Muscles PART 2.docx

8 Pages
122 Views

Department
Cellular, Anatomical and Physiological Sciences
Course Code
CAPS 391
Professor
Bruce Matheson

This preview shows pages 1,2 and half of page 3. Sign up to view the full 8 pages of the document.
Description
Muscles PART 2 Neuromuscular Junction 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 they innervate. 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. Excitation-Contraction Coupling 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 myofibrils. 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 bridges. 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 actin myofilaments 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 heads. 5) Cross Bridges Release > ATP molecule binds to each of the myosin heads causing them to detach from actin. 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. Muscle Relaxation 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* Muscle Twitch 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 Motor Units 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
More Less
Unlock Document

Only pages 1,2 and half of page 3 are available for preview. Some parts have been intentionally blurred.

Unlock Document
You're Reading a Preview

Unlock to view full version

Unlock Document

Log In


OR

Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


OR

By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.


Submit