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1 Anatomy & Physiology Seventh Edition Chapter 09 Muscles and Muscle Tissues...

1 Anatomy & Physiology Seventh Edition Chapter 09 Muscles and Muscle Tissues Reminder-Lab Exam week of 10/14 View in D2L Materials > Content > Animations > Muscle 1, 2, 3 (problem #2 slide 4) Based on slides by Karen Dunbar Kareiva Based on slides by Karen Dunbar Kareiva © 2020 Pearson Education  2 Muscle Tissue Topics  Three types of muscle tissue  Skeletal muscle as an organ, with connective tissue, nerves, and vascular epithelium  Skeletal muscle cell modifications and specialized proteins  Sliding filament mechanism of contraction  Neuromuscular junction leads to muscle fiber excitation action potentials, which initiates excitation- contraction coupling which initiates sliding filaments and the cross bridge cycling of myosin & actin  Muscle twitch and summation  Recruitment and motor units  Isotonic and isometric contractions  Energy sources to fuel contractions  Factors influencing force of contraction  Velocity and duration of different fiber types  byContrast Based on slides smooth/cardiac/skeletal muscle mechanisms Karen Dunbar Kareiva  3 Characteristics of Muscle Tissue  Nearly half of body’s mass  Can transform chemical energy (A TP) into directed mechanical energy, which is capable of exerting force  All muscles share four main characteristics:  Excitability (responsiveness): ability to receive and respond to stimuli  Contractility: ability to shorten forcibly when stimulated  Extensibility: ability to be stretched  Elasticity: ability to recoil to resting length  Terminologies: Myo, mys, and sarco are prefixes for muscle Based on slides by Karen Dunbar Kareiva  Muscle Tissue - Comparison of 4 Skeletal, Cardiac, and Smooth Muscle Based on slides by Karen Dunbar Kareiva  5 Muscle Functions  Four important functions 1. Produce movement: responsible for all locomotion and manipulation  Example: walking, digesting, pumping blood 2. Maintain posture and body position 3. Stabilize joints 4. Generate heat as they contract Based on slides by Karen Dunbar Kareiva  6 Muscle as an Organ: Nerve and Blood Supply  Each skeletal muscle receives a nerve, artery, and veins  “Consciously controlled” or “voluntary” muscle has nerves supplying every fiber to control activity  Contracting muscle fibers require huge amounts of oxygen and nutrients  Also need waste products removed quickly Based on slides by Karen Dunbar Kareiva  7 Muscle as Organ:Connective Tissue Sheaths  Each skeletal muscle, as well as each muscle fiber, is covered in connective tissue  Support cells and reinforce whole muscle  Sheaths from external to internal:  Epimysium: dense irregular connective tissue surrounding entire muscle; may blend with fascia  Perimysium: fibrous connective tissue surrounding fascicles (groups of muscle fibers)  Endomysium: fine areolar connective tissue surrounding each muscle fiber Based on slides by Karen Dunbar Kareiva  8 Muscle Fiber Microanatomy and Sliding Filament Model (animation) skip to 16  These are cells that have modified structures and specialized proteins as compared to the prototypical cell  Skeletal muscle fibers are long, cylindrical cells that contain multiple nuclei  Sarcolemma: muscle fiber plasma membrane  Sarcoplasm: muscle fiber cytoplasm  Contains many glycosomes for glycogen storage, as well as myoglobin for O2 storage  Modified organelles  Myofibrils  Sarcoplasmic reticulum  T tubules Based on slides by Karen Dunbar Kareiva  9 Animation - Muscle #3 Cross- bridge cycle  Anatomy of a Sarcomere https://mediaplayer.pearsoncmg.com/assets/sci-ip2 -cbc-anatomy-of-sarcomere Based on slides by Karen Dunbar Kareiva  10 Animation - Muscle #2 Excitation-Contraction Coupling  Structures Responsible For Excitation-Contraction Coupling https://mediaplayer.pearsoncmg.com/assets/sci-ip2 -ecc-structures-responsible-for-ecc Based on slides by Karen Dunbar Kareiva  11 Sarcoplasmic Reticulum and T Tubules (animation)  T tubules  Tube formed by protrusion of sarcolemma deep into cell interior  Increase muscle fiber’s surface area greatly  Lumen continuous with extracellular space  Allow electrical nerve transmissions to reach deep into interior of each muscle fiber  Tubules penetrate cell’s interior at each A–I band junction between terminal cisterns  Triad: area formed from terminal cistern of one sarcomere, T tubule, and terminal cistern of neighboring sarcomere  When an electrical impulse passes by, T tubule proteins change shape, causing SR proteins to change shape, causing release of calcium into cytoplasm Based on slides by Karen Dunbar Kareiva  12 Myofibrils (animation)  Myofibrils are densely packed, rodlike elements  Single muscle fiber can contain 1000s  Accounts for ~80% of muscle cell volume  Myofibril features  Striations  Sarcomeres  Myofilaments  Molecular composition of myofilaments Based on slides by Karen Dunbar Kareiva  13 Myofibrils (animation)  Striations: stripes formed from repeating series of dark and light bands along length of each myofibril  A bands: dark regions  H zone: lighter region in middle of dark A band  M line: line of protein (myomesin) that bisects H zone vertically  I bands: lighter regions  Z disc (line): coin-shaped sheet of proteins on midline of light I band Based on slides by Karen Dunbar Kareiva  14 Myofibrils (animation)  Sarcomere  Smallest contractile unit (functional unit) of muscle fiber  Contains A band with half of an I band at each end  Consists of area between Z discs  Individual sarcomeres align end to end along myofibril, like boxcars of train Based on slides by Karen Dunbar Kareiva  15 Myofibrils (animation)  Myofilaments  Orderly arrangement of actin and myosin myofilaments within sarcomere  Actin myofilaments: thin filaments  Extend across I band and partway in A band  Anchored to Z discs  Myosin myofilaments: thick filaments  Extend length of A band  Connected at M line  Sarcomere cross section shows hexagonal arrangement of one thick filament surrounded by six thin filaments Based on slides by Karen Dunbar Kareiva  16 Myofibrils (animation)  Molecular composition of myofilaments  Thick filaments: composed of protein myosin that contains two heavy and four light polypeptide chains  Heavy chains intertwine to form myosin tail  Light chains form myosin globular head  During contraction, heads link thick and thin filaments together, forming cross bridges  Myosins are offset from each other, resulting in staggered array of heads at different points along thick filament Based on slides by Karen Dunbar Kareiva  17 Myofibrils (animation)  Molecular composition of myofilaments  Thin filaments: composed of fibrous protein actin  Actin is polypeptide made up of kidney-shaped G actin (globular) subunits  G actin subunits bear active sites for myosin head attachment during contraction  G actin subunits link together to form long, fibrous F actin (filamentous)  Two F actin strands twist together to form a thin filament  Tropomyosin and troponin: regulatory Based on slides by Karen Dunbar proteins Kareiva bound to actin  18 Myofibrils  (animation) Molecular composition of myofilaments  Other proteins help form the structure of the myofibril  Elastic filament: composed of protein titin  Holds thick filaments in place; helps recoil after stretch; resists excessive stretching  Dystrophin  Links thin filaments to proteins of sarcolemma  Nebulin, myomesin, C proteins bind filaments, or sarcomeres together  Maintain alignment of sarcomere Based on slides by Karen Dunbar Kareiva  19 Clinical—Homeostatic Imbalance  Duchenne muscular dystrophy (DMD) is most common and serious form of muscular dystrophies, muscle-destroying diseases that generally appear during childhood  Inherited as a sex-linked recessive disease, so almost exclusively in males (1 in 3600 births)  Appears between 2 and 7 years old when boy has difficulty coordinating movement and falls frequently  Disease progresses from extremities upward, finally affecting head, chest muscles, and cardiac muscle.  With supportive care, people with DMD can live into 30s and beyond Based on slides by Karen Dunbar Kareiva  20 Clinical—Homeostatic Imbalance  Caused by defective gene for dystrophin, a protein that links thin filaments to extracellular matrix and helps stabilize sarcolemma  Sarcolemma of DMD patients tears easily, allowing entry of excess calcium which damages contractile fibers  Inflammation follows and regenerative capacity is lost resulting in increased apoptosis of muscle cells and drop in muscle mass Based on slides by Karen Dunbar Kareiva  Sliding Filament Model 21 of Contraction (animation)  In the relaxed state, thin and thick filaments overlap only slightly at ends of A band  Sliding filament model of contraction states that during contraction, thin filaments slide past thick filaments, causing actin and myosin to overlap more  Neither thick nor thin filaments change length, just overlap more  When nervous system stimulates muscle fiber, myosin heads are allowed to bind to actin, forming cross bridges, which cause sliding (contraction) process to begin Based on slides by Karen Dunbar Kareiva  Sliding Filament 22 Model of Contraction (animation)  Cross bridge attachments form and break several times, each time pulling thin filaments a little closer toward center of sarcomere in a ratcheting action  Causes shortening of muscle fiber  Z discs are pulled toward M line  I bands shorten  Z discs become closer  H zones disappear  A bands move closer to each other Based on slides by Karen Dunbar Kareiva  23 Backgroun d and Overview (animation ) skip to 28  The Big Picture—Four steps must occur for skeletal muscle to contract: 1. Events at neuromuscular junction 2. Muscle fiber excitation Based on slides by Karen Dunbar Kareiva 3. Excitation-contraction coupling  24 Animation - Muscle #1 Excitation at the Neuromuscular Junction  Motor Neurons Control Muscle Contraction: https://mediaplayer.pearsoncmg.com/assets/secs-ip2-nmj-motor-neurons-con trol-muscle-contraction  The Neuromuscular Junction: https://mediaplayer.pearsoncmg.com/assets/secs-ip2-nmj-the-neuromuscular -junction  Release of Neurotransmitter: https://mediaplayer.pearsoncmg.com/assets/secs-ip2-nmj-release-of-neurotra nsmitter  Generation of End Plate Potential: https://mediaplayer.pearsoncmg.com/assets/secs-ip2-nmj-generation-of-end- plate-potential  Stopping the Signal: https://mediaplayer.pearsoncmg.com/assets/secs-ip2-nmj-stopping-the-signa l Based on slides by Karen Dunbar Kareiva  Muscle Excitation at the Neuromuscular Junction – Summary: https://mediaplayer.pearsoncmg.com/assets/secs-ip2-nmj-summary  25 A&P Flix™: Events at the Neuromuscular Junction  https://mediaplayer.pearsoncmg.com/assets/ch09_ 9.4a_mariebhap11ge Based on slides by Karen Dunbar Kareiva  Muscle Fiber Contraction 26 Background and Overview  Decision to move is activated by brain, signal is transmitted down to spinal cord to motor neurons which then activate muscle fibers  Neurons and muscle cells are excitable cells capable of action potentials  Excitable cells are capable of changing resting membrane potential voltages  AP crosses from neuron to muscle cell via the neurotransmitter acetylcholine (ACh) Based on slides by Karen Dunbar Kareiva  27 Background and Overview  Ion channels  Play the major role in changing of membrane potentials  Two classes of ion channels:  Chemically gated ion channels—opened by chemical messengers such as neurotransmitters  Example: ACh receptors on muscle cells  Voltage-gated ion channels—open or close in response to voltage changes in membrane potential Based on slides by Karen Dunbar Kareiva  28 Background and Overview  Axon terminal (end of axon) and muscle fiber are separated by gel-filled space called synaptic cleft  Stored within axon terminals are membrane-bound synaptic vesicles  Synaptic vesicles contain neurotransmitter acetylcholine (ACh)  Infoldings of sarcolemma, called junctional folds, contain millions of ACh receptors  NMJ consists of axon terminals, synaptic cleft, and junctional Based on slides by Karen Dunbar Kareiva folds  29 Events at the Neuromuscular Junction 1. AP arrives at axon terminal 2. Voltage-gated calcium channels open, calcium enters motor neuron 3. Calcium entry causes release of A Ch neurotransmitter into synaptic cleft 4. ACh diffuses across to ACh receptors (Na+ chemical gates) on sarcolemma 5. ACh binding to receptors, opens gates, allowing N a+ to enter resulting in end plate potential 6. Acetylcholinesterase degrades A Ch Based on slides by Karen Dunbar Kareiva  30 Clinical—Homeostatic Imbalance  Many toxins, drugs, and diseases interfere with events at the neuromuscular junction  Example: myasthenia gravis: disease characterized by drooping upper eyelids, difficulty swallowing and talking, and generalized muscle weakness  Involves shortage of Ach receptors because person’s ACh receptors are attacked by own antibodies  Suggests this is an autoimmune disease Based on slides by Karen Dunbar Kareiva  31 Generation of an Action Potential Across the Sarcolemma  Resting sarcolemma is polarized, meaning a voltage exists across membrane  Inside of cell is negative compared to outside  Action potential is caused by changes in electrical charges  Occurs in three steps 1. Generation of end plate potential 2. Depolarization 3. Repolarization Based on slides by Karen Dunbar Kareiva  32 Generation of an Action Potential Across the Sarcolemma 1. End plate potential  ACh released from motor neuron binds to ACh receptors on sarcolemma  Causes chemically gated ion channels (ligands) on sarcolemma to open  Na+ diffuses into muscle fiber  Some K+ diffuses outward, but not much  Because Na+ diffuses in, interior of sarcolemma becomes less negative (more positive)  Results in local depolarization called end plate potential Based on slides by Karen Dunbar Kareiva  Generation of an Action Potential 33 Across the Sarcolemma 2. Depolarization: generation and propagation of an action potential (AP)  If end plate potential causes enough change in membrane voltage to reach critical level called threshold, voltage-gated Na+ channels in membrane will open  Large influx of Na+ through channels into cell triggers A P that is unstoppable and will lead to muscle fiber contraction  AP spreads across sarcolemma from one voltage-gated N a+ channel to next one in adjacent areas, causing that area to depolarize Based on slides by Karen Dunbar Kareiva  Generation of an Action Potential 34 Across the Sarcolemma 3. Repolarization: restoration of resting conditions  Na+ voltage-gated channels close, and voltage-gated K+ channels open  K+ efflux out of cell rapidly brings cell back to the initial resting membrane voltage  Refractory period: muscle fiber cannot be stimulated for a specific amount of time, until repolarization is complete  Ionic conditions of resting state are restored by Na+-K+ pump  Na+ that came into cell is pumped back out, and K+ that flowed outside is pumped Based on slides by Karen back into cell Dunbar Kareiva  35 Excitation-Contraction (E-C) Coupling (animation) skip to 40  Excitation-contraction (E-C) coupling: events that transmit AP along sarcolemma (excitation) are coupled to sliding of myofilaments (contraction)  AP is propagated along sarcolemma and down into T tubules, where voltage-sensitive proteins in tubules stimulate Ca2+ release from SR  Ca2+ release leads to contraction  AP is brief and ends before contraction is seen Based on slides by Karen Dunbar Kareiva  36 Animation - Muscle #2 Excitation-Contraction Coupling  Introduction To Excitation-Contraction Coupling https://mediaplayer.pearsoncmg.com/assets/sci-ip2-ecc-introduc tion-to-ecc  Structures Responsible For Excitation-Contraction Coupling https://mediaplayer.pearsoncmg.com/assets/sci-ip2-ecc-structur es-responsible-for-ecc  Action Potential Causes Calcium Ion Release https://mediaplayer.pearsoncmg.com/assets/spi-ip2-ecc-action-p otential-causes-calcium-ion-release  Role of Calcium in Excitation-Contraction Coupling https://mediaplayer.pearsoncmg.com/assets/sci-ip2-ecc-role-of-c alcium-in-ecc  Summary Based on slides by Karen Dunbar Kareiva https://mediaplayer.pearsoncmg.com/assets/sci-ip2-ecc-summar y  37 A&P Flix™: Excitation- Contraction Coupling  https://mediaplayer.pearsoncmg.com/assets/apf-ex citation-contraction-coupling Based on slides by Karen Dunbar Kareiva  38 Muscle Fiber Contraction: Cross Bridge Cycling (animation) skip to 46  At low intracellular Ca2+ concentration:  Tropomyosin blocks active sites on actin  Myosin heads cannot attach to actin  Muscle fiber remains relaxed  Voltage-sensitive proteins in T tubules change shape, causing sarcoplasmic reticulum (S R) to release Ca2+ to cytosol Based on slides by Karen Dunbar Kareiva  39 Animation - Muscle #3 Cross- bridge-cycle  Introduction to Cross Bridge Cycling https://mediaplayer.pearsoncmg.com/assets/sci-ip2-c bc-introduction  Anatomy of a Sarcomere https://mediaplayer.pearsoncmg.com/assets/sci-ip2-c bc-anatomy-of-sarcomere  Sliding Filament Mechanism of Contraction https://mediaplayer.pearsoncmg.com/assets/sci-ip2-c bc-sliding-filament-mechanism-of-contraction  Cross Bridge Cycle https://mediaplayer.pearsoncmg.com/assets/sci-ip2-c bc-cross-bridge-cycle  Relaxation of the Sarcomere Based on https://mediaplayer.pearsoncmg.com/assets/sci-ip2-c slides by Karen Dunbar Kareiva  40 A&P Flix™: Cross Bridge Cycle  https://mediaplayer.pearsoncmg.com/assets/apf-cr oss-bridge-cycle Based on slides by Karen Dunbar Kareiva  41 Muscle Fiber Contraction: Cross Bridge Cycling (animation)  At higher intracellular Ca2+ concentrations, Ca2+ binds to troponin  Troponin changes shape and moves tropomyosin away from myosin-binding sites  Myosin heads are then allowed to bind to actin, forming cross bridge  Cycling is initiated, causing sarcomere shortening and muscle contraction  When nervous stimulation ceases, C a2+ is pumped back into SR, and contraction ends Based on slides by Karen Dunbar Kareiva  42 Muscle Fiber Contraction: Cross Bridge Cycling (animation)  Four steps of the cross bridge cycle 1. Cross bridge formation: high- energy myosin head attaches to actin thin filament active site 2. Working (power) stroke: myosin head pivots and pulls thin filament toward M line 3. Cross bridge detachment: ATP attaches to myosin head, causing cross bridge to detach 4. Cocking of myosin head: energy from hydrolysis of ATP “cocks” myosin head into high-energy state This energy will be used for power stroke in the next cross bridge cycle Based on slides by Karen Dunbar Kareiva  43 Clinical—Homeostatic Imbalance  Rigor mortis  3–4 hours after death, muscles begin to stiffen  Peak rigidity occurs about 12 hours postmortem  Intracellular calcium levels increase because A TP is no longer being synthesized, so calcium cannot be pumped back into SR  Results in cross bridge formation  ATP is also needed for cross bridge detachment  Results in myosin head staying bound to actin, causing constant state of contraction  Muscles stay contracted until muscle proteins break down, causing myosin to release Based on slides by Karen Dunbar Kareiva  The Muscle Twitch 44  Muscle twitch: simplest contraction resulting from a muscle fiber’s response to a single action potential from motor neuron  Muscle fiber contracts quickly, then relaxes  Three phases of muscle twitch  Latent period: events of excitation-contraction coupling  No muscle tension seen  Period of contraction: cross bridge formation  Tension increases  Period of relaxation: Ca2+ reentry into S R  Tension declines to zero  Muscle contracts faster than it relaxes Based on slides by Karen Dunbar Kareiva  45 The Muscle Twitch  Differences in strength and duration of twitches are due to variations in metabolic properties and enzymes between muscles  Example: eye muscles contraction are rapid and brief, whereas larger, fleshy muscles (calf muscles) contract more slowly and hold it longer Based on slides by Karen Dunbar Kareiva  46 Graded Muscle Responses  Normal muscle contraction is relatively smooth, and strength varies with needs  A muscle twitch is seen only in lab setting or with neuromuscular problems, but not in normal muscle  Graded muscle responses vary strength of contraction for different demands  Required for proper control of skeletal movement  Responses are graded by:  Changing frequency of stimulation (temporal summation)  Changing strength of stimulation (motor unit recruitment) Based on slides by Karen Dunbar Kareiva  47 Graded Muscle Responses  Muscle response to changes in stimulus frequency  Wave (temporal) summation results if two stimuli are received by a muscle in rapid succession  Muscle fibers do not have time to completely relax between stimuli, so twitches increase in force with each stimulus  Additional Ca2+ that is released with second stimulus stimulates more shortening Based on slides by Karen Dunbar Kareiva  48 Graded Muscle Responses  Muscle response to changes in stimulus frequency  If stimuli frequency increases, muscle tension reaches near maximum  Produces smooth, continuous contractions that add up (summation)  Further increase in stimulus frequency causes muscle to progress to sustained, quivering contraction referred to as unfused (incomplete) tetanus  If stimuli frequency further increase, muscle tension reaches maximum  Referred to as fused (complete) tetanus because contractions “fuse” into one smooth sustained contraction plateau  Prolonged muscle contractions lead to muscle fatigue Based on slides by Karen Dunbar Kareiva  49 The Motor Unit  Motor unit consists of the motor neuron and all muscle fibers (four to several hundred) it supplies  Smaller the fiber number, the greater the fine control  Muscle fibers from a motor unit are spread throughout the whole muscle, so stimulation of a single motor unit causes only weak contraction of entire muscle Based on slides by Karen Dunbar Kareiva  50 Graded Muscle Responses  Muscle response to changes in stimulus strength  Recruitment (or multiple motor unit summation): stimulus is sent to more muscle fibers, leading to more precise control  Types of stimulus involved in recruitment:  Subthreshold stimulus: stimulus not strong enough, so no contractions seen  Threshold stimulus: stimulus is strong enough to cause first observable contraction  Maximal stimulus: strongest stimulus that increases maximum contractile force  All motor units have been recruited Based on slides by Karen Dunbar Kareiva  51 Graded Muscle Responses  Muscle response to changes in stimulus strength  Recruitment works on size principle  Motor units with smallest muscle fibers are recruited first  Motor units with larger fibers are recruited as stimulus intensity increases  Largest motor units are activated only for most powerful contractions  Motor units in muscle usually contract asynchronously  Some fibers contract while others rest Based on slides by Karen Dunbar Kareiva  Helps prevent fatigue  52 Muscle Tone  Constant, slightly contracted state of all muscles  Due to spinal reflexes  Groups of motor units are alternately activated in response to input from stretch receptors in muscles  Keeps muscles firm, healthy, and ready to respond Based on slides by Karen Dunbar Kareiva Isotonic and Isometric 53 Contractions  Isotonic contractions: muscle changes in length and moves load  Isotonic contractions can be either concentric or eccentric:  Concentric contractions: muscle shortens and does work  Example: biceps contract to pick up a book  Eccentric contractions: muscle lengthens and generates force  Example: laying a book down causes biceps to lengthen while generating a force Based on slides by Karen Dunbar Kareiva Isotonic and Isometric Contractions 54  Isometric contractions  Load is greater than the maximum tension muscle can generate, so muscle neither shortens nor lengthens  Electrochemical and mechanical events are same in isotonic or isometric contractions, but results are different  In isotonic contractions, actin filaments shorten and cause movement  In isometric contractions, cross bridges generate force, but actin filaments do not shorten  Myosin heads “spin their wheels” on same actin-binding site Based on slides by Karen Dunbar Kareiva  55 Energy for Contraction and ATP Providing Energy for Contraction  ATP supplies the energy needed for the muscle fiber to:  Move and detach cross bridges  Pump calcium back into S R  Pump Na+ out of and K+ back into cell after excitation-contraction coupling  Available stores of ATP depleted in 4–6 seconds  ATP is the only source of energy for contractile activities; therefore, it must be regenerated quickly Based on slides by Karen Dunbar Kareiva  56 Providing Energy for Contraction  ATP is regenerated quickly by three mechanisms:  Direct phosphorylation of ADP by creatine phosphate (CP)  Anaerobic pathway: glycolysis and lactic acid formation  Aerobic pathway Based on slides by Karen Dunbar Kareiva  57 Providing Energy for Contraction  Direct phosphorylation of ADP by creatine phosphate (CP)  Creatine phosphate is a unique molecule located in muscle fibers that donates a phosphate to ADP to instantly form ATP  Creatine kinase is enzyme that carries out transfer of phosphate  Muscle fibers have enough A TP and CP reserves to power cell for about 15 seconds Creatine phosphate + ADP → creatine + ATP Based on slides by Karen Dunbar Kareiva  58 Providing Energy for Contraction  Anaerobic pathway: glycolysis and lactic acid formation  ATP can also be generated by breaking down and using energy stored in glucose  Glycolysis: first step in glucose breakdown  Does not require oxygen  Glucose is broken into 2 pyruvic acid molecules  2 ATPs are generated for each glucose broken down  Low oxygen levels prevent pyruvic acid from entering aerobic respiration phase  Normally, pyruvic acid enters mitochondria to start aerobic respiration phase; however, at high intensity activity, oxygen is not available  Bulging muscles compress blood vessels, impairing oxygen delivery  In the absence of oxygen, referred to as anaerobic Based on slidesglycolysis, pyruvic acid is converted to lactic acid by Karen Dunbar Kareiva  59 Providing Energy for Contraction  Anaerobic pathway: glycolysis and lactic acid formation  Lactic acid  Diffuses into bloodstream  Used as fuel by liver, kidneys, and heart  Converted back into pyruvic acid or glucose by liver  Anaerobic respiration yields only 5% as much ATP as aerobic respiration but produces A TP 2½ times faster Based on slides by Karen Dunbar Kareiva  60 Providing Energy for Contraction  Aerobic Respiration  Produces 95% of ATP during rest and light-to-moderate exercise  Slower than anaerobic pathway  Consists of series of chemical reactions that occur in mitochondria and require oxygen  Breaks glucose into CO2, H2O, and large amount ATP (32 can be produced)  Fuels used include glucose from glycogen stored in muscle fiber, then bloodborne glucose, and free fatty acids  Fatty acids are main fuel after 30 minutes of exercise Based on slides by Karen Dunbar Kareiva  Providing Energy for Contraction 61  Energy systems used during sports  Aerobic endurance  Length of time muscle contracts using aerobic pathways  Light-to-moderate activity, which can continue for hours  Anaerobic threshold  Point at which muscle metabolism converts to anaerobic pathway Based on slides by Karen Dunbar Kareiva  62 Muscle Fatigue  Fatigue is the physiological inability to contract despite continued stimulation  Possible causes include:  Ionic imbalances can cause fatigue  Levels of K+, Na+, and Ca2+ can change disrupting membrane potential of muscle cell  Increased inorganic phosphate (P i) from CP and ATP breakdown may interfere with calcium release from SR or hamper power  Decreased ATP and increased magnesium  As ATP levels drop, magnesium levels increase and this can interfere with voltage-sensitive T tubule proteins  Decreased glycogen  Lack of ATP is rarely a reason for fatigue, except in severely stressed muscles Based on slides by Karen Dunbar Kareiva  63 Excess Postexercise Oxygen Consumption  For a muscle to return to its pre-exercise state:  Oxygen reserves are replenished  Lactic acid is reconverted to pyruvic acid  Glycogen stores are replaced  ATP and creatine phosphate reserves are resynthesized  All replenishing steps require extra oxygen, so this is referred to as excess postexercise oxygen consumption (EPOC)  Formerly referred to as “oxygen debt” Based on slides by Karen Dunbar Kareiva  Force of Muscle Contractions 64  Force of contraction depends on number of cross bridges attached, which is affected by four factors: 1. Number of muscle fibers stimulated (recruitment): the more motor units recruited, the greater the force 2. Relative size of fibers: the bulkier the muscle, the more tension it can develop. Muscle cells can increase in size (hypertrophy) with regular exercise 3. Frequency of stimulation: the higher the frequency, the greater the force 4. Degree of muscle stretch: muscle fibers with sarcomeres that are 80–120% their normal resting length generate more force  If sarcomere is less than 80% resting length, filaments overlap too much, and force decreases  If sarcomere is greater than 120% of resting length, filaments do not overlap enough so force decreases Based on slides by Karen Dunbar Kareiva  65 Factors That Increase the Force of Skeletal Muscle Contraction Based on slides by Karen Dunbar Kareiva  66 Length-Tension Relationships of Sarcomeres in Skeletal Muscles Based on slides by Karen Dunbar Kareiva  Factors Influencing Velocity and Duration 67 of Skeletal Muscle Contraction  How fast a muscle contracts and how long it can stay contracted is influenced by: Muscle fiber type Load Recruitment Based on slides by Karen Dunbar Kareiva  68 Velocity and Duration of Contraction  Muscle fiber type  Classified according to two characteristics 1. Speed of contraction—slow or fast fibers according to:  Speed at which myosin ATPases split ATP  Pattern of electrical activity of motor neurons 2. Metabolic pathways used for A TP synthesis  Oxidative fibers: use aerobic pathways  Glycolytic fibers: use anaerobic glycolysis Based on slides by Karen Dunbar Kareiva  69 Velocity and Duration of Contraction  Muscle fiber type  Based on these two criteria, skeletal muscle fibers can be classified into three types:  Slow oxidative fibers, fast oxidative fibers, or fast glycolytic fibers  Most muscles contain mixture of fiber types, resulting in a range of contractile speed and fatigue resistance  All fibers in one motor unit are the same type  Genetics dictate individual’s percentage of each Based on slides by Karen Dunbar Kareiva  70 Velocity and Duration of Contraction  Muscle fiber type  Different muscle types are better suited for different jobs  Slow oxidative fibers: low-intensity, endurance activities  Example: maintaining posture  Fast oxidative fibers: medium-intensity activities  Example: sprinting or walking  Fast glycolytic fibers: short-term intense or powerful movements  Example: hitting a baseball Based on slides by Karen Dunbar Kareiva  71 Structural and Functional Characteristics of the Three Types of Skeletal Muscle Fibers Based on slides by Karen Dunbar Kareiva  Velocity and Duration of Contraction 72  Load and recruitment  Load: muscles contract fastest when no load is added  The greater the load, the shorter the duration of contraction  The greater the load, the slower the contraction  Recruitment: the more motor units contracting, the faster and more prolonged the contraction Based on slides by Karen Dunbar Kareiva  73 Smooth Muscle  Found in walls of most hollow organs:  Respiratory, digestive, urinary, reproductive, circulatory (except in smallest of blood vessels) except heart  Most organs contain two layers of sheets with fibers oriented at right angles to each other  Longitudinal layer: fibers run parallel to long axis of organ  Contraction causes organ to shorten  Circular layer: fibers run around circumference of organ  Contraction causes lumen of organ to constrict  Alternating contractions and relaxations of layers mix and squeeze substances through lumen of hollow organs Based on slides by Karen Dunbar Kareiva  Smooth muscle fibers are spindle- Differences 74 shaped fibers Between  Thin and short compared with skeletal muscle fibers which Smooth and are wider and much longer Skeletal  Only one nucleus, no striations Muscle Fibers  Lacks connective tissue sheaths  Contains endomysium only  Contain varicosities (bulbous swellings) of nerve fibers instead of neuromuscular junctions  Varicosities store and release neurotransmitters into a wide synaptic cleft referred to as a diffuse junction  Innervated by the autonomic nervous system Based on slides by Karen Dunbar Kareiva Differences Between Smooth and 75 Skeletal Muscle Fibers  Smooth muscle has less elaborate S R, and no T tubules  SR is less developed than in skeletal muscle  SR does store intracellular Ca2+, but most calcium used for contraction has extracellular origins  Sarcolemma contains pouchlike infoldings called caveolae  Caveolae contain numerous Ca2+ channels that open to allow rapid influx of extracellular Ca2+ Based on slides by Karen Dunbar Kareiva  76 Differences Between Smooth and Skeletal Muscle Fibers  Smooth muscle fibers are usually electrically connected via gap junctions, whereas skeletal muscle fibers are electrically isolated  Gap junctions are specialized cell connections that allow depolarization to spread from cell to cell  There are no striations and no sarcomeres, but they do contain overlapping thick and thin filaments Based on slides by Karen Dunbar Kareiva  77 Differences Between Smooth and Skeletal Muscle Fibers  Smooth muscle also differs from skeletal muscle in the following ways:  Thick filaments are fewer and have myosin heads along entire length  Ratio of thick to thin filaments (1:13) is much lower than in skeletal muscle (1:2)  Thick filaments have heads along entire length, making smooth muscle as powerful as skeletal muscle  No troponin complex  Does contain tropomyosin, but not troponin  Protein calmodulin binds Ca2+ Based on slides by Karen Dunbar Kareiva  Differences Between Smooth and 78 Skeletal Muscle Fibers  Thick and thin filaments arranged diagonally  Myofilaments are spirally arranged, causing smooth muscle to contract in corkscrew manner  Intermediate filament–dense body network  Contain lattice-like arrangement of noncontractile intermediate filaments that resist tension  Dense bodies: proteins that anchor filaments to sarcolemma at regular intervals  Correspond to Z discs of skeletal muscle  During contraction, areas of sarcolemma between dense bodies bulge outward  Make muscle cell look puffy Based on slides by Karen Dunbar Kareiva  79 Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle Based on slides by Karen Dunbar Kareiva  80 Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle Based on slides by Karen Dunbar Kareiva  81 Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle Based on slides by Karen Dunbar Kareiva  82 Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle Based on slides by Karen Dunbar Kareiva  83 Contraction of Smooth Muscle  Mechanism of contraction  Slow, synchronized contractions  Cells electrically coupled by gap junctions  Action potentials transmitted from fiber to fiber  Some cells are self-excitatory (depolarize without external stimuli)  Act as pacemakers for sheets of muscle  Rate and intensity of contraction may be modified by neural and chemical stimuli Based on slides by Karen Dunbar Kareiva  84 Contraction of Smooth Muscle  Mechanism of contraction  Contraction in smooth muscle is similar to skeletal muscle contraction in the following ways:  Actin and myosin interact by sliding filament mechanism  Final trigger is increased in intracellular Ca2+ level  ATP energizes sliding process  Contraction stops when Ca2+ is no longer available Based on slides by Karen Dunbar Kareiva  85 Contraction of Smooth Muscle  Mechanism of contraction  Contraction in smooth muscle is different from skeletal muscle in the following ways:  Some Ca2+ still obtained from S R, but mostly comes from extracellular space  Ca2+ binds to calmodulin, not troponin  Activated calmodulin then activates myosin kinase (myosin light chain kinase)  Activated myosin kinase phosphorylates myosin head, activating it  Leads to cross bridge formation with actin Based on slides by Karen Dunbar Kareiva  86 Contraction of Smooth Muscle  Mechanism of contraction  Stopping smooth muscle contraction requires more steps than skeletal muscle  Relaxation requires:  Ca2+ detachment from calmodulin  Active transport of Ca2+ into SR and extracellularly  Dephosphorylation of myosin to inactive myosin Based on slides by Karen Dunbar Kareiva  87 Sequence of Events in Excitation- Contraction Coupling of Smooth Muscle Based on slides by Karen Dunbar Kareiva  88 Contraction of Smooth Muscle  Energy efficiency of smooth muscle contraction  Slower to contract and relax but maintains contraction for prolonged periods with little energy cost  Slower ATPases  Myofilaments may latch together to save energy  Most smooth muscle maintain moderate degree of contraction constantly without fatiguing  Referred to as smooth muscle tone  Makes ATP via aerobic respiration pathways Based on slides by Karen Dunbar Kareiva  89 Contraction of Smooth Muscle  Regulation of contraction  Controlled by nerves, hormones, or local chemical changes  Neural regulation  Neurotransmitter binding causes either graded (local) potential or action potential  Results in increases in Ca2+ concentration in sarcoplasm  Response depends on neurotransmitter released and type of receptor molecules  One neurotransmitter can have a stimulatory effect on smooth muscle in one organ, but an inhibitory effect in a different organ Based on slides by Karen Dunbar Kareiva  90 Contraction of Smooth Muscle  Regulation of contraction  Hormones and local chemicals  Some smooth muscle cells have no nerve supply  Depolarize spontaneously or in response to chemical stimuli that bind to G protein– linked receptors  Chemical factors can include hormones, high CO2, pH, low oxygen  Some smooth muscles respond to both neural and chemical stimuli Based on slides by Karen Dunbar Kareiva  91 Contraction of Smooth Muscle  Special features of smooth muscle contraction  Response to stretch  Stress-relaxation response: responds to stretch only briefly, then adapts to new length  Retains ability to contract on demand  Enables organs such as stomach and bladder to temporarily store contents  Length and tension changes  Can contract when between half and twice its resting length  Allows organ to have huge volume changes without becoming flabby when relaxed Based on slides by Karen Dunbar Kareiva Types of Smooth Muscle 92  Smooth muscle varies in different organs by: 1. Fiber arrangement and organization 2. Innervation 3. Responsiveness to various stimuli  Unitary smooth muscle  Commonly referred to as visceral muscle  Possess all common characteristics of smooth muscle:  Arranged in opposing (longitudinal and circular) sheets  Innervated by varicosities  Often exhibit spontaneous action potentials  Electrically coupled by gap junctions  Respond to various chemical stimuli  Multiunit smooth muscle  Located in large airways in lungs, large arteries, arrector pili muscles, and iris of eye  Very few gap junctions, and spontaneous depolarization is rare  Similar to skeletal muscle in some features  Independent muscle fibers  Innervated by autonomic nervous system, forming motor units  Graded contractions occur in response to neural stimuli that involve recruitment  Different from skeletal muscle because, like unitary smooth muscle, is Based on slides by Karen Dunbar Kareiva