Anatomy chapter 9

myo-

macroscopic

mys-

tissue layer

sarco-

cellular components

skeletal muscles 

organs attached to bones and skin 

muscle fibers

longest of all muscle and are striated (stripes)

cardiac muscle

-only in heart

-striated

-involuntary

smooth muscle

-hollow organs

-not striated

-involuntary

excitability 

ability to receive and respond to stimuli 

contractility

ability to shorten forcibility

extensibility

ability to be stretched

elasticity

ability to recoil to resting length

muscle functions 

-produce movement 

-maintain posture 

-stabilize joints 

-generate heat 

skeletal

-nerves and blood supply

-connective tissue sheaths

-attachments

nerves and blood

-receives a nerve, artery, and vein

-supply every fiber to control

-muscle fibers require huge amount of oxygen and nutrients

tissue sheaths

-support cells and reinforce muscle

epimysium 

dense irregular tissue surrounded by entire muscle 

perimysium

fibrous connective surrounding fascicles

endomysium

fine areolar connective surrounding each fiber

attachments

attach bones or other structures

direct (fleshy) attachments 

epimysium fused to periosteum or perichondrium 

indirect attachments

wrapping extends beyond muscle

tendons

rope like; connect bone to muscle

ligaments

aponeurosis; bone to bone

muscle fibers 

long, cylindrical cells (multiple nuclei)  

sarcolema

muscle fiber plasma membrane

sarcoplasm

muscle fiber cytoplasm

-contain glycosomes for glycogen storage and myoglobin for oxygen

specialized structure order

-muscle (organ)

-fascicles (bundles)

-myofibers (cells)

-myofibrils (organelles)

-myofilaments (actin and myosin)

myofibrils (organelle) 

-packed, rod-like cells 

-features: striations, sarcomeres, myofilaments, molecular composition of myofilaments 

-striated 

A bands

-dark bands

H zone

lighter region in middle of A bands

M line

line of myomesin that bisects H zone

I bands 

lighter bands 

Z disc

coin shaped actin filaments on midline of I band

sarcomere

-smallest unit

-contains an A band with half an I band at each band (between Z disc)

-align end to end along myofibril

myofilaments

-arrangement of actin and myosin

-cross section shows hexagon (thick) surrounded by 6 thin filaments

actin (myofilaments)

-thin 

-extend across I band 

-anchored to Z disc 

myosin (myofilaments)

-thick

-extend the length of the A band

-connect at M line

myofibrils

molecular composition of myofilaments

Myosin (myofibrils)

-thick

-heavy form tail

-light form the head

-offset each other

cross bridges

heads linking with thin filaments

actin (myofibrils)

-thin

-polypeptide with G actin subunits

-link to form long F actin (filaments)

-2 F strands twist to form thin filaments

tropomyosin and troponin 

proteins bound to actin 

titin

holds in place

dystrophin

links filaments to proteins

DMD

-muscle dystrophy

-children

-defective gene for dystrophin

sarcoplasmic reticulum and tubules 

-tubules penetrate the interior at A-I band junction 

t tubules

formed by protrusion of the sarcolemma deep into the cell interior

-increase surface area

-lumen

-nerve transmission to reach each fiber

triad

area formed from the terminal cistern of the sarcomere, t-tubule, and cistern

sarcoplasmic reticulum and tubules relationships

-membrane that protrudes into the intermembrane space

-SR proteins control calcium channels

-T tubules change when the pulse passes

Sliding filament model for contraction

-bridges inactive=filaments stops

-model states during contraction, thin filaments slide past thick filaments, causing actin and myosin to overlap

-I bands shorten

-Z discs closer

-H zones disappear

-A bands closer to each other

relaxed muscle

thin and thick filaments overlap only at ends of A bands

shortening 

tension across cross-bridges on thin filaments exceeds forces opposing shortening  

chemically gated channel

open by chemical messengers (neurotransmitters)

voltage gated channel

open/close in response to voltage changes

anatomy of motor neurons and neuromuscular

-somatic travels for CNS to muscle (divides into branches)

-axons travel ends on a fiber forming the neuromuscular junction of the motor end plate (fiber has 1 junction with 1 neuron)

4 steps for muscle contraction 

1.neuromuscular junction event 

2.muscle fiber excitation 

3.excitation contraction coupling 

4.cross-bridge cycling

event at neuromuscular junction

1.actin potential arrives

2. voltage-gated channel open; calcium enters

3.calcium helps release acetylcholine (AcH) into cleft

4.AcH diffuses across AcH receptors on sarcolemma

5.Ach binds; ion channels open; sodium enters

6.acetylcholinesterase degrades Ach

action potential

-resting is polarized (voltage exists) (inside is negative)

-AP is caused by changes in electrical charges

1.generation of end plate potential

2.depolarization (becomes negative)

3.reploarization (becomes positive)

excitation contraction (E-C) coupling

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

-AP is propagated and down into t tubules where voltage- sensitive proteins in tubules stimulate ca2+ release from SR

contraction: cross bridge cycling 

-formation needs ca2+

-low concentration ca2+ (tropomyosin blocks active sites on actin)

-high concentration ca2+ binds to troponin (changes shapes and moves tropmyosin away from myosin binding sites) 

cross-bridge formation

high-energy myosin heads attached to actin thin filament active sites

working (power) strokes

heads pivots and pulls thin filaments toward M line

cross-bridge detattachment

ATP attaches to myosin head, causing bridge to dethatch

cocking of myosin head

energy from the hydrolysis of ATP “cocks” myosin head into high-energy state 

contraction as a whole

-contraction produces muscle tension (force exerted)

-load=opposing force muscle to contract

-vary in response to stimuli

motor unit (1 nerve)

-contains axons with 100s of motor neurons (axon branches into terminals)

-consists of motor neurons and all muscle fibers (4 to 100s)

-small fiber # great fine control

-fibers from the motor unit are spread throughout the whole muscle, so stimulation of a single motor unit causes a weak contraction of the entire muscles

muscle twitch

simple contraction from fiber response to 1 actin potential from neuron (quick contraction)

-strength and duration vary due to difference metabolic properties and enzymes

latent phase (MT)

excitation-contraction coupling ( no tension)

period of contract (MT)

cross-bridge form (tension up)

relaxation phase (MT)

ca2+ reentry into SR (tension down to 0)

graded muscle contractions

vary strength contraction (proper control)

graded contraction (frequency)

-wave (temporal) contraction results if 2 stimuli are reached by a muscle

-do not have time to completely relax

-additional ca2+ release with 2nd stimulus more shortening

-increase stimuli= maximum reached (summation and quivering)

-fused tetanus because contraction fused into 1 smooth sustained contraction plateau (muscle fatigue)

graded muscle contraction (strength)

-recruitment (muscle motor unit summation) stimulus sent to fibers, more precise control

-works on size principle 

-smallest fibers are first

-larger fibers once stimulus intensifies 

-largest fibers only for powerful contractions 

-contract asynchronously to prevent fatigue 

subthreshold 

not strong yet; no contractions 

threshold

strong to cause 1st observable contraction

maximal

strongest; increases max contractile force

muscle tone

-contracted state

-spinal reflexes (fibers alternatively activated in response to input from stretch receptors in muscles)

-firm, healthy,ready to respond

isotonic contraction

shortens, muscle tension exceeds load

isometric contraction 

no shortening; tension increases 

-load is greater than the maximum tension muscle can generate (no shorten or lengthen)

concentric contraction (isotonic)

shortens; works

eccentric (iostonic)

lengthens; generates force

electrochemical and mechanical events

isotonic - actin filaments shorten and move

isometric- cross bridges generate force, but actin filaments dont shorten (myosin heads spin on binding site)

ATP for muscle contractions

-providing energy ( ATP supplies the energy needed for muscle fiber to: move, detach, pump calcium, pump na+ out, K+ in)

-available stores at ATP depleted

-only source (ATP); regenerate quick

aerobic

muscle contracts using aerobic paths (light/ moderate activity)

anaerobic 

muscle metabolism converts to anaerobic paths 

muscle fatigue

inability to contract despite continued stimulation

-causes

• imbalances with K+, Na+, Ca2+ levels changing, disrupting membrane potential

• inorganic phosphate from CP and ATP breakdown

• decreased ATP and increased SR magnesium (voltage, sensitive)

• low glycogen

-lack of ATP (rare occasion)

excess postexercise oxygen consumption

-return pre-exercise state

• oxygen reserves are replenished

• lactate→ pyruvate

• glycogen stores replaced

• ATP and creatine phosphate reserves are resynthesized

-replenishing steps require extra O2 which is excess postexercise oxygen consumption (EPOC)

velocity and duration of contraction

-speed of contraction (slow/fast)

-pattern of electrical activity of motor neurons

-metabolic pathways used for ATP synthesis

-oxidative :aerobic

-glycolytic: anaerobic

aerobic repiration

-mitochondria

anaerobic respiration

-no mitochondria

slow oxidative 

low intensity (posture)

fast oxidative

medium intensity (walking)

fast glycolytic

intense/powerful (hitting baseball)

load

muscles contract fastest when no load is added

recruitment 

the more motor units contracting, the faster and more prolonged the contraction

smooth muscles

-not in heart

-sheets of tight fibers (2 layers)

-longitudinal and circular

-spindle-shaped

-lacks a nucleus and striations tissue sheaths