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Chapter 10:

Muscle Tissue

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Muscle Tissue

• A primary tissue type, divided into:– skeletal muscle

• Voluntary striated muscle, controlled by nerves of the central nervous system

– cardiac muscle• Involuntary striated muscle

– smooth muscle• Involuntary nonstriated muscle

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Characteristics of all Muscle Tissues

1. Specialized Cells: - elongated, high density of myofilaments =

cytoplasmic microfilaments of actin and myosin

2. Excitability/Irritability: - receive and respond to stimulus

3. Contractility: - shorten and produce force upon stimulation

4. Extensibility: - can be stretched

5. Elasticity: - recoil after stretch

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Skeletal Muscle Tissue

• Skeletal muscles make up 44% of body mass

• Skeletal muscle = an organ– composed of:

• skeletal muscle cells (fibers) and CT• nerves and blood vessels

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Functions of Skeletal Muscles

1. Produce skeletal movement2. Maintain posture and upright

position3. Support soft tissues4. Guard entrances and exits5. Maintain body temperature by

generating heat6. Stabilize joints

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Muscle Tissue Organized at the Tissue Level

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Formation of Skeletal Muscle Fibers

• Skeletal muscle cells are called fibers

Figure 10–2

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Skeletal Muscle Anatomy

• Each muscle is innervated by one nerve: – Nerve must branch and contact each

skeletal muscle fiber (cell)

• One artery, branches into extensive capillaries around each fiber:– supply oxygen– supply nutrients– remove wastes.

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Organization of Connective Tissues

Figure 10–1

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Organization of Connective Tissues• Muscles have 3 layers of connective

tissues that hold the muscle together:1. Epimysium

- covers the muscle (exterior collagen layer), separates muscle from other tissues, composed of collagen, connects to deep fascia

2. Perimysium- composed of collagen and elastin, has associated blood vessels and nerves, bundles muscle fibers into groups called fascicles

- perimysium covers a fascicle

3. Endomysium- composed of reticular fibers, contains capillaries, nerve fibers and satellite cells (= stem cells repair), surrounds individual muscle fibers

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Muscle Attachments

• Endomysium, perimysium, and epimysium come together:– at ends of muscles– to form connective tissue attachment

to bone matrix– Tendon = cord-like bundles– Aponeurosis = sheet-like

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How would severing the tendon attached to a muscle affect the muscle’s ability to move a body

part?

A. Uncontrolled movement would result from a severed tendon.

B. Movement would be greatly exaggerated with no tendon.

C. No movement is possible without a muscle to bone connection.

D. Limited movement would result.

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Muscle

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Skeletal Muscle Fibers

• Huge cells: – up to 100 µm diameter, 30 cm long

• Multinucleate• Formed by fusion of 100s of myoblasts• Nuclei of each myoblast retained to

provide enough mRNA for protein synthesis in large fiber

• Unfused myoblasts in adult = satellite cells

• Satellite cells are capable of division and fusion to existing fibers for repair but cannot generate new fibers

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Organization of Skeletal Muscle Fibers

Figure 10–3

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Skeletal Muscle Fibers

• Cell membrane = sarcolemma• Sarcolemma maintains separation of electrical

charges resulting in a transmembrane potential• Na+ pumped out of the cell creating positive

charge on the outside of the membrane• Negative charge from proteins on inside give

muscle fibers a resting potential of -85mV• If permeability of the membrane is altered, Na+

will flow in causing a change in membrane potential

• Change in potential will signal the muscle to contract

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Transverse Tubules

• Tubes of sarcolemma called transverse tubules (T tubules) reach deep inside the cell to transmit changes in transmembrane potential to structures inside the cell

• Transmit action potential through cell• Allow entire muscle fiber to contract

simulataneously

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Skeletal Muscle Fibers

• Cytoplasm = sarcoplasm: – rich in glycosomes (glycogen granules)

and myoglobin (binds oxygen)• Fiber is filled with myofibrils extending

the whole length of the cell• Myofibrils consist of bundles of

myofilaments• Myofilaments are responsible for

muscle contraction – made of actin and myosin proteins

• 80% of cell volume

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Organization of Skeletal Muscle Fibers

Figure 10–3

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Skeletal Muscle Fibers• Actin:

– makes up the thin filament• Myosin:

– makes up the thick filament• When thick and thin filaments

interact, contraction occurs

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Skeletal Muscle FibersSarcoplasm contains networks of SER called

sarcoplasmic reticulum (SR)• Sarcoplasmic Reticulum:

– A membranous structure surrounding each myofibril – Function:

• store calcium and help transmit action potential to myofibril

– SR forms chambers (terminal cisternae) attached to T-tubules – Cisternae

• Concentrate Ca2+ (via ion pumps) • Release Ca2+ into sarcomeres to begin muscle

contraction

• All calcium is actively pumped from sarcoplasm to SR (SR has 1000X more Ca2+ than sarcoplasm)

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Skeletal Muscle Fibers• Triads are located repeated along the

length of myofilaments– Triads = T-tubule wrapped around a

myofibril sandwiched between two terminal cisternae of SR • Formed by 1 T tubule and 2 terminal cisternae

of SR

• Triads are located on both ends of a sarcomere– Sarcomere = smallest functional unit of a

myofibril

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Sarcomere

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• Each muscle = ~ 100 fascicles

• Each fascicle = ~ 100 muscle fibers

• Each fiber (cell) = ~ 1 thousand

myofibrils

• Each myofibril = ~ 10 thousand

sarcomeres

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The structural components of a

sarcomere.

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Sarcomeres

• The contractile units of muscle• Structural units of myofibrils • Form visible patterns within

myofibrils

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SarcomeresComposed of: 1. Thick filaments – myosin 2. Thin filaments – actin 3. Stabilizing proteins: -hold thick and thin filaments in place 4. Regulatory proteins: - control interactions of thick and thin

filaments

Organization of the proteins in sarcomere causes striated appearance of the muscle fiber

Figure 10–4

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Muscle Striations

• A striped or striated pattern within myofibrils:– alternating dark, thick filaments (A

bands) and light, thin filaments (I bands)

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Regions of the Sarcomere1. A-band:

- whole width of thick filaments, looks dark microscopically

2. M line: at midline of sarcomere- Center of each thick filament, middle of A-band- Attaches neighboring thick filaments

3. H-zone: - Light region on either side of the M line- Contains thick filaments only

4. Zone of overlap:- ends of A-bands- place where thin filaments intercalate between thick

filaments (triads encircle zones of overlap)

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Regions of the Sarcomere3. I-band:

- Contains thin filaments outside zone of overlap - Not whole width of thin filaments

4. Z lines/disc: - the centers of the I bands

- constructed of Actinins- Anchor thin filaments and bind

neighboring sarcomeres- Constructed of Titin Proteins

- Bind thick filaments to Z-line, stabilize the filament

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Why does skeletal muscle appear striated when viewed through a

microscope?

A. Z lines and myosin filaments align within the tissue.

B. Glycogen reserves are linearly arranged.

C. Capillaries regularly intersect the myofibers.

D. Actin filaments repel stain, appearing banded.

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• Sarcomere Function– Transverse tubules encircle the

sarcomere near zones of overlap– Ca2+ released by SR causes thin and

thick filaments to interact

• Muscle Contraction– Is caused by interactions of thick and

thin filaments– Structures of protein molecules

determine interactions

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Thin Filament

Figure 10–7a

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Thin Filaments (5-6 nm diameter)

• Made of 4 proteins:1. Actin2. Nebulin

- Holds F actin strands together- F-actin (filamentous) consists of rows of G-actin

(globular)- Each G-actin has an active site that can bind to myosin

3. Tropomyosin- Covers the active sites on G actin to prevent actin–

myosin binding

4. Troponin: holds tropomyosin on the G-actin- Also has receptor for Ca2+:

- when Ca2+ binds to the troponin-tropomyosin complex it causes the release of actin allowing it to bind to myosin

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Troponin and Tropomyosin

Figure 10–7b

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Initiating Contraction

• Ca2+ binds to receptor on troponin molecule

• Troponin–tropomyosin complex changes

• Exposes active site of F actin

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Thick Filament

Figure 10–7c

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Thick Filaments (10-12 nm diameter)

• Composed of:– bundled myosin molecules – titin strands that recoil after stretching

• Each Myosin has three parts1. Tail:

- tails bundled together to make length of

thick filament- all point toward M-line

2. Hinge: - flexible region, allows movement for

contraction

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Thick Filaments (10-12 nm diameter)

3. Head: - hangs off tail by hinge, will bind actin at

active site.

- No heads in H-zone- also contains core of titin:

- elastic protein that attaches thick filaments to Z-line

- Titin holds thick filament in place and aid elastic recoil of muscle after stretching- Each thick filament is surrounded by a hexagonal arrangement of thin filaments

with which it will interact

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The Myosin Molecule

Figure 10–7d

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Myosin Action

• During contraction, myosin heads:– interact with actin filaments, forming

cross-bridges – pivot, producing motion

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Sliding Filaments

Figure 10–8

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Sliding Filament TheoryContraction of skeletal muscle is due to thick filaments and thinfilament sliding past each other

– not compression of the filaments1. H-zones and I-bands decrease width during contraction2. Zones of overlap increase width3. Z-lines move closer together4. A-band remains constantSliding causes shortening of every sarcomere in every myofibril

in every fiberOverall result = shortening of whole skeletal muscle

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The components of the neuromuscular

junction, and the events involved in the neural

control of skeletal muscles.

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Skeletal Muscle Contraction

1. Excitation2. Excitation-

Contraction Coupling

3. Contraction4. Relaxation

Figure 10–9 (Navigator)

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1. Excitation and the Neuromuscular Junction

• Excitation of muscle fiber is controlled by the nervous system at the neuromuscular junction using neurotransmitter

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The Neuromuscular Junction

• Is the location of neural stimulation• Action potential (electrical signal):

– travels along nerve axon– ends at synaptic terminal

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Components of Neuromuscular Junction

Neuromuscular Junction:- where a nerve terminal interfaces with a muscle fiber at

the motor end plate - one junction per fiber: control of fiber from one

neuron1. Synaptic Terminal:

- expanded end of the axon, contains vesicles of neurotransmitters Acetylcholine (Ach)

2. Motor End Plate:- specialized sarcolemma that contains Ach receptors

and the enzyme acetylcholinesterase (AchE)3. Synaptic Cleft:

- space between the synaptic terminal and motor end plate where neurotransmitters are released

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Skeletal Muscle: Neuromuscular Junction

Figure 10–10a, b (Navigator)

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2. Skeletal Muscle Excitation

Figure 10–10c

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The Neurotransmitter

• Acetylcholine or ACh:– travels across the synaptic cleft – binds to membrane receptors on

sarcolemma (motor end plate)– causes sodium–ion rush into

sarcoplasm– is quickly broken down by enzyme

(acetylcholinesterase or AChE)

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Action Potential

• Generated by increase in sodium ions in sarcolemma

• Travels along the T tubules• Leads to excitation–contraction

coupling

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The Process of Contraction

• Neural stimulation of sarcolemma:– causes excitation–contraction

coupling

• Cisternae of SR release Ca2+:– which triggers interaction of thick and

thin filaments– consuming ATP and producing tension

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3. Excitation–Contraction Coupling

• Action potential reaches a triad:– releasing Ca2+

– triggering contraction

• Requires myosin heads to be in “cocked” position:– loaded by ATP energy

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The key steps involved in the contraction of a

skeletal muscle fiber.

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Exposing the Active Site1. The action potential of

the transverse tubules reaches a triad and causes the release of calcium ions from the cisternae of the SR into the sarcoplasm around the zones of overlap of the sarcomeres

2. Calcium binds to troponin on the thin filaments

3. Troponin pulls tropomyosin off the active sites of the actin so that cross bridges can form.

Figure 10–11

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The Contraction Cycle

Figure 10–12 (1 of 4)

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5 Steps of the Contraction Cycle

1. Exposure of active sites2. Formation of cross-bridges3. Pivoting of myosin heads4. Detachment of cross-bridges5. Reactivation of myosin

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The Contraction Cycle

Figure 10–12 (2 of 4)

1. Actin, free of tropomyosin, binds to myosin via its active site

2. Cross bridges are formed * Actin active sites are bound to myosin heads

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The Contraction Cycle

Figure 10–12 (3 of 4)

3. Myosin heads have been pre-primed for movement via ATP energy prior to cross bridge formation and are pointed away from the M line. Upon actin binding, the myosin heads pivot toward the M line in an event called the power stroke, which pulls the thick filament along the thin filament

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The Contraction Cycle

• Myosin ATPase uses ATP to break the cross bridges releasing the myosin head from the actin active site, and resets the myosin head pointed away from the M-line

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The Contraction Cycle

• The myosin head is now primed to interact with a new active site on actin

• Myosin can carry out 5 power strokes per second while calcium and ATP are available.

• Each power stroke shortens the sarcomere by 1%

Figure 10–12 (Navigator) (4 of 4)

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Fiber Shortening

• As sarcomeres shorten, muscle pulls together, producing tension

Figure 10–13

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Contraction Duration

• Depends on:– duration of neural stimulus– number of free calcium ions in

sarcoplasm– availability of ATP

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4. Relaxation

1. Ca2+ reabsorbed by sarcoplasmic reticulum

2. Ca2+ ions detach from troponin3. Troponin, without Ca2+, pivots

tropomyosin back onto active sites on actin, no cross bridges can form

4. Sarcomeres stretch back out:- Gravity- Opposing muscle contractions- Elastic recoil of titin protein

Result: Muscle returns to Resting Length

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A Review of Muscle Contraction

Table 10–1 (1 of 2)

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A Review of Muscle Contraction

Table 10–1 (2 of 2)

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Rigor Mortis• A fixed muscular contraction after death• Caused when:

– SR can not absorb Ca2+ : • ion pumps cease to function• calcium builds up in the sarcoplasm

– Ca2+ bind troponin– Tropomyosin frees actin– Cross bridges from– No ATP to detach myosin head because ATP is

already all used up• fixed cross bridge

• Contractions occur until necrosis releases lysosomal enzymes which digest cross bridges

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Disease of Muscle Contraction

1. Botulism/Botox:- Bacteria Clostridium botulinum (grows in

improperly canned foods) produces botulinum toxin- Toxin prevents the release of Ach at the

neuromuscular junction- Results in flaccid paralysis

2. Tetanus:- Bacteria Clostridium tetani (grows in soil) produces

tenanus toxin:- Toxin causes over stimulation of motor neurons

- Results in spastic paralysis

3. Myasthenia gravis:- Autoimmune disease- Causes loss of Ach receptors muscles become

non-responsive

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KEY CONCEPT

• Skeletal muscle fibers shorten as thin filaments slide between thick filaments

• Free Ca2+ in the sarcoplasm triggers contraction

• SR releases Ca2+ when a motor neuron stimulates the muscle fiber

• Contraction is an active process• Relaxation and return to resting length is

passive

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Where would you expect the greatest concentration of Ca2+ in resting

skeletal muscle to be?

A. T tubulesB. surrounding the

mitochondriaC. within sarcomeresD. cisternae of the

sarcoplasmic reticulum

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How would a drug that interferes with cross-bridge formation affect

muscle contraction?

A. interferes with contractionB. slows contractionC. speeds contractionD. increases strength of

contraction

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Predict what would happen to a muscle if the motor end plate

failed to produce acetylcholinesterase.

A. Muscle would lose strength.

B. Muscle would be unable to contract.

C. Muscle would lock in a state of contraction.

D. Muscle would contract repeatedly.

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What would you expect to happen to a resting skeletal muscle if the

sarcolemma suddenly became very permeable to Ca2+?

A. increased strength of contraction

B. decreased cross bridge formation

C. decreased ability to relaxD. both A and C

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The mechanism responsible for tension production in a muscle

fiber, and the factors that determine the peak

tension developed during a contraction.

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Tension Production

• Muscle tension:– Force exerted by contracting muscle– Force is applied to a load

• Load = weight of the object being acted upon

• For a single muscle fiber contraction is all–or–none:– as a whole, a muscle fiber is either

contracted or relaxed

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Tension of a Single Muscle Fiber

• Once contracting tension depends on:

1. The number of pivoting cross-bridges2. The fiber’s resting length at the time

of stimulation

3. The frequency of stimulation

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Resting Length• Greatest tension produced at optimal resting length

– Optimal resting length = Optimum overlap – Overlap determines the number of pivoting cross-bridges

• Enough overlap, so that myosin can bind actin, not so much that thick filaments crash into Z-lines

Figure 10–14

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Why is it difficult to contract a muscle that has been

overstretched?

A. Myosin filaments break.B. Crossbridges can not be

formed.C. Z lines are unable to

sustain contractile forces.D. Tendons lose elasticity.

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Frequency of Stimulation

• Twitch = single contraction due to a single neural stimulation, 3 phases:

1. Latent period: post stimulation but no tension- Action potential moves across the sarcolemma- Ca2+ is released

2. Contraction phase: peak tension production- Ca2+ bind- Active cross bridge formation

3. Relaxation phase: decline in tension- Ca2+ is reabsorbed- Cross bridges decline

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Myogram• A graph of twitch tension

development

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Twitch

• Single twitch will not produce normal movement

– requires many cumulative twitches

• Repeat stimulation will result in higher tension due to Ca2+ not being fully absorbed - Ca2+ more cross bridges

• Types of Frequency Stimulation1. Treppe2. Wave summation

a. Incomplete Tetanusb. Complete Tetanus

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Treppe

• Stepping up of tension production to max level with repeat stimulation of the same fiber following relaxation phase

• Repeated stimulations immediately after relaxation phase:– stimulus frequency < 50/second

• Causes a series of contractions with increasing tension

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Treppe

• A stair-step increase in twitch tension

Figure 10–16a

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Wave Summation• Repeat stimulation before relaxation phase

ends resulting in more tension production than max treppe– stimulus frequency > 50/second

• Typical muscle contraction• Increasing tension or summation of twitches

Figure 10–16b

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Incomplete Tetanus

• Rapid cycles of contraction and relaxation produces max tension

• Twitches reach maximum tension

Figure 10–16c

Cardiac muscle incomplete tetanus Only to prevent seizure of heart

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Complete Tetanus

• Relaxation eliminated, continuous contraction• Fiber is in prolonged state of contraction

– Produces 4x more tension than maximum treppe– Quick to fatigue

Figure 10–16d

Most Skeletal muscle complete tetanus when contracting

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During treppe, why does tension in a muscle gradually increase even

though the strength and frequency of the stimulus are constant?

A. Increased blood flow improves contraction.

B. Sarcomeres shorten with each contraction.

C. Calcium ion concentration increases with successive stimuli.

D. Generated heat improves contraction.

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The factors that affect peak tension production during the contraction of an entire skeletal muscle,

and the significance of the motor unit in this

process.

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Tension Produced by Whole Skeletal Muscles

• Depends on:1. Internal tension produced by sarcomeres

- Not all the tension is transferred to the load, some of it is lost due to the elasticity of muscle tissues

2. External tension exerted by muscle fibers on elastic extracellular fibers- Tension applied to the load

3. Total number of muscle fibers stimulated

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Total Number of Muscle Fibers Stimulated

• Each skeletal muscle has thousands of fibers organized into motor units

• Motor units = all fibers controlled by a single motor neuron– Axon branches to contact each fiber

• Number of fibers in a motor unit depends on the function– Fine control: 4/unit (e.g. eye muscles)– Gross control: 2000/unit (e.g. leg muscles)

• Fibers from different units are intermingled in the muscle so that the activation of one unit will produce equal tension across the whole muscle

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Motor Units in a Skeletal Muscle

Figure 10–17

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Recruitment (Multiple Motor Unit Summation)

• In a whole muscle or group of muscles, smooth motion and increasing tension is produced by slowly increasing size or number of motor units stimulated

• Recruitment = order of activation of a motor unit– Slower weaker units are activated first– Strong units are added to produce steady

increases in tension

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Contraction Skeletal Muscle

• During sustained contraction of a muscle– Some units rest while others contract to avoid

fatigue

• For maximum tension, all units in complete tetanus – Leads to rapid fatigue

• Muscle tone = maintaining shape/definition of the muscle– Some units are always contracting– Exercise = Increase # of units contraction

Increase in metabolic rate Increase in speed of recruitment (better

tone)

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KEY CONCEPT

• Voluntary muscle contractions involve sustained, tetanic contractions of skeletal muscle fibers

• Force is increased by increasing the number of stimulated motor units (recruitment)

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The types of muscle contractions.

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Contraction Skeletal Muscle

• All contractions produce tension but not always movement

1. Isotonic Contractions:- Muscle length changes resulting in

movement

2. Isometric Contractions- Tension is produced with no

movement

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Isotonic Contraction• If muscle tension > resistance:

– muscle shortens (concentric contraction)

• If muscle tension < resistance:– muscle lengthens (eccentric contraction)

Figure 10–18a, b

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Isometric Contraction

• Skeletal muscle develops tension, but is prevented from changing lengthNote: Iso = same, metric = measure

Figure 10–18c, d

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Return to Resting Length

• Expansion via:1. Elastic recoil after contraction

- The pull of elastic elements (tendons and ligaments)

- Expands the sarcomeres to resting length

2. Opposing muscle contractions- Reverse the direction of the original motion

3. Gravity- Opposes muscle contraction to return a

muscle to its resting state

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Can a skeletal muscle contract without shortening? Explain.

A. Yes; isotonic contractions produce no movement.

B. No; resistance is always less than force generated.

C. Yes; concentric contractions are common.

D. No; contraction implies movement.

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The mechanisms by which muscle fibers obtain

energy to power contractions.

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Muscle Metabolism

• 1 fiber ~15 million thick filaments• 1 thick filament ~ 2500 ATP/sec• 1 glucose (aerobic respiration) = 36 ATP• Each fiber needs 1x1012 glucose/sec to

contract• ATP unstable, muscles store respiration

energy on creatine as Creatine Phosphate (CP)

• Creatine phosphokinase transfers P from CP at ADP when ATP is needed to reset myosin for next contraction

• Each cell as only ~20 sec of energy reserved

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ATP and CP

• Adenosine triphosphate (ATP): – the active energy molecule

• Creatine phosphate (CP):– the storage molecule for excess ATP

energy in resting muscle• Energy recharges ADP to ATP:

– using the enzyme creatine phosphokinase (CPK)

• When CP is used up, other mechanisms generate ATP

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Muscle Metabolism

• At Rest:– Use glucose and fatty acids with O2 (from

blood) aerobic respiration•Resulting ATP is used to CP reserves•Excess glucose is stored as glycogen

• Moderate Activity:– CP used up

– Glucose and fatty acids with O2 (from blood) are used to generate ATP (aerobic respiration)

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Muscle Metabolism

• High Activity:– O2 not delivered adequately

– Glucose from glycogen reserves are used for ATP via fermentation (glycolysis only)•Pyruvic acid is converted to lactic acid•Excess lactic acid production leads to

muscle cramps

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ATP Generation

• Cells produce ATP in 2 ways:– aerobic metabolism of fatty acids in the

mitochondria (At rest and Moderate activity)• Is the primary energy source of resting muscles• Breaks down fatty acids • Produces 34 ATP molecules per glucose molecule

– anaerobic glycolysis (fermentation) in the cytoplasm (High activity)• Is the primary energy source for peak muscular

activity• Produces 2 ATP molecules per molecule of

glucose• Breaks down glucose from glycogen stored in

skeletal muscles

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Muscle Metabolism

Figure 10–20a

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Muscle Metabolism

Figure 10–20b

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Muscle Metabolism

Figure 10–20c

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Muscle Metabolism

Figure 10–20 (Navigator)

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Factors that contribute to muscle fatigue, and the stages and mechanisms

involved in muscle recovery.

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Muscle Fatigue

• When muscles can no longer perform a required activity (contraction), they are fatigued

1. Depletion of reserves - glycogen, ATP, CP

2. Decreased pH due to:- lactic acid production

3. Damage to sarcolemma and sarcoplasmic reticulum

4. Muscle exhaustion and pain

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To restore function, cell need:

1. Intracellular energy reserves- Glycogen and CP

2. Good Circulation- Nutrients in, wastes out

3. Normal O2 levels4. Normal pH

- Lactic Acid Disposal

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Normal pHLactic Acid Disposal

- Lactic acid diffuses into the blood- Filtered out by the liver- Converted back to glucose through

the Cori Cycle- Returned to blood for use by cells- When O2 returns

- Remaining lactic acid in the muscle is converted to glucose and used in aerobic cellular respiration

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KEY CONCEPT

• Skeletal muscles at rest metabolize fatty acids and store glycogen

• During light activity, muscles generate ATP through aerobic breakdown of carbohydrates, lipids or amino acids

• At peak activity, energy is provided by anaerobic reactions that generate lactic acid as a byproduct

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Muscle fibers and physical conditioning that relate to

muscle performance.

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Muscle Performance• Power:

– the maximum amount of tension produced• Endurance:

– the amount of time an activity can be sustained

• Power and endurance depend on:1. Types of muscle fibers

A. Fast Glycolytic Fibers (fast twitch)B. Slow Oxidative Fibers (slow twitch)C. Intermediate/Fast Oxidative Fibers

2. Physical conditioningA. Aerobic ExerciseB. Resistance Exercise

121

Fiber Types

• Types of fibers in a muscle are genetically determined and mixed

1. Fast glycolytic Fibers (fast twitch)- Myosin ATPase work quickly- Anaerobic ATP production: glycolysis only- Large diameter fibers- More myofilaments and glycogen- Few mitochondria- Fast to act, powerful, but quick to fatigue- Catabolize glucose only

122

Fiber Types

2. Slow Oxidative Fibers (slow twitch)- Myosin ATPases work slowly- Specialized for aerobic respiration

- Many mitochondria- Extensive blood supply - Myoglobin (red pigment, binds oxygen)

- Smaller fibers for better diffusion- Slow to contract, weaker tension, but resist

fatigue- Catabolize glucose, lipids, and amino acids

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Fiber Types

3. Intermediate/Fast Oxidative Fibers- Qualities of both fast glycolytic and

slow oxidative fibers- Fast acting but perform aerobic

respiration so to resist fatigue- Physical conditioning can convert

some fast fibers into intermediate fibers for stamina

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Fast versus Slow Fibers

Figure 10–21

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Comparing Skeletal Muscle Fibers

Table 10–3

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Muscles and Fiber Types

• White muscle:– mostly fast fibers– pale (e.g., chicken breast)

• Red muscle:– mostly slow fibers – dark (e.g., chicken legs)

• Most human muscles:– mixed fibers– pink

127

Physical Conditioning

1. Aerobic Exercise: - Increase Capillary Density- Increase Mitochondria and myoglobinBoth then:- Increase efficiency of muscle metabolism- Increase strength and stamina- Decrease fatigue

2. Resistance Exercise:- Results in Hypertrophy:

- fibers increase in diameter but not number- Increase glycogen, myofibrils, and myofilaments

results in increase tension production

128

Physical Conditioning

• Growth Hormone (pituitary) and Testosterone (male sex hormone)– Stimulate synthesis of contractile proteins

• Results in Muscle Enlargement

• Epinephrine – Stimulates increase muscle metabolism

• Results in increase force of contraction

• Without stimulation muscles will atrophy– Fibers shrink due to loss of myofilament

proteins– Loss: up to ~5%/day

129

KEY CONCEPT

• What you don’t use, you loose • Muscle tone indicates base activity in

motor units of skeletal muscles• Muscles become flaccid when inactive

for days or weeks• Muscle fibers break down proteins,

become smaller and weaker• With prolonged inactivity, fibrous tissue

may replace muscle fibers

130

Why would a sprinter experience muscle fatigue before a marathon

runner would?

A. Sprinters cannot utilize ATP for long periods of time.

B. Sprinters’ muscles are most efficient aerobically.

C. Sprinters’ muscles are most efficient anaerobically.

D. Sprinters’ muscles are weaker.

131

Which activity would be more likely to create an oxygen

debt: swimming laps or lifting weights?

A. swimming lapsB. lifting weightsC. both A and BD. neither A nor B

132

Which type of muscle fibers would you expect to predominate in the large leg

muscles of someone who excels at endurance activities, such as cycling or

long-distance running?

A. slow fibersB. fast fibersC. nonvascular fibersD. thick, glycogen-laden fibers

133

Cardiac Muscle Tissue

134

Cardiac Muscle Tissue

• Cardiac muscle is striated, found only in the heart

Figure 10–22

135

Cardiac Muscle Tissue• Forms the majority of heart tissue• Cells = cardiocytes• One or two nuclei• No cell division• Long branched cells• Myofibrils organized into sarcomeres (striated)• No triads (no terminal cisternae)• Transverse tubules encircle Z-lines• Aerobic Respiration Only• Mitochondria and myoglobin rich• Glycogen and lipid energy reserves• Intercalated discs at cell junctions (gap junctions

and desmosomes) – allow transmission of action potentials – link myofibrils from on cardiocyte (cell) to the

next

136

Coordination of Cardiocytes

• Because intercalated discs link heart cells mechanically, chemically, and electrically, the heart functions like a single, fused mass of cells

137

4 Functions of Cardiac Tissue

1. Automaticity:– contraction without neural stimulation– Automatically due to control by pacemaker cells

• These cells generate action potentials spontaneously

2. Pace and amount of contraction tension:– Can be adjusted and controlled by the nervous

system

3. Extended contraction time- Contraction is 10x longer than skeletal muscle

4. Only twitches, no complete tetanus- Prevention of wave summation and tetanic

contractions by cell membranes

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Smooth Muscle Tissue

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Structure of Smooth Muscle

• Nonstriated tissue

Figure 10–23

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Smooth Muscle Tissue• Lines hollow organs

– Regulates blood flow and movement of materials in organs

• Forms errector pili muscles• Usually organized into two layer

1. Circular2. Longitudinal

• Spindle shaped cells• Single central nucleus• Cells capable of division• No myofibrils, sarcomeres, or T tubules• SER/ER throughout cytoplasm• No tendons

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Smooth Muscle Tissue

• Thick filaments (myosin fibers) scattered– Myosin fibers have more heads per thick

filament• Thin filaments are attached to dense

bodies on desmin cytoskeleton (web)• Adjacent cells attach at dense bodies

with gap junctions (firm linkage and communication)– Dense bodies transmit contractions from

cell to cell• Contraction compresses the whole cell

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Smooth Muscle in Body Systems

• Forms around other tissues • In blood vessels:

– regulates blood pressure and flow• In reproductive and glandular systems:

– produces movements • In digestive and urinary systems:

– forms sphincters– produces contractions

• In integumentary system:– arrector pili muscles cause goose bumps

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Smooth Excitation-Contraction• Different than striated muscle:

– no troponin so active sites on actin are always exposed

• Events:1. Stimulation causes Ca2+ release from SR2. Ca2+ binds calmondulin in the sarcoplasm

- Calmondulin = CALcium MODULated proteIN

3. Calmondulin activates myosin light chain kinase, this complex phosphorylates myosin

4. MLC Kinase converts ATP ADP to cock myosin head

5. Cross bridge form contraction, cells pull toward center

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Smooth Excitation-Contraction

Stimulation is by involuntary control from- Autonomic Nervous System- Hormones- Other Chemical FactorsSkeletal Muscle = Motor NeuronsCardiac Muscle = Automatically

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Characteristics of Skeletal, Cardiac, and Smooth Muscle

Table 10–4

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Why are cardiac and smooth muscle contractions more affected by

changes in extracellular Ca2+ than are skeletal muscle contractions?

A. Extracellular Ca2+ inhibits actin.

B. Crossbridges are formed extracellularly.

C. Most calcium for contractions comes from SR stores.

D. Most calcium for contractions comes from extracellular fluid.

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Smooth muscle can contract over a wider range of resting lengths than skeletal muscle can. Why?

A. Smooth muscle sarcomeres are longer.

B. Myofilament arrangement is less organized in smooth muscle.

C. Smooth muscle cells are shorter.

D. Smooth muscle actin is longer.

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Effects of Aging

• Skeletal Muscle fibers become thinner– Decrease myofibrils, Decrease reserves = Decrease in strength and endurance

and Increase in fatigue

- Decrease cardiac and smooth muscle function = Decrease cardiovascular performance

- Increase fibrosis (CT):- Skeletal muscle less elastic

- Decrease ability to repair- Decrease satellite cells- Increase scar formation

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SUMMARY • 3 types of muscle tissue:

– skeletal– cardiac– smooth

• Functions of skeletal muscles• Structure of skeletal muscle cells:

– endomysium– perimysium– epimysium

• Functional anatomy of skeletal muscle fiber:– actin and myosin

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SUMMARY

• Nervous control of skeletal muscle fibers:– neuromuscular junctions – action potentials

• Tension production in skeletal muscle fibers:– twitch, treppe, tetanus

• Tension production by skeletal muscles:– motor units and contractions

• Skeletal muscle activity and energy:– ATP and CP– aerobic and anaerobic energy

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SUMMARY

• Skeletal muscle fatigue and recovery• 3 types of skeletal muscle fibers:

– fast, slow, and intermediate

• Skeletal muscle performance:– white and red muscles– physical conditioning

• Structures and functions of:– cardiac muscle tissue– smooth muscle tissue