lecture 7 review

excitability

• accept an electrical signal

• properties of skeletal muscle

conductivity

• electrical excitation spreads

• properties of skeletal muscle

contractility

• long cells shorten

  • Generate pulling force

• properties of skeletal muscle

elasticity

• cells recoil after being stretched

• properties of skeletal muscle

extensibility

• extend in respond to contraction of the opposing muscle cells (stretch)

• properties of skeletal muscle

tissue

• a group of cells of similar structure that perform a common function

• 4 types:

  • epithelial tissue

  • connective tissue

  • muscle tissue

  • nervous tissue

skeletal muscle

• Striated

  • Strongest, but fatigue quickest

• Elongated muscle fibers

• Voluntary contraction (controlled by brain consciously)

• in skeleton and skin

cardiac muscle

• Striated

• Branched cells

• Involuntary contraction

• in heart

smooth muscle

• Nonstriated

  • Weakest, but don’t fatigue.

• Fusiform (spindle) shaped

• Involuntary

• in walls of organs

tendon

attaches muscle to bone, skin, or another muscle

aponeurosis

thin, flattened sheet of tendon

bone markings

• where tendons attach to bones (ex/ tubercle)

  • origin

  • insertion

origin

• the less mobile attachment of a muscle (anchor)

• bone markings

insertion

• the more mobile attachment of a muscle (moves)

• bone markings

agonist

prime mover responsible for a specific movement

synergist

• a muscle that assists the agonist in performing an action

• all have same motion (ex/ elbow flexion)

antagonist

• a muscle that opposes the action of the agonist

• exact opposite action (ex/ elbow extension)

epimysium

• Dense irregular CT

• Surrounds the whole muscle

• Continuous with tendons

perimysium

• Moderately dense irregular CT

• Surrounds fascicles (groups of muscle fibers)

endomysium

• Areolar CT

• Surrounds individual muscle fibers

sarcolemma

plasma membrane of skeletal muscle

t-tubules

deep invaginations of sarcolemma

Sarcoplasmic reticulum

• specialized smooth ER

• Stores/releases calcium ions for muscle contraction

triad

one T-tubule flanked sarcoplasmic reticulum

myofibrils

• contractile organelles composed of myofilaments

  • 80% of cytoplasm

  • Long row of repeating segments (sarcomeres)

striations

• caused by protein filament arrangement in sarcomere

• are created by organization of thick and thin myofilaments

  • A band

  • I band

thick filaments

• composed of myosin protein twisted together.

  • Tails are connected in the center.

  • Myosin heads project outward along the length.

    • Can bind exposed myosin-binding sites on actin during contraction.

• in sarcomeres

thin filament

• composed mainly of actin protein

  • Actin protein. has myosin-binding sites.

  • Tropomyosin proteins coil around band, blocking binding sites.

  • Troponin sits on top of tropomyosin, keeping it in place

z-disk

• band of protein on ends of sarcomere that maintain organization (holds actin proteins and titin)

  • One Sarcomere is the distance between two Z-disks

titin

• connects ends of thick filaments to Z-disk (holds thick filament)

  • Used to recoil muscle after contraction or extension

A band

“dark band” where thick myofilaments exist

I band

“light band” where no thick myofilaments exist

Muscle size

changes due to changing levels of proteins (myofibrils get bigger or smaller)

muscle hypertrophy

• growth in muscle size (exercise)

• Exercise creates small tears that are repaired by building more protein strands

muscle atrophy

decrease in muscle size

motor unit

• a single neuron and all the muscle fibers it controls

  • Each muscle fiber is controlled by one neuron

  • A single neuron can innervate multiple fibers

• The strength of muscle contraction is determined by recruitment of motor units

• Neuromuscular Junction (NMJ)

• the point where a neuron and muscle fiber meet

• Action Potential

• Excitability

action potential

the “electrical signal” that passes from the neuron to the muscle cell

step 1: excitation

• Action potential in neuron “passes” to muscle cell

• Action potential travels through sarcolemma and down T-tubules

• Sliding Filament Theory

step 2: Excitation-Contraction Coupling

• Action potential triggers the release of Ca2+ from sarcoplasmic reticulum

• Ca2+ binds troponin, moving tropomyosin off myosin-binding sites of actin

• Sliding Filament Theory

step 3: contraction

• Myosin heads bind actin proteins

• Power Stroke

  • ATP molecule used to power this movement.

• The heads detach and repeat this motion several times

  • A new ATP molecule binds to release the myosin head from actin (rigor mortis)

• Myosin pulls thin filaments towards center

• Sarcomere contracts as filaments overlap

  • The length of filaments doesn’t change!

• Sliding Filament Theory

power stroke

• Activated myosin heads pivot, sliding thin & thick filaments across each other

  • step 3: contraction

mechanism of relaxation

• Action potential in neuron stops

• Action potential in muscle cell stops

• Ca2+ sequestered back into the sarcoplasmic reticulum

• Tropomyosin goes back into place, blocking myosin-binding sites on actin

• Myosin detaches from thin filament.

• Titin protein recoils sarcomere back to original size