Chapter #10 Muscle Tissue (copy)

Skeletal Muscle

This tissue is packaged into skeletal muscles, organs that are attached to bones and skin.

Skeletal muscle fibers are the longest of all muscles and have striations (stripes)
Also called voluntary muscle: can be consciously controlled
Contract rapidly; tire easily; powerful
Keywords for skeletal muscle: skeletal, striated, and voluntary

Cardiac Muscle

This tissue is found only in heart

Makes up bulk of heart walls

Striated

Involuntary: cannot be controlled consciously

Contracts at steady rate due to heart’s own pacemaker, but nervous system can increase rate

Key words for cardiac muscle: cardiac, striated, and involuntary

Smooth Muscle

This tissue is found in walls of hollow organs

Examples: stomach, urinary bladder, and airways

Not striated

Involuntary: cannot be controlled consciously

Key words for smooth muscle: visceral, nonstriated and involuntary

Muscle Tissue Comparisons

Skeletal Muscle ( Explained)

Skeletal muscle is an organ made up of different tissues with three features: nerve and blood supply, connective tissue sheaths, and attachments

Each muscle receives a nerve, artery, and veins

Consciously controlled skeletal muscle has nerves supplying every fiber to control activity

Contracting muscle fibers require huge amounts of oxygen and nutrients

Also need waste products removed quickly

Each skeletal muscle, as well as each muscle fiber, is covered in connective tissue

Support cells and reinforce whole muscle

Sheaths from external to internal:

Epimysium »Perimysium»Endomysium

Epimysium (skeletal muscle)

dense irregular connective tissue surrounding the entire muscle; may blend with fascia

Perimysium (skeletal muscle)

fibrous connective tissue surrounding fascicles (groups of muscle fibers)

Endomysium (skeletal muscle)

fine areolar connective tissue surrounding each muscle fiber

Sarcolemma (Skeletal Muscle Fiber Microanatomy)

muscle fiber plasma membrane

Sarcoplasm (Skeletal Muscle Fiber Microanatomy)

: muscle fiber cytoplasm

Myofibrils (Skeletal Muscle Fiber Microanatomy)

Myofibrils are densely packed, rodlike elements
Single muscle fiber can contain 1000s
Accounts for ~80% of muscle cell volume

Myofibril features Striations, Sarcomeres, Myofilaments, Molecular composition of myofilaments

Sacromere

Smallest contractile unit (functional unit) of muscle fiber

A bands (Sacromere)

dark regions

I bands (Sacromere)

lighter regions

Z disc/line (Sacromere)

coin-shaped sheet of proteins on midline of light I band

M line (Sacromere)

line of protein (myomesin) that bisects H zone vertically

H zone (Sacromere)

lighter region in middle of dark A band

All muscles share four main characteristics:

1. Excitability (responsiveness): ability to receive and respond to stimuli

2. Contractility: ability to shorten forcibly when stimulated

3. Extensibility: ability to be stretched

4. Elasticity: ability to recoil to resting length

Four important functions of muscle

Produce movement: responsible for all locomotion and manipulation
Example: walking, digesting, pumping blood

Maintain posture and body position

Stabilize joints

Generate heat as they contract

ONLY skeletal and smooth muscle cells are elongated and referred to as…

muscle fibers

Striations

stripes formed from repeating series of dark and light bands along length of each myofibril

Myofilaments

Orderly arrangement of actin and myosin myofilaments within sarcomere

Actin myofilaments

thin filaments Extend across I band and partway in A band and Anchored to Z discs

Myosin myofilaments

thick filaments Extend length of A band Connected at M line

Sarcomere cross section shows hexagonal arrangement of one thick filament surrounded by six thin filaments

Sarcomere cross section shows hexagonal arrangement of one thick filament surrounded by six thin filaments

Thick filaments (myofilaments)

composed of protein myosin that contains two heavy and four light polypeptide chains

Heavy chains intertwine to form myosin tail

Light chains form myosin globular head

During contraction, heads link thick and thin filaments together, forming cross bridges

Myosins are offset from each other, resulting in staggered array of heads at different points along thick filament

Thin filaments (myofilaments)

composed of fibrous protein actin

Actin is polypeptide made up of kidney-shaped G actin (globular) subunits

G actin subunits bears active sites for myosin head attachment during contraction

G actin subunits link together to form long, fibrous F actin (filamentous)

Two F actin strands twist together to form a thin filament

Tropomyosin and troponin (myofilaments)

regulatory proteins bound to actin

Elastic filament (myofilaments)

composed of protein titin

Holds thick filaments in place; helps recoil after stretch; resists excessive stretching

Dystrophin
Links thin filaments to proteins of sarcolemma

Nebulin, myomesin, C proteins bind filaments or sarcomeres together
Maintain alignment of sarcomere

Sarcoplasmic reticulum

network of smooth endoplasmic reticulum tubules surrounding each myofibril and Most run longitudinally

Terminal cisterns form perpendicular cross channels at the A–I band junction

SR functions in regulation of intracellular Ca2+ levels and Stores and releases Ca2+

T tubules Tube

formed by protrusion of sarcolemma deep into cell interior
Increase muscle fiber’s surface area greatly
Lumen continuous with extracellular space
Allow electrical nerve transmissions to reach deep into interior of each muscle fiber

Tubules penetrate cell’s interior at each A–I band junction between terminal cisterns

Triad

area formed from terminal cistern of one sarcomere, T tubule, and terminal cistern of neighboring sarcomere

Triad relationships

T tubule contains integral membrane proteins that protrude into intermembrane space (space between tubule and muscle fiber sarcolemma)

Tubule proteins

act as voltage sensors that change shape in response to an electrical current

SR cistern membranes

have integral membrane proteins that protrude into intermembrane space
SR integral proteins control opening of calcium channels in SR cisterns

When an electrical impulse passes by, T tubule proteins change shape, causing SR proteins to change shape, causing release of calcium into cytoplasm

Excitation Contraction Coupling

1. Muscle moving = nervous system releases Accetylcholine

2. Accetylcholine binds with Accetylcholine receptor on the sarcolemma

3. This allows Na+ to come in (DEPOLARIZATION)

4. Voltage gates are opened, which allows more sodium in

5. The cell is depolarized to the point of allowing calcium out

6. This causes actin and myosin to come together.

Decision to move is activated by….

brain, signal is transmitted down spinal cord to motor neurons which then activate muscle fibers

Neurons and muscle cells are

excitable cells capable of action potential

Excitable cells

are capable of changing resting membrane potential voltages

AP crosses from neuron to muscle cell via the

neurotransmitter acetylcholine (ACh)

Contraction

the activation of cross bridges to generate force

Shortening occurs when tension generated by cross bridges on thin filaments exceeds forces opposing shortening

Contraction ends when cross bridges become inactive

In the relaxed state,

thin and thick filaments overlap only slightly at ends of A band

Sliding filament model of contraction states

that during contraction, thin filaments slide past thick filaments, causing actin and myosin to overlap more
Neither thick nor thin filaments change length, just overlap more

When nervous system stimulates muscle fiber

myosin heads are allowed to bind to actin, forming cross bridges, which cause sliding (contraction) process to begin

Cross bridge attachments form and break several times, each time pulling thin filaments a little closer toward center of sarcome in a ratcheting action
Causes shortening of muscle fiber

Z discs are pulled toward M line I bands shorten Z discs become closer H zones disappear and A bands move closer to each other

Depolarization

generation and propagation of an action potential (AP)

If end plate potential causes enough change in membrane voltage to reach critical level called threshold, voltage-gated Na+ channels in membrane will open

Large influx of Na+ through channels into cell triggers AP that is unstoppable and will lead to muscle fiber contraction

AP spreads across sarcolemma from one voltage-gated Na+ channel to next one in adjacent areas, causing that area to depolarize

Repolarization

restoration of resting conditions

Na+ voltage-gated channels close, and voltage-gated K+ channels open

K+ efflux out of cell rapidly brings cell back to initial resting membrane voltage

Refractory period: muscle fiber cannot be stimulated for a specific amount of time, until repolarization is complete

Ionic conditions of resting state are restored by Na+-K+ pump

Na+ that came into cell is pumped back out, and K+ that flowed outside is pumped back into cell

Large influx of Na+ leads to….

muscle contration

Refractory period

muscle fiber cannot be stimulated for a specific amount of time, until repolarization is complete

Excitation-contraction (E-C) coupling

events that transmit AP along sarcolemma (excitation) are coupled to sliding of myofilaments (contraction)

AP is propagated along sarcolemma and down into T tubules, where voltage-sensitive proteins in tubules stimulate Ca2+ release from SR
Ca2+ release leads to contraction

AP is brief and ends before contraction is seen

Depolarization/Repolarization Chart

1. Resting membrane potential of sarcolemma is -90mV

2. The threshold is reached when ACh receptors, which are chemically gated ion channels. Na+ enters changing the RMP fro -90mV to -65mV

   1. THRESHOLD VALUE: -65mV

3. Depolarization: occurs at voltage-gated Na+ channels on sacrolemma. RMP goes from -65mV to +30mV

4. Repolarization occurs due to closure of voltage-gated Na+ channels and opening of voltage-gated K+ channels. This changes the RMP from +30 to -90mV

Resting membrane potential of sarcolemma is

-90mV

THRESHOLD VALUE

-65mV

At low intracellular Ca2+ concentration: (1)

Tropomyosin blocks active sites on actin
Myosin heads cannot attach to actin
Muscle fiber remains relaxed

Voltage-sensitive proteins in T tubules change shape… (2)

causing sarcoplasmic reticulum (SR) to release Ca2+ to cytosol

At higher intracellular Ca2+ concentrations, Ca2+… (3)

binds to troponin

Troponin changes shape and moves tropomyosin away from myosin-binding sites

Myosin heads is then allowed to bind to actin, forming cross bridge

Cycling is initiated, causing sarcomere shortening and muscle contraction

When nervous stimulation ceases, Ca2+ is pumped back into SR, and contraction ends

Four steps of the cross bridge cycle of sarcomere

1. Cross bridge formation: high-energy myosin head attaches to actin thin filament active site

1. Working (power) stroke: myosin head pivots and pulls thin filament toward M line

1. Cross bridge detachment: ATP attaches to myosin head, causing cross bridge to detach

1. Cocking of myosin head: energy from hydrolysis of ATP “cocks” myosin head into high-energy state
   This energy will be used for power stroke in next cross bridge cycle

Binding site for actin

myosin head

When calcium is binded to actin….

actin and myosin come together

ATP binds and

causes release of myosin head

then ATP is hydrolyzed and another crossbridge is formed

Summary of Exciation-Coupling and Depolarization/Repolarization

1. When we think about contracting the muscle, the signal travels down axon of alpha motor neuron. This depolarization causing Ca2+ channels to open up

2. Ca2+ binds to vesicle containing ACH

3. ACh binds to ACh receptor, allowing Na+ in.

4. Local depolarization opens up voltage-gated Na+ channels.

5. The sarcolemma is depolarized with Na+

6. Depolarization travels down T tubule, which causes Ca2+ to difuse

7. Ca2+ binds to troponin which exposed myosin binding sites on actin

8. Crossbridge of myosin and actin form

9. To release this contraction ADP is added

Depolarization

Na+ in

Repolarization

K+ out

Contraction

produces muscle tension, the force exerted on load or object to be moved

may/may not shorten muscle

Force and duration vary in response to stimuli of different frequencies and intensities

Isometric contraction

no shortening; muscle tension increases but does not exceed load

Isotonic contraction

muscle shortens because muscle tension exceeds load

Motor nerve

Each muscle is served by at least one

contains axons of up to hundreds of motor neurons
Axons branch into terminals, each of which forms NMJ with single muscle fiber

Motor unit

is the nerve-muscle functional unit

Motor unit consists of the motor neuron and all muscle fibers (four to several hundred) it supplies
Smaller the fiber number, the greater the fine control

Muscle fibers from a motor unit are

spread throughout the whole muscle, so stimulation of a single motor unit causes only weak contraction of entire muscle

Muscle twitch

simplest contraction resulting from a muscle fiber’s response to a single action potential from motor neuron
Muscle fiber contracts quickly, then relaxes

Twitch can be observed and recorded as a

myogram

Tracing

line recording contraction activity

Three phases of muscle twitch

1. Latent period: events of excitation-contraction coupling No muscle tension seen

2. Period of contraction: cross bridge formation Tension increases

3. Period of relaxation: Ca2+ reentry into SR Tension declines to zero

Muscle….

contracts faster than it relaxes

Differences in strength and duration of twitches are due

to variations in metabolic properties and enzymes between muscles

Example: eye muscles contraction are rapid and brief, whereas larger, fleshy muscles (calf muscles) contract more slowly and hold it longer

START ON THIS BRIEL BRIEL