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)