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31 Cards in this Set
- Front
- Back
Nerve signal arrices at synaptic knob causing calcium channels to open and calscium ions to enter
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Excitation
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Calcium ions trigger exocytosis of synaptc vesicles which release ACh into synaptic cleft
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Excitation
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ACh binds to receptors on motor end plate allowing sodium ions to enter muscle fiber and potassium ions to leave muscle fiber
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Excitation
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Movement of ions across sarcolemma creates muscle action potential to excite muscle fiber
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Excitation
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Muscle actin potential spreads through T-tubules into sarcoplasm
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Excitation-Contraction Coupling
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Calcium-release channels in sarcoplasmic reticulum open in calcium ions diffues into sarcoplasm
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Excitation-Contraction Coupling
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Calcium ions bind to troponin molecules on thin filaments causing them to change shape
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Excitation-Contraction Coupling
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Troponin-tropomyosin complex shifts to new position exposingmyosin-binding sites on actin filament so cross-bridges can form
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Excitation-Contraction Coupling
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Thin actin filaments slide inward over thick myosin filaments causing sarcomere to shorten
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Sliding filament mechanism
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ATP attaches to ATP-binding site on myosin head and is split by myosin ATPase to energize head
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Sliding filament mechanism
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Myosin head attaches to binding site on actin toform cross bridge
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Sliding filament mechanism
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Myosin head swivels toward center of sarcomere creating a power stroke
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Sliding filament mechanism
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Second ATP attaches to ATP-binding site on myosin head allowing it to detach from actin filament
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Sliding filament mechanism
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Myosin head forms new cross-bridge farther along thin filament to produce another power stroke
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Sliding filament mechanism
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Cycle is repeatred over and over to shorten sarcomere as long as ATP and calcium ions are present
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Sliding filament mechanism
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When nerve signals no longer arrive at NMJ, synaptic knob stops releasing ACh
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Relaxation
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Acetylcholine is broken into fragments by acetylcholinesterase
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Relaxation
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Calcium ions are actively transported out of sarcoplasm and back into sarcoplasmic reticulum where they bind to calsequestrin
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Relaxation
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Calcium ions dissociate from troponin and troponin-tropomyosin complex moves back into position to block myosin-binding sites on actin
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Relaxation
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When a person dies, calcium ions leak into sarcoplasm and bind to troponin to initiate cross-bridge formation triggeing rigor mortis within three to four hours
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Relaxation
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Force of muscle contraction depends on sarcomere length within muscle before contraction begins
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Length-tension relationship
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Maximum tension is developed when resting length of sarcomere is optimal due to degree of overlap between thick and thin filaments
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Lenth-tension relationship
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If sarcomere is over-streched, littl overlap exists between thik and thin filamens and few cross-bridges form and muscle tension falls to zero
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Length-Tension Relationship
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If sarcomere is contracted, too much overlap exists between thick and thin filaments and thick filaments crumple as they are compressed against Z discs and muscle tension falls to zero
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Length-Tension Relationship
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Nerve signal will stimulate individual muscle fiber to contract with less than maximum force so total tension produced depends on frequency of stimulation of fiber
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Motor Units
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Nerve signal will stimulate all muscle fibers in a motor unit to contract in unison
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Motor Units
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Contraction does not always involve shortening muscle but could produce only internal tension
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Isometric and isotonic contractions
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muscle fibers exert constant tension but change lengths as load is moved
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Isotonic contraction
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muscle shorens and pulls on tendon to produce movement and decrease angle at joint
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Concentrc isotonic contraction
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Muscle lengthens to maintain tension as joint angle increases
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Eccentric isotonic contraction
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Musle fibers remain same length but increase tension as load is supported
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Isometric contracion
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