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Movement, Stability, Communication, Control of body openings and passages, Heat Production (as much as 85%). |
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Layer of areolar connective tissue that surrounds muscle fibers. Allows room for blood capillaries and nerves. |
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Group of muscle fibers and their surrounding endomysium. Visible to the naked eye as the muscle's "grain." |
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Connective tissue sheath that surrounds the muscle as a whole. |
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Connective tissue sheath that surrounds and separates fascicles. |
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Separates adjacent muscles. |
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Hypodermis - Separates muscle from skin. Can contain or be dominated by adipose tissue. |
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Collagen fibers of the epimysium are continuous with the periosteum. Red muscle tissue seems to appear directly from the bone. Ex. intercostal muscles. |
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Collagen fibers of the epimysium continue as a strong fibrous tendon that merges into the periosteum of a nearby bone. |
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In skeletal muscle, a single multi-nuclei cell. |
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Excitable – responds to stimuli by changing membrane potential.
Contractile – muscles shorten to produce force. Extensible – muscles can stretch.
Elastic – stretched muscles return to original length. |
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Plasma membrane of a muscle fiber. |
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Cytoplasm of a muscle fiber. |
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Bundles of parallel myofilaments made of actin and myosin. Take up most of the muscle fiber's space and allow for contraction. |
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Red pigment in a muscle fiber that stores oxygen needed for muscle activity. |
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Smooth ER of a muscle fiber. Forms network around myofibrils and stores Ca2+ for muscle contraction. Has end sacs called terminal cisternae that traverse the muscle fiber. Two terminal cisternae are associated with one transverse tubule. |
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Transverse Tubules (T-tubules) |
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Definition
Infoldings of a muscle fiber's sarcolemma that travel throughout the muscle fiber's interior. They allow ECF to get close to myofibrils and the SR. |
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Filaments made of myosin. |
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Filaments made of actin. Active sites on the actin subunits are covered by tropomyosin. Tropomyosin has a small calcium binding protien called troponin attached to it. |
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Made of titin. They anchor thick filaments to the z-disc. |
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Segment of a myofibril from one z-disc to the next. It is the contractile unit of the muscle. |
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Dark band of thick filaments. Overlaps some thin filaments. |
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Light band of thin filaments. No overlap with thick filaments. |
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A lighter band within the A band where there is no overlap with thin filaments. |
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Dark, narrow band in the middle of an I band. Made of titin and connected to the sarcolemma by way of the cytoskeleton. |
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A somatic motor neuron and all of the muscle fibers it innervates. |
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The synapse between a nerve fiber and a muscle fiber. |
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Depression on the sarcolemma where the axon terminal (synaptic knob) sits. There is a gap between the terminal and the sarcolemma called the synaptic cleft. There are many folds in the motor end plate with many ACh receptors. |
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Steps in the Sliding Filament Mechanism |
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Definition
Myosin begins in a low energy form with the head bent toward the tail, bound to molecule of ATP.
1) (reach) Myosin hydrolyzes ATP. Energy released from ATP changes myosin to a high-energy extended shape.
2) (grab) High-energy myosin binds to actin – forms the myosin-actin cross-bridge.
3) (pull) Myosin returns to the low energy state – the power stroke – myosin bends back toward the tail, pulling actin with it.
4) (release) Myosin binds to new ATP causing it to releases the actin (myosin can’t release actin if there is no ATP – causes rigor mortis after death).
Each myosin can pull 5 times per second. Contraction continues as long as the neuron continues to signal and ATP is available. |
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Definition
Z discs are pulled closer together – makes sarcomere shorter.
I bands get shorter – thin filaments do not change length, but overlap with thick filaments.
H bands disappear – thin filaments pulled together until they overlap the thick filaments.
A bands stay the same – no change in the length of the thick filaments.
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Steps Involved in Muscle Relaxation |
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Definition
1) Neuron stops signaling.
2) Calcium is pumped back into the sarcoplasmic reticulum.
3) Calcium releases troponin.
4) Tropomyosin moves back over the actin to prevent myosin binding.
5) Sarcomeres return to original length. Titin compressed during contraction, pushes back like a spring when myosin releases actin. Contraction of an opposing muscle pulls the muscle back to its original length.
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Steps for Excitation, Coupling, Contraction, & Relaxation |
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Definition
1) signal in the neuron causes release of ACh into the synaptic cleft 2) ACh binds to receptors at the motor end plate of the muscle fiber ACh receptors are ligand-gated Na+ channels that open when ACh binds 3) Na+ rushes into the cell causes change in membrane potential right at the NMJ 4) change in membrane potential opens voltage-gated ion channels lets Na+ in and K+ out and changes the membrane potential near the NMJ opens more voltage-gated ion channels, changes potential a further from NMJ positive feedback mechanism continues to open more channels, cause more change 5) results in an action potential opening of channels and change in membrane potential is positive feedback mechanism spreads along the entire sarcolemma now the muscle is excited, how does this cause muscle contraction? Excitation-contraction coupling: 6) action potential spreads along sarcolemma and down the T tubules 7) opens voltage-gated calcium channel in the T tubules 8) opens ryanodine receptors in sarcoplasmic reticulum ryanodine receptors are calcium channels connected to T tubule channels when T tubule channels are activated, ryanodine receptors open releases lots of calcium into the sarcoplasm 9) calcium binds to troponin 10) tropomyosin moves off the active sites on the actin filaments so myosin can bind Contraction: 11) myosin hydrolyzes ATP and takes high-energy extended shape (reach) 12) high-energy myosin binds to actin (grab) 13) myosin returns to the low energy state and pulls actin with it (pull) 14) myosin binds to new ATP – causes it to releases the actin (release) 15) steps 11-14 repeat until signal to contract stops (or ATP is gone) Relaxation: 16) neuron stops releasing ACh 17) ACh in synaptic cleft is broken down by acetylcholinesterase 18) Na+/K+ pump returns muscle fiber to resting membrane potential 19) calcium is pumped back into the sarcoplasmic reticulum 20) tropomyosin moves back over the actin active sites 21) titin pushes sarcomeres back to original length |
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Mitochondria use glucose and oxygen to produce CO2, H2O, and ATP:
1 C6H12O6 + 6 O2 → 6 CO2 + 6 H2O + 32-36 ATP Glycogen stored in muscle provides glucose and myoglobin provides oxygen. Produces energy for regular activities. Sudden intense activity uses up all the oxygen more quickly than it is replaced. Takes time for respiratory/cardiovascular systems to respond to need for oxygen. Resting muscles have enough ATP for a few seconds of intense activity. |
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Glucose is used without oxygen to produce a little ATP:
1 C6H12O6 → 2 C3H6O3 (lactic acid) + 2 ATP
Very inefficient use of glucose, but provides ATP for 30-40 seconds of intense activity. Allows respiratory/cardiovascular system time to increase oxygen supply. |
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Definition
Steal phosphate from another molecule. A phosphate is transferred creatine phosphate to ADP to make ATP:
creatine-P + ADP → creatine + ATP
A phosphate is transferred from ADP to ADP to make ATP:
ADP + ADP → AMP + ATP
Provides energy for 5-10 seconds of intense activity. |
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Definition
Weakness and loss of contraction due to prolonged use.
Muscles are unable to contract and eventually fail.
Factors contributing to muscle fatigue:
Muscle runs out of glycogen leading to less ATP synthesis.
Less ATP to power Na/K pumps to maintain membrane potential.
Lactic acid lowers pH and inhibits enzymes needed to make ATP.
Neurons run out of ACh to stimulate contraction. |
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Definition
Extra oxygen needed to recover after strenuous exercise.
Need oxygen to:
Synthesize resting levels of ATP and creatine-P.
Turn lactic acid back into glucose in the liver. Replace oxygen reserves bound to myoglobin and hemoglobin.
Supply oxygen for increased metabolic rate caused by activity. |
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