Muscular System

general structure and physiology

3 types of muscular tissue

skeletal

cardiac

smooth

skeletal muscle tissue

only voluntary muscle, most skeletal muscles move bone

striated— alternating light and dark bands

functions of muscular tissue

producing body movement (walking/running/etc.)

stabilizing body positions (posture)

moving substances within the body (heart pumping, digestive tract)

generating heat (shivering)

properties that enable muscles to function

excitability

contractility

extensibility

elasticity

excitability

ability to respond to stimuli

contractility

ability to contract forcefully when stimulated

extensibility

ability to stretch without being damaged

elasticity

ability to return to an original length

epimysium

outermost layer that surrounds numerous bundles of fascicles (dense irrefular connective tissue)

perimysium

separates 10-100 muscles into bundles called fascicles

endomysium

separates individual muscle fibers from one another (areolar loose connective tissue)

fascia

sheet of connective tissue that separates neighboring muscles or muscle groups from each other and the subcutaneous tissue

• lines body wall and limbs

• surrounds and supports muscles and other organs

skeletal muscle cells

• arise from mesenchyme as myoblasts

• replicate then fuse to form mature muscle fiber (do NOT do mitosis)

• same number of cells as at birth throughout lifetime

• has hundreds of nuclei

indirect attachment (tendon)

bridges the gap between muscle ends and bony attachment

ligament

a cord that attaches a bone to another bone

aponeurosis

broad, flattened tendon

somatic motor neuron

neurons that stimulate skeletal muscle to contract

direct attachment (fleshy)

no tendon between muscle and bone (little separation)

muscle seems to emerge directly from the bone

muscle origin

bony attachment at stationary end of muscle (nonmoveable end)

muscle belly

thicker, middle region of muscle between origin and insertion

muscle insertion

bony attachment to mobile end of the muscle (moveable end)

action

the effects produced by a muscle (to produce or prevent movement)

prime mover (agonist)

muscle that produces most of the force during join action

synergist

muscle that aids the prime mover

• stabilizes the nearby joint

• modifies the direction of movement

antagonist

opposed the prime mover

• relaxes to give prime mover control over action

• prevents excessive movement and injury

antagonistic pairs

muscles that act on opposite sides of a joint

fixator

muscle that prevents movement of bone

intrinsic muscles

contained within a region, such as the hand (in the structure they’re controlling

• both origin and insertion are in the same region

extrinsic muscles

act on a designated region, but has its origin somewhere else (found outside the structure it controls)

sarcolemma

plasma membrane of muscle fiber

transverse tubules

tunnel-like extensions of the sarcolemma of muscle fiber

sarcoplasm

cytoplasm of muscle fiber

myoglobin

a cytoplasmic protein that binds oxygen

glycogen

a polymer of glucose

sarcoplasmic reticulum (SR)

a network of membranous sacs around the myofibrils

• stores calcium ions

myofibrils

contractile organelles

3 proteins of myofibrils and their functions

contractile proteins

• generate force during contraction

regulatory protein

• switch the contraction process on and off

Structural protein

• align the thick and thin filaments properly

• provide elasticity/extensibility

• link myofibrils to sarcolemma

contractile proteins

myosin

actin

myosin

thick filaments

• function as motor protein

• convert ATP to energy of motion

• heads of myosin go outward to grab

actin

thin filaments

• provide the site for the myosin head to grab onto

• tropomyosin and troponin are also part of the thin filament

structural proteins

titin

dystrophin

titin

stabilize the position of myosin (elasticity)

dystrophin

links thin filaments to the sarcolemma

A-Band

both zones of overlap and H-band (dark area in center)

H-band

just myosin (on either side is a zone of overlap)

I-band

actin (light areas)

Z-disc

the thick dark line running down the center of the I-band

• also the end of the sarcomere

M-line

midline

regulatory proteins

tropomyosin and troponin

tropomyosin

covers the myosin binding sites, keeps myosin from engaging with the actin

troponin

binds to tropomyosin

• the presence of calcium causes tropomyosin to uncover the myosin binding sites, allowing contractions to start

in the presence of Ca++

• myosin heads attach to and progressively pull the thin filaments toward the center of the sarcomere

• leading to shortening the entire muscle (contraction)

synaptic end bulb

end of the nerve that triggers muscle contraction

synaptic cleft

space between the nerve and the muscle

synaptic vesicles

sacs suspended in the synaptic end bulb containing molecules of the transmitter acetylcholine (Ach)

neuromuscular junction (NMJ)

where the synaptic bulb and sarcolemma communicate with each other

neurotransmitter

chemical released by the initial cell communicating with the second cell

motor end plate

the region of the muscle cell membrane opposite the synaptic end bulbs that contain the acetylcholine receptors

STEPS when a nerve impulse triggers a muscle action potential

1. release acetylcholine (ACh)

nerve impule arrives at synaptic end bulbs and causes the synaptic vesicles to release ACh into the synaptic cleft.

2. activation of the ACh receptors

binding of ACh to the receptor on the motor end plate opens an ion channel that allows flow of Na+ to the inside of the muscle

3. production of muscle action potential

this Na+ flow triggers a muscle action potential that causes the Ca++ to be released from the sarcoplasmic reticulum

4. termination of ACh activity

ACh effects only last briefly because it is rapidly broken down by acetylcholinestrase (AChE)

• AChE breaks down ACh which closes the Na+ channel which then ceases the release of Ca++

Botulinum toxin (neuroparalyzer)

blocks release of ACh from synaptic vesicles (no signal = no contraction)

is also used as medicine and cosmetic treatment

curare

sits on Na+ channels blocking ACh from binding

• ACh is still released but without it being able to bind there is still no muscle contraction

Derivatives of this are used in surgery to relax muscles

anticholinesterase

slow actions of acetylcholinesterase adn reomval of ACh

• can strengthen weak muscle contractions

lots of ATP is needed for…

power the contraction cycle

pump Ca++ into the sarcoplasmic reticulum

3 ways muscle fibers can get ATP

1. creatine phosphate (substrate level phosphorylation) (makes 1 ATP)

2. anaerobic cellular respiration (fermentation) (makes 2 ATP)

3. aerobic cellular respiration (makes about 30-34 ATP)

substrate level phosphorylation

enzyme binds to ADP and another chemical with a phosphate

• the phosphate comes off and joins ADP forming ATP

2 enzyme systems that control phosphate transfers

1. Myokinase— transfers phosphate from one ADP to another, converting the latter to ATP

2. Creatine kinase— obtains phosphate from phosphate-storage molecule, creatine phosphate, and gives it to ADP

creatine phosphate

first and quickest way to get ATP but lasts the shortest time

• phosphate is taken off the creatine kinase and added to ADP to form ATP

phosphagen system

synthesis of creatine phosphate into ATP (lasts about 3-15 sec)

anaerobic fermentation

muscles obtain glucose (from blood and their own stored glycogen)

• converts glucose to lactate

anaerobic (lactate) threshold

the point at which lactate becomes detectable in the blood (enough ATP for 30-40 sec)

aerobic respiration

activity that lasts longer than half a minute

• pyruvic acid entering the mitochondria is completely oxidized and generates ATP, water, carbon dioxide, and heat

how many molecules of ATP does aerobic respiration yield

30-34

ATP synthesis during exercise order

1. burn through myoglobin to get oxygen

2. use up creatine phosphate (phosphagen system)

3. anaerobic fermentation (glycogen-lactate system)

4. aerobic respiration

muscle fatigue

progressive weakness from prolonged use of muscles

VO2 max

the point at which the rate of oxygen consumption plateaus and does not increase further with added workload.

Excess Post exercise Oxygen Consumption (EPOC)

meets metabolic demand also known as oxygen debt— replace what was used up

• oxygen from myoglobin

• phosphate from creatine phosphate

• oxygen to liver that is disposing of lactate

2 different muscle fibers (dependent on myoglobin content)

red muscle fibers

white muscle fibers

red muscle fibers

darker in color

high myoglobin content

contains more mitochondria

good blood supply

good for aerobic respiration = lasts longer

white muscle fibers

lower myoglobin count

lighter in color

stores lots of glycogen

anaerobic respiration = generates ATP faster

3 main types of fibers:

slow oxidative fibers (slow twitch)

fast oxidative-glycolytic fibers (intermediate fibers)

fast glycolytic fibers (fast twitch

slow oxidative fibers (SO)

smallest in diameter = weakest

red muscle fibers (more myoglobin)

slow speed of contraction and very resistant to fatigue

best for prolonged, sustained contraction (like maintaining posture/endurance)

fast oxidative glycolytic fibers (FOG)

intermediate in diameter (in between)

have lots of myoglobin and blood capillaries (red-pink)

speed of contraction is a little faster

muscle that you train (from getting more mitochondria and generating more ATP)

fast glycolytic fibers (FG)

largest in diameter = strongest, most powerful contractions

low myoglobin and blood capillaries count (white)

few mitochondria

intense anaerobic movements for short duration (heavy lifting)

single nerve impulse produces

a single muscle action potential (same signal every time there is no stronger and weaker signals)

Maximum tensions (force) depends on

rate at which nerve impulses arrive

amount of stretch before contraction

nutrient and oxygen availability

size of motor unit

motor unit

a motor neuron and the muscle fiber it stimulates

• comes out of spinal cord into the muscles forming neuromuscular junctions

twitch contraction

the brief contraction of the muscle fibers in a motor unit in response to an action potential

latent period

the brief delay between the stimulus of the nerve and the muscle contraction

contraction period

calcium binds to the troponin revealing the myosin binding sites on actin and cross bridges are formed

relaxation period

calcium is transported back to SR and the binding sites are covered by tropomyosin as the heads detach from actin

muscle tone

a small amount of tension in the muscle due to weak contractions of motor units

• keeps skeletal muscles firm

• maintains posture

isotonic contraction

tension developed remains constant while the muscle changes it’s length

• body movements and moving objects

concentric

muscle shortens

eccentric

muscle lengthens

isometric contraction

tension generated is not enough for the object to be moved and the muscle doesn’t change length

• holding book steady with your arm outstretched

myasthenia gravis

body attacks the sodium channels (blocking the ACh receptors) which results in less Na+ resulting in less Ca++ which causes a weaker muscle contraction

treatment for myasthenia gravis

cholinesterase inhibitors slows breakdown of ACh allowing it to stimulate the muscles for longer

Duchenne muscular dystrophy

most lethal

sex-linked only found in males caused by mutation in dystrophin gene

• sarcolemma tears every time muscle contracts which forms fat where muscle should be

• no cure— most die by 20

muscle cramps

result of inadequate blood flow, low electrolytes, overuse, or dehydration