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BIOL 273 - Unit 3 - Muscles

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BIOL 273
Vivian Dayeh

Biol 273: Unit 3- Muscle Notes Muscles have two common functions: 1. To generate motion 2. To generate force Muscle Types There are 3 types of muscles 1. Cardiac Muscles: found only in the heart and moves blood through the circulatory system (Cardiac and Skeletal are both striated muscles because they alternate light and dark bands) 2. Skeletal muscles: attached to the bones of the skeleton, enabling these muscles to control body movement 3. Smooth Muscles: the primary muscle of internal organs and tubes, such as stomach, urinary bladder, and blood vessels; functions in influencing the movement of material into, out of, and within the body; not striated due to the arrangement of contractile fibers within muscle cells Cardiac Muscles >involuntary >has features of both skeletal and smooth muscle >striated and have a sarcomere structure >electrically linked together; gap junctions are connected in specialized cell junctions known as intercalated disks >under sympathetic and parasympathetic control and hormone control >most is contractile, but about 1% of the myocardial cells are specialized to generate action potentials spontaneously >the heart has the ability to contract without any outside signals; the signal for contraction is myogenic (originating within the heart muscle itself) >Autorhythmic cells: specialized myocardial cells which produce the signal for myocardial contraction; aka pace-makers because they set the rate of the heartbeat >smaller and contain few contractile fibers >Differences when compared to Skeletal Muscle 1. Cardiac muscle fibers are much smaller than skeletal muscle fibers and usually have a single nucleus per fiber 2. Individual cardiac muscle cells branch and join neighbouring cells end-to-end to create a complex network  Intercalated disks: cell junctions; consist of interdigitated membranes; two components, desmosomes and gap junctions  Desmosomes: strong connections that tie adjacent cells together, allowing force created in one cell to be transferred to the adjacent cell 3. Gap junctions in the intercalated disks electrically connect cardiac muscle cells to one another; allow waves of depolarization to spread rapidly from cell to cell, so that all the heart muscle cells contract almost simultaneously  Cardiac muscle resembles single-unit smooth muscle 4. T-tubules of myocardial cells are larger than those of skeletal muscle, and they branch inside the myocardial cells 5. Myocardial SR is smaller than that of skeletal muscle, reflecting the fact that cardiac muscle depends in part on extracellular Ca2+ to initiate contraction; resembles smooth muscle 6. Mitochondria occupy about 1/3 the cell volume of a cardiac contractile fiber, a reflection of the high energy demand of these cells; cardiac muscle consumes approx. 70- 80% of the oxygen delivered to it by the blood, more than twice the amount extracted by other cells in the body >action potentials originate in the pace maker cells, and spreads into the contractile cells through gap junctions 2+ >contraction force is determined by how much Ca is bound to troponin in the cell Excitation-Contraction coupling (EC coupling) [FIG.14.9] 1. Action potential enters from adjacent cell  Action potential enters a contractile cell , moves across the sarcolemma and into the t-tubules 2+ 2+ 2. Voltage-gated Ca channels open. Ca enters the cell  Opens voltage-gated L-type Ca channels+ 3. Ca induces Ca release through ryanodine receptor-channels (RyR) 2+ 4. Local release causes Ca spark 5. Summed Ca sparks create a Ca signal2+ 2+ 2+  Ca -induced Ca2+ release(CICR) since the myocardial RyR channels open in response to Ca binding 2+ 6. Ca ions bind to troponin to initiate contraction 7. Relaxation occurs when Ca unbinds from troponin 2+ 2+ 8. Ca is pumped back into the SR for storage with the help of Ca -ATPase 9. Ca is exchanged with Na by the Na -Ca exchanger (NCX) + + + 10. Na gradient is maintained by the Na -K -ATPase Myocardial Action Potentials> Contractile Cells >the rapid depolarization phase of the action potential is the result of Na+ entry and the steep re-polarization phase is due to K+ leaving the cell 2+ >myocardial cells have longer action potentials due to Ca entry Phase 4: Resting membrane potential >stable resting potential of about -90mV Phase 0: depolarization >wave of depolarization through gap junctions causes a more positive membrane potential >voltage-gated Na channels open, allowing Na to enter the cell and rapidly depolarize it >membrane reaches approx. +20mV before the channels close Phase 1: Initial re-polarization >Na channels close, and the cell begins to repolarize as K leaves through open K channels + Phase 2: the Plateau >initial repolarization is very brief >the action potential then flattens into a plateau as the results of two events: + >a decrease in K permeability >an increase in Ca permeability 2+ 2+ >Ca channels have been slowly opening in phase 0 and 1, when they finally open, Ca enters the cell; at the + same time, some “fast” K channels close >combination of Ca influx and decreased K efflux causes the action potential to flatten out 2+ >the influx of Ca lengthens the total duration of a myocardial action potential >typically lasts 200 msec or more >the longer action potential helps to prevent tetanus; this is important because the heart must relax so the ventricles can fill with blood >refractory period: the time following an action potential during which a normal stimulus cannot trigger a second action potential Phase 3: Rapid Re-polarization >plateau ends when Ca channels close and K permeability increases once more >when the slow K channels open, K exits rapidly, returning the cell to its resting potential Phase 4: Resting membrane potential >Autorhythmic Cells >pacemaker potential: an unstable membrane potential which starts at -60 mV and slowly drifts upward toward the threshold; it never ‘rests’ at a constant value >Ifchannels: when the cell membrane potential is -60 mV, these channels open; they are permeable to both K+ and Na+ >they allow current (I) to flow and because of their unusual properties >belong to the family of HCN channels or hyperpolarization-activated cyclic nucleotide-gated channels >when they open at negative membrane potentials Na+ influx exceeds K+ efflux >the Ifchannels gradually close and one set of Ca2+ channels open as the membrane potential becomes more positive + >the depolarization phase is due to the opening of voltage-gated Na channels + >the repolarization phase is due to the resultant efflux of K >the speed with which the pacemaker cells depolarize determine the rate at which the heart contract, or the heart rate Skeletal Muscles >often described as voluntary muscles; they contract with conscious direction >contract only in response to a signal from a somatic motor neuron; cannot initiate their own contraction, nor is it influenced directly by hormones > generate heat and contribute to homeostasis of body temperature >40% of total body weight >attach to bones via tendons made of collagen >origin of muscle: the end of the muscle that is attached closest to the trunk or to the more stationary bone >insertion of muscle: the more distal or more mobile attachment >contraction of a skeletal muscle moves the skeleton >flexor muscle: if the center of the connected bones are brought close together when the muscle contracts; movement is called flexion >extensor muscle: if the bones move away from each other when the muscle contracts; movements is called extension >Antagonistic muscle groups: flexor-extensor pairs; most joints in the body have both flexor and extensor muscles> contracting muscles can pull the bone in one direction but need another muscle to counteract the initial movement >Skeletal muscles are made up of muscle fibres: long, cylindrical cell with up to several hundred nuclei; the largest cells in the body; created by the fusion of multiple individual embryonic muscle cells >Satellite Cells: lie just outside the muscle fiber membrane; activate and differentiate into muscle when needed for muscle growth and repair >each skeletal muscle is sheathed in connective tissue as well as the entirety of the muscle >fascicles contain groups of bundled muscle fibres >relatively uniform throughout the body Muscle Fibre >Sarcolemma = the cell membrane of a muscle fiber >Sarcoplama = the cytoplasm >myofibrils = highly organized bundles of contractile and elastic proteins that carry out the work of contraction > Sarcoplasmic Reticulum (SR) = a form of modified endoplasmic reticulum that wraps around each myofibril >consists of longitudinal tubules with enlarges regions called the terminal cisternae >it concentrates and sequesters Ca 2+ 2+ > Ca release from the SR creates calcium signals that play a key role in contraction in all types of muscle >the terminal cisternae are adjacent and associated with transverse tubules or T-tubules >One T-tubule + two flanking terminal cisternae =a Triad >T-tubule membranes are a continuation of the muscle fiber membrane> lumen is continuous with the extracellular fluid >allow action potentials to move rapidly from the cell surface into the interior of the fiber so that they reach the terminal cisternae nearly simultaneously >Without T-tubules, the action potential would reach the center of the fibre only by conduction of the action potential through the cytosol, a slower and less direct process that would delay the response time of the muscle fiber >Mitochondria provide a lot of the ATP for muscle contraction through oxidative phosphorylation of glucose and other biomolecules Myofibrils >One muscle fibre can contain thousands of myofibrils >composed of several types of proteins: contractile (myosin and actin), regulatory (tropomyosin and troponin), and giant accessory proteins (titin and nebulin) >Myosin: a motor protein with the ability to create movement; thick filaments >composed of protein chains that intertwine to form a long tail and a pair of tadpole-like heads >the tail is stiff white the protruding myosin heads have an elastic hinge region where the heads join the rods; the hinge allows the heads to swivel around their point of attachment >each head has two protein chains: a heavy motor domain chain and a smaller light chain >Motor Domain chain: binds ATP and uses the energy from ATP’s high-energy phosphate bond to create movement >acts as an enzyme- therefore it is considered a myosin ATPase >contains a binding site for actin >Thick Filament is approx. 250 myosin molecules and is arranged so that myosin heads are clustered at each end of the filament, and the central region of the filament is a bundle of myosin tails >Actin: a protein that makes up the thin filaments of the muscle fibre >G-actin is a globular protein molecule; multiple G-actin molecules polymerize to form long chains or filaments called F-actin > 2 F-actin polymers twist together creating the thin filaments of the myofibrils >Myosin Crossbridges connect thick and thin filaments and form when myosin heads bind to actin >G-actin molecules have a single myosin-binding site and >myosin heads have a single actin-binding site and a single ATP binding site >Two states: >low-force (relaxed muscles) >high-force (contracting muscles) >Sarcomere: the contractile unit of a myofibril; forms the repeating light and dark bands >Z Disks: a sarcomere is made up of two Z disks and the filaments in between; they are zigzag protein structures that serve as the attachment site for thin filaments >I Bands: the lightest colour bands; represent a region occupied only by thin filaments; a Z disk runs through the middle of every I Band, so each half is in a different Sarcomere; Isotropic: reflects light uniformly >A Band: the darkest colour bands; encompass the entire length of the thick filament; thick and thin filaments overlap at the ends of the A Band, whereas the center only contains thick filaments; anisotropic: they scatter light unevenly >H Zone: the central region of the A Band is lighter than the edges of the A band because it is only occupied by thick filaments >M Line: represents proteins that form the attachment site for thick filaments; equivalent to the Z disk for think filaments; divides an A Band in half >each thin filament is surrounded by 3 thick filaments, and 6 thin filaments surround a thick filament >Titin: a huge elastic molecule and the largest known protein, composed of more than 25,000 amino acids; one stretches from a Z disk to the next M line; Two functions: >stabilizes the position of the contractile filaments > Its elasticity returns stretched muscles to their resting length >Nebulin: an inelastic giant protein that lies alongside thin filaments and attaches to the Z disk; helps to align the actin filaments of the sarcomere with Titin >A calcium signal initiates the power stroke, when myosin crossbridges swivel and push the actin filaments toward the center of the sarcomere >at the end of the power stroke, each myosin head releases actin, then swivels back and binds to a new actin molecule, ready to start another contractile cycle >during contraction, the heads do not all release at the same time or the fibers would slide back to their starting position >Myosin ATPase converts the chemical bond energy of ATP into the mechanical energy of crossbridge motion; it hydrolyzes ATP to ADP + inorganic Phosphate and the energy released is trapped by myosin and stored as potential energy in the angle between the myosin head and the long axis of the myosin filament> myosin heads in this position are said to be “cocked” or ready to rotate Muscle Contractions >muscle tension: the force created by contracting muscles >load: a weight or force that opposes contraction of a muscle >Contraction: the creation of tension in a muscle; requires energy input from ATP >Relaxation: the release of tension created by contraction 1. Events at the Neuromuscular junction> convert an acetylcholine signal from a somatic motor neuron into an electrical signal in the muscle fibre 2. Excitation-Contraction (E-C) coupling> the process in which muscle action potentials initiate calcium signals that in turn activate a contraction-relaxation cycle 3. Contraction-Relaxation Cycle (at the molecular level)> the sliding filament theory of contraction >twitch: one contraction-relaxation cycle; a single action potential evokes a single twitch; does not represent the maximum force that a muscle fiber can develop The Sliding Filament Theory >the sliding filament theory proposes that overlapping actin and myosin filaments of fixed length slide past one another in an energy-requiring process, resulting in muscle contraction >relaxed state: large I band, and an A band the size of the thick filament >contracted state: the thick and thin filaments slide past each other; Z disks move closer together; I band and H zone almost disappear entirely >the length of the A band remains constant even though the sarcomere can shorten or extend Calcium Signals and Myosin movement [F IG 12.8-12.9] >Troponin: a calcium-binding complex of three proteins; controls the positioning of an elongated protein polymer, tropomyosin >Tropomyosin wraps around actin filaments and partially covers actin’s myosin-binding sites> ‘off’ position > it must be switched to an ‘on’ position before contraction can occur >Relaxed state: myosin head cocked; tropomyosin partially blocks binging site on actin; myosin is weakly bound to actin >for relaxation to occur, Ca concentrations in the cytosol must decrease 2+ 2+ >by the law of mass action, when Ca concentration decreases, Ca will unbind to Troponin C >SR pumps Ca back into its lumen using a Ca -ATPase 2+ > as the cytosolic concentration of calcium decreases, the equilibrium between bound and unbound Ca is disturbed; this results in calcium releasing from troponin >Initiation of Contraction: a calcium signal initiates contraction 1. Ca levels increase in cytosol 2+ 2+ 2. Ca binds to troponin (TN)> Troponin C binds reversibly to Ca 3. Troponin C-Ca complex pulls tropomyosin away from actin’s myosin-binding site 4. Myosin binds strongly to actin and completes power stroke 5. Actin filament moves >Rigor state: where the myosin heads are tightly bound to G-actin molecules; no nucleotide (ATP/ADP) is bound to myosin; in a living muscle it occurs for only a brief period of time because their muscle fiber has a sufficient supply of ATP that quickly binds to myosin once ADP is released >after death, when metabolism stops and ATP supplies are exhausted, muscles are unable to bind more ATP, so they remain in the tightly bound rigor state; it persists for a day or so after death, until enzymes within the decaying fiber begin to break down the muscle proteins> ie. Rigor Mortis >steps of myosin movement along actin filaments 1. ATP binds and myosin detaches: an ATP molecule binds to the myosin head; ATP-binding decreases the actin- binding affinity of myosin, and myosin releases from actin 2. ATP hydrolysis provide energy for the myosin head to rotate and reattach to actin: the ATP-binding site on the myosin head closes around ATP and hydrolyzes it to ADP +Pi, which remains attached to myosin as energy released by ATP hydrolysis rotates the myosin head until it forms a 90° angle with the long axis of the filaments; in this new position, myosin binds to a new actin that is 1-3 molecules away from where it started  This crossbridge is weak and low-force because tropomyosin is partially blocking actin’s binding site  Most resting muscle fibers are in this state, cocked and prepared to contract, and just waiting for a calcium signal 3. The Power Stroke: begins after Ca binds to troponin to uncover the rest of the myosin-binding site  Crossbridges are now strong, and high-force bonds as myosin releases Pi> allows the head to swivel  Myosin heads swing toward the M line, sliding the attached actin filament along with them  Aka crossbridge tilting because the myosin head and hinge region tilt from 90° to 45° angle 4. Myosin releases ADP: at the end of the power stroke; with ADP gone, the myosin head is again tightly bound to actin in the rigor state Excitation-Contraction coupling [F IG 12.10] >Excitation-Contraction coupling has 4 major events: 1. Acetylcholine (ACh) is released from the somatic motor neuron  ACh binds to ACh receptor-channels on the motor end plate of the muscle fiber  When the gated channels open, they allow both Na and K to cross the membrane + +  Na influx exceeds K efflux because the addition of net positive charge to the muscle fiber depolarizes the membrane creating an end-plate potential (EPP) 2. Ach initiates an action potential in the muscle fiber  Normally EPP always reach threshold and initiates a muscle action potential  The action potential travels across the surface of the muscle fiber and into the t-tubules by the + sequential opening of voltage-gated Na channels>  similar to the conduction of action potentials in axons, although action potentials in skeletal muscles are conducted more slowly than action potentials in myelinated axons 3. The muscle action potential triggers calcium release from the sarcoplasmic reticulum  Action potential in t-tubule alters conformation of DHP receptor  T-tubule membrane contains a voltage-sensing L-type calcium channel called a Dihydropyridine (DHP) receptor 2+  These channels are mechanically linked to Ca release channels in the adjacent SR  The SR Ca release channel are called ryanodine receptors (RyR)  DHP receptor opens RyR Ca release channels in sarcoplasmic reticulum, and Ca enters cytoplasm  The depolarization of an action potential reaches a DHP receptor and the receptor changes conformation; this change opens the RyR Ca release channels 2+  Stored Ca then flows down its electrochemical gradient into the cytosol, where it initiates contraction 4. Calcium combines with troponin and initiates contraction 2+  Ca binds to troponin, allowing actin-myosin binding  Myosin heads execute power stroke  Actin filament slides toward center of sarcomere  Sarcoplasmic reticulum Ca -ATPase pumps Ca back into SR  Decrease in free cytosolic [Ca ] causes Ca to unbind to troponin  Tropomyosin re-covers binding site. When myosin heads release, elastic elements pull filaments back to their relaxed position >Latent Period: short delay between the muscle action potential and the beginning of muscle tension development; represents the time required for calcium release and binding to troponin ATP: Energy >muscles require energy for: >crossbridge movement and release during contraction 2+ >pumping Ca back into the SR during relaxation >restoring Na and K to the extracellular and intracellular compartments >the amount of ATP in a muscle fiber at any time is sufficient for approx. 8 twitches >Phosphocreatine is a backup energy source; a molecule whose high-energy phosphate bonds are created from creatine and ATP when muscles are at rest >when muscles become active, phosphocreatine transfers its phosphate group to ADP to create more ATP to power muscles >creatine kinase (CK): an enzyme which transfers the phosphate group to ADP from phosphocreatine; aka creatine phosphokinase (CPK) >elevated blood levels of CPK indicate damage to skeletal or cardiac muscles > → → >Carbohydrates, particularly glucose, are the most rapid and efficient source of energy for ATP production >glucose is metabolized through glycolysis to pyruvate > In the presence of adequate oxygen, pyruvate goes into the citric acid cycle, producing about 30 ATP for each molecule of glucose >in the absence of adequate oxygen, muscle fiber metabolism relies more on anaerobic glycolysis >glucose is metabolized to lactate with a yield of only 2 ATP per glucose >it is quicker than aerobic glycolysis >Fatty acids can produce energy > Always requires oxygen >during rest and light exercise, muscles burn fatty acids along with glucose > Relatively slow and cannot produce ATP rapidly enough to meet the energy needs of muscle fibers during heavy exercise >Proteins: >normally not a source of energy for muscle contraction >most amino acids found in muscle fibers are used to synthesize proteins rather than to produce ATP >Even intense exercise uses only 30% of the ATP in a muscle fiber Muscle Fatigue >Fatigue: a reversible condition in which a muscle is no longer able to generate or sustain the expected power output >influenced by the intensity and duration of the contractile activity, by whether the muscle fiber is using aerobic or anaerobic metabolism, by the composition of the muscle, and by the fitness level of the individual >central fatigue: arise in the central nervous system >includes subjective feelings of tiredness and a desire to cease activity >pH levels as a factor in central fatigue probably applies only in cases of maximal exertion >neural causes for fatigue could arise either from communication failure at the neuromuscular junction or from failure of the CNS command neurons >ie. If ACh is not synthesizes in the axon terminal fast enough to keep up with neuron firing rate, neurotransmitter release at the synapse decreases; the muscle EPP fails to reach the threshold value needed to trigger a muscle fiber action potential, resulting in contraction failure >can be associated with neuromuscular disease, but it is probably not a factor in normal exercise >peripheral fatigue: arise anywhere between the neuromuscular junction and the contractile elements of the muscles >most experimental evidence suggests that muscle fatigue arises from excitation-contraction failure in the muscle fiber rather than from failure of control neurons or neuromuscular transmission >fatigue in submaximal exertion> caused by the depletion of muscle glycogen stores which would be affecting an aspect of contraction besides ATP >Fatigue in short-duration maximal exertion: >1. Increased levels of inorganic phosphate (produced when ATP and phosphocreatine are used for energy in the muscle fiber); elevated cytoplasmic Pi may slow Pi release from myosin and thereby alter the power stroke 2+ 2+ >2. Elevated phosphate levels decrease Ca release because the phosphate combines with Ca to become calcium phosphate >ion imbalances have been implicated in fatigue >During maximal exercise: K leaves the muscle fiber with each action potential; K concentrations rise in the extracellular fluid of the t-tubules; this shift alters the membrane potential of the muscle fiber >changes in Na -K -ATPase activity + >the accumulation of H from ATP hydrolysis contributes to acidosis >the factors that cause fatigue are still uncertain Muscle Fibers and Speed [F IG12.15] >the speed to which a muscle fiber contracts is determined by the isoform of myosin ATPase present in the fiber’s thick filaments >the duration of contraction also varies according to fiber type; twitch duration is determined largely by how fast the SR removes Ca from the cytosol >Oxidative fibers rely primarily on oxidative phosphorylation
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