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Chapter 12 Notes

by: MBattito

Chapter 12 Notes BIOL 3160

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These notes cover the material for chapter 12 covered in lecture and from the textbook
Human Physiology
Dr. Tamara McNutt-Scott
Class Notes
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This 10 page Class Notes was uploaded by MBattito on Sunday March 6, 2016. The Class Notes belongs to BIOL 3160 at Clemson University taught by Dr. Tamara McNutt-Scott in Fall 2015. Since its upload, it has received 37 views. For similar materials see Human Physiology in Biological Sciences at Clemson University.


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Date Created: 03/06/16
Chapter 12: Mechanisms of Contraction and Neural Control  Ability to use chemical energy to produce force and movement is resent to a limited extend in most cells o In muscle cells it has become dominant  Force generation and movement by muscle can be used in a variety of ways in the human body o Movement within external environment o Regulate internal environment o Speech o Drawing a picture o Twiddling your thumbs o Typing these notes Structure of Skeletal Muscle  Epimysium: outer sheath formed by fibrous connective tissue fibers within tendon extending around muscle  Fascicles: subdivisions of the muscle body formed by the epimysium extending into it o Perimysium: connective tissue sheath surrounding each fascicle o Myo-fibers: muscle fibers that each fascicle is composed of o Sarcolemma: plasma membrane surrounding the myo- fibers o Endomysium: thin connective tissue layer enveloping the sarcolemma of each myo-fiber  Basement membrane – or basal lamina  Connective tissue of tendons, epimysium, perimysium and endomysium are all continuous  therefore muscle fibers do not normally pull out of the tendon when contracted  Skeletal muscle fibers are multinucleate  Most distinctive feature if their striated appearance produced by alternating dark and light bands o A bands: dark bands o I bands: light bands  Z lines: thin dark lines seen in the middle of the I bands Motor End Plate and Motor Unit  Motor end plate: specialized region of the sarcolemma of the muscle fiber at the neuromuscular junction o Motor neuron stimulates the muscle fiber to contract by liberating acetylcholine at the junction  End plate potential: depolarization at the motor end plate that causes action potential o Depolarization of a motor axon terminal causes exocytosis of ACh into the synaptic cleft  bind to several thousand nicotinic ACh receptors on the motor end plate  binding causes ACh receptor ion channels to open  end plate potential  Motor unit: each somatic motor neuron with all of the muscle fibers that it innervates  Graded contractions: varied number of motor units activated o Activated by rapid, asynchronous contractions for smooth, sustained contraction  Smaller motor unit allows for a finer control of skeletal muscle contraction  Smaller motor unit are activated first and stimulated by lower level excitatory input than larger motor units o Smaller motor units are used most often o Recruitment: process of activating larger and larger motor units  used when contractions of greater strength of required  Two processes occur when you gradually increase the force of a muscle contraction: o Motor units involved are stimulated asynchronously at a greater frequency  summation of contractions o Recruitment of additional larger motor units  Can occur at the same time  Increase the force of contraction Mechanisms of Contraction  Cross bridges between thick and thin filaments cause sliding of the filaments – thus muscle tension and shortening o Activity of the cross bridges is regulated by calcium availability o Availability of calcium is increased by action potentials produced by the sarcolemma  Myofibrils: subunits that compose each muscle cell o ~1 micrometer in diameter o Extend in parallel rows o So densely packed that other organelles are restricted to the narrow cytoplasmic spaces between adjacent myofibrils  Dark A and light I bands are seen within each myofibril and stacked vertically from one side of the muscle fiber to the other o Individual myofibrils are not visible with an ordinary light microscope  entire muscle fiber seems to be striated  Myofilaments: small structures contained in each myofibril o A bands: thick filament  Primarily composed of myosin  H band in the center  M line in the center of the H band o I bands: thin filament  Primarily composed of actin  Z-lines in the center of each I band o I bands overlap A bands at the edges – causes outside of A band to appear darker  H bands: the center lighter region of A bands that contains only thick filament  Sarcomere: smallest contractile unit of muscle o Subunits from Z line to Z line o M line in the center of the sarcomere is produced by protein filaments at the center of the thick filament  Serve to anchor the thick filaments so they stay together during contraction o Titin: largest protein in the human body  Each protein has its terminal end in a Z disc – spring- like portion running through the I band and a longer portion bound to the M line  The spring-like portion is highly folded and unfolds when the sarcomere is stretched  Contributes to their elastic recoil  allows muscle to return to resting length when relaxed  Contraction: refers to the activation of force–generating sites within muscle fibers Sliding Filament Theory of Contraction 1. A myofiber with its myofibrils shortens by movement of the insertion toward the origin of the muscle 2. Shortening of the myofibrils is caused by shortening of the sarcomeres 3. Shortening of the sarcomeres is accomplished by sliding of the myofilaments – the length of each myofilament remains constant 4. Sliding of the filaments is produced by asynchronous power strokes of myosin cross bridges, which pull the thin filaments (actin) over the thick filaments (myosin) 5. The A bands remain the same length during contraction, but are pulled toward the origin of the muscle 6. Adjacent A bands are pulled closer together as the I bands between them shorten 7. The H bands shorten during contraction as the thin filaments on the sides of the sarcomeres are pulled toward the middle Interaction between thin and thick filament  Cross bridges are part of the myosin proteins that extend from the axis of the thick filaments to form “arms” that terminate in globular “heads”  Myosin has 2 globular heads that serve as cross bridges on either side o Each head is oriented opposite of each other so when actin is attached on either side it can pill the actin from each side toward the center  Each myosin head contains an ATP-binding site closely associated with an actin-binding site o Each head functions as a myosin ATPase enzyme o ATP must be split into ADP and P before the myosin heads can bind to actin o The position of the myosin head changes and now has the potential energy required for a contraction  Once the myosin head forms a cross bridge with actin, myosin is dephosphorylated o Causes a conformational change and the cross bridge produces a power stroke – the force that pulls the thi filament toward the center of the A band  After the power stroke, ADP is released and a new ATP is attached so myosin can detach from actin  The cycle will repeat itself to reach required overall contraction  During contraction, only a portion of cross bridges are attached at any given time – thus, power strokes are not in synchrony  Force produced by each power stroke is constant, but when the muscle’s load is greater, the number of cross bridges engaged in power strokes is increased to generate more force Regulation of Contraction:  Regulation of cross bridge attachment to actin is a function of 2 regulatory molecules associated with the thin filament o Tropomyosin: lies within groove between G-actin monomers  Covers binding site for myosin in relaxed muscle o Troponin: 3 protein complex:  TnT: binds to tropomyosin  TnI: inhibits the binding of cross bridges to actin  TnC: binds calcium  Responsible for moving tropomyosin – requires interaction of troponin with calcium  F-actin: actin filament that is a polymer formed of 300-400 G- actin subunits arranged in a double row and twisted into a helix Role of Calcium in Muscle Contraction  In a relaxed muscle calcium concentration in the sarcoplasm is very low o Sarcoplasm: cytoplasm of muscle cell  When a muscle cells is stimulated to contract, calcium concentrations quickly rise in the sarcoplasm o Some of the calcium binds to the troponin causing a conformational change that moves it and tropomyosin out of the way  allows actin to bind to the cross bridge  Calcium is the go signal for contracting – highly regulated  Calcium is only released when a signal is given through a neuromuscular junction  Other reasons to keep calcium levels low: o Signal transduction o Promotes the breakdown of glycogen within the muscle cell so there is glucose for ATP o Calcium and phosphate form crystals that make your bone too hard  Calcium is tightly regulated – observe regulation by 2 intracellular proteins: o Calsequestrin within the sarcoplasmic reticulum o Calmodulin within sarcoplasm Excitation-Contraction Coupling:  Muscle contraction begins when sufficient intracellular calcium levels are reached  Relaxation is produced by active calcium transport out of sarcoplasm and into the sarcoplasmic reticulum o Sarcoplasmic reticulum: modified endoplasmic reticulum consisting of interconnected sacs and tubes that surround each myofibril within the muscle cell  Terminal cisternae: expanded portions of the sarcoplasmic reticulum where most of the calcium is stored in relaxed muscle fibers  Calcium release channels (Ryanodine receptor): membrane channels from the sarcoplasmic reticulum into the sarcoplasm o 10x larger than voltage-gated Ca2+ channels permitting a very high rate of calcium diffusion  Transverse tubules (T tubules): narrow membranous tunnels formed from and continuous with sarcolemma o Open to the extracellular environment through pores in the cell surface and are able to conduct action potentials  Skeletal muscle fibers are electrically activated by the release of ACh from axon terminals at the motor end plate  End plate potentials are produced and generate action potentials  T tubules contain voltage-gated calcium channels (DHP receptors) o Respond to membrane polarization  DHP receptors change shape when T tubules conduct action potentials  direct coupling between these channels on the T tubules and the calcium release channels in the sarcoplasmic reticulum o The channels on the T tubules directly causes the calcium release channels to open  releases calcium into cytoplasm and stimulating contraction  Excitation-contraction coupling: process by which action potentials cause contractions o Electromechanical release mechanism: excitation- contraction coupling mechanism in skeletal muscle  Voltage gated calcium channels are the calcium release channels are physically (mechanically) coupled  DHP is voltage gated  Ryanodine is mechanically gated  Calcium induced calcium release channels: calcium release channels on the membrane of the sarcoplasmic reticulum that open in response to a rise in calcium concentration in the cytoplasm o Most calcium that is released is from these channels  To stop cross-bridge cycle, the production of action potentials must cease o SERCA pumps: sarcoplasmic/endoplasmic reticulum calcium ATPase pumps  Active transport pumps that accumulate calcium so that it is sequestered from the cytoplasm  Prevents calcium from binding to troponin – tropomyosin blocks actin binding site  Requires ATP  Two absolutes you must have for contraction: o Calcium o ATP – not only needed for contraction, but also relaxation in the form of making sure the pumps are running Mechanics of Skeletal Muscle  Skeletal contractions typically produce bone movement at joints, which act as levers to move load against which the muscle tension is exerted o Tension: the force exerted on an object (the load) by the contracting muscle o Load and tension are opposing forces o Load > tension = no movement  Isometric contraction (constant length) – does not mean there is no tension being generated; the cells are still contracting just not sliding o Tension > load = movement  Isotonic contraction (constant tension)  Concentric  Eccentric: lengthening  Series-elastic component: during contraction, non-contractile parts of muscle and connective tissue of tendon are being pulled – have elasticity – when distending force released, then “spring back” to resting lengths  Absorb some of the tension as muscle contractions Muscle Twitch:  Mechanical response of a muscle to a single action potential/electrical stimulus  Muscle contractions are graded responses o In general, muscle contraction can be grades in 2 ways  Changing the strength of the stimulus  Threshold stimulus: weakest stimulation at which motor unit is stimulated to contract  Maximal stimulus: strongest stimulus to recruit all motor units to contract  Changing frequency of stimulation  Latent period: time it takes for the action potential to go from the motor neuron to activate the dhp and get contraction started  Period of contraction: when actin and myosin are interacting with each other  Period of relaxation: point where calcium is being taken off – vacuuming up extra calcium Incomplete and Complete Tetanus:  If 2 identical stimuli are delivered to a muscle in rapid succession, the 2 nd twitch will be stronger than the first  wave summation o Occurs because subsequently induced contractions occur before muscle can relax  summing the contractions  With increasingly faster rate of stimulation, muscle relaxation is shorter and increases calcium – leading to incomplete tetanus  When a “fusion frequency” of stimulation is reached with no visible relaxation between successive twitches complete tetanus is attained Treppe:  Warming up period  make the muscles ready to work  Staircase pattern observed when muscle fibers first stimulated to contract o Stimulus strength constant  Due to: o Increasing amounts of calcium available in sarcoplasm o Heat generated from muscle work increases enzyme efficiency in muscle o Muscle more pliable Force-Velocity Curve:  Lighter objects are moved faster than heavier objects o Inverse relationship between force opposing muscle contraction and velocity of muscle shortening o Lighter object: steep slope o Heavier object: less steep slope  What does this curve represent physiologically? o Actin and myosin interactions cause muscles to move – the shortening velocity is determined by the rate of the cross- bridges undergoing their cycling activity Length-Tension Relationship  Muscle contraction strength can be influenced by a variety of fatos o Fiber numbers activated, stimulus frequency, muscle fiber thickness, length of muscle fiber at rest  An “ideal” resting length for striated muscle fibers that results in maximum force generation Energy Requirements for Skeletal Muscle:  Skeletal muscle cannot store ATP, so it must have metabolic mechanisms in place to meet demand once contractile activity begins  Metabolism of Skeletal Muscle: o Skeletal muscles metabolize anaerobically for the first 45- 90 seconds of moderate to heavy exercise o Aerobic respiration contributes the major portion of the skeletal muscle energy requirements following the first 2 minutes of exercise  Oxygen is important for ATP generation in a working muscle  Observe maximal capacity for aerobic exercise in an individual – dependent on the maximum rate of oxygen consumption by the body  maximal oxygen uptake or aerobic capacity  Lactate threshold: also defines intensity of exercise o Percentage of the maximal oxygen uptake at which a significant rise in blood lactate levels occurs  Oxygen Debt: o Includes oxygen that was withdrawn from savings deposits – hemoglobin in blood and myoglobin in muscle – the extra oxygen required for metabolism by tissues warmed during exercise, and the oxygen needed for the metabolism of the lactic acid produced dring anaerobic metabolism o Repaid by the heavy breathing following exercise Muscle Fatigue:  Defined as any exercise-induced reduction in the ability of muscle to generate force/power (reversible) o Observe increase in extracellular potassium concentration during maximal contraction o Reduces membrane potential, thus interferes with ability to generate action potentials  Causes (due to exercise type): o Depleting of muscle glycogen o Reduced ability of sarcoplasmic reticulum to release calcium o “Others” – increase in phosphate, increase decrease in ATP  In humans, fatigue is experienced before muscles fatigue o Central fatigue: muscle fatigue caused by changes in the central nervous system rather than by fatigue of the muscles themselves  Muscle fatigue has 2 major components: o Peripheral component: fatigue in the muscles themselves o Central component: fatigue in the CNS that causes reduced activation of muscles by motorneurons Types of Skeletal Muscle Fibers:  Skeletal muscle is classified on the basis of contraction speed o Fiber types:  Slow-twitch (type I fibers): suited for prolonged contractions  Intermediate fibers  Fast-twitch (type II fibers): suited for rapid, intense movements  Fibers differ in mechanical and metabolic characteristics  Human muscles are a mixture of fiber types o Gives muscle a range of contraction speed, varying resistance levels to fatigue and performance Muscle Damage and Repair  Observe resident stem cells in skeletal muscle o Satellite cells:  “Leftover” from embryological development  Located outside muscle fibers o Permits some degree of repair and regeneration  Ability declines with age o Sarcopenia: loss of muscle tissue as a normal part of the aging process  Myostatin: transforming growth factor – Beta family, also know as GDF-8 o Paracrine regulator inhibits satellite cells and muscle growth (myokine) Neural control of skeletal muscle and reflexes:  Muscle tone: state of tension in resting muscle  Gamma motor neuron activity maintained to keep muscle spindle under proper tension Cardiac Muscle  Striated, short branched muscle fibers  Electrically coupled via gap junctions o Electrical impulse conducted along axis from cell to cell o Functional syncytium: behave as a single functional unit o Contract to fullest extent  Pacemaker cells o Spontaneously depolarize o Set contractile rate o Modified by autonomic innervation  Excitation-contraction coupling o Calcium induced calcium release  Different from skeletal muscle – no “direct” interaction between T tubules and sarcoplasmic reticulum  Slower process Smooth Muscle  Non-striated o No sarcomeres but actin and myosin are present  Thin filaments are long  Dense bodies  Sites of attachment for thin filaments  Connected by intermediate filaments  Thick filaments vertically stacked  Sliding can occur along entire length of thin filament


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