A&P: Skeletal and Smooth Muscle

skeletal muscle

striated, voluntary. attached to skeleton, contraction causes movement of bones

skeletal muscles not attached to bones

tongue, diaphragm

skeletal muscle homeostasis

breathing, procuring food, generation of heat, movement from harm

smooth muscle

not striated, involuntary. walls of hollow organs and tubes (digestive tract, blood vessels, airway, bladder). slow, sustained contractions

cardiac muscle

striated, involuntary. heart, pumps blood

tendon

connective tissue that attaches muscle to bone

skeletal muscle levels of organization

muscle, fascicle, muscle fiber, myofibril, sarcomere, myofilament

fascicle

bundle of muscle fibers wrapped in connective tissue

muscle fiber

a single muscle cell, cylinder shaped, runs length of muscle

myofibril

make up muscle fibers, consist of sarcomeres, banded in appearance

sarcolemma

muscle cell membrane

sarcoplasm

cytoplasm of a muscle cell

sarcomere

contractile unit of a muscle fiber

myofilaments

actin and myosin

z line

a dark thin protein band to which actin filaments are attached, marking the boundaries between adjacent sarcomeres

i band

thin filaments only (light band)

a band

entire length of thick filament (dark band)

h zone

thick filaments only

m line

middle of sarcomere to which the thick filaments are attached

cross bridges

myosin head, which connects thick filaments and thin filaments during a contraction

regulatory proteins

tropomyosin and troponin, regulate interaction of actin and myosin

anchor proteins

anchor cytoskeleton proteins to the sarcolemma, each other, and EC matrix

α-actinin

anchors actin filaments to the Z-line

titin

elastic protein that interconnects Z line to the M line, stabilizes myosin filaments, largest known protein

dystrophin-associated glycoproteins

anchor contractile elements to muscle fiber membrane and muscle

myosin structure

thick filament. tail with two heads, one actin binding site and one myosin ATPase site

cross bridges are oriented

toward the Z line

thin filament consists of

actin, troponin, tropomyosin

actin structure

spherical protein, two strands twist together to form backbone of thin filament

tropomyosin

threadlike protein that spirals around actin. at rest it covers myosin bridge sites to prevent interaction and contraction

troponin

holds tropomyosin in position. 3 subunits, one binds to tropomyosin, one holds tropomyosin on active sites, one binds calcium

when calcium binds to troponin

it changes the protein shape to pull tropomyosin off cross bridge binding sites myosin can interact with actin

neuromuscular junction

junction between a motor neuron terminal and a skeletal muscle fiber

neuromuscular transmission

1. nerve action potential is propagated to the axon terminal

2. depolarization of axon terminal opens voltage gated Ca++ channels and Ca++ enters the cell

3. Ca++ triggers exocytosis of vesicles containing ACh

4. ACh diffuses across the gap and binds to nicotinic cholinergic receptors

5. non-specific cation channels open, large diffusion of Na+ (some K+ out) into the cell cause depolarization to generate EPP

6. EPP opens voltage gated Na+ channels in muscle cell membrane to generate muscle cell action potential

7. ACh is metabolized

acetylcholine (ACh)

choline acetyltransferase combines choline and acetyl-CoA, synthesized and stored in nerve terminal

choline

obtained from diet, transported into nerve terminals

acetylcholinesterase (AChE)

splits ACh, choline is reused

MEPP

miniature end plate potential, generated by spontaneous release of ACh

EPP

end plate potential

respiratory arrest is caused by

continuous depolarization of respiratory muscles or prevention of contraction

black widow spider venom

rapid release of ACh, prolonged depolarization causing respiratory failure

botulinum toxin

blocks ACh release, continuous relaxation. respiratory failure

curare

reversibly binds to ACh receptor, prevents ACh from binding, no muscle contraction. respiratory failure

organophosphates

inhibits AChE, ACh accumulates causing continuous stimulation. respiratory failure

myasthenia gravis

autoimmune disease, immune system produces antibodies against ACh end plate receptors that inhibit or destroy them, muscles become weak

NMBD

neuromuscular blocking drugs

nondepolarizing NMBD

block ACh receptors to relax skeletal muscles. tubocuranine, pancuronium, rocuronium.

depolarizing NMBD

blocks ACh receptos and cause blockage of channel. succinylchloride

excitation-contraction coupling

events that take place from the initiation of the muscle cell action potential to the release of Ca++ from the SR

sarcoplasmic reticulum

specialized endoplasmic reticulum of muscle cells

lateral sacs

expanded regions of sarcoplasmic reticulum, associated with T-tubules and involved in the storage and release of Ca++

T-tubules

extensions of the sarcolemma that extend deep into the muscle cell, action potentials travel down these

muscle cell action potential travels down T-tubule, signal is passed to SR which

opens Ca++ channels, releasing Ca++ into the sarcoplasm

Ca++ release channel

located on lateral sac of SR, open in response to voltage gated activation of dihyrdropyridine receptors to release Ca++ into sarcoplasm

dihydropyridine receptor

voltage gated channels located on T tubules, activated by muscle cell action potentials

steps of Ca++ release

1. muscle cell action potential is propagated down membrane and T tubules

2. depolarization activates dihydropyridine receptors

3. Ca++ release channels open and Ca++ enters cell

4. released Ca++ opens more channels in SR

5. Ca++ initiates contraction

6. Ca++ ATPase pumps Ca++ back into SR

sarcoplasmic Ca++ concentration is a balance of

the rate at which Ca++ enters the cell from the lateral sacs and the rate at which Ca++ is pumped back in

relaxed muscle

cross bridge binding site on actin is physically covered by troponin-tropomyosin complex

excited muscle

Ca++ binds to troponin, troponin-tropomyosin complex is pulled aside to expose cross-bridge binding site. binding of actin and myosin cross bridge triggers power stroke that pulls thin filament inward during contraction

sliding filament theory

filaments do not shorten, only sarcomere length shortens. cross bridge pulls actin and Z lines toward center of sarcomere

cross bridge cycling

1. Ca++ is present, energized cross bridge binds to site on actin

2. power stroke, pull thin filament towards the center of sarcomere, releases ADP and Pi

3. ATP binds to ATPase site on cross bridge, causing detachment and energizing cross bridge

4. energized cross bridge binds to a more distant site, power stroke and cycling are repeated

role of ATP in muscle contraction

binds to ATPase to allow detachment of myosin, splitting of ATP provides energy for crossbridge to carry out another cycle, active transport of Ca++ back into SR

complete shortening

repeated cycles of cross bridges, all power strokes are towards center of sarcomere, cross bridges do not stroke in unision

relaxation of muscle

end of muscle cell action potentials and Ca++ is pumped back into SR

steps in muscle cell contraction

1. AP is propagated down motor nerve fiber to nerve terminal

2. ACh is released

3. ACh binds to nicotinic receptors on end=plate

4. ligand-gated ion channels open and Na+ diffuse in to depolarize end-plate and generate EPP

5. EPP generates muscle cell AP

6. muscle cell AP propagated along membrane and T tubules

7. Ca++ channels open and release Ca++ into sarcoplasm initiating contraction

8. Ca++ pumped back into SR

tension in contractile elements is transmitted to

tendons to move the bones

origin

end attached to more stationary part

insert

end attached to the part that moves

motor unit

motor neuron and all of the muscle fibers it innervates

the more motor units that are activated

the more fibers are contracted and the stronger the contraction

the more frequent the action potentials

the more calcium is released

tetanus

maximal sustained contraction

length-tension relationship

number of cross bridges that can interact with actin

optimum length

the length at which a muscle can exert maximum tension (usual resting length)

isometric contraction

tension developed but no shortening, load is greater than muscle tension

isotonic contraction

muscle tension remains constant and muscle fibers shorten, lift the load

most contractions begin with

isometric until the tension overcomes the load you are lifting and contraction becomes isotonic

load

force exerted on a muscle by an object

the greater the load

the slower the contraction speed

work output of muscles

work=force x distance. energy consumed becomes heat

extension

straightening of a limb

flexion

bending of a limb

sources of ATP

stored ATP and creatine phosphate

creatine phosphate

energy storage molecule in muscle tissue. reacts with ADP to form ATP and creatine, providing immediate supply of ATP for short, high intensity contractile effort

anaerobic glycolysis

provides 2 ATP per molecule of glucose. forms lactic acid which causes muscle soreness. used for short, high intensity exercise

oxdative phosphorylation

provides 32-34 ATP per molecule glucose. used for prolonged, endurance exercise

muscle fatigue

exercising muscles cannot maintain tension due to accumulation of lactic acid or depletion of energy reserves

delay or prevention of fatigue

fibers differ in resistance to fatigue, recruit motor units most resistant, as well as asynchronous recruitment of motor units

neuromuscular fatigue

motor neurons can not synthesize ACh fast enough

central fatigue

occurs when the CNS no longer adequately activates motor neurons

oxygen debt after stopping exercise

continue to breathe deeply and rapidly, ATP restores creatine phosphate, lactic acid to pyruvic acid to ATP or back to glucose

types of muscle fibers

slow oxidative, fast oxidative, fast glycolytic

most muscles contain a mixture of

fiber types in different proportions

mixture of fiber types is determined by

type of activity and genetics

speed of contraction

determined by speed in which ATPase splits ATP

fast twitch

hydrolyzed ATP faster, completes more cross bridge cycles per second and sarcomeres shorten faster

slow twitch

hydrolyzes ATP slowly, slower rate of cross bridge cycles

adaptation of skeletal muscle

type of exercise establishes neuronal pattern of activity and adaptation of muscle fibers

aerobic exercise increases

number of mitochondria and capillaries

high intensity, short duration exercise increases

synthesis of actin and myosin protein, increasing diameter of fast glycolytic fibers