Kin2230-Muscles.pdf

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Department
Kinesiology
Course
Kinesiology 2230A/B
Professor
Glen Belfry
Semester
Fall

Description
MUSCLES There are more than 430 muscles in the body. Muscles are organized in opposing pairs. For every movement about a joint, you need an opposite muscle to move it back to its resting position. Remember, muscles only contract! Types of Muscles • Skeletal (**We are most concerned with skeletal muscle) • Voluntary muscle • Controlled consciously • 3 different types of skeletal muscles • Different nomenclatures exist, but they’re all based on metabolic characteristics • Eg. SO, FOG, FG; ST, FTa, FTb; Type 1, Type 2a, Type 2b • Slow oxidative: contract slowly; primarily oxidative (aerobic) • Fast oxidative glycolytic: have the ability to produce energy in significant amounts oxidatively (aerobically) as well as produce energy glycolytically (anerobically) • These fibers provide a huge performance advantage - we can use energy both aerobically and anaerobically • Fast glycolytic: very little oxidative (aerobic) capacity; able to produce tremendous amounts of power; will produce lactate • The time that these fibers can work at maximal rates is very limited • Has an origin and insertion, on either side of a joint • Cardiac • Controls itself with assistance from the nervous and endocrine systems • Only found within the heart • Myocardial muscle cells attach to adjacent myocardial cells - they do not have an origin and insertion point • Smooth • Involuntary muscle • Controlled unconsciously • In the walls of blood vessels and internal organs **Muscle fibers are a single cells made up of myofibrils (different types of proteins - actin and myosin) Connective Tissue •Epymisium: tissue surrounding the whole muscle •Perimysium: surrounds approximately 150 fibers •Endomysium: separates individual fibers •Fasiculus: a group of fibers •Connective tissues from the different coverings of the muscle (epymisium, perimysium, endomysium) come together as the tendon that attaches to the bone •We need to be able to transmit the force of the muscle contraction to the bone in order to move the joint •As the myofibrils contract, the force of contraction transfers through the entire muscle and eventually to the bone •Muscles attach to bones via tendons •Muscles have two attachments: the origin (non-movable) and the insertion (movable) Scaffolding Proteins • Several scaffolding proteins are also involved in muscle structure • They give the muscle strength and form - they help muscles keep their shape • Scaffolding proteins are also binding sites for proteins involved in signaling cascades • Binding sites are located in the area between titin and nebulin • Titin - associated with myosin filaments • Nebulin - associated with actin filaments Dystrophin Dimer and Muscular Dystrophy LOOK THIS UP! • The dystrophin dimer is the attachment that allows the contraction of actin/myosin to be transferred to the plasmalemma (ie. the transferring of force to the whole muscle) • Muscular dystrophy is a degenerative disease of the muscle - progressive muscle weakness • Dystrophin dimer begins to disintegrate • Actin/myosin filaments are still fully functional (they can still shorten) • We have lost the link to the outer membrane of the cell (ie. we have lost the ability for the whole muscle body to contract and shorten) • Shortening and contraction is not relayed through to the muscle and bone An Individual Sarcomere • A sarcomere spans from one Z-line to another Z-line • Z-lines are anchor points to adjacent sarcomeres • The function that the muscle is required to perform (ie. the force being generated) will dictate how many sarcomeres will be involved in that particular movement • Nebulin lies on either side of the actin filaments • Titin lies along the myosin filaments • The M-line is the middle anchor point within an individual sarcomere • We get shortening from the Z-line to the M-line This is a muscle fibre cross-section. It shows you how many muscle fibres are associated with a muscle. Each of these muscle fibres can act independently; we don’t need to recruit all muscle fibres for each movement. The contractile proteins within a muscle are: • Thick filament - myosin • Thin filament - actin, troponin, tropomyosin • Tropomyosin wraps around the actin filament • Troponin molecules cover the sites where myosin heads will bind with the actin Alpha motor neurons are the type of neurons that elicit shortening of the actin/myosin complex. Initiation of Muscle Contraction •Nerve is depolarized •Action potential moves along nerve •Action potential crosses neuromuscular junction •Action potential enters muscles and causes calcium release Action Potentials •Action potential: a rapid and sustained depolarization of the nerve membrane •Membrane must first reach threshold before an action potential can occur •Action potential is propagated along the nerve •Depolarization refers to the change in polarity from negative to positive •Repolarization refers to the change in polarity form positive to negative •Threshold - a certain degree of movement of charges that must occur across the membrane of the muscle cells before an action potential can be generated Resting Membrane Potential • RMP: resting membrane potential • Negative charge inside the cell (-70mV)...resulting from: • Higher membrane permeability to K+ than Na+ - more K+ in the cell, more Na+ outside the cell • Membrane proteins are negative and impermeable to membrane - this is where the negative charge within the cell comes from What does this mean? • Cl- repelled exits • Positive charge outside the cell - associated with Na+ Generation of an Action Potential What triggers this •Start with a depolarization - change in polarity across the cell membrane from the inside of the depolarization? cell to the outside of the cell •As the AP is propagated, the change in polarity affect voltage-gated Na+ channels - sodium channels open - influx of sodium into the cell •Membrane has high permeability to potassium - even at rest, K+ is high within the cell •For a brief moment, we have the accumulation of Na+ and K+ within the cell - this gives us the actual AP - movement of positive charge (in the form of Na+ from the outside of the cell into the cell) •As potassium leaves the cell (through channels, due to increase membrane permeability), this brings us back to that negative environment within the cell •But now we need to get the potassium back into the cell and sodium out of the cell before an action potential can be expressed at this location again • We use to the Na/K pump - need ATP for this to work because we’re pumping against the concentration gradient • Pumping K+ back into the cell and pumping Na+ out of the cell read up about this! • hyperpolarization, refractory period • Propagation • Change in polarity is going to open up the adjacent sodium channels • Propagation is the change in polarity along the nerve tissue • Change in polarity is a change in voltage - remember, these sodium channels are ‘voltage-gated’ Nerve Function • Myelinated fibers (have a myelin sheath) and unmyelinated fibers (no myelin sheath) • Myelinated sheath allows for faster conduction of AP along the axon • Ie. Action potentials are faster in myelinated fibers compared to unmyelinated fibers • Myelin sheath provides insulation - prevent loss of charge/ polarity to surrounding environment (predominantly water) • Unmyelinated axons propagate APs at a much slower rate • Myelin sheath: 80% fat/lipids, 20% protein • Nodes of Ranvier: the short spaces in between adjacent sheathes Saltatory Conduction • In myelinated axons, action potentials do not propagate as waves, but recur at successive nodes and in effect “hop” along the axons watch the video • **KNOW the difference between continuous conductions http:// (unmyelinated) and saltatory conduction (myelinated) www.blackwellpublishing.com/ • There is a period of time, as the AP travels along the nerve, where you’re unable to generate an AP matthews/actionp.html • When the polarity is reversed, you can’t initiate an AP • This is called the refractory period • Need to wait for complete repolarization before you can conduct the next AP • Saltatory conduction: refers to the movement of an AP along a myelinated fiber • AP can ‘hop’ from one myelinated section to the next myelinated section • Myelinated fibers are found within the nervous system when an impulse must travel long distances or when fast action of a particular muscle group is required (ie. quadriceps muscle and hamstring muscle groups for running) • The gaps between myelin sheath cells are called Nodes of Ranvier • The electrical impulse jumps from one node to the next in 120m/s - this is called saltatory conduction • Large diameter nerve fibers conduction impulses faster than smaller diameter fibers but are harder to activate • Large muscle groups will have much larger nerve fibres innervating those muscle, but they will also require much more stimulation to activate these fibers • Notice the difference in insulating qualities between these different fibers Synapses • Synapses are interfaces between the nerve fiber and the subsequent tissue (or subsequent nerve) • A synapse carries information from one nerve to another • The information may be inhibitory or excitatory • Summed effect of inputs determines whether or not an action potential occurs • Spatial summation - impulses from several neurons at the same time • Increase frequency of stimulation from different nerve fibres • Input coming down different dendrites • Temporal summation - several impulses from one neuron over time • Input coming down the same dendrite • Frequency of input from one nerve fiber • Once we become proficient at particular movements (ie. in sports) - the things you’re required to do have become so automatic, don’t need to use our brain to coordinate movements - they become spinal cord reflexes • Synapses are specialized junction cells of the nervous system that signal to each other and to non-nerve cells such as those in muscles or glands • Chemical synapse: eg. release of chemicals at the NMJ • In the heart, gap junctions are a form of electrical synapse • Although the heart has innervation from the sympathetic NS, it is able to propagate the action potential the myocardium itself - myocardium will spontaneously depolarize and the depolarization can pass from one myocardial cell to the next through these gap junctions Transmission of Nerve Impulse at the Neuromuscular Junction watch the video • “How does the body change the stimulus so it can go from a nerve fibre to a muscle fibre?” http:// • At the NMJ, you still have the AP arriving at the nerve terminal • Voltage-gated channels specific to calcium open and Ca2+ flows into the presynaptic terminal highered.mcgra • Calcium influx causes release of ACh from vesicles • ACh is released into the presynaptic cleft w-hill.com/sites/ • ACh moves across the junction • SODIUM channels open in response to ACh - **These sodium-channels ARE NOT voltage-gated** • ACh binds to receptors on sodium channels, which enables sodium to enter the muscle membrane - causes 0072437316/ depolarization of the muscle membrane • The surface of the muscle cell has the ability to depolarize and propagate an action potential (like it would in a student_view0/ nerve cell) chapter45/ • ACh-esterase - splits ACh into acetic acid and choline • Choline is reabsorbed and binds to acetic acid and is stored as ACh until the next stimulus is received • The action potential is now in the sarcolemma membrane...it will travel the length of the muscle fibers animations.html • As it does so, it will travel down the T-tubules, which allows entry of the AP within the muscle fiber itself • Intracellular tubule system - Transverse Tubule System # • Runs perpendicular to myofibrils • Like the vasculature • Surround individual muscle fibers • Partial function is spreading action potential • Depolarization from outer regions to deep areas • Allows AP to get into all areas of the muscle • Once in the T-tubules, the action potential will travel down the sarcoplasmic reticulum...this will lead to the release of Ca2+ • Sarcoplasmic reticulum • Extensive network of tubular channels • Runs parallel to myofibrils • Each tubule terminates in a saclike vesicle that stores Ca2+ • Depolarization triggers the release of Ca2+ which activates actin filaments • Contraction will be maintained until Ca2+ is reabsorbed into the SR • During fatigue...as pH changes, Ca2+ release becomes inhibited and Ca2+ uptake becomes inhibited • Tetanus occurs - muscle is neither contracting or relaxing **One muscle fiber can be 12cm long!!** (Diameter of muscle fibers is quite small) watch the video Spinal Cord Injuries http://highered.mcgraw- hill.com/sites/0072437316/ student_view0/chapter45/ animations.html • What are the effects of location of the injury on function?? • The higher the injury in the spinal cord...greater limb dysfunction you’re going to see • Cervical injury - lose all limb function, still have ability to see, think, breathe • Thoracic injury (mid-chest, abdominal) - lose lower limb function • Lumbar injury - some minimal leg function • Coccyx - some dysfunction in the legs • Cervical, thoracic, lumbar, sacral injuries.... • Lose function in the areas below the injury Role of Action Potential and Ca2+ in Muscle Contraction •The SR functions to... •1) Uptake calcium from the sarcoplasm •2) Release calcium into the sarcoplasm to initiate contraction •3) Sequester it during relaxation •T-tubules are connected to the SR (this is where Ca2+ is stored) •Ca2+ release leads to contraction of the muscle •Contraction will continue to occur as long as there is Ca2+ •Ca2+ reabsorption will stop contraction **What happens when Ca2+ is released from the sarcoplasmic reticulum??** • We know that ATP is required for 1) muscle contraction... • But a significant amount of ATP is also required to 2) sequester Ca2+ back into the sarcoplasmic reticulum • Ca2+ ATPase pump -functions to pump back into SR • ATP is also used in nerve fibers to 3) power the Na+/K+ pump which is involved in repolarization of the nerve membrane • >> Summary picture: 1. Synaptic transmission at the NMJ 2. AP travels along muscle membrane and down T-tubules 3. AP reached SR and triggers release of Ca2+ 4. Ca2+ facilitates actin-myosin interaction 5. Muscle contraction 6. Ca2+ sequestered back into SR through the Ca2+ ATPase pump Muscle Triad • On both sides of a T-tubule are dilated end sacs of the sarcoplasmic reticulum called the terminal cisternae • A T-tubule together with its two terminal cisternae is called a muscle triad • Within the muscle... • >> Picture shows T-tubule in between 2 areas of sarcoplasmic reticulum, which make up a muscle triad Mechanism of Muscular Contraction -SLIDING FILAMENT HYPOTHESIS • We’re looking at the movement of actin and myosin filaments to shorten the muscle....transfer of force through connective tissue that connect to bone and result in in a movement of a joint • Z-line - outside anchor points; separate adjacent sarcomeres; make up the borders of the sarcomere • H zone - within the A-band; zone of myosin that is NOT superimposed by the thin filaments • H zone will get smaller and eventually disappear with contraction • Actin are moving towards each other • I-band - zone of actin that is NOT superimposed by thick filaments • Pulling z-lines together, pulling adjacent sarcomere towards each other • I-band gets smaller during contraction • A band- contains the entire length of myosin • **THIS DOES NOT CHANGE!!! - length of myosin itself does not change!!! • Muscle is pulling in both directions - you’re pulling on the origin and pulling on the insertion • Both sides coming towards the central Z-line • Remember, within a muscle there are tens of thousand of sarcomeres that are all shortening • Myosin heads are swiveling and pulling the actin Not really sure what the main point of this slide is...? filaments towards each other • Different areas within the muscle are contracting at different times; different cross-bridges are going to be formed at different times? GO OVER THIS!! Mechanism for Myosin-Actin Interaction watch this video • Tropomyosin winds around the actin filaments and covers the myosin-binding http://biology.berkeley.edu/ bio1a/topic/Muscle_Motility/ sites on the actin filaments actin_myosin.html • There are only specific areas on the actin where the myosin heads will bind • Troponins are attached to the tropomyosin and contained binding sites for Ca2+ • Mechanism begins when the Ca2+ binds to the troponin • Tropomyosin shifts to uncover binding sites on actin so that myosin head can now interact with the actin filament • Magnesium ion activates myosin head causing release of phosphorus ion from ATP leaving ADP and causing the myosin head to contract • ATP binds to myosin head - this releases the myosin head from the actin • Mg2+ stimulates ATP hydrolysis! - myosin head reset to extended length • Release of phosphate initiates the power stroke • ADP is released by conformational change of the power stroke • Myosin is then in a flexed, actin-bound state until a new ATP binds (ie. think of rigor mortis occurring when ATP is depleted) • Energy is provided for cross-bridge movement when P splits from ATP • Detachment of myosin cross-bridges from actin filament occurs when ATP is joined to actomyosin complex -> returns to its original state • Key enzyme:myosin ATPase - splits ATP making energy available for contraction • Fast twitch fibers have increased activity of myosin ATPase • Amount of myosin ATPase will determine the twitch characteristics of the muscle fiber • The more of this enzyme is available, the more ATP can be hydrolyzed, the more energy can be released - this is going to be a faster twitching fiber Summary • Actin and myosin proteins... • Myosin is the thick filament to which myosin heads are attached • Troponin and tropomyosin part of the actin - these regulate contact between myosin and actin filaments during contraction • Troponin - increased affinity to Ca2+....Ca2+ and troponin triggers myofibrils to interact and slide past each other (Mg activates myosin-ATP hydrolysis) • Tropomyosin - prevents premature coupling of actin/myosin • Sarcomere - repeating unit between two z-lines...functional unit of the cell Important Contractile Properties • Length-tension relationship • There is an optimal muscle length for maximum force production • Functional characteristic of the muscle - related to number of cross-bridges can be formed • Biomechanics perspective - there are certain limb/joint angles that will allow you to generate the most amount of force • If the muscle is in a lengthened position... • This is a very weak position • Fewest cross-bridges being made - remember, more cross-bridges = more force • Low force at full extension • If the muscle is in a shortened position... • All the cross-bridges that can be made have been made - you can’t generate any more force • Low force at full flexion •Trying to stay away from limb angles that will result in a lengthened muscle or avery shortened muscle •With these maximal positions we can generate the most amount of force - in sports, we’re concerned with what angles and what limb positions are the best and then trying to fit this into different techniques in sports •90-120 degrees is optimal... •All muscle groups act in a similar fashion •Most powerful in this mid-range • Force-velocity relationship • Highest force is generated at the slowest velocity - related to the time it takes for cross-bridges to be formed • 1) Increased velocity...decreased time for cross-bridge formation, less force • As velocity increases, the force you can generate decreases • 2) Greater force...need to recruit more fibers and make more cross- bridges • 3) Greater force...fibre shortening times are longer • Force you can generate is dictated by the number of cross-bridges you can make - it takes a finite amount of time for the cross-bridges to be made • Poweris defined as force per unit time • POWER = [force x distance (work)] / time • To be more powerful, you’re doing work in a shorter time - this is important in a lot of sports! • When do we generate the most power??? - mid-range velocity • Isometric contraction - no change in length • Can produce a tremendous amount of force • As the muscle shortens and moves faster, the less force you will be able to generate • You can generate a lot of force if you go slowly • If you want to generate a lot of force, you have to slow down velocity • Slower movement = can form more cross-bridges • Faster movement = less time to make cross-bridges, can’t generate as much force • Looking at the different velocities that are capable in the different fiber types • ST = slower velocity • FT = faster velocity • Related to amount of myosin ATPase in the muscle itself • more ATPase = release more energy faster = more energy per unit time = generate more power • LENGTH-TENSION: Looking at the angle of the joints...trying to find angles that give us the most amount of force • First picture: all her joint angles are in the optimal position to produce the maximal amount of force • Second picture: now the quadriceps and gastrocnemius are in a lengthened position, which means they are going to be really weak...in this position, movement is very slow •FORCE-VELOCITY •Discus throwing - all these athletes are huge! •Looking at power sports - why is it important to be big?? •With increased velocity you’re going to make fewer cross- bridges; fewer cross-bridges means you’re generating less force •If you’re bigger, you’re going to have more cross-bridges (more contractile proteins) - at high velocities, you’re going to only be using a low percentage of these cross-bridges but because you have so many more to begin with you can generate more force Types of Muscle Contraction • Isotonic - constant resistance (dynamic) • Force remains the same as you go through the motion (eg. climbing a rope) • Isometric - constant length (static) • (eg. rugby scrum) • Isokinetic - constant speed, changing load • Eccentric - lengthening contraction • You’re probably 2-3x stronger eccentrically than you are concentrically • Concentric - shortening contraction • >> This graph is looking at both eccentric and concentric contractions with different velocities • Remember that when velocity is 0, this is an isometric contraction (muscle is contracting but there’s no movement around the joint) • Fast concentric contractions - generating very little force • Fast eccentric contractions - generating lots of force • We can generate much more force eccentrically than we can concentrically • From a practical perspective...if you have a situation where a bigger person is trying to move a smaller person...a smaller person can generate a lot of force if they’re being slowly pushed backwards by a larger person - this is because moving backwards is primarily eccentric (think about your hamstrings lengthening...) and moving forwards is primarily concentric • Eg. hockey, basketball (guarding), football (offensive linesman) Motor Units • A motor unit is a motor nerve and all the muscle fibres innervated by it • May be spread throughout the muscle - in many other species (ie. rodents), they tend to have fairly homogenous muscle groups • All fibers within a given motor unit share the same characteristics • Ie. same metabolic characteristics/profile - they’re all going to be ST/FT etc. because it is dependent on innervation - and they’re all innervated by the same nerve... • Motor units are of different sizes and allow graded contraction - this is related to function • Small motor units will have a small number of fibers associated with a particular motor nerve • Eg. Eye movement, typing, writing notes • Number of fibers associated with these motor units is very few, forces generated are very small and these are very precise movements • Large motor units will have hundreds or thousands of fibers being innervated by one nerve • Needing to generate very large amounts of force • Sizes of motor units differ due to fiber size and number • Recruited from smallest to largest he didn’t talk about this in lecture • Fibers in the same motor unit: same enzymatic profile and same twitch characteristics • >> This is picture looking at... • A) One nerve innervating a number of different fibers • B) You can also have a mixture of different fiber types/ motor units within the same muscle matrix - this is what we see in human muscle • ^^ Looking at human muscle...we know that they’re many hundreds of fibers within a muscle • Trying to determine how big a particular motor unit is: • How many fibers are associated with that one particular nerve? • Stimulate the nerve (electrostimulation) for a number of minutes until we’re sure that all the glycogen within the innervated muscle fibers has been utilized • Stained for glycogen • White fibers are those that are glycogen depleted • We can determine which fibers are associated with that particular nerve by picking out the ‘white fibers’ • You can have a large number of muscle fibers being innervated by that one nerve • Remember, function will be dependent on how many fibers are actually being innervated • >> Another example
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