muscle physiology

Step 3 of Cross Bridge Cycle

"power stroke" triggered and actin filaments are pulled towards center of the sarcomere

muscle contraction: sliding filament mechanism

- Contracting muscle fibers exert a pulling tension, shortening in length - Caused when thick & thin filaments slide over each other - Requires the presence of ATP and is triggered by the presence of Ca2+

cardiac muscle

1 or 2 nuclei; branch; intercalated discs form direct cytoplasmic connection end to end

event 5 at neuromuscular junction

ACh binding opens ion channels that allow passage of Na+ into the muscle fiber and K+ out of the muscle fiber. More Na+ Ions enters than K+ ions exit, producing a local change in the membrane potential (end plate potential

Event 4 at Neuromuscular Junction

ACh diffuses acrosses the synaptic cleft and binds to its receptors on the sarcolemma

event 6 at neuromuscular junction

ACh effects are terminated by its breakdown in the synaptic cleft by acetylcholinesterase and diffusion away from the junction

Step 4 of Cross Bridge Cycle

ATP binds to myosin which detaches myosin from actin

a band (dark)

H zone (thick filaments only)

sarcomeres shorten

I bands shorten; H zones shorten; Zone of overlap increases

Muscle Excitation-Contraction Coupling

This all occurs at a neuromuscular junction. (includes end bulbs of motor neuron, synaptic cleft, and motor end plate) Involves a nerve action potential, end plate potential, and muscle action potential. Acetylcholine is the neurotransmitter (excitatory).

extensibility

ability of muscle to stretch without being damaged

excitability

ability to respond to stimuli

Elasticity

ability to return to original length and shape after contraction

contractile proteins

actin and myosin

Event 1 at Neuromuscular Junction

action potential arrives at axon terminal of motor neuron

event 1 of action potential propagation

an end plate potential generated at neuromuscular junction

Endomysium

areolar connective tissue that wraps around each muscle fiber; contains nerves and blood vessels;

event 3 at neuromuscular junction

ca2+ entry causes ACh (a neurotransmitter) to be released by exocytosis

contraction

cross-bridge cycle and sliding of myofilaments

perimysium

dense irregular tissue that wraps muscle fibers into muscle fascicules

event 2 of action potential propagation

depolarization: generating and propagating an action potential

excitation

events that transmit the action potential along the sarcolemma

myosin

motor protein; thick filament; 2 binding sites

actin

moved by myosin; thin filaments; 1 binding site

skeletal muscle

multinucleated; unbranched

Step 2 of Cross Bridge Cycle

myosin binds to actin, forming crossbridge

Step 1 of Cross Bridge Cycle

myosin head start in cocked position with ADP+P

no ACh or Ca2+

no contration

Epimysium

outmost layer of dense irregular tissue, minimizes friction against bones and other muscles

sarcomeres

repeating unites of myofibrils, and are the functional units of skeletal muscle

event 3 of action potential propagation

repolarization: restoring the sarcolemma to its initial polarized state (negative inside, positive outside)

z-discs

separate sarcomeres

smooth muscle

single nucleus; unbranched

m line

supporting proteins

Contractility

tension generated when muscle forcefully contracts

Tropomyosin

thin filament; blocks myosin binding; bound by troponin

I band (light)

thin filaments only

structural proteins

titin, nebulin, desmin, and dystrophin

troponin

triplet molecules; 3 binding sites; allows myosin binding

regulatory proteins

tropomyosin and troponin

Event 2 at Neuromuscular Junction

voltage-gated Ca2+ channels open. Ca2+ enters the axon terminal, moving down it electrochemical gradient

a band (dark)

zone of overlap (overlap of thick and thin filaments)