Muscles PART 2
Aps carried by motor neurons cause Aps to be produced in muscle fibers based on events of NMJ. Axons
of motor neurons carry Aps from brain/spinal cord to skeletal muscle fibers, branch each to one muscle
fiber to innervate. Near muscle fiber, axon branch forms cluster of enlarged terminals that rest in
invagination of sarcolemma to form NMJ (synapse) > axon terminals/area of muscle fiber sarcolemma
Axon terminal > presynaptic terminal
Muscle fiber > synaptic cleft
Muscle plasma membrane in the area of the junction > postsynaptic membrane (motor-end-plate).
Presynaptic terminal > mitochondria, small spherical sacs (synaptic vesicles).
Synaptic vesicles > contain acetylcholine, organic molecule of acetic acid + choline (neurotransmitter).
Neurotransmitter > substance released from presynaptic membrane, diffuses across synaptic cleft,
alters activity of postsynaptic cell. Stimulate OR inhibit AP in postsynaptic membrane by binding to
ligand gated channels.
When AP reaches presynaptic terminal, voltage gated Ca+ channels open and Ca diffuses into cell.
Causes contents of synaptic vesicles to be secreted by exocytosis from presynaptic terminal into
synaptic cleft. Ach then diffuses across cleft, binds to receptors in postsynaptic membrane. Ligand gated
Na channels open, increase permeability of membrane to Na+. Sodium ions diffuse into the cell, causing
depolarization. If depolarization reaches threshold, AP is generated along postsynaptic membrane.
Ach unbinds from ligand gated Na channels (then close), acetylcholinesterase is attached to postsynaptic
membrane and removes Ach from synaptic cleft by breaking it down to acetic acid + choline. (keeps Ach
from accumulating in synaptic cleft where it would be a constant stimulus to postsynaptic terminal,
producing continuous contractions in the muscle fiber). Ensures only ONE pre and post synaptic AP are
yielded. Choline is symported w/ sodium into presynaptic terminal, recycled to make Ach. Acetic acid
diffuses away from synaptic cleft. Ach reformed within presynaptic terminal using acetic acid generated
from metabolism and form choline recycled from synaptic cleft. Ach then taken in by synaptic vesicles.
Mechanism by which an AP causes contraction of a muscle fiber. (involves sarcolemma, T tubules,
sarcoplasmic reticulum, Ca+, troponin).
T tubules project into tubules, wrap around sarcomeres where actin/myosin myofilaments overlap.
Lumen of T tubules filled with ECF and continuous w/ exterior of muscle fiber. Sarcoplasmic reticulum is enlarged near T tubules (terminal cisternae). T tubule + 2 adjacent terminal
cisternae = triad*
Sarcoplasmic reticulum actively transports Ca+ into its lumen. Concentration of Ca in the sarcoplasmic
reticulum is much higher than sarcoplasm of resting muscle fiber.
E-C coupling > starts at NMJ w/ production of AP in the sarcolemma. AP propagated along sarcolemma
of muscle fiber and into T tubules. T tubules carry AP into interior of muscle fiber, cause Ca channels in
terminal cisternae of the SR to open. Ca channels open, Ca rapidly diffuses into sarcoplasm surrounding
Ca ions bind to Ca binding sites on Troponin molecules of actin myofilaments. Ca-troponin combination
causes troponin-tropomyosin to move deeper into the groove between 2 F actin strands, exposing
active sites on actin myofilaments. Heads of myosin molecules bind to exposed active sites to form cross
bridges. Movement of cross bridges results in contraction *
Cross Bridge Movement
Forces actin myofilament (where myosin molecule heads are attached) to slide over surface of myosin
myofilament. After movement, myosin heads release from actin and return to original position and
forms another cross bridge on different site on actin myofilament, movement, release of cross bridge,
return to original position. (Cross Bridge Cycling – during a single contraction).
LEAD UP TO CROSS BRIDGE FORMATION
1) AP produced @ neuromuscular junction propagated along sarcolemma of skeletal muscle.
Depolarization spreads along membrane of T tubules.
2) Depolarization of T tubules causes gated Ca channels in SR to open, increased permeability of SR
to Ca+ (especially in terminal cisternae). Calcium ions diffuse from SR into sarcoplasm.
3) Calcium ions released from SR bind to troponin molecules. Troponin molecules bound to G actin
molecules are released, causing tropomyosin to move, ecpose active sites on G actin.
4) Active sites on G actin are exposed, heads of myosin myofilaments bind to the, forming cross
One ATP energy required for each cross bridge formation, movement, release.
1) ADP + phosphate bound to head of myosin molecules at rest.
2) Exposure of active sites > Ca binds to troponins, tropomyosins move, exposing active sites on
3) Cross Bridge Formation > myosin heads bind to exposed active sites on actin myofilaments to
form cross bridges, phosphates released from myosin heads. 4) Power Stroke > energy in myosin heads is used to move myosin heads causing actin
myofilaments to slide past myosin myofilaments, ADP molecules are released from myosin
5) Cross Bridges Release > ATP molecule binds to each of the myosin heads causing them to detach
6) Hydrolysis of ATP > myosin ATPase portion of the myosin heads split ATP and ADP and
phosphate, which remain attached to the myosin heads.
7) Recovery Stroke > heads of myosin molecules return to resting position, energy Is stored in
heads of myosin molecules. If Ca are still attached to troponins, cross bridge
formation/movement are repeated. Cycle occurs during muscle contractions. Not all cross
bridges form/release simultaneously.
Active transport of Ca back into SR
Ca concentration decreases in sarcoplasm, ions diffuse away from troponin, troponin-tropomyosin
complex re-establishes its position, blocks active sites on actin molecules. Cross bridges cannot
reform, muscles relax.
Takes longer to relax than contract > reuptake of Ca by active transport takes longer than diffusion
of Ca, requires ATP*
Single, brief contraction/relaxation cycle.
Lag phase > time between application of stimulus to motor neuron and beginning of contraction
Contraction phase > time during which contraction occurs
Relaxation phase > time which relaxation occurs
Single motor neuron + muscle fibers it innervates, vary based on # of muscle fibers they contain,
sensitivity to stimuli for contractions
# of motor units > delicate/precise movements = less muscle fibers, less precise/more powerful =
more muscle fibers. Fewer fibers in motor units of muscle = greater control
Stimulus strength/motor unit response > Force of contraction increased in SUMMATION: increasing
force of contraction of muscle fibers within muscle, and RECRUITMENT: increasing number of
muscle fibers contracting.
Treppe > stimulated muscle fiber when stimulated contracts with greater force with each
subsequent stimulus (in muscle fiber that has rested for a long period), muscle is maximally stimulated at low frequency, allows complete relaxation between stimuli, successive contractions
are stronger and stronger.
Treppe > increased Ca levels around myofibrils. Ca released by first stimulus not completely taken
up by SR before second stimulus (releases additional Ca). Ca concentration in sarcoplasm increases
slightly during the first few muscle contractions, makes contraction more efficient (more ions
available to bind to troponin). Warming up * inc blood flow to muscles, increased heat production.
Multiple-motor-unit summation > relationship between increasedstimulus strength + increased # of
contracting motor units. (force of contraction increases as more are stimulated).
Subthreshold Stimulus > not strong enough to casue AP in any axon in a nerve, NO contraction
Threshold Stimulus > (increased stimulus), strong enough to produce AP in single motor unit axon,
all fibers of motor unit contract.
Submaximal Stimuli > progressively stronger stimuli, produces AP in axons of additional motor units.
Maximal Stimuli > produces Aps in axons of all motor units of that muscle.
Stimulus Frequency and Whole Muscle Contraction
AP is completed before contraction phase is completed. Relaxation of muscle fiber is not required
before second AP can stimulate second contraction. Frequency of Aps increase in muscle fiber,
frequency of contraction increases until period of Sustained Contraction (TETANUS)
Incomplete Tetanus > muscle fibers partially relax between contractions
Complete Tetanus > muscle fibers produce APs quickly, no relaxation occurs
Multiple Wave Summation > frequency of contractions increases, increased tension produced.
Sarcoplasm and CT of muscle have some elasticity. During each muscle twitch, some tension of
contracting muscle fiber is used to stretch elastic, the rest to lift the load. Relaxation starts before
elastic components are stretched. Muscle stimulated by high frequency, elastic e