Biology 111 Muscle and Muscle Tissue Part 2 PDF

BIOL 111: MUSCLE AND MUSCLE TISSUE Instructor: Dr. Pamela Paynter-Armour  OBJECTIVES Identify the requirements for Skeletal Muscle Contraction Describe the events at the Neuromuscular Junction Describe the events in Generation of an Action Potential Discuss...

BIOL 111: MUSCLE AND MUSCLE TISSUE Instructor: Dr. Pamela Paynter-Armour  OBJECTIVES Identify the requirements for Skeletal Muscle Contraction Describe the events at the Neuromuscular Junction Describe the events in Generation of an Action Potential Discuss the Excitation-Contraction (E-C) Coupling events Describe the anatomy and physiology of smooth muscles  REQUIREMENTS FOR SKELETAL MUSCLE CONTRACTION 1. Activation: neural stimulation at a neuromuscular junction 2. Excitation-contraction coupling: Generation and propagation of an action potential along the sarcolemma Final trigger: a brief rise in intracellular Ca2+ levels (Meeking, 2010).  EVENTS AT THE NEUROMUSCULAR JUNCTION Skeletal muscles are stimulated by somatic motor neurons Axons of motor neurons travel from the central nervous system via nerves to skeletal muscles Each axon forms several branches as it enters a muscle Each axon ending forms a neuromuscular junction with a single muscle fiber (Meeking, 2010).  Myelinated axon Action of motor neuron potential (AP) Axon terminal of Nucleus neuromuscular junction Sarcolemma of the muscle fiber 1 Action potential arrives at axon terminal of motor neuron. Ca2+ Synaptic vesicle Ca2+ 2 Voltage-gated Ca2+ channels containing ACh open and Ca2+ enters the axon Mitochondrion terminal. Synaptic Axon terminal of motor neuron cleft Fusing synaptic vesicles (Meeking, 2010).  NEUROMUSCULAR JUNCTION Where motor neuron meets muscle fiber Components Synaptic knob Synaptic vesicles Acetylcholine (ACh) Motor end plate ACh receptors Synaptic cleft Acetylcholinesterase (McKinley & O'Loughlin, n.d.) 6  7 (McKinley & O'Loughlin, n.d.)  NEUROMUSCULAR JUNCTION Situated midway along the length of a muscle fiber Axon terminal and muscle fiber are separated by a gel-filled space called the synaptic cleft Synaptic vesicles of axon terminal contain the neurotransmitter acetylcholine (ACh) Junctional folds of the sarcolemma contain ACh receptors (Meeking, 2010).  EVENTS AT THE NEUROMUSCULAR JUNCTION Nerve impulse arrives at axon terminal ACh is released and binds with receptors on the sarcolemma Electrical events lead to the generation of an action potential (Meeking, 2010).  DESTRUCTION OF ACETYLCHOLINE ACh effects are quickly terminated by the enzyme acetylcholinesterase Prevents continued muscle fiber contraction in the absence of additional stimulation (Meeking, 2010).  Myelinated axon Action of motor neuron potential (AP) Axon terminal of Nucleus neuromuscular junction Sarcolemma of the muscle fiber 1 Action potential arrives at axon terminal of motor neuron. Ca2+ Synaptic vesicle Ca2+ 2 Voltage-gated Ca channels 2+ containing ACh open and Ca2+ enters the axon Mitochondrion terminal. Axon terminal Synaptic of motor neuron cleft 3 Ca2+ entry causes some Fusing synaptic synaptic vesicles to release vesicles their contents (acetylcholine) Junctional by exocytosis. ACh folds of sarcolemma 4 Acetylcholine, a neurotransmitter, diffuses across Sarcoplasm of the synaptic cleft and binds to muscle fiber receptors in the sarcolemma. 5 ACh binding opens ion Na+ K+ Postsynaptic membrane channels that allow simultaneous ion channel opens; passage of Na+ into the muscle ions pass. fiber and K+ out of the muscle fiber. 6 ACh effects are terminated Ach– Degraded ACh Na+ Postsynaptic membrane by its enzymatic breakdown in ion channel closed; the synaptic cleft by ions cannot pass. acetylcholinesterase. Acetyl- cholinesterase K+ (Meeking, 2010). Figure 9.8  EVENTS IN GENERATION OF AN ACTION POTENTIAL 1. Local depolarization (end plate potential): ACh binding opens chemically (ligand) gated ion channels Simultaneous diffusion of Na+ (inward) and K+ (outward) More Na+ diffuses, so the interior of the sarcolemma becomes less negative Local depolarization – end plate potential (Meeking, 2010). EVENTS IN GENERATION OF AN ACTION POTENTIAL 2. Generation and propagation of an action potential: End plate potential spreads to adjacent membrane areas Voltage-gated Na+ channels open Na+ influx decreases the membrane voltage toward a critical threshold If threshold is reached, an action potential is generated (Meeking, 2010).  EVENTS IN GENERATION OF AN ACTION POTENTIAL Local depolarization wave continues to spread, changing the permeability of the sarcolemma Voltage-regulated Na+ channels open in the adjacent patch, causing it to depolarize to threshold (Meeking, 2010).  EVENTS IN GENERATION OF AN ACTION POTENTIAL 3. Repolarization:  Na+ channels close and voltage- gated K+ channels open  K+ efflux rapidly restores the resting polarity  Fiber cannot be stimulated and is in a refractory period until repolarization is complete  Ionic conditions of the resting state are restored by the Na+-K+ pump (Meeking, 2010).  Axon terminal Open Na+ Closed K+ Channel Channel Synaptic Na+ cleft ACh Na+ K+ K+ ++ + ACh ++ + + Action potential + +++ + n Na+ K+ tio 2 Generation and propagation of za l a ri the action potential (AP) po de of e Wav Closed Na+ Open K+ Channel Channel 1 Local depolarization: Na+ generation of the end plate potential on the sarcolemma K+ Sarcoplasm of muscle fiber 3 Repolarization (Meeking, 2010).  Axon terminal Open Na+ Closed K+ Channel Channel Synaptic Na+ cleft ACh K+ Na + K + ++ + + +++ ACh n ++ + + Action potential + Na+ K+ tio iza l ar d ep o of ve Wa 1 Local depolarization: generation of the end plate potential on the sarcolemma Sarcoplasm of muscle fiber (Meeking, 2010).  Axon terminal Open Na+ Closed K+ Channel Channel Synaptic Na+ cleft ACh K+ Na + K + ++ + + +++ ACh n ++ + + Action potential + Na+ K+ tio iza 2 Generation and propagation of the l ar action potential (AP) d ep o of ve Wa 1 Local depolarization: generation of the end plate potential on the sarcolemma Sarcoplasm of muscle fiber (Meeking, 2010).  Closed Na+ Open K+ Channel Channel Na+ K+ 3 Repolarization (Meeking, 2010).  (Meeking, 2010). Axon terminal Open Na+ Closed K+ Channel Channel Synaptic Na+ cleft ACh Na+ K+ K+ ++ + ACh ++ + + Action potential + +++ + n Na+ K+ tio 2 Generation and propagation of za l a ri the action potential (AP) po de of e Wav Closed Na+ Open K+ 1 Channel Channel Local depolarization: Na+ generation of the end plate potential on the sarcolemma K+ Sarcoplasm of muscle fiber 3 Repolarization  Na+ channels close, K+ channels Depolarization open due to Na+ entry Repolarization due to K+ exit Na+ channels open Threshold K+ channels close (Meeking, 2010).  EXCITATION- CONTRACTION (E-C) COUPLING Sequence of events by which transmission of an AP along the sarcolemma leads to sliding of the myofilaments Latent period: Time when E-C coupling events occur Time between AP initiation and the beginning of contraction (Meeking, 2010).  EVENTS OF EXCITATION- CONTRACTION (E-C) COUPLING AP is propagated along sarcomere to T tubules Voltage-sensitive proteins stimulate Ca2+ release from SR Ca2+ is necessary for contraction (Meeking, 2010).  MECHANISM OF CONTRACTION 1. Calcium binds to TnC 2. Conformational change in troponin exposes myosin binding site on actin 3. Myosin binds to actin 4. ATP cleavage causes myosin to bend 5. This causes actin filament to move pass myosin 6. A new ATP binds to myosin head. This causes head to de-attach and swing back on hinge(Donley, 2004)  Setting the stage Axon terminal of motor neuron Synaptic cleft Action potential is generated ACh Sarcolemma Terminal cisterna of SR Muscle fiber Ca2+ Triad One sarcomere (Meeking, 2010).  Steps in E-C Coupling: Sarcolemma Voltage-sensitive T tubule tubule protein 1 Action potential is propagated along the sarcolemma and down the T tubules. Ca2+ release channel 2 Calcium ions are released. Terminal cisterna of SR Ca2+ Actin Troponin Tropomyosin Ca2+ blocking active sites Myosin 3 Calcium binds to troponin and removes the blocking action of tropomyosin. Active sites exposed and ready for myosin binding 4 Contraction begins Myosin cross bridge The aftermath (Meeking, 2010).  1 Action potential is propagated along the sarcolemma and down Steps in the T tubules. E-C Coupling: Sarcolemma Voltage-sensitive T tubule tubule protein Ca2+ release channel Terminal cisterna of SR Ca2+ (Meeking, 2010).  1 Action potential is propagated along the sarcolemma and down Steps in the T tubules. E-C Coupling: Sarcolemma Voltage-sensitive T tubule tubule protein Ca2+ release channel 2 Calcium ions are Terminal released. cisterna of SR Ca2+ (Meeking, 2010).  Actin Troponin Tropomyosin Ca2+ blocking active sites Myosin The aftermath (Meeking, 2010).  Actin Troponin Tropomyosin Ca2+ blocking active sites Myosin 3 Calcium binds to troponin and removes the blocking action of tropomyosin. Active sites exposed and ready for myosin binding The aftermath (Meeking, 2010).  Actin Troponin Tropomyosin Ca2+ blocking active sites Myosin 3 Calcium binds to troponin and removes the blocking action of tropomyosin. Active sites exposed and ready for myosin binding 4 Contraction begins Myosin cross bridge The aftermath (Meeking, 2010).  Steps in E-C Coupling: Sarcolemma Voltage-sensitive T tubule tubule protein 1 Action potential is propagated along the sarcolemma and down the T tubules. Ca2+ release channel 2 Calcium ions are released. Terminal cisterna of SR Ca2+ Actin Troponin Tropomyosin Ca2+ blocking active sites Myosin 3 Calcium binds to troponin and removes the blocking action of tropomyosin. Active sites exposed and ready for myosin binding 4 Contraction begins Myosin cross bridge The aftermath (Meeking, 2010).  ROLE OF CALCIUM (CA2+) IN CONTRACTION At low intracellular Ca2+ concentration: Tropomyosin blocks the active sites on actin Myosin heads cannot attach to actin Muscle fiber relaxes (Meeking, 2010).  ROLE OF CALCIUM (CA2+) IN CONTRACTION At higher intracellular Ca2+ concentrations: Ca2+ binds to troponin Troponin changes shape and moves tropomyosin away from active sites Events of the cross bridge cycle occur When nervous stimulation ceases, Ca2+ is pumped back into the SR and contraction ends (Meeking, 2010).  CROSS BRIDGE CYCLE Continues as long as the Ca2+ signal and adequate ATP are present Cross bridge formation—high-energy myosin head attaches to thin filament Working (power) stroke—myosin head pivots and pulls thin filament toward M line (Meeking, 2010).  CROSS BRIDGE CYCLE Cross bridge detachment—ATP attaches to myosin head and the cross bridge detaches “Cocking” of the myosin head— energy from hydrolysis of ATP cocks the myosin head into the high- energy state (Meeking, 2010).  Thin filament Actin Ca2+ ADP Myosin Pi cross bridge Thick filament Myosin 1 Cross bridge formation. ADP ADP Pi Pi ATP hydrolysis The power (working) 2 stroke. 4 Cocking of myosin head. ATP ATP 3 Cross bridge detachment. (Meeking, 2010).  Actin Ca2+ Thin filament ADP Myosin Pi cross bridge Thick filament Myosin 1 Cross bridge formation. (Meeking, 2010).  ADP Pi 2 The power (working) stroke. (Meeking, 2010).  ATP 3 Cross bridge detachment. (Meeking, 2010).  ADP Pi ATP hydrolysis 4 Cocking of myosin head. (Meeking, 2010).  Thin filament Actin Ca2+ ADP Myosin Pi cross bridge Thick filament Myosin 1 Cross bridge formation. ADP ADP Pi ATP Pi hydrolysis 4 Cocking of myosin head. 2 The power (working) stroke. ATP ATP 3 Cross bridge detachment. (Meeking, 2010).  SOME SITES SHOWING ANIMATIONS OF MUSCLE CONTRACTION http://www.physioviva.com/movies/muscle_struc-func-h uman/index.html http://www.brookscole.com/chemistry_d/templates/ student_resources/shared_resources/animations/ muscles/muscles.html  ALL-OR-NONE PRINCIPLE All-or-none principle: A muscle fiber either contracts completely or does not contract at all. When a motor unit is stimulated, all its fibers contract at the same time. The total force exerted by the muscle depends on the number of activated motor units. (McKinley & O'Loughlin, n.d.)  CONTRACTION Isometric length of the muscle does not change because the tension produced never exceeds the resistance (load) tension is generated, but not enough to move the load Isotonic tension produced exceeds the resistance (load), and the muscle fibers shorten, resulting in movement (McKinley & O'Loughlin, n.d.) 46  THREE TYPES OF SKELETAL MUSCLE FIBERS Fast are large in diameter contain large glycogen reserves densely packed myofibrils relatively few mitochondria called white fibers due to lack of myoglobin majority of skeletal muscle fibers in the body Intermediate resemble fast fibers; however have a greater resistance to fatigue Slow smaller and they contract more slowly called red fibers because due to myoglobin (McKinley & O'Loughlin, n.d.) SMOOTH MUSCLE Visceral (Smooth) Found in the internal organs of the body such as the digestive system, respiratory system, blood vessels, and eyes. Contract to cause movement in these systems Involuntary: function without conscious thought or control Smooth Muscle Contraction Resembles skeletal muscle contraction interaction between actin and myosin both use calcium and ATP both depend on impulses Different from skeletal muscle contraction smooth muscle lacks troponin smooth muscle depends on calmodulin two neurotransmitters affect smooth muscle acetlycholine and norepinephrine hormones affect smooth muscle stretching can trigger smooth muscle contraction smooth muscle slower to contract and relax smooth muscle more resistant to fatigue  SMOOTH MUSCLE Found in visceral organs, arteries and veins, iris of the eye Each cell is surrounded by reticular fibers and a basal lamina These harnesses help to convey force started by smooth muscle contraction (Donley, 2004)  SMOOTH MUSCLE Composed of short muscle fibers that have a fusiform shape and single centrally located nucleus. Thick and thin filaments are not precisely aligned so no visible striations or sarcomeres are present. Z discs are absent - thin filaments are attached to dense bodies by elements of the cytoskeleton. (McKinley & O'Loughlin, n.d.)  SMOOTH MUSCLE Sarcoplasmic reticulum is sparse. Transverse tubules are absent. Contraction is slow, resistant to fatigue, and usually sustained for an extended period of time. Takes longer than skeletal muscle to contract and relax. Contraction is under involuntary control. (McKinley & O'Loughlin, n.d.) (McKinley & O'Loughlin, n.d.) 58  SMOOTH MUSCLE No T-tubules, SR is poorly developed Actin and myosin are no organized into lattice network. Excitation-contraction coupling- Calcium binds to calmodulin Causes phosphorylation of myosin light chain kinase No tropomyosin (Donley, 2004) (Donley, 2004)  Contraction in smooth muscle is controlled by phosphorylation of myosin (Donley, 2004) Figure 10—30. Drawing of a segment of smooth muscle. All cells are surrounded by a net of reticular fibers. In cross section, these cells show various diameters.  Figure 10—33. Smooth muscle cells relaxed and contracted. Cytoplasmic filaments insert on dense bodies located in the cell membrane and deep in the cytoplasm. Contraction of these filaments decreases the size of the cell and promotes the contraction of the whole muscle. During the contraction the cell nucleus is deformed. (Donley, 2004)  MUSCLE ATROPHY Reduction in muscle size, tone, and power. Due to reduced stimulation, it loses both mass and tone. Muscle becomes flaccid, and its fibers decrease in size and become weaker. Even a temporary reduction in muscle use can lead to muscular atrophy. (McKinley & O'Loughlin, n.d.)  MUSCLE HYPERTROPHY An increase in muscle fiber size. Muscle size may be improved by exercising. Repetitive, exhaustive stimulation of muscle fibers results in more mitochondria, larger glycogen reserves, and an increased ability to produce ATP. Ultimately, each muscle fiber develops more myofibrils, and each myofibril contains a larger number of myofilaments. (McKinley & O'Loughlin, n.d.) § RIGOR MORTIS (DEATH RIGOR) Symptom: stiffening of the body beginning 3 to 4 hours after death Causes: Calcium activates myosin-actin cross- bridging and muscle contracts, but can not relax. Mechanisms: muscle relaxation requires ATP and ATP production is no longer produced after death Thick and thin filaments remain rigidly cross- linked. Fibers remain contracted until myofilaments decay, proteins break down. Take home message-- Cross bridge detachment is ATP required University of Tennessee at Martin. (n.d.).  IDENTIFY THE MUSCLE Cardiac Smooth Skeletal 1. What is the basic functional unit of skeletal muscle tissue? a) the muscle fibre b) the sarcomere c) the myofibril d) the sarcoplasmic reticulum 2. IN MUSCLE CONTRACTION, THIS ION IS ESSENTIAL (a) Cl (b) Ca (c) K (d) Na  3. MUSCLES UTILIZED FOR CONTROLLING THE FLOW OF ALL SUBSTANCES WITHIN LUMEN ARE GROUPED AS (a) hormonal system (b) skeletal system (c) cardiac muscles (d) smooth muscles  4. TENDONS CONNECT BONE AND a) Bone b) Ligaments c) Muscle d) Cartilage  5. WHICH OF THE FOLLOWING IS NOT A KIND OR TYPE OF MUSCLE? a) Cardiac b) Skeletal c) Sesamoids. d) Smooth  REFERENCES Career and Technical Education. (n.d.). Muscle and Muscle Tissues. Retrieved from http://cte.unt.edu/content/files/_HS/cur riculum/Muscle_and_Tissues.ppt Donley. (2004).Muscle Tissue. Retrieved from https://www.google.tt/#q=muscle+an d+muscle+tissue+ppt  REFERENCES CONT’D McKinley & O'Loughlin. (n.d.). Muscle Tissue and Organization. Retrieved from http://www.google.tt/url? sa=t&rct=j&q=&esrc=s&frm=1&source=web&cd=1 0&ved=0CFsQFjAJ&url=http%3A%2F %2Ffaculty.orangecoastcollege.edu%2Fhapp %2Fpresentations%2Fbio220%2FMcKinley %2FCh10%2520Muscle%2520Tissue.ppt&ei=K- dfUr67Ko3- 8QSmmoGgAw&usg=AFQjCNE_1QdYorcXKbsiOpdBYs 5N98IVzw Meeking, J. (2010). Muscles and Muscle Tissue. Retrieved from  REFERENCES CONT’D Shier, D., Butler, J. and Lewis, R. (n.d.). Muscular System. Retrieved from http://www.google.tt/url? sa=t&rct=j&q=&esrc=s&frm=1&sourc e=web&cd=10&ved=0CFoQFjAJ&url= http%3A%2F%2Fwww.rtmsd.org %2Fcms%2Flib %2FPA01000204%2FCentricity %2FDomain %2F170%2Fchapt09_lecture.ppt&ei=N OtfUt7hIoKE9QScsoCgDg&usg=AFQjC NHpXAt5DsPap6KoLqVL1erYlylg5Q  REFERENCES CONT’D University of Tennessee at Martin. (n.d.). Chapter 11– Muscular Tissue. Retrieved from http://www.google.tt/url? sa=t&rct=j&q=&esrc=s&frm=1&sourc e=web&cd=1&ved=0CCUQFjAA&url= http%3A%2F%2Fwww.utm.edu %2Fstaff%2Fdonalds%2Fa-p- 1%2Flecture-notes%2Fch11-Muscular- tissue.ppt&ei=z- NbUryiJYiGkQf7t4CIAw&usg=AFQjCNFC dQI5oZ7wjTC3z9HDi9RO39YHXQ&bvm =bv.53899372,d.eW0