontraction.

Cardiac Muscle


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Stress-relaxation response

when stretched, initially contracts & then tensiondecreases to what is needed

stretch hollow organs as they fill & yet pressureremains fairly constant

when empties, muscle rebounds & walls firm up

Muscle Comparisons


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Regeneration of Muscle


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g

Skeletal muscle fibers cannot divide after 1st year growth is enlargement of existing cells

Cardiac muscle fibers cannot divide or regenerate

all healing is done by fibrosis (scar formation)

Smooth muscle fibers (regeneration is possible) cells can grow in size (hypertrophy)

some cells (uterus) can divide (hyperplasia)

new fibers can form from stem cells in BV walls


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Aging and Muscle Tissue

Skeletal muscle starts to be replaced by fat beginning at 30

use it or lose it

Slowing of reflexes & decrease in maximal strength

Change in fiber type to slow oxidative fibers may be due tolack of use or may be result of aging


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Abnormal Contractions

Spasm = involuntary contraction of single muscle

Cramp = a painful spasm

Tic = involuntary twitching of muscles normally

under voluntary control--eyelid or facial muscles Tremor = rhythmic, involuntary contraction of

opposing muscle groups

Fasciculation = involuntary, brief twitch of a motor

unit visible under the skin


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Muscle Fatigue

Any exercise induced reduction in the ability to maintainmuscle to generate force or power. Sustained muscle contraction fatigue is due to an accumulation

of ECF K

+

. Repolarization phase of AP.

During moderate exercise fatigue occurs when slow-twitch fibers deplete their glycogen reserve.

Fast twitch fibers are recruited, converting glucose to

lactic acid. Interferes with Ca2+ transport.

Central fatigue:

chapte 3 muscle

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