Chapter 10 Lecture Outline

Transcription

1 Chapter 10 Lecture Outline See separate PowerPoint slides for all figures and tables preinserted into PowerPoint without notes. Copyright McGraw-Hill Education. Permission required for reproduction or display. 1

2 10.1a Functions of Skeletal Muscle Body movement Move bones, make facial expressions, speak, breathe, swallow Maintenance of posture Stabilize joints, maintain body position Protection and support Package internal organs and hold them in place Regulating elimination of materials Circular sphincters control passage of material at orifices Heat production Help maintain body temperature 2

3 10.1b Characteristics of Skeletal Muscle Tissue Excitability: ability to respond to a stimulus by changing electrical membrane potential Conductivity: involves sending an electrical change down the length of the cell membrane Contractility: exhibited when filaments slide past each other Enables muscle to cause movement Elasticity: ability to return to original length following a lengthening or shortening Extensibility: ability to be stretched 3

4 10.2a Gross Anatomy of Skeletal Muscle What is the hierarchy of structures in a muscle? A whole muscle contains many fascicles A fascicle consists of many muscle fibers o A muscle fiber is a muscle cell In addition to the muscle cells, a skeletal muscle contains nerves, blood vessels, and connective tissue 4

5 Structural Organization of Skeletal Muscle Figure

6 10.2a Gross Anatomy of Skeletal Muscle Connective tissue components Three concentric layers of wrapping o Epimysium Dense irregular connective tissue wrapping whole muscle o Perimysium Dense irregular connective tissue wrapping fascicle Houses many blood vessels and nerves o Endomysium Areolar connective tissue wrapping individual fiber Delicate layer for electrical insulation, capillary support, binding of neighboring cells 6

7 10.2a Gross Anatomy of Skeletal Muscle Connective tissue components (continued) Attachments of muscle to bone (or to skin or to another muscle) can be tendons or aponeuroses o o Tendon: cordlike structure of dense regular connective tissue Aponeurosis: thin, flattened sheet of dense irregular tissue 7

8 10.2a Gross Anatomy of Skeletal Muscle Connective tissue components (continued) Deep fascia o Sheet of dense irregular connective tissue o Located external to epimysium o Separates different muscles while binding them together o Contains nerves, blood vessels, and lymph vessels Superficial fascia o Areolar and adipose tissue o Located superficial to deep fascia o Separates muscles from skin 8

9 10.2a Gross Anatomy of Skeletal Muscle Blood vessels and nerves Skeletal muscle has extensive blood vessels o Deliver oxygen and nutrients, removing waste products Skeletal muscle is innervated my somatic neurons o Axons of neurons branch, terminate at neuromuscular junctions o Can allow for voluntary control of contraction 9

10 10.2b Microscopic Anatomy of Skeletal Muscle What are the parts of a muscle cell (fiber)? Sarcoplasm (cytoplasm) o Has typical organelles plus contractile proteins and other specializations Multiple nuclei (individual cells are multinucleated) o o Cell is formed in embryo when multiple myoblasts fuse Some nearby myoblasts become undifferentiated satellite cells for support and repair of muscle fibers Sarcolemma (plasma membrane) o o Has T-tubules (transverse tubules) that extend deep into the cell Sarcolemma and its T-tubules have voltage-gated ion channels that allow for conduction of electrical signals 10

11 Development of Skeletal Muscle Figure

12 Structure and Organization of a Skeletal Muscle Fiber 12

13 Structure and Organization of a Skeletal Muscle Fiber Figure 10.3c 13

14 10.2b Microscopic Anatomy of Skeletal Muscle Parts of a muscle cell (continued) Sarcoplasm includes o Myofibrils (hundreds to thousands per cell) Bundles of myofilaments (contractile proteins) enclosed in sarcoplasmic reticulum Make up most of the cell s volume o Sarcoplasmic reticulum Internal membrane complex similar to smooth endoplasmic reticulum Terminal cisternae: blind sacs of sarcoplasmic reticulum» Serve as reservoirs for calcium ions» Combine in twos with central T-tubule to form triads 14

15 10.2b Microscopic Anatomy of Skeletal Muscle Sarcoplasmic reticulum (continued) Has pumps that import Ca 2+ into sarcoplasmic reticulum where it binds to calmodulin and calquestrin Has channels that allow Ca 2+ to be released into surrounding sarcoplasm to trigger contraction Figure 10.3d 15

16 10.2b Microscopic Anatomy of Skeletal Muscle Myofibrils contain thick and thin filaments Thick filaments o Consist of bundles of many myosin protein molecules Each myosin molecule has two heads and two intertwined tails Heads have binding site for actin of thin filaments and ATPase site Heads point toward ends of the filament 16

17 10.2b Microscopic Anatomy of Skeletal Muscle Myofibrils contain thick and thin filaments (continued) Thin filaments o Consist mostly of two twisted strands of fibrous actin (F-actin) o Each strand is a necklace of hundreds of actin globules (G-actin) o Each G-actin has a myosin binding site to which myosin heads attach during contraction o Troponin and tropomyosin are regulatory proteins of thin filament Tropomyosin: twisted stringlike protein covering actin in a noncontracting muscle Troponin: globular protein attached to tropomyosin When Ca 2+ binds to troponin it pulls tropomyosin off actin allowing contraction 17

18 Molecular Structure of Thick and Thin Filaments Figure

19 10.2b Microscopic Anatomy of Skeletal Muscle Organization of a sarcomere Myofilaments arranged in repeating units, sarcomeres Composed of overlapping thick and thin filaments Delineated at both ends by Z discs o o Specialized proteins perpendicular to myofilaments Anchors for thin filaments The positions of thin and thick filaments give rise to alternating I-bands and A-bands 19

20 10.2b Microscopic Anatomy of Skeletal Muscle Organization of a sarcomere (continued) I bands o o o A band o o o Light-appearing regions that contain only thin filaments Bisected by Z disc Get smaller when muscle contracts (can disappear with maximal contraction) Dark-appearing region that contains thick filaments and overlapping thin filaments Contains H zone and M line Makes up central region of sarcomere 20

21 10.2b Microscopic Anatomy of Skeletal Muscle Organization of a sarcomere (continued) H zone: central portion of A band o Only thick filaments present; no thin filament overlap o Disappears with maximal muscle contraction M line: middle of H zone o Protein meshwork structure o Attachment site for thick filaments Figure 10.5a 21

22 Structure of a Sarcomere Figure 10.5 b 22

23 10.2 Microscopic Anatomy of Skeletal Muscle Organization of a sarcomere (continued) Other structural and functional proteins o Connectin (Titin) Extends from Z disc to M line Stabilizes thick filaments and has springlike properties (passive tension) o Dystrophin Anchors some myofibrils to sarcolemma proteins Abnormalities of this protein cause muscular dystrophy 23

24 10.2b Microscopic Anatomy of Skeletal Muscle Mitochondria and other structures associated with energy production Muscle fibers have abundant mitochondria for aerobic ATP production Myoglobin within cells allows storage of oxygen used for aerobic ATP production Glycogen is stored for when fuel is needed quickly Creatinine phosphate can quickly give up its phosphate group to help replenish ATP supply 24

25 10.2c Innervation of Skeletal Muscle Fibers Motor unit: a motor neuron and all the muscle fibers it controls Figure 10.6a 25

26 10.2c Innervation of Skeletal Muscle Fibers Motor unit (continued) Axons of motor neurons from spinal cord (or brain) innervate numerous muscle fibers The number of fibers a neuron innervates varies o o Small motor units have less than five muscle fibers Allow for precise control of force output Large motor units have thousands of muscle fibers Allow for production of large amount of force (but not precise control) Fibers of a motor unit are dispersed throughout the muscle (not just in one clustered compartment) 26

27 10.2c Innervation of Skeletal Muscle Fibers Neuromuscular junction Location where motor neuron innervates muscle Usually mid-region of muscle fiber Has synaptic knob, synaptic cleft, motor end plate Figure 2.7a 27

28 Structure and Organization of a Neuromuscular Junction Figure 10.7b 28

29 10.2c Innervation of Skeletal Muscle Fibers Neuromuscular junction (continued) Synaptic knob Expanded tip of the motor neuron axon Houses synaptic vesicles o Small sacs filled with neurotransmitter acetylcholine (ACh) Has Ca 2+ pumps in plasma membrane o Establish calcium gradient, with more outside the neuron Has voltage-gated Ca 2+ channels in membrane o Ca 2+ flows into cell (down concentration gradient) if channels open 29

30 10.2c Innervation of Skeletal Muscle Fibers Neuromuscular junction (continued) Motor end plate Specialized region of sarcolemma with numerous folds Has many ACh receptors o Plasma membrane protein channels o Opened by binding of ACh o Allow Na + entry and K + exit Synaptic cleft Narrow fluid-filled space Separates synaptic knob from motor end plate Acetylcholinesterase resides here o Enzyme that breaks down ACh molecules 30

31 10.2d Skeletal Muscle Fibers at Rest Muscle fibers exhibit resting membrane potential (RMP) Fluid inside cell is negative compared to fluid outside cell RMP of muscle cell is about 90 mv RMP set by leak channels and Na + /K + pumps (voltage-gated channels are closed) Figure

32 Overview of Events in Skeletal Muscle Contraction Figure

33 10.3a Neuromuscular Junction: Excitation of a Skeletal Muscle Fiber What is the first step in the process of contraction? Neuron excites muscle fiber Calcium enters synaptic knob o Nerve signal travels down axon, opens voltage-gated Ca 2+ channels o Ca 2+ diffuses into synaptic knob o Ca 2+ binds to proteins on surface of synaptic vesicles Synaptic knob releases ACh o Vesicles merge with cell membrane at synaptic knob: exocytosis o Thousands of ACh molecules released from about 300 vesicles 33

34 10.3a Neuromuscular Junction: Excitation of a Skeletal Muscle Fiber Neuron excites muscle fiber (continued) ACh binds to its receptors at motor end plate o ACh diffuses across cleft, binds to receptors, excites fiber Figure

35 Clinical View: Myasthenia Gravis Autoimmune disease, primarily in women Antibodies bind to ACh receptors in neuromuscular junctions Receptors removed from muscle fiber by endocytosis Results in decreased muscle stimulation Rapid fatigue and muscle weakness Eye and facial muscles often involved first May be followed by swallowing problems, limb weakness 35

36 10.3b Sarcolemma, T-tubules, and Sarcoplasmic Reticulum: Excitation-Contraction Coupling Stimulation of the fiber is coupled with the sliding of filaments Coupling includes the end-plate potential (EPP), muscle action potential, and release of Ca 2+ from the sarcoplasmic reticulum 36

37 10.3b Sarcolemma, T-tubules, and Sarcoplasmic Reticulum: Excitation-Contraction Coupling 37

38 10.3b Sarcolemma, T-tubules, and Sarcoplasmic Reticulum: Excitation-Contraction Coupling End-plate potential (EPP) ACh receptors are chemically gated channels that open when ACh binds to them Na + diffuses into the cell through the channels (while a little K + diffuses out) Cell membrane briefly becomes less negative at the end plate region EPP is local but it does lead to the opening of voltage-gated ion channels in the adjacent region of the sarcolemma 38

39 10.3b Sarcolemma, T-tubules, and Sarcoplasmic Reticulum: Excitation-Contraction Coupling Initiation and propagation of action potential along the sarcolemma and T-tubules An action potential is a rapid rise (depolarization) and fall (repolarization) in the charge of the membrane o EPP reaches threshold by causing nearby voltage-gated Na + channels to open Na + diffuses into the cell through voltage-gated channels o Cell depolarizes: becomes less negative, eventually becomes +30 mv o This results in the opening of adjacent voltage-gated Na + channels and more Na + entry o A chain reaction occurs as depolarization is propagated down the membrane and T-tubules 39

40 10.3b Sarcolemma, T-tubules, and Sarcoplasmic Reticulum: Excitation-Contraction Coupling Initiation and propagation of action potential along the sarcolemma and T-tubules (continued) Just after Na + channels open, they close and voltage-gated K + channels open o K + diffuses out of the cell o Cell repolarizes: returns to 90mV o Repolarization is then propagated down the membrane and T-tubules While the cell is depolarizing and repolarizing it is in a refractory period unable to respond to another stimulation 40

41 10.3b Sarcolemma, T-tubules, and Sarcoplasmic Reticulum: Excitation-Contraction Coupling Events of an action potential at the sarcolemma Fig

42 10.3b Sarcolemma, T-tubules, and Sarcoplasmic Reticulum: Excitation-Contraction Coupling Release of Ca 2+ from the sarcoplasmic reticulum Action potential opens voltage-gated Ca 2+ channels of sarcoplasmic reticulum Ca 2+ diffuses out of cisternae into sarcoplasm Ca 2+ interacts with myofilaments triggering contraction 42

43 10.3c Sarcomere: Crossbridge Cycling When Ca 2+ binds to troponin, it triggers crossbridge cycling Troponin and tropomyosin move so actin is exposed Figure

44 10.3c Sarcomere: Crossbridge Cycling Crossbridge cycling: four repeating steps 1) Crossbridge formation Myosin head attaches to exposed binding site on actin 2) Power stroke Myosin head pulls thin filament toward center of sarcomere ADP and P i released 3) Release of myosin head ATP binds to myosin head causing its release from actin 4) Reset myosin head ATP split into ADP and P i by myosin ATPase Provides energy to cock the myosin head 44

45 10.3c Sarcomere: Crossbridge Cycling Figure

46 10.3c Sarcomere: Crossbridge Cycling Crossbridge cycling (continued) Cycling continues as long as Ca 2+ and ATP are present Results in sarcomere shortening as Z discs move closer together Narrowing (or disappearance) of H zone and I band Thick and thin filaments remain the same length but slide past each other 46

47 Sarcomere Shortening Figure

48 Clinical View: Muscular Paralysis and Neurotoxins Tetanus Spastic paralysis caused by toxin from Clostridium tetani Blocks release of inhibitory neurotransmitter in spinal cord, resulting in overstimulation of muscles Vaccination prevents this life-threatening condition Botulism Muscular paralysis caused by toxin from Clostridium botulinum Prevents release of ACh at synaptic knobs Although toxin ingestion can be life-threatening, careful injections of it can treat spasticity (e.g., due to cerebral palsy) or can be used for cosmetic purposes (diminishing wrinkles) 48

49 10.3d Skeletal Muscle Relaxation Events in muscle relaxation Termination of nerve signal and ACh release from motor neuron Hydrolysis of ACh by acetylcholinesterase Closure of ACh receptor causes cessation of end plate potential No further action potential generation Closure of calcium channels in sarcoplasmic reticulum Return of Ca 2+ to sarcoplasmic reticulum by pumps Return of troponin to original shape Return of tropomyosin blockade of actin s myosin binding sites Return of muscle to original position due to its elasticity 49

50 10.4a Supplying Energy for Skeletal Muscle Contraction Muscle cells have only a little ATP in storage Stored ATP is spent after about 5 seconds of intense exertion Three ways to generate ATP in skeletal muscle fiber Immediate supply via phosphate transfer Short-term supply via glycolysis Long-term supply via aerobic cellular respiration 50

51 10.4a Supplying Energy for Skeletal Muscle Contraction Immediate supply of ATP: phosphate (P i ) transfer Myokinase transfers P i from one ADP to another Creatine kinase transfers P i from creatine phosphate to ADP Figure

52 10.4a Supplying Energy for Skeletal Muscle Contraction Short-term supply of ATP: glycolysis Does not require oxygen Glucose (from muscle s glycogen or through blood) is converted to two pyruvate molecules 2 ATP released per glucose molecule Occurs in cytosol 52

53 10.4a Supplying Energy for Skeletal Muscle Contraction Long-term supply of ATP: aerobic cellular respiration Requires oxygen Occurs within mitochondria Pyruvate oxidized to carbon dioxide o Transfer of chemical bond energy to NADH and FADH 2 o Energy used to generate ATP by oxidative phosphorylation Produces a net of 30 ATP Triglycerides can also be used as fuel to produce ATP o More ATP from triglycerides with longer fatty acid chains 53

54 Metabolic Processes for Generating ATP Figure

55 10.4a Supplying Energy for Skeletal Muscle Contraction Source of ATP depends on intensity and duration of exercise For a 50-meter sprint (less than 10 seconds) o ATP supplied primarily by phosphate transfer system For a 400-meter sprint (less than a minute) o ATP supplied primarily by glycolysis after first few seconds For a 1500-meter run (more than a minute) o ATP supplied primarily by aerobic processes after first minute 55

56 Utilization of Immediate, Short-Term, and Long-Term Energy Sources Figure

57 10.4b Oxygen Debt Oxygen debt Amount of additional oxygen needed after exercise to restore pre-exercise conditions Additional oxygen required to o Replace oxygen on hemoglobin and myoglobin o Replenish glycogen o Replenish ATP and creatine phosphate o Convert lactic acid back to glucose 57

58 10.5a Criteria for Classification of Muscle Fiber Types Muscle fibers are categorized by two criteria 1. Type of contraction generated 2. Primary means used for supplying ATP 58

59 10.5a Criteria for Classification of Muscle Fiber Types Type of contraction generated Differences in power, speed, and duration o Power related to diameter of muscle fiber (larger are more powerful) o Speed and duration related to type of myosin ATPase (some catalyze faster), quickness of action potential propagation, and quickness of Ca 2+ release and reuptake by sarcoplasmic reticulum Fast-twitch fibers are more powerful and have quicker and briefer contractions than slow twitch fibers 59

60 10.5a Criteria for Classification of Muscle Fiber Types Primary means for supplying ATP Oxidative versus glycolytic fibers o Oxidative fibers (fatigue-resistant) use aerobic cellular respiration Extensive capillaries Many mitochondria Large supply of myoglobin (red fibers) o Glycolytic fibers (fatigable) use anaerobic cellular respiration Fewer capillaries Fewer mitochondria Smaller supply of myoglobin (white fibers) Large glycogen reserves 60

61 10.5b Classification of Muscle Fiber Types Three types of skeletal muscle fibers 1. Slow oxidative fibers (type I) o Contractions are slower and less powerful o High endurance since ATP supplied aerobically o About half the diameter of other fibers, red in color due to myoglobin 2. Fast oxidative fibers (type IIa, intermediate) o Contractions are fast and powerful o Primarily aerobic respiration, but delivery of oxygen lower o Intermediate size, light red in color 3. Fast glycolytic fibers (type IIb, fast anaerobic) o Contractions are fast and powerful o Contractions are brief, as ATP production is primarily anaerobic o Largest size, white in color due to lack of myoglobin 61

62 10.5c Distribution of Muscle Fiber Types A single muscle contains a mixture of fiber types There are variations in proportions of fiber types in different muscle groups Hand muscles have a high percentage of fast glycolytic fibers for quickness Back muscles have a high percentage of slow oxidative fibers to continually maintain postural support 62

63 10.5c Distribution of Muscle Fiber Types Long-distance runners Higher proportion of slowoxidative fibers in legs Sprinters Higher percentage of fast glycolytic fibers Determined primarily by genes Determined partially by training Figure

64 10.6 Measurement of Skeletal Muscle Tension Muscle tension Tension is the force generated when a muscle is stimulated to contract Lab experiments measure tension and graph it (myogram) Fig

65 10.6a Muscle Twitch A twitch is a brief contraction to a single stimulus The minimum voltage that triggers a twitch is threshold stimulus Periods of the twitch Latent period o Time after stimulus but before contraction begins o No change in tension Contraction period o Time when tension is increasing o Begins as power strokes pull thin filaments Relaxation period o Time when tension is decreasing to baseline o Begins with release of crossbridges o Generally lasts a little longer than contraction period 65

66 10.6b Motor Unit Recruitment Muscle is stimulated repeatedly As voltage increases, more units are recruited to contract Figure

67 10.6b Motor Unit Recruitment Recruitment is also called multiple motor unit summation It explains how muscles exhibit varying degrees of force Recruit just a few motor units to lift a pencil Recruit many motor units to lift a suitcase Above a certain voltage, all units are recruited, and so maximum contraction occurs (regardless of how much higher voltage is) 67

68 What is treppe? 10.6c Treppe, Wave Summation, Incomplete Tetany, and Tetany An increase in twitch tension when stimuli occur times per second Voltage is the same for each stimulus and relaxation is complete for each twitch Twitches get stronger due to o Insufficient time to remove all Ca 2+ between twitches o Increased heat improves enzyme efficiency Figure 10.23b 68

69 10.6c Changes in Stimulus Frequency: Treppe, Wave Summation, Incomplete Tetany, and Tetany Wave summation (temporal summation) If stimulus frequency set at about 20 per second o Relaxation is not completed between twitches o Contractile forces add up to produce higher tensions Incomplete tetany and tetany If frequency is increased further, myogram exhibits incomplete tetany o Tension increases and twitches partially fuse If frequency is increased further still (e.g., per second), myogram exhibits tetany o Tension trace is a smooth line without relaxation High frequency stimuli lead to fatigue (decreased tension production) 69

70 Skeletal Muscle Response to Change in Stimulation Frequency Figure 10.23c 70

71 10.7a Muscle Tone Muscle tone Resting tension in a muscle Generated by involuntary nervous stimulation of muscle Some motor units stimulated randomly at any time Change continuously so units not fatigued Do not generate enough tension for movement Decreases during deep sleep 71

72 10.7b Isometric and Isotonic Contractions Isometric contraction Although tension is increased, it is insufficient to overcome resistance Muscle length stays the same E.g., holding a weight while arm doesn t move Isotonic contraction Muscle tension overcomes resistance resulting in movement Tone stays constant, but length changes Concentric contraction o Muscle shortens as it contracts o E.g., in the biceps brachii when lifting a load Eccentric contraction, subtype o Muscle lengthens as it contracts o E.g., in the biceps brachii when lowering a load 72

73 Isometric Versus Isotonic Contraction Figure

74 Clinical View: Isometric Contraction and Increase in Blood Pressure Sustained isometric contractions o Associated with increase in blood pressure May be a concern for those with baseline high blood pressure E.g., shoveling snow o General peripheral constriction (from cold) elevates pressure o Isometric contractions of shoveling also increase pressure 74

75 10.7c Length-Tension Relationship The tension a muscle produces depends on its length at the time of stimulation Fiber at resting length generates maximum contractile force o Optimal overlap of thick and thin filaments Fiber at a shortened length generates weaker force o Filament movement is limited (already close to Z disc) Fiber at an extended length generates weaker force o Minimal thick and thin filament overlap for crossbridge formation 75

76 Length-Tension Curve Figure

77 10.7d Muscle Fatigue Fatigue: reduced ability to produce muscle tension Primarily caused by a decrease in glycogen stores during prolonged exercise Other possible causes of fatigue Problems of excitation at neuromuscular junction o Insufficient Ca 2+ to enter synaptic knob o Decreased number of synaptic vesicles Problems with excitation contraction coupling o Altered ion concentrations impair action potential conduction and Ca 2+ release from sarcoplasmic reticulum Problems with crossbridge cycling o Excessive P i slows release of P i from myosin head o Less Ca 2+ available for troponin (some Ca 2+ is bound to P i ) 77

78 10.8a Effects of Exercise What changes occur in muscle in response to exercise? Endurance exercise leads to better ATP production (e.g., more mitochondria) Resistance exercise leads to hypertrophy o o o Muscle increases in size due to increases in synthesis of contractile proteins Muscle also increases glycogen reserves and mitochondria Also appears to stimulate limited amount of hyperplasia (increase in number of fibers) What changes result from lack of exercise? Atrophy: decrease in size due to lack of use o o E.g., someone wearing a cast Initially reversible, but becomes permanent if extreme 78

79 10.8b Effects of Aging Loss of muscle mass with age Slow loss begins in person s mid-30s due to decrease in activity Decreased size, power, and endurance of skeletal muscle Loss in fiber number and diameter (decrease in myofibrils) Decreased oxygen storage capacity Decreased circulatory supply to muscles with exercise Reduced capacity to recover from injury Decreased number of satellite cells Fibrosis: muscle mass often replaced by dense regular connective tissue o Decreased flexibility 79

80 Clinical View: Anabolic Steroids as Performance-Enhancing Compounds Anabolic steroids Synthetic substances that mimic testosterone Require prescription for legal use Stimulate manufacture of muscle proteins Popular performance enhancers Side effects include o Increased risk of heart disease and stroke o Kidney damage and liver tumors o Testicular atrophy, breast development in males o Acne, high blood pressure, aggressive behavior o Growth of facial hair and menstrual irregularities in women 80

81 Cardiac muscle cells 10.9 Cardiac Muscle Tissue Short, branching fibers One or two nuclei Striated (contain sarcomeres) Many mitochondria use aerobic respiration Intercalated discs join ends of neighboring fibers o Discs contain desmosomes and gap junctions Contractions started by heart s autorhythmic pacemaker cells Heart rate and contraction force influenced by autonomic nervous system 81

82 Cardiac Muscle Figure

83 10.10a Location of Smooth Muscle Smooth muscle is found in a variety of organ systems with a variety of roles In blood vessels of cardiovascular system o Helps regulate blood pressure and flow In bronchioles of respiratory system o Controls airflow to alveoli In intestines of digestive system o Mixes and propels materials In ureters of urinary system o Propels urine from kidneys to bladder In uterus of female reproductive system o Delivers baby Several other locations and functions 83

84 Location of Smooth Muscle Figure

85 10.10b Microscopic Anatomy of Smooth Muscle Smooth muscle cells have fusiform shape Wide in the middle with tapered ends Smaller than skeletal muscle fibers Sarcolemma has varied types of Ca 2+ channels (gated by chemicals, voltage, etc.) Transverse tubules absent Surface area increased by caveolae (flasklike invaginations) Sarcoplasmic reticulum sparse Outside of cell is important source of Ca 2+ 85

86 Microscopic Anatomy of Smooth Muscle Figure

87 10.10b Microscopic Anatomy of Smooth Muscle Arrangement of anchoring proteins and contractile proteins of smooth muscle Cytoskeleton composed of extensive intermediate filaments o Dense bodies: points where intermediate filaments interact within sarcoplasm o Dense plaques: points where intermediate filaments attach on inner sarcolemma Contractile proteins o Arranged between dense bodies and dense plaques o Oriented at oblique angles to longitudinal axis of cell o Contraction causes a twisting motion Lack sarcomeres and Z discs (smooth = no striations) 87

88 10.10b Microscopic Anatomy of Smooth Muscle Like skeletal muscle, smooth muscle filaments have actin, myosin, and troponin Unlike skeletal muscle, smooth muscle Filaments have myosin heads along their entire length; can form many crossbridges Filaments have latchbridge mechanism: myosin attaches to actin for extended time without burning extra ATP Has calmodulin: protein that binds Ca 2+ to trigger contraction Has myosin light-chain kinase (MLCK): enzyme that phosphorylates myosin heads when activated by calmodulin Has myosin light-chain phosphatase: enzyme that dephosphorylates myosin head (required for relaxation) 88

89 Smooth Muscle Contraction Figure

90 10.10c Smooth Muscle Contraction Steps of contraction Stimulus leads to opening of voltage-gated Ca 2+ channels Ca 2+ enters sarcoplasm and binds to calmodulin Calcium-calmodulin complex binds to MLCK MLCK phosphorylates myosin head Myosin head attaches to actin, hydrolyzes ATP, pulls on actin o Process is repeated frequently so that cell shortens 90

91 10.10c Smooth Muscle Contraction Relaxation of smooth muscle Cessation of stimulation Removal of Ca 2+ from sarcoplasm Dephosphorylation of myosin by myosin light-chain phosphatase Can be slow to relax due to latchbridge mechanism 91

92 10.10c Smooth Muscle Contraction Smooth muscle contraction characteristics Long latent period o Takes time to phosphorylate myosin head o Slow ATPase activity Long duration o Slow calcium pumps o Need for dephosphorylation of myosin head o Latchbridge mechanism Slowness fits its functional requirements o Extended contractions maintain continuous tone E.g., in walls of blood vessels 92

93 10.10c Smooth Muscle Contraction Smooth muscle contraction characteristics (continued) Fatigue-resistant Energy requirements low compared to skeletal muscle ATP supplied through aerobic cellular respiration Can maintain contraction without ATP through latchbridge mechanism 93

94 10.10c Smooth Muscle Contraction Smooth muscle contraction characteristics (continued) Length-tension curve Exhibits broader curve than skeletal muscle o Lacks limitations due to Z discs o Myosin heads present in center of thick filaments Can contract forcefully not only at rest, but also o when compressed to half resting length o when stretched to double resting length E.g., allows emptying bladder regardless of amount of urine 94

95 10.10d Controlling Smooth Muscle Control of smooth muscle Autonomic (involuntary) nervous system secretes transmitters o Muscle s response depends on neurotransmitter present and muscle s receptor for it o E.g., smooth muscle of bronchioles contracts in response to ACh and relaxes in response to norepinephrine Response to stretch o Myogenic response is contraction in reaction to stretch o Stress-relaxation response is relaxation after prolonged stretch Other stimulating factors include: o Various hormones, low ph, low O 2, high CO 2, certain drugs GI tract smooth muscle can be stimulated by pacemaker cells 95

96 10.10e Functional Categories Two categories of smooth muscle: multiunit and single unit Multiunit smooth muscle Arranged in units that receive stimulation to contract individually Found in o Iris and ciliary muscles of the eye o Arrector pili muscles in skin o Larger air passageways in respiratory system o Walls of larger arteries Degree of contraction depends on number of motor units activated 96

97 10.10e Functional Categories Single-unit (visceral) smooth muscle Stimulated to contract in unison as cells linked by gap junctions Form two or three sheets in wall of hollow organ More common type; locations include o Walls of digestive, urinary, and reproductive tracts o Portions of respiratory tract o Most blood vessels 97

98 10.10e Functional Categories Stimulation of single-unit smooth muscle Occurs through varicosities swellings of autonomic neurons Varicosities contain synaptic vessels with one type of neurotransmitter o Either ACh or norepinephrine Receptors scattered across the sarcolemma Numerous smooth muscle cells stimulated simultaneously Stimulation spread from cell to cell via gap junctions so contraction is synchronous 98

99 Multiunit and Single-Unit Smooth Muscle Figure