9 Skeletal Muscle Tissue

© 2011 Pearson Education, Inc.

PowerPoint® Lecture Presentations prepared byAlexander G. CheroskeMesa Community College at Red Mountain

9Skeletal Muscle Tissue


Section 1: Functional Anatomy of Skeletal Muscle Tissue

• Learning Outcomes

• 9.1 Describe the organization of skeletal muscle at the tissue level.

• 9.2 Identify the structural components of a sarcomere.

• 9.3 Describe the structural components of a thin filament and a thick filament.

• 9.4 Identify the components of the neuromuscular junction, and summarize the events involved in

the neural control of skeletal muscles.

• 9.5 Describe the role of ATP in a muscle contraction, and explain the steps involved in the

contraction of a skeletal muscle fiber.



• Muscle tissue

• One of the four primary tissue types

• Consists chiefly of muscle cells specialized for contraction

• Three types

1. Cardiac• In heart propelling blood through blood vessels

2. Smooth• Move fluids and solids along digestive tract

• Regulate diameters of small arteries

• Other functions



• Muscle tissue (continued)

• Three types (continued)

3. Skeletal

• Move body by pulling on bones

• Each cell is a single muscle fiber

• Each muscle is an organ

• Primarily muscle cells plus connective tissues, nerves, and blood vessels

© 2011 Pearson Education, Inc.Figure 9 Section 1

Skeletal Muscle Tissue

Cardiac Muscle Tissue

Smooth Muscle Tissue

Skeletal muscle tissue contractionsmove the body by pulling on bonesof the skeleton, making it possiblefor us to walk, dance, bite an apple,or play the ukulele.

Cardiac muscle tissue contractionsin the heart propel blood throughthe blood vessels.

Smooth muscle tissue contractionsmove fluids and solids along thedigestive tract and regulate thediameters of small arteries, amongother functions.



• Skeletal muscle tissue functions

• Produce skeletal movements

• Pull tendons and move bones

• Maintain posture and body position

• Skeletal muscle tension maintains body posture

• Support soft tissues

• Support weight of visceral organs and shield internal tissues from injury



• Skeletal muscle tissue functions (continued)• Guard entrances and exits

• Openings of digestive and urinary tracts encircled by skeletal muscle (sphincters)

• Provide voluntary control of swallowing, defecation, and urination

• Maintain body temperature• Some energy used for muscle contraction is released

as heat

• Provide nutrient reserves• Amino acids from muscle fibers can be released into

circulation and used to produce glucose and energy


Module 9.1: Skeletal muscle anatomy

• Skeletal muscle

• Complex organ containing:

• Skeletal muscle fibers (contraction)

• Connective tissues (harness contractile forces)

• Blood vessels (nourish muscle fibers)

• Nerves (control contractions)



• Skeletal muscle connective tissues

• Tendon

• Bundle of collagen fibers that attach muscle to bone

• Collagen fibers extend into bone matrix providing firm attachment

• Also occurs as a sheet (= aponeurosis)

• Epimysium (epi-, on + mys, muscle)

• Dense layer of collagen fibers surrounding entire muscle

• Separates muscle from surrounding tissues and organs

• Connected to deep fascia



• Skeletal muscle connective tissues (continued)

• Perimysium (peri-, around)

• Fibrous layer that divides muscle into compartments or bundles of cells (= fascicles)

• Contains collagen and elastin fibers, blood vessels, and nerves

• Endomysium (endo-, inside)

• Surrounds individual muscle cells or fibers

• Loosely interconnects adjacent muscle fibers

• Contains capillaries, myosatellite (stem) cells, and axons of neurons that control muscle fibers



Animation: Muscle Physiology: Muscle Layers

Animation: Anatomy of Skeletal Muscles



• Skeletal muscle cell development

• Myoblasts (myo-, muscle + blastos, formative cell) fuse, forming multinucleate cells

• Develop into skeletal muscle fibers

• Each skeletal muscle fiber nucleus represents a myoblast

• Not all myoblasts fuse into developing muscle fibers

• Some remain in endomysium and help muscle repair


Myosatellite cell

Immaturemuscle fiber

Nuclei

Myosatellite cell

Up to 30 cmin length

Mature skeletalmuscle fiber

The multinucleate cells begindifferentiating into skeletalmuscle fibers as they enlarge andbegin producing the proteinsinvolved in muscle contraction.

Over time, most of the myoblasts fusetogether to form larger multinucleate cells.However, a few myoblasts remain within thetissue as myosatellite cells, even in adults.

Muscle fibers develop through thefusion of embryonic mesodermalcells called myoblasts.

Myoblasts

The development of a skeletal musclefiber from myoblast to maturity

Figure 9.1 4 – 5



• Mature muscle cell characteristics

• Very large cells

• Can have diameter of 100 µm and length of 30 cm (12 in.)

• Each contains hundreds of nuclei just internal to plasma membrane (sarcolemma) (sarkos, flesh + lemma, husk)

• Genes in nuclei control production of enzymes and structural proteins for contraction

• Many nuclei = many genes = faster production

• Cytoplasm = sarcoplasm

© 2011 Pearson Education, Inc.Figure 9.1 5 – 6

Myofibrils

Sarcoplasm

Mitochondria

Sarcolemma

Nuclei

Myosatellite cell

Up to 30 cmin length

Mature skeletalmuscle fiber

A mature skeletal muscle fiber


Module 9.1 Review

a. Define tendon and aponeurosis.

b. Describe the connective tissue layers associated with skeletal muscle tissue.

c. How would severing the tendon attached to a muscle affect the muscle’s ability to move a body part?


Module 9.2: Skeletal muscle fiber anatomy

• Myofibrils

• Cylindrical structures 1–2 µm in diameter and as long as muscle fiber

• Hundreds to thousands comprise an individual muscle cell

• Each is banded and gives the skeletal muscle cells their banded appearance

• Made of protein filaments (= myofilaments)

• Thin filaments (primarily actin)

• Thick filaments (primarily myosin)

© 2011 Pearson Education, Inc.Figure 9.2 1

The myofibril, the source of a muscle fiber’s striations

Myofibril

Sarcolemma

Sarcoplasm

Skeletal muscle fiber

Nuclei


Sarcolemma

Mitochondria

A section of a muscle fiber, revealingits myofibrils, each of which iscomposed of myofilaments

Myofibril

Thin filament

Thick filament



• Myofilament structure

• Have repeating functional units called sarcomeres (sarkos, flesh + meros, part)

• Approximately 10,000 sarcomeres/myofibril

• Each sarcomere has a 2-µm resting length

• Zone of overlap• Thin and thick filaments interspersed

• Z lines• Boundary of adjacent sarcomeres

• Interconnect thin filaments from adjacent sarcomeres

• Consist of proteins (actinins)



• Myofilament structure (continued)

• A band

• Dense sarcomere region containing thick filaments

• I band

• Contains thin filaments (no thick)

• Extends from A band of one sarcomere to the next A band

• M line

• Connects central portion of each thick filament

• H band

• Lighter region around M line

• Contains only thick filaments (no thin)


Sarcomeres, the repeatingfunctional units of myofilaments

Arrangementof filaments inzone of overlap

A band I band

Z lineM line Sarcomere

H band

Myofibril



• Specialized parts of skeletal muscle cells

• Sarcolemma

• Separates sarcoplasm from interstitial fluid

• Maintains distribution of positive and negative charges on either side

• = Transmembrane potential

• All cells have a characteristic transmembrane potential

• Large changes in skeletal muscle transmembrane potential lead to contraction

• Are transmitted along entire muscle cell surface



• Specialized parts of skeletal muscle cells (continued)

• Transverse tubules (T tubules)

• Narrow tubes from sarcolemma extending into sarcoplasm

• Transmembrane potential changes travel along T tubules to cell interior

• Encircle each sarcomere




• Sarcoplasmic reticulum (SR)

• Similar to smooth endoplasmic reticulum of other cells

• Forms tubular network around each myofibril

• On either side of T tubule, forms expanded chambers (terminal cisternae)

• T tubule + terminal cisternae = triad


The transverse tubules and the sarcoplasmic reticulum

Transverse tubules (T tubules)T tubule encircling sarcomereat zone of overlap

Sarcolemma

Transverse tubule

Terminal cisternae

TriadPosition of M line




• Sarcoplasmic reticulum (SR) (continued)

• Contains pumps moving calcium from sarcoplasm to SR

• SR calcium occurs as free ions and bound to proteins

• SR calcium concentrations can be 40,000× that of sarcoplasm

• Muscle contraction begins with SR calcium release


Sarcoplasmic reticulum (SR)Ca2+

Gated calciumchannel (closed)

Calcium ionpump

Sarcoplasm

The membrane of the sarcoplasmic reticulum, which contains calcium ion pumps


Module 9.2 Review

a. Define transverse tubules.

b. Describe the structural components of a sarcomere.

c. Where would you expect the greatest concentration of Ca2+ to be in a resting skeletal muscle?


Module 9.3: Thick and thin filaments

• Thin filaments

• Attached to Z lines with actinin

• 5–6 µm in diameter, 1 µm in length

• Primarily actin

• Individual G-actin molecules (with active site for binding myosin) link together to form F-actin (filamentous)

• F-actin strand held together with nebulin



• Thin filaments (continued)

• Also contain two regulatory proteins

1. Tropomyosin

• Covers G-actin active sites and prevents actin–myosin interaction

• Attached to troponin

2. Troponin

• Consists of three subunits

1. Binds to tropomyosin (forms complex)

2. Binds to G-actin (maintains position on actin)

3. Binds two calcium ions (for activation during contraction)

Animation: Muscle Physiology: Troponin


A longitudinal section of a sarcomere

Myofibril

Z line Thin filament Thick filament

The structure of thin filamentsActinin Z line

The attachment of thin filaments tothe Z line at either end of a sarcomere

F-actin

G-actinNebulin

Tropomyosin

Troponin

Active site

A thin filament, which is primarily composed ofactin associated with other interacting proteins



• Thick filaments

• 10–12 nm in diameter and 1.6 µm long

• Have core of titin

• Connect to Z lines

• Are elastic and recoil after stretching

• Contain ~300 myosin molecules



• Thick filaments (continued)

• Myosin molecule

• Has long tail bound to other myosin molecules

• Has two globular subunits (= free head)

• Forms cross-bridges with actin during contraction

• Connection between head and tail allows a hinge-like (pivot) motion

Animation: Muscle Physiology: Muscle Proteins

Animation: Muscle Physiology: Myosin Parts



• Sliding filament theory

• When muscles contract, thin filaments slide past thick filaments, and

1. H bands and I bands get smaller

2. Zones of overlap get larger

3. Z lines approach each other

4. A bands remain constant

• Sliding occurs in all sarcomeres of a myofibril

• Myofibril gets shorter

• Muscle cell gets shorter

Animation: Muscle Physiology: Sarcromeres


Sarcomere at rest

Z line Z lineH band

I band A band

The sliding filament theory

I band A band

Z line Z lineH band

Sarcomere contraction and filament sliding



Module 9.3 Review

a. Describe the components of thin filaments and thick filaments.

b. What gives skeletal muscle its striated appearance?

c. Briefly describe the sliding filament theory.


Module 9.4: Neuromuscular junction

• Neuromuscular junction (NMJ)

• Intercellular connection between motor neuron and skeletal muscle fiber

• Muscle fiber contracts only under control from the NMJ

• Only one NMJ per muscle fiber• Although one motor neuron axon may branch to control

multiple muscle cells

A&P Flix: Events at the Neuromuscular Junction


Motor endplate

Synaptic terminal

Sarcoplasmicreticulum

Myofibril

Motor neuron

Axon

Motor end plate

Path of electricalimpulse (action

potential)

Neuromuscularjunction

Myofibril

Muscle fiber

The structural relationship between a skeletalmuscle fiber and its lone neuromuscular junction

Figure 9.4 1



• Neuromuscular junction (NMJ) (continued)

• Consists of:

1. Synaptic terminal of neuron

• Has vesicles filled with neurotransmitter (acetylcholine [ACh])

• Changes permeability of sarcolemma

2. Motor end plate of muscle fiber

1. Has junctional folds (creases)

2. Contains acetylcholinesterase (AChE), an enzyme that breaks down ACh

• Synaptic cleft (space between neuron and muscle fiber)

• Also contains AChE


Synaptic cleft

VesiclescontainingACh (red)

Motor end plate

AChE

Junctional fold

The locations of ACh and AChE ina resting neuro-muscular junction



• Activities at the neuromuscular junction

1. Electrical impulse (action potential) at the synaptic terminal causes vesicles of ACh to fuse with neuron plasma membrane

• = Exocytosis of ACh

2. ACh diffuses across synaptic cleft and binds to receptors in motor end plate

• ACh binding allows Na+ to diffuse into the cell

3. Sarcolemma generates action potential

• AChE inactivates receptors by quickly removing ACh from synaptic cleft


Arriving actionpotential

Junctionalfold

The arrival of an action potential,the stimulus for ACh release


Sarcolemma ofmotor end plate

Exocytosis of ACh into the synapticcleft in response to arriving actionpotential


Diffusion of ACh molecules andtheir binding to receptors on themotor end plate

Na+

Na+

Na+

AChreceptor site


Actionpotential

AChE

Generation of an action potential bythe sudden inrush of sodium ions,and the breakdown of ACh by AChE



• Action potential in the muscle cell

• Action potential (AP) generated at motor end plate sweeps across sarcolemma

• Effect is almost immediate since AP is an electrical event

• Event is brief since ACh has been removed and no other stimulus occurs until another AP at motor end plate

• Action potential sweeps down T tubules and causes calcium to be released from SR to sarcomeres causing muscle contraction

• = Excitation-contraction coupling

Animation: Muscle Fiber Contraction



Excitation-contraction coupling,the dumping of calcium ions ontosarcomeres as a result of themovement of an action potentialdown the T tubule

T tubule

Sarcoplasm

Sarcoplasmicreticulum (SR)

Ca2+ Ca2+


Module 9.4 Review

a. Describe the neuromuscular junction.

b. How would a drug that blocks acetylcholine release affect muscle contraction?

c. Predict what would happen if there were no AChE in the synaptic cleft.


Module 9.5: Muscle fiber contraction cycle

• Resting sarcomere

• Each myosin head is already “energized” and “cocked” (heads pointing away from M line)

• Energy supplied by breakdown of ATP by myosin

• Myosin acting as an ATPase

• Breakdown products (ADP and P) still attached to myosin head


Resting Sarcomere

Contraction Cycle Begins

Myosin head

Troponin

ActinTropomyosin



• Steps of muscle fiber contraction cycle

1. Contraction cycle begins

• Arrival of calcium ions at zone of overlap

2. Active-site exposure

• Calcium binds to troponin• Weakens bond between actin and troponin–

tropomyosin complex

• Troponin changes position, exposing active sites on actin

3. Cross-bridge formation

• Myosin heads bind to exposed active sites on actin forming cross-bridges



• Steps of muscle fiber contraction cycle (continued)

4. Myosin head pivoting

• Stored energy within myosin head releases and head pivots toward M line

• = Power stroke

• ADP and P are released from myosin head

5. Cross-bridge detachment

• Attachment of new ATP causes release of myosin from actin

• Exposes active site again for formation of another cross-bridge

6. Myosin reactivation

• New ATP broken down and head “recocks”



A&P Flix: The Cross Bridge Cycle

Animation: Muscle Physiology: Intracellular Calcium Proteins



• Contracted sarcomere

• Entire cycle repeated as long as Ca2+ concentrations remain high and ATP is available

• Calcium levels remain high as long as action potentials continue down T tubules

• Once stimulus is removed

• SR calcium channels close

• Calcium pumps move Ca2+ from sarcoplasm into terminal cisternae

• Troponin–tropomyosin complex moves to cover active sites, preventing further cross-bridge formation

Animation: Muscle Physiology: Muscle Cycles of Attachment and Detachment


Module 9.5 Review

a. What molecule supplies the energy for a muscle contraction?

b. List the interrelated steps that occur once the contraction cycle has begun.

c. What triggers myosin reactivation?


Section 2: Functional Properties of Skeletal Muscle Tissue


• 9.6 Describe the mechanism responsible for tension production in a muscle fiber, and discuss the

factors that determine the peak tension developed during a contraction.

• 9.7 Discuss the factors that affect peak tension production during the contraction of an entire

skeletal muscle, and explain the significance of the motor unit in this process.

• 9.8 Compare the different types of muscle contractions.




• 9.9 Describe the mechanisms by which muscle fibers obtain the energy to power

contractions.

• 9.10 Describe the factors that contribute to muscle fatigue, and discuss the stages and

mechanisms involved in the muscle’s subsequent recovery.

• 9.11 Relate the types of muscle fibers to muscle performance.

• 9.12 CLINICAL MODULE Explain the physiological factors responsible for muscle

hypertrophy, atrophy, and paralysis.



• Review• Neural control

• Skeletal muscle fibers contract when stimulated by motor neuron at neuromuscular junction

• Stimulus is an action potential (AP) at synaptic terminal

• Excitation-contraction coupling• AP causes release of ACh into synaptic cleft• ACh binds to motor end plate receptors opening Na+

channels• Leads to AP in sarcolemma

• AP travels along T tubules causing release of Ca2+ from terminal cisternae of SR



• Review (continued)

• Excitation-contraction coupling (continued)

• Contraction cycle begins and continues as long as ATP is available and APs are still produced at motor end plate

• Thick and thin filaments interact, shortening sarcomeres/muscle fibers/muscle

• Contraction of entire muscle produces a pull or tension


Module 9.6: Tension and muscle length

• Variance in tension that a muscle fiber produces depends on resting length of sarcomere and stimulation time• Does not depend on number of sarcomeres contracted

• All sarcomeres are stimulated and contract together• = Muscle fiber “on” (producing tension) or “off” (relaxed)

• Stretched or compressed compared to optimal resting length, produces less tension

• Normal sarcomere length range is 75%–130% of optimal

• Muscle arrangement, connective tissues, and bones usually prevent too much stretching or compression



• Tension within optimal sarcomere lengths

• Maximum number of cross-bridges can form

• Produces greatest tension

• Tension at increased (stretched) sarcomere lengths

• Reduction in tension due to reduction in size of zone of overlap and number of cross-bridges

• At extreme lengths, no zone of overlap exists and no tension can be generated

• Normally prevented by titin filaments (tie thick filaments to Z lines) and connective tissues



• Tension at decreased (compressed) sarcomere lengths

• Reduces tension as sarcomeres have little area to shorten before thin filaments collide with or overlap with thin filaments from opposite side

• When sarcomeres are fully compressed (thick filaments contacting Z lines), no tension can be produced


A decrease in the restingsarcomere length reducestension because stimulatedsarcomeres cannot shortenvery much before the thinfilaments extend across thecenter of the sarcomere andcollide with or overlap the thinfilaments of the opposite side.

Sarcomeres produce tensionmost efficiently within anoptimal range of lengths. Whenresting sarcomere length iswithin this range, the maximumnumber of cross-bridges canform, producing the greatesttension.

An increase in sarcomere lengthreduces the tension produced byreducing the size of the zone of overlapand the number of potentialcross-bridge interactions.

When the zone of overlap is reduced tozero, thin and thick filaments cannotinteract at all. The muscle fiber cannotproduce any active tension, and acontraction cannot occur. Suchextreme stretching of a muscle fiber isnormally prevented by titin filaments(which tie the thick filaments to the Zlines) and by the surroundingconnective tissues.

Normalrange

Decreased length Increased sarcomere length

Tension productionfalls to zero whenthe thick filamentsare jammed againstthe Z lines and thesarcomere cannotshorten further.

Te

ns

ion

(p

erc

en

t o

f m

axim

um

)

Figure 9.6 1



• Muscle twitch

• Single stimulus-contraction-relaxation sequence in a muscle fiber

• Vary in duration depending on:

• Muscle type

• Muscle location

• Internal and external conditions

• Other factors

• Can be viewed on myograms (graph of tension development in muscle fibers)


Ten

sio

n

StimulusTime (msec)

A myogram, a graph of tension development in muscle fibers

Eye muscle Deep muscleof the calf



• Twitch phases

• Latent period

• Action potential sweeps across sarcolemma

• SR releases calcium ions

• Contraction cycle has not begun (= no tension)

• Contraction phase

• Tension rises to peak

• Calcium binds to troponin allowing cross-bridge formation between myosin head and active site on actin



• Twitch phases (continued)

• Relaxation phase

• Calcium levels fall

• Active sites covered by tropomyosin

• Number of cross-bridges decline with detachment


Ten

sio

n

The phases of a 40-msec twitch in a muscle fiber from thegastrocnemius muscle

Maximum tension development

Restingphase Stimulus

Contractionphase

Relaxationphase

Time (msec)

The latent periodbegins at stimulationand typically lasts about2 msec. During thisperiod, an actionpotential sweeps acrossthe sarcolemma, and thesarcoplasmic reticulumreleases calcium ions.The muscle fiber doesnot produce tensionduring the latent period,because the contractioncycle has yet to begin.

In the contractionphase, tension rises toa peak. As the tensionrises, calcium ions arebinding to troponin, active sites on thinfilaments are beingexposed, andcross-bridgeinteractions areoccurring.

The relaxation phaselasts about 25 msec.During this period, calciumlevels are falling, activesites are being covered bytropomyosin, and thenumber of activecross-bridges is decliningas they detach. As a result,tension returns to restinglevels.


Module 9.6 Review

a. Name a factor that affects the amount of tension produced when a skeletal muscle contracts.

b. Explain two key concepts of the length–tension relationship.

c. For each portion of a myogram tracing a twitch in a stimulated gastrocnemius (calf) muscle fiber, describe the events that occur within the muscle.


Module 9.7: Developing peak tension

• Two factors determine amount of tension produced by a skeletal muscle

1. Amount of tension produced by each muscle fiber

• Dependent on stimulation frequency

2. Total number of muscle fibers stimulated



• Effects of stimulation frequency on tension

• Treppe (German for staircase)

• Stimulation of skeletal muscle fiber immediately after relaxation phase produces increasing maximum tension

• Continues for first 30–50 stimulations

• Most skeletal muscles do not demonstrate treppe


Treppe

Time

Ten

sio

n

Maximum tension (in treppe) KEY

= Stimulus



• Effects of stimulation frequency on tension (continued)

• Wave summation

• Stimulation of skeletal muscle fiber before relaxation phase completion produces increasing maximum tension

• = Addition of one twitch to another

• Duration of twitch determines maximum time available to produce wave summation


Time

Ten

sio

nWave summation

KEY

= Stimulus



• Effects of stimulation frequency on tension (continued)

• Incomplete tetanus (tetanos, convulsive tension)

• Wave summation producing almost peak tension

• Complete tetanus

• Wave summation where stimulation frequency eliminates relaxation phase and produces peak tension• SR cannot reclaim Ca2+ making contraction continuous

• Seldom occurs in normal functioning muscles


KEY

= Stimulus

Ten

sio

n

Time

Incomplete tetanus

Maximum tension (in tetanus)


KEY

= Stimulus

Ten

sio

n

Time

Complete tetanus



• Effects of muscle fiber number on tension

• Typical muscle has thousands of muscle fibers

• Groups of muscle fibers controlled by one motor neuron = motor unit

• Size of motor unit varies with muscle control

• Examples:

• External eye muscle (fine control): 4–6 muscle cells

• Leg muscle (gross control): 1000–2000 muscle cells

• Muscle fibers of different motor units are intermingled



• Effects of muscle fiber number on tension (continued)

• Motor units

• Recruitment

• Movements begin with the smallest motor units

• As movement continues, more and larger motor units are stimulated to contribute producing greater tension

• Asynchronous motor unit summation

• Motor units activated on a rotating basis to maintain a sustained contraction


The structure of a motor unit, which consists of all the muscle fiberscontrolled by a single motor neuron

Spinal cord

Cell bodies ofmotor neurons

Axonsof motorneurons

Motornerve

Intermingled muscle fibers fromdifferent motor units

KEY

Motor unit 1

Motor unit 2

Motor unit 3Figure 9.7 5


Asynchronous motor unit summationduring a sustained contraction

Tension in tendon

Motor unit 1

Motor unit 2

Motor unit 3

Ten

sio

n

Time



• Effects of muscle fiber number on tension (continued)

• Motor units (continued)

• Muscle tone

• Variable number of motor units always active to produce low level tension (not enough to produce movement)

• Regulated at subconscious level

• Activated muscle fibers use energy and therefore can affect metabolism by a small amount


Module 9.7 Review

a. Define motor unit.

b. Describe the relationship between the number of fibers in a motor unit and the precision of body movements.

c. Compare incomplete tetanus with wave summation.


Module 9.8: Isotonic and isometric contractions

• Isotonic contraction (iso-, equal + tonos, tension)

• Tension rises, until muscle length changes, then remains constant

• Examples: lifting an object, walking, running

• Concentric contraction

• Muscle tension overcomes load and muscle shortens

• Speed of contraction inversely related to load

• Eccentric contraction

• When load is more than peak tension produced, muscle lengthens

• Rate of elongation varies with difference in load/tension


A concentric isotonic contraction

Tendon

Musclecontracts(isotonic

contraction)

2 kg

2 kg


Time

Musclelength

(percentof resting

length)

Muscletension

(kg)

Contractionbegins

Musclerelaxes

Amountof load

Resting length

Muscle tension and length changes during aconcentric isotonic contraction

Peak tensionproduction


The inverse relationship between speed of musclecontraction and load on the muscle

Load (kg)

Sp

eed

of

mu

scle

co

ntr

acti

on


An eccentric isotonic contraction

6 kg

6 kg

Support removed,contraction begins


Musclelength

(percentof resting

length)

Muscletension

(kg)

Peak tensionproduction

Resting length

Time

Support removed,contraction begins

Muscle tension and length changes during an eccentricisotonic contraction

When the eccentriccontraction ends,the unopposed loadstretches themuscle until eitherthe muscle tears, atendon breaks, orthe elastic recoil ofthe skeletal muscleis sufficient tooppose the load.


Module 9.8: Isotonic and isometric contractions

• Isometric contraction (metric, measure)

• Muscle length does not change and tension never exceeds load

• Contracting muscle bulges but not as much as during isotonic contraction

• Individual muscle fibers shorten only due to connective tissues stretching

• Example: postural muscle contractions


6 kg 6 kg

An isometric contraction

Musclecontracts(isometric

contraction)


Musclelength

(percentof resting

length)

Contractionbegins

Muscletension

(kg)

Time

Resting length

productionPeak tension

Muscle tension and length dynamicsduring an isometric contraction


Module 9.8 Review

a. Define isotonic contraction and isometric contraction.

b. Can a skeletal muscle contract without shortening? Why or why not?

c. Explain the relationship between load and speed of muscle contraction.


Module 9.9: ATP production in muscles

• Three sources of ATP in muscles

1. Glycolysis (anaerobic: does not require oxygen)

• Occurs in sarcoplasm

• Produces 2 ATP and 2 pyruvate molecules for each glucose

2. Aerobic metabolism

• Provides 95% of ATP demands of resting muscle cell

• Occurs in mitochondria• Primarily through electron transport chain activity

• Produces 17 ATP for each pyruvate


The sites and processes of ATP production in cells

Glycolysis

Glucose CYTOPLASM

MITOCHONDRION

MATRIX

Citric acidcycle

Pyruvate

Aerobic metabolism

Electrontransportsystem

ADP +phosphate



• Three sources of ATP in muscles (continued)

3. Creatine phosphate (CP)

• Creatine assembled from amino acids

• Facilitates regeneration of ATP

• ADP + CP ATP + C




• Muscles store few high-energy molecules

• ATP

• CP

• Most energy stored as glycogen

• May account for 1.5% of total muscle weight

• Enables extended periods of muscle contractions



• ATP demand and production at different activity levels

• At rest

• Demand for ATP is low

• Surplus ATP produced by mitochondria

• Used to build up CP and glycogen reserves

• At moderate activity levels

• Demand for ATP increases

• ATP production by mitochondria (aerobic metabolism) meets demand



• ATP demand and production at different activity levels (continued)

• At peak activity levels

• Mitochondria can provide only ~1/3 ATP demand

• Glycolysis provides most ATP

• Excess pyruvate converts to lactic acid (dissociates into lactate and H+)

• Decreases intracellular pH

• Can affect enzymatic activities and cause fatigue


Module 9.9 Review

a. Identify three sources of energy utilized by muscle fibers.

b. How do muscle cells continuously synthesize ATP?

c. Under what conditions do muscle fibers produce lactic acid?


Module 9.10: Muscle fatigue and recovery

• Fatigue

• When a muscle can no longer perform at the required activity level

• Decline in pH is a major factor

• Decreases calcium/troponin binding

• Alters enzyme activities



• Under conditions of insufficient oxygen

• Glycolysis quickly produces ATP

• Lowers pH due to lactic acid buildup

• Faster ATP production than aerobic metabolism

• Only until glycogen reserves are depleted (1–2 min)

• Less efficient than aerobic metabolism

• Only 4%–6% of energy captured from conversion of glucose to pyruvate

• Elevates body temperature

• Triggers increased sweating


Glycolysis, which enables a skeletal muscle to continue contractingeven when insufficient oxygen is available

OXYGEN INSUFFICIENT Glycogen

Glucose

Pyruvate Lactate

Glycolysis(anaerobic)

CYTOPLASM

MITOCHONDRION

Citric acidcycle


Figure 9.10 1



• Under conditions of available oxygen

• During recovery period, intracellular conditions return to normal (can take hours to days)

• Oxygen available in abundance

• ATP production primarily through aerobic metabolism

• More efficient than glycolysis

• Fiber captures ~42% of energy released

• Heat produced

• ~85% of heat needed for normal body temperature

• Lactate converted back to pyruvate

• Pyruvate can be used to generate ATP by mitochondria or used to aid synthesis of glucose and glycogen reserves


Glycogen OXYGEN AVAILABLE

Glucose

Pyruvate Lactate

MITOCHONDRION

Citric acidcycle


CYTOPLASM

Aerobic metabolism, which is much more efficient than glycolysis

70% convertedback to glucose

30% broken down for energy

Figure 9.10 2



• Lactate cycling

• During peak activity

• Lactate produced by muscle fibers diffuses into blood

• Liver begins process of • Lactate pyruvate glucose

• 30% of pyruvate converted to ATP by mitochondria

• 70% of pyruvate converted to glucose

• Ultimately, glucose is released into blood by liver and returns to muscle cells

• = Cori cycle



• Lactate cycling (continued)

• During recovery period

• Liver continues converting lactate to glucose and returning to cells via blood

• Glucose absorbed by skeletal muscle fibers and replenishes glycogen reserves

• From producing ATP in muscle cells and liver, body oxygen demand is high• Oxygen debt (excess postexercise oxygen

consumption: EPOC)

• Amount of oxygen needed to return to pre-exertion conditions


The production of lactate during peak activity, its conversion to glucose in the liver, and the rebuilding ofglycogen reserves in the muscles during recovery

Lactate

Pyruvate Glucose

Glucose

Pyruvate

Lactate

Glucose

70–80%

20–30%LIVER

MUSCLE

Glycogen reserves in muscle

Peak Activity Recovery

Much of the large amounts of lactateproduced during peak exertion diffusesout of the muscle fibers and into thebloodstream. The liver absorbs this lactateand begins converting it into pyruvate.

This process continues after exertion has ended, because lactatelevels within muscle fibers remain relatively high, and lactatecontinues to diffuse into the bloodstream. After the absorbedlactate is converted to pyruvate in the liver, roughly 30 percent ofthe new pyruvate molecules are broken down in themitochondria, providing the ATP needed to convert the remaining 70 percent of pyruvate molecules into glucose. The glucose molecules are then released into the circulation, where they are absorbed by skeletal muscle fibers and used to rebuild their glycogen reserves.

Figure 9.10 3


Module 9.10 Review

a. Define oxygen debt (excess postexercise oxygen consumption).

b. What two processes are crucial in repaying a muscle’s oxygen debt during the recovery period?

c. After strenuous exercise, what causes the “burning” sensation in skeletal muscles?


Module 9.11: Skeletal muscle fiber types

• Three major types of skeletal muscle fibers

1. Fast fibers

• Reach peak tensions in <0.01 sec

• Large in diameter

• Have densely packed myofibrils, large glycogen reserves, few mitochondria

• Powerful

• Fatigue rapidly since most ATP produced anaerobically


Fast fibers in cross section LM x 171



• Three major types of skeletal muscle fibers (continued)

2. Slow fibers

• Half diameter of fast fibers

• Take 3× as long to contract compared to fast fibers

• Can maintain longer sustained contractions

• Primarily use aerobic metabolism for ATP production• Increased oxygen reserves due to:

• Extensive capillary network

• Myoglobin pigment (stores O2 like hemoglobin)

• Are dark red


LM x 171Slow fibers in cross section

Figure 9.11 2



• Three major types of skeletal muscle fibers (continued)

3. Intermediate fibers

• More closely resemble fast fibers

• Contain little myoglobin

• Relatively pale

• But more capillaries and more fatigue resistant


Fast (W) and slow (R) fibers in longitudinal section

LM x 783




• Most muscles have a mixture of fiber types

• Percentages of each type vary

• According to muscle function

• Back and calf muscles dominated by slow fibers

• Eye or hand may have no slow fibers

• According to genetics

• Percentage of fast to slow inherited

• According to physical training

• Percentage of intermediate to fast can be modified with athletic training


Module 9.11 Review

a. Identify the three types of skeletal muscle fibers.

b. Why would a sprinter experience muscle fatigue before a marathon runner would?

c. Which type of muscle fiber would you expect to predominate in the large leg muscles of someone who excels at endurance activities, such as cycling or long-distance running?


CLINICAL MODULE 9.12: Factors and clinical conditions affecting muscles

• Hypertrophy

• Increase in muscle size due to:

• Increase in myofilaments

• Increase in myofibril size

• Increase in mitochondria

• More glycogen and glycolytic enzymes

• As a result of repeated exhaustive stimulation

• Can be promoted by administration of steroid hormones



• Atrophy

• Decrease in muscle size, tone, and power

• As a result of decreased stimulation such as during:

• Paralysis by spinal injury

• Damage to nervous system

• Having body part in cast after bone fracture

• Initially reversible, but after prolonged disuse, muscle fibers can die and not be replaced



• Clinical conditions

• Polio

• Virus attacks motor neurons of brain and spinal cord causing paralysis (lost of voluntary movement)

• Tetanus

• Toxin from bacteria (Clostridium tetani) that suppresses the mechanism inhibiting motor neuron activity

• Thrives in low-oxygen areas like deep punctured tissues

• Results in sustained, powerful contractions of affected muscles

• Severe tetanus can have 40%–60% mortality

• Deaths rare due to immunization in U.S.



• Clinical conditions (continued)

• Botulism

• Toxin from bacteria (Clostridium botulinum) that blocks ACh release at neuromuscular junctions

• Acquired through bacteria-contaminated food

• Myasthenia gravis

• Loss of ACh receptors at neuromuscular junctions

• Results in progressive weakness



• Clinical conditions (continued)

• Rigor mortis

• Generalized muscle contraction shortly after death (2–7 hours)

• Begins with small muscles of face, neck, and arms

• Due to depletion of ATP, leaving myosin cross-bridges attached to actin

• Ends 1–6 days later as muscular tissue decomposes


Four clinical conditions thataffect skeletal muscles

Polio: a virus affects motor neurons in thespinal cord and brain, causing muscleatrophy and paralysis

Tetanus: the bacterium Clostridium tetani releases apowerful toxin that suppresses the mechanism thatinhibits motor neuron activity, causing sustained, powerful contraction of skeletal muscles throughoutthe body

Botulism: ingestion of a toxin produced by the bacteriumClostridium botulinum paralyzes skeletal muscles by preventingACh release at neuromuscular junctions

Myasthenia gravis: loss of ACh receptors at the neuromuscularjunctions results in progressive muscular weakness

Figure 9.12 3


CLINICAL MODULE 9.12 Review

a. Define muscle hypertrophy and muscle atrophy.

b. Six weeks after Fred broke his leg the cast is removed, and as he steps down from the exam table, his leg gives way and he falls. Propose a logical explanation.

c. Explain how the flexibility or rigidity of a dead body can provide a clue about a murder victim’s time of death.

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9 Skeletal Muscle Tissue

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