8 Muscles Intro

8/19/2019 8 Muscles Intro

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Chapter 8Histology andPhysiology of

Muscles

Skeletal Muscle Fibers


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Functions of the Muscular System

1. Body movement (Skeletal Muscle)2. Maintenance of posture (Skeletal

Muscle)

3. Respiration (Skeletal Muscle)4. Production of body heat (Skeletal

Muscle)

5. Communication (Skeletal Muscle)6. Constriction of organs and vessels

(Smooth Muscle)

7. Heartbeat (Cardiac Muscle)


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Functional Characteristics of Muscle

1. Contractility: the ability to shorten

forcibly

2. Excitability: the ability to receive andrespond to stimuli

3. Extensibility: the ability to be stretched

or extended

4. Elasticity: the ability to recoil and

resume the original resting length


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Types of Muscle Tissue

• The three types of muscle tissue areskeletal, smooth, and cardiac

• These types differ in

– Structure – Location

– Function

– Means of activation

• Each muscle is a discrete organcomposed of muscle tissue, blood vessels,nerve fibers, and connective tissue


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Types of Muscle Tissue

• Skeletal muscles are responsible for most bodymovements

– Maintain posture, stabilize joints, and generate heat

• Smooth muscle is found in the walls of hollow

organs and tubes, and moves substances throughthem

– Helps maintain blood pressure

– Squeezes or propels substances (i.e., food, feces) through

organs

• Cardiac muscle is found in the heart and pumps

blood throughout the body


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Tab. 8.1


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Skeletal Muscle Structure

• Skeletal muscle cells are elongated and areoften called skeletal muscle fibers

• Each skeletal muscle cell contains several nucleilocated around the periphery of the fiber nearthe plasma membrane

• Fibers appear striated due to the actin andmyosin myofilaments

• A single fiber can extend from one end of amuscle to the other

• Contracts rapidly but tires easily

• Is controlled voluntarily (i.e., by consciouscontrol)


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• Fascia is a general term for connective tissue sheets• The three muscular fascia, which separate and

compartmentalize individual muscles or groups of

muscles are:

– Epimysium: an overcoat of dense collagenous

connective tissue that surrounds the entire muscle

– Perimysium: fibrous connective tissue that surrounds

groups of muscle fibers called fascicles (bundles)

– Endomysium: fine sheath of connective tissue

composed of reticular fibers surrounding each muscle

fiber


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• The connective tissueof muscle provides a

pathway for blood

vessels and nerves toreach muscle fibers

Fig. 8.1


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• The connectivetissue of muscle

blends with other

connective tissuebased structures,

such as tendons,

which connect

muscle to bone

Fig. 8.2


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• Muscle Fibers – Terminology

• Sarcolemma: muscle cell plasma membrane

• Sarcoplasm: cytoplasm of a muscle cell• Myo, mys, and sarco: prefixes used to refer to

muscle

– Muscle contraction depends on two kinds of

myofilaments: actin and myosin• Myofibrils are densely packed, rod-like contractile

elements

• They make up most of the muscle volume


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Fig. 8.2


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• Actin (thin) myofilaments consist of two helicalpolymer strands of F actin (composed of G actin),

tropomyosin, and troponin

• The G actin contains the active sites to whichmyosin heads attach during contraction

• Tropomyosin and troponin are regulatory subunits

bound to actin

Fig. 8.2


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• Myosin (thick) myofilaments consist of myosinmolecules

• Each myosin molecule has – A head with an ATPase, which breaks down ATP

– A hinge region, which enables the head to move

– A rod

• A cross-bridge is formed when a myosin head bindsto the active site on G actin

Fig. 8.2


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• Sarcomeres – The smallest contractile unit of a muscle

– Sarcomeres are bound by Z disks that hold actin

myofilaments

– Six actin myofilaments surround a myosin myofilament

– Myofibrils appear striated because of A bands and I

bands

Fig. 8.2


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• Thick filaments: extend the entire length of an A band• Thin filaments: extend across the I band and partway

into the A band

• Z-disc: a coin-shaped sheet of proteins (connectins) thatanchors the thin filaments and connects myofibrils to oneanother

• Thin filaments do not overlap thick filaments in the lighterH zone

• M lines appear darker due to the presence of the protein

desmin• The arrangement of myofibrils within a fiber is so

organized a perfectly aligned repeating series of dark Abands and light I bands is evident


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Fig.

8.3bc


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Sliding Filament Model

• Actin and myosin myofilaments do not change in lengthduring contraction

• Thin filaments slide past the thick ones so that the actinand myosin filaments overlap to a greater degree – Upon stimulation, myosin heads bind to actin and sliding begins

– Each myosin head binds and detaches several times duringcontraction (acting like a ratchet to generate tension and propelthe thin filaments to the center of the sarcomere)

• In the relaxed state, thin and thick filaments overlap onlyslightly

• As this event occurs throughout the sarcomeres, themuscle shortens

• The I band and H zones become narrower duringcontraction, and the A band remains constant in length


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Fig. 8.4


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• Actin and myosin myofilaments in a relaxedmuscle (below) and a contracted muscle are the

same length. Myofilaments do not change

length during muscle contraction

Fig. 8.4


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• During contraction, actin myofilaments at eachend of the sarcomere slide past the myosinmyofilaments toward each other. As a result,the Z disks are brought closer together, and the

sarcomere shortens

Fig. 8.4


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• As the actin myofilaments slide over the myosinmyofilaments, the H zones (yellow) and the Ibands (blue) narrow. The A bands, which areequal to the length of the myosin myofilaments,do not narrow because the length of the myosin

myofilaments does not change

Fig. 8.4


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• In a fully contracted muscle, the ends ofthe actin myofilaments overlap at the

center of the sarcomere and the H zone

disappears

Fig. 8.4


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Physiology of Skeletal Muscle Fibers

• Membrane Potentials – The nervous system stimulates muscles to contract

through electric signals called action potentials

– Plasma membranes are polarized, which means there

is a charge difference (resting membrane potential)across the plasma membrane

– The inside of the plasma membrane is negative as

compared to the outside in a resting cell

– An action potential is a reversal of the restingmembrane potential so that the inside of the plasma

membrane becomes positive


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• Ion Channels – Assist with the production of action potentials

• Ligand-gated channels

• Voltage-gated channels


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Fig. 8.5


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Fig. 8.6


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• Action Potentials – Depolarization results from an increase in thepermeability of the plasma membrane to Na+

– If depolarization reaches threshold, an actionpotential is produced

– The depolarization phase of the action potentialresults from the opening of many Na+ channels

Fig. 8.6


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• Action Potentials – The repolarization phase of the action

potential occurs when the Na+ channels close

and K+ channels open briefly

Fig. 8.6


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Fig. 8.6


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• Action Potentials – Occur in an all-or-none fashion

• A stimulus below threshold produces no action

potential

• A stimulus at threshold or stronger will produce an

action potential

– Propagate (travel) across plasma membranes


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• Nerve Stimulus of Skeletal Muscle – Skeletal muscles are stimulated by motor

neurons of the somatic nervous system

– Axons of these neurons travel in nerves tomuscle cells

– Axons of motor neurons branch profusely as

they enter muscles

– Each axonal branch forms a neuromuscular

junction with a single muscle fiber


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• The neuromuscular junction is formed from: – Axonal endings

• Have small membranous sacs (synaptic vesicles)

• Contain the neurotransmitter acetylcholine (ACh)

– Motor end plate of a muscle• Specific part of the sarcolemma

• Contains ACh receptors

• Though exceedingly close, axonal ends and

muscle fibers are always separated by a spacecalled the synaptic cleft


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Fig. 8.7


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1. An action potential (orangearrow) arrives at thepresynaptic terminal andcauses voltage-gated Ca2+

channels in the

presynaptic membrane toopen

2. Calcium ions enter thepresynaptic terminal andinitiate the release of the

neurotransmitteracetylcholine (ACh) fromsynaptic vesicles

3. ACh is released into thesynaptic cleft by exocytosis

Fig. 8.8

Neuromuscular Junction Physiology


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channels in the





Fig. 8.8



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channels in the





Fig. 8.8



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4. ACh diffuses across thesynaptic cleft and binds toligand-gated Na+ channels onthe postsynaptic membrane

5. Ligand-gated Na+ channels

open and Na+ enters thepostsynaptic cell, causing thepostsynaptic membrane todepolarize. If depolarizationpasses threshold, an action

potential is generated alongthe postsynaptic membrane

6. ACh is removed from theligand-gated Na+ channels,which then close

Fig. 8.8



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Fig. 8.8



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Fig. 8.8


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7. The enzyme acetylcholinesterase,which is attached to the postsynaptic

membrane, removes acetylcholine

from the synaptic cleft by breaking it

down into acetic acid and choline

8. Choline is symported with Na

+

intothe presynaptic terminal, where it

can be recycled to make ACh.

Acetic acid diffuses away from the

synaptic cleft

9. ACh is reformed within the

presynaptic terminal using acetic

acid generated from metabolism and

choline recycled from the synaptic

cleft. ACh is then taken up by the

synaptic vesicles

Fig. 8.8



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7. The enzyme acetylcholinesterase,which is attached to the postsynaptic

membrane, removes acetylcholine

from the synaptic cleft by breaking it

down into acetic acid and choline

8. Choline is symported with Na

+

intothe presynaptic terminal, where it

can be recycled to make ACh.

Acetic acid diffuses away from the

synaptic cleft

9. ACh is reformed within the

presynaptic terminal using acetic

acid generated from metabolism and

choline recycled from the synaptic

cleft. ACh is then taken up by the

synaptic vesicles

Fig. 8.8



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7. The enzyme acetylcholinesterase,which is attached to the postsynapticmembrane, removes acetylcholinefrom the synaptic cleft by breaking itdown into acetic acid and choline

8. Choline is symported with Na+ into

the presynaptic terminal, where itcan be recycled to make ACh.

Acetic acid diffuses away from thesynaptic cleft

9. ACh is reformed within thepresynaptic terminal using acetic

acid generated from metabolism andcholine recycled from the synapticcleft. ACh is then taken up by thesynaptic vesicles

Fig. 8.8



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Fig. 8.8

E it ti C t ti C li


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Excitation-Contraction Coupling

• In order to contract, a skeletal musclemust:

– Be stimulated by a nerve ending

– Propagate an electrical current, or actionpotential, along its sarcolemma

– Have a rise in intracellular Ca2+ levels, the

final trigger for contraction

• Linking the electrical signal to the

contraction is excitation-contraction

coupling

E it ti C t ti C li


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•Invaginations of the sarcolemma form T tubules, whichwrap around the sarcomeres and penetrate into the cell’s

interior at each A band –I band junction

• Sarcoplasmic reticulum (SR) is

an elaborate, smooth

endoplasmic reticulum thatmostly runs longitudinal and

surrounds each myofibril

– Paired terminal cisternae form

perpendicular cross channels – Functions in the regulation of

intracellular calcium levels

• A triad is a T tubule and two

terminal cisternaeFig. 8.9

E it ti C t ti C li


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1. An action potential produced at the

presynaptic terminal in theneuromuscular junction is propagatedalong the sarcolemma of the skeletalmuscle. The depolarization alsospreads along the membrane of the Ttubules

2. The depolarization of the T tubule

causes gated Ca2+

channels in theSR to open, resulting in an increasein the permeability of the SR to Ca2+,especially in the terminal cisternae.Calcium ions then diffuse from theSR into the sarcoplasm

3. Calcium ions released from the SR

bind to troponin molecules. Thetroponin molecules bound to G actinmolecules are released, causingtropomyosin to move, exposing theactive sites on G actin

4. Once active sites on G actinmolecules are exposed, the heads of

the myosin myofilaments bind tothem to form cross-bridges

E it ti C t ti C li


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causes gated Ca2+






E it ti C t ti C li


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causes gated Ca2+






E it ti C t ti C li


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causes gated Ca2+






E it ti C t ti C li


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causes gated Ca2+

channels in the SRto open, resulting in an increase in thepermeability of the SR to Ca2+,especially in the terminal cisternae.Calcium ions then diffuse from the SRinto the sarcoplasm




the myosin myofilaments bind to themto form cross-bridges


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Fig. 8.11


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Fig. 8.11


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Fig. 8.11


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Fig. 8.11


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Fig. 8.11


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Fig. 8.11


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Muscle Relaxation


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Muscle Relaxation

• Calcium ions are transported back into thesarcoplasmic reticulum

• Calcium ions diffuse away from troponin

and tropomyosin moves, preventingfurther cross-bridge formation

Muscle Twitch


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Muscle Twitch

• The contraction of amuscle as a result of

one or more muscle

fibers contracting• Has lag, contraction,

and relaxation

phases

Table 8.2


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Strength of Muscle Contraction


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• For a given condition, a muscle fiber or motor

unit contracts with a consistent force in response

to each action potential

• For a whole muscle, stimuli of increasingstrength result in graded contractions of

increased force as more motor units are

recruited (multiple motor unit summation)

• Stimulus of increasing frequency increase theforce of contraction (multiple-wave summation)

M t U it


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Motor Unit

Fig. 8.13



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• Incomplete tetanus is partial relaxation betweencontractions, and complete tetanus is no

relaxation between contractions

• The force of contraction of a whole muscleincreases with increased frequency of

stimulation because of an increasing

concentration of Ca2+ around the myofibrils

• Treppe is an increase in the force of contractionduring the first few contractions of a rested

muscle

M lti l M t U it S ti i M l


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Multiple Motor Unit Summation in a Muscle

Fig. 8.14

M lti l W S ti


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Multiple-Wave Summation

Fig. 8.15

Treppe


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Treppe

Fig. 8.15


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Types of Muscle Contraction


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Types of Muscle Contraction

• Isometric contractions cause a change in muscletension but no change in muscle length

• Isotonic contractions cause a change in musclelength but no change in muscle tension

• Concentric contractions are isotonic contractionsthat cause muscles to shorten

• Eccentric contractions are isotonic contractionsthat enable muscles to shorten

• Muscle tone is the maintenance of a steadytension for long periods

• Asynchronous contractions of motor unitsproduce smooth, steady muscle contractions


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Muscle Length and Tension


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Muscle Length and Tension

Fig. 8.17

• Muscle contracts

with less than

maximum force if

its initial length is

shorter or longer

than optimal


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Fatigue


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Fatigue

• The decreased ability to do work• Can be caused by

– The central nervous system (psychologicfatigue)

– Depletion of ATP in muscles (muscularfatigue)

• Physiologic contracture (the inability of

muscles to contract or relax) and rigormortis (stiff muscles after death) resultfrom inadequate amounts of ATP


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Energy Sources


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Energy Sources

• Creatine phosphate – ATP is synthesized

when ADP reacts

with creatine

phosphate to formcreatine and ATP

– ATP from this

source providesenergy for a short

time

Fig. 8.18

Energy Sources


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Energy Sources

• Anaerobic respiration – ATP synthesized provides

energy for a short time at

the beginning of exercise

and during intenseexercise

– Produces ATP less

efficiently but more rapidly

than aerobic respiration

– Lactic acid levels increase

because of anaerobic

respiration

Fig. 8.18

Energy Sources


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Energy Sources

• Aerobic respiration – Requires oxygen

– Produces energy

for muscle

contractions under

resting conditions

or during

endurance exercise

Fig. 8.18


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Fig. 8.18


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Speed of Contraction


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Speed of Contraction

• The three main types of skeletal musclefibers are

– Slow-twitch oxidative (SO) fibers

– Fast-twitch glycolytic (FG) fibers – Fast-twitch oxidative glycolytic (FOG) fibers

• SO fibers contract more slowly than FG

and FOG fibers because they have slowermyosin ATPases than FG and FOG fibers

Fatigue Resistance


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Fatigue Resistance

• SO fibers are fatigue-resistant and rely onaerobic respiration

– Many mitochondria, a rich blood supply, andmyoglobin

• FG fibers are fatigable – Rely on anaerobic respiration and have a high

concentration of glycogen

• FOG fibers have fatigue resistanceintermediate between SO and FG fibers

– Rely on aerobic and anaerobic respiration

Functions


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Functions

• SO fibers maintain posture and are involved withprolonged exercise – Long-distance runners have a higher percentage of

SO fibers

• FG fibers produce powerful contractions of shortduration – Sprinters have a higher percentage of FG fibers

• FOG fibers support moderate-intensity

endurance exercises – Aerobic exercise can result in the conversion of FGfibers to FOG fibers


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Tab. 8.3

Muscular Hypertrophy and Atrophy


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Muscular Hypertrophy and Atrophy

• Hypertrophy is an increase in the size ofmuscles – Due to an increase in the size of muscle fibers

resulting from an increase in the number of myofibrilsin the muscle fibers

• Aerobic exercise – Increases the vascularity of muscle

– Greater hypertrophy of slow-twitch fibers than fast-twitch fibers

• Intense anaerobic exercise

– Greater hypertrophy of fast-twitch fibers than slow-twitch

• Atrophy is a decrease in the size of muscle – Due to a decrease in the size of muscle fibers or a

loss of muscle fibers

Effects of Aging on Skeletal Muscle


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Effects of Aging on Skeletal Muscle

• By 80 years of age 50% of the musclemass is gone

– Due to a loss in muscle fibers

– Fast-twitch muscle fibers decrease in numbermore rapidly than slow-twitch fibers

• Can be dramatically slowed if people

remain physically active

Types of Smooth Muscle


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ypes o S oot usc e

• Visceral smooth muscle fibers have manygap junctions and contract as a single unit

• Multiunit smooth muscle fibers have fewgap junctions and function independently

– Found in the walls of hollow visceral organs,such as the stomach, urinary bladder, andrespiratory passages

– Forces food and other substances throughinternal body channels

– It is not striated and is involuntary

Regulation of Smooth Muscle


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g

• Contraction is involuntary – Multiunit smooth muscle contracts when

externally stimulated by nerves, hormones, or

other substances

– Visceral smooth muscle contracts

autorhythmically or when stimulated externally

• Hormones are important in regulating

smooth muscle

Structure of Smooth Muscle Cells


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• Spindle-shaped with a single nucleus• Have actin and myosin myofilaments

– Actin myofilaments are connected to dense bodies

and dense areas

• Not striated

• No T tubule

system and

most have lessSR than skeletal

muscle

• No troponin

Contraction and Relaxation of Smooth Muscle


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• Calcium ions enter the cell to initiatecontraction

– Bind to calmodulin

– Activate myosin kinase, which transfers a

phosphate group from ATP to myosin – When phosphate groups are attached to

myosin, cross-bridges form

• Relaxation results when myosinphosphatase removes a phosphate groupfrom the myosin molecule


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Fig. 8.19


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Functional Properties of Smooth Muscle


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p

• Pacemaker cells are autorhythmic smooth musclecells that control the contraction of other smoothmuscle cells

• Smooth muscle cells contract more slowly thanskeletal muscle cells

• Smooth muscle tone is the ability of smooth muscleto maintain a steady tension for long periods withlittle expenditure of energy

• Smooth muscle in the walls of hollow organsmaintain a relatively constant pressure on the

contents of the organ despite changes in contentvolume

• The force of smooth muscle contraction remainsnearly constant despite changes in muscle length

Cardiac Muscle Cells


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Cardiac Muscle Cells

• Occurs only in the heart

• Is striated like skeletal muscle but is notvoluntary

• Have a single nucleus

• Connected by intercalated disks that allowingthem to function as a single unit

• Capable of autorhythmicity

• Contracts at a fairly steady rate set by theheart’s pacemaker

• Neural controls allow the heart to respond tochanges in bodily needs


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Tab. 8.1


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Documents

8 Muscles Intro