CH. 9 Muscular Tissue - Dr. Jones

sarcoplasm

muscle cell cytoplasm

muscle fiber

long muscle cell

excitability (responsiveness)

contractility (shorten forcibly)

extensibility (stretched)

elasticity (recoil to resting length)

four main characteristics of muscles

oxygen and glucose

what do muscle fibers need to contract?

epimysium

-dense irregular connective tissue

-surrounding entire muscle; may blend with fascia

perimysium

-fibrous connective tissue

-surrounding fascicles (groups of muscle fibers)

endomysium

-fine areolar connective tissue

-surrounding each muscle fiber

-deepest of connective tissue wrapping

direct (fleshly) attachments

epimysium fused to periosteum of bone or perichondrium of cartilage

indirect attachments

connective tissue wrappings extend beyond muscle such as:

• rope-like tendon (like a cord)

• sheet-like aponeurosis (flatten out)

sarcolemma

muscle fiber plasma membrane

myoglobin

oxygen binding protein found only in muscle

glycosomes

specialized vesicles for glycogen storage in muscle

myofribrils

a muscle cell is a bundle of densely packed ___.

(smaller than fiber)

perimysium

Separate bundle of fasicles

endomysium

separate muscle fibers

myofibril

Responsible for striations in muscle fiber

sarcomere

divides myofibril into sections

-smallest contractile unit of muscle fiber

myofilament

myofibril is a bundle of ___.

-consists of proteins that make up striations (light and dark)

actin myofilament

thin filament - I band

myosin myofilament

thick filament - A band

M line

divide sarcomere into a right and left side

H zone

zone of sarcomere that has no actin, only myosin

cross bridges

when actin and myosin touch = contraction

tropomyosin and troponin

control proteins bound to ACTIN

-act as gatekeepers if actin and myosin ever get to touch

dystrophin

holds actin in proper position for good overlap (alignment)

-responsible for dystrophy if mutated

duchenne muscular dystrophy (DMD)

-sex-linked recessive gene (mother to son); exclusive to males

-child is clumsy and falls frequently

-caused by defective gene for dystriophin (links thin filaments to matrix which helps stabilize sarcolemma)

sarcoplasmic reticulum

Network of smooth endoplasmic reticulum tubules surrounding each MYOFIBRIL

-runs length of muscle fiber

-only responds to electrical stimulation

-stores calcium

sarcoplasmic reticulum

stores Ca²⁺ when the fiber is at rest

T tubules

allow electrical nerve transmissions to reach deep into the interior of each muscle fiber

-”transverse”

-portions of plasma membrane weave in and around each myofibril so they can receive electrical stimulation

contraction

the activation of cross bridges to generate force

tension

shortening occurs when __ is generated by cross bridges

ends

contraction __ when cross bridges become inactive

sliding filament model of contraction

thin filaments slide past thick filaments, causing actin and myosin to overlap

-neither thick nor thin filaments change length, just overlap

cross bridge shortening of muscle fiber

-I bands shorten

-Z discs become closer

-H zones disappear

-A bands move closer to each other

action potentials

big electrical signals

-stimulate skeletal muscle

acetylcholine (ACh)

what neurotransmitter action potential uses (chemical)

chemically-gated ion channels

ion channel opened by chemical messengers such as neurotransmitters

Ex. ACh receptors on muscle cells

voltage-gated ion channels

ion channel receptor open or close in response to electrical changes in membrane potential

axons

long, threadlike extensions of motor neurons > travel from central nervous system to skeletal muscle

(long tail of neuron-which is in brain)

neuromuscular junction

where neuron and muscle meet

-also called motor end plate

-equal to amt muscle fibers

axon terminal

end of axon

synaptic cleft

gel-filled space between axon terminal and muscle

synatic vesicles

contain acetylcholine (ACh) neurotransmitter

acetylcholine (ACh)

can diffuse over synaptic cleft which bind to muscle via receptors

Action potential arrives at axon terminal

1st event at neuromuscular junction

voltage-gated CALCIUM channels open, calcium enters motor neuron

2nd event at neuromuscular junction

after action potential arrives at axon terminal, what happens next?

calcium entry causes RELEASE of acetylcholine (ACh) neurotransmitter into synaptic cleft

3rd event at neuromuscular junction

after voltage-gated calcium channels open due to action potential and calcium enters motor neuron, what happens next with calcium?

ACh diffuses across to ACh RECEPTORS (chemical gates) on the sarcolemma

4th event at neuromuscular junction

after calcium causes the release of ACh into the synaptic cleft, what happens to the ACh?

ACh binds to ACh receptors on the muscle, which OPENS the gates, allowing Na+ (sodium) to enter muscle; results in end plate potential

5th event at neuromuscular junction

after ACh diffuses across ACh receptors what happens next?

acetylcholinesterase

an enzyme that breaks down the neurotransmitter acetylcholine (ACh), terminating any nerve signals responsible for muscle contraction

myasthenia gravis

autoimmune disease which immune system destroys ACh receptors

-weakened contraction of muscle.. need to get channels on muscle to open via ACh first!)

negative

the inside of a muscle fiber is more ___ than the outside

end plate potential

local depolarization (becomes more positive)

-ACh released from motor neuron bind to ACh receptors on sarcolemma

-chemically gated ion channels (ligands) on sarcolemma to open

-ACh diffuse into muscle fiber; causing interior of sarcolemma to become less negative (MORE POSITIVE)

Na+

outside of muscle cell there is lots of ___ compared to inside

K+

inside of muscle cell there is more __ compared to outside

-70mV

voltage when muscle is at rest

-55-50mV

point of no return - voltage threshold ; muscle contraction

repolarization

restoration of resting conditions (back to negative)

-K+ go out of cell rapidly bringing cell back to initial resting membrane voltage

refractory period

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

depolarization

Na+ entry to a cell causes…?

repolarization

K+ exiting a cell causes..?

contraction

Ca+ release leads to ___.

Ca+

what do you need to remove troponin and tropomyosin in order for actin and myosin to overlap (cross bridge) - create contraction?

ATP

what enable the actin-myosin cross-bridge to detach?

rigor mortis

3-4 hours after death muscles begin to stiffen

-actin myosin connected, nothing to release it due to no ATP

load

opposing force to muscle contraction; what the muscle is working against

nerve

groups of axons of neuron

muscle twitch

single action potential in muscle

latent period

delay of action potential of neuron; no muscle tension seen

period of contraction

cross bridge formation; tension increase

period of relaxation

reentry into sarcoplasmic reticulum; tension declines to zero slowly

muscle tone

constant, slightly contracted state of all muscles

-keeps muscle steady, healthy, ready to respond

isometric contraction

no shortening; not enough to overcome load

-muscle tension increases but does not exceed load

-load is greater than max tension muscle can generate ex. when you stand up

isotonic contraction

muscle shortens because muscle tension exceeds load

-muscle changes length and moves load

-concentric or eccentric

concentric contraction

isotonic contraction

-muscle shorten and does work

ex. biceps contract to pick up a book

eccentric contraction

muscle lengthens and generates force

ex. laying a book down causes biceps to lengthen while generating a force

disuse atrophy

degeneration and loss of mass

-due to immobilization or loss of neural stimulation (nervous system not able to convey signal)

ex. cast over leg allow bone to heal but muscle weakens over time

top-down

muscular development occurs head to toe or ___.

-a baby can lift its head before it can walk

myoblast-like skeletal muscle satellite cells

limited regenerative abiity

cardiomyocytes

can divide at a modest rate, but if injured is mostly replacced by connective tissue

smooth muscle

regenerates throughout life

sarcopenia

loss of muscle mass

-age 30

intermittent claudication

limping