Chapter 11 Muscles PDF
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This document provides information on muscle tissues. It details different types of muscles such as skeletal, cardiac, and smooth, their functions, characteristics, anatomy and related topics of the human body. The document also covers muscle attachments, muscle proteins and the sliding filament theory. It is suitable for secondary school biology students.
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Chapter 11 Muscles & Muscle Tissue "We cannot become what we need to be by remaining what we are“ - Max DePree - The Muscular System ❑ 600 Skeletal muscles ❑ Most attached to bones ❑ Muscles shorten by converting the chemical energy of ATP into mechanical energ...
Chapter 11 Muscles & Muscle Tissue "We cannot become what we need to be by remaining what we are“ - Max DePree - The Muscular System ❑ 600 Skeletal muscles ❑ Most attached to bones ❑ Muscles shorten by converting the chemical energy of ATP into mechanical energy Myology: Study of Muscles Introduction to Muscle 3 Types of muscle: 1. Skeletal (voluntary, Striated, multinucleated) 2. Cardiac (heart: Striated, branched, involuntary) 3. Smooth (hollow organs, involuntary, non- striated) Functions of Muscles 1. Movement of body parts and organ contents 2. Stability: maintain posture and prevent unwanted movement (fixing a joint) 3. Communication - speech, expression & writing 4. Control of openings and passageways 5. Body heat production: Skeletal muscles produce upto 85% of body heat Characteristics of Muscle 1. Responsiveness (excitability or irritabiity) – Receive and respond to stimuli (chemical signals, stretch) or other signals with electrical changes across the plasma membrane 2. Conductivity – Local electrical change triggers a wave of excitation that travels along the muscle fiber 3. Contractility -- shorten when stimulated 4. Extensibility -- capable of being stretched 5. Elasticity -- returns to its original resting length after being stretched Anatomy of Skeletal Muscle Skeletal muscle cell (also called muscle fiber) – 10 to 100 µm in diameter, up to 30 cm long Bundled together in groups called fascicles Skeletal muscle is composed of 2 types of tissue: 1. Muscular Tissue 2. Connective Tissue Connective Tissues of a Muscle 1. Epimysium (outside the muscle) – Covers whole muscle belly – Blends into connective tissue that separates muscles 2. Perimysium (around the muscle) – Slightly thicker layer of connective tissue – Surrounds a bundle of cells called a fascicle 3. Endomysium (within the muscle) – Thin layer of tissue surrounding each cell/fiber – Allows room for capillaries and nerve fibers Epimysium Bone Epimysium Perimysium Tendon Endomysium Muscle fiber in middle of a fascicle (b) Blood vessel Fascicle (wrapped by perimysium) Endomysium (between individual muscle fibers) Perimysium Fascicle Muscle fiber Muscle Attachments 2 ways a muscle can attach to bone: 1. Direct (fleshy) attachment to bone – Epimysium is continuous with periosteum – Intercostal muscles 2. Indirect attachment to bone – Epimysium continues as tendon that merges into periosteum as perforating fibers – Biceps brachii muscle – Stress will tear the tendon before pulling the tendon loose from either muscle or bone Anatomy of Skeletal Muscle Voluntary striated muscle attached to bones Skeletal muscle cell (also called muscle fiber) – 10 to 100 µm in diameter, up to 30 cm long Exhibits alternating light and dark bands (striations – striated muscle) – Reflects overlapping arrangement of internal contractile proteins Under conscious control Epimysium Bone Perimysium Tendon Endomysium Muscle fiber in middle of a fascicle Fascicle Fascicle Muscle fiber Sarcolemma Mitochondrion Myofibril Diagram of part of a muscle fiber showing the myofibrils. One myofibril is extended from the cut end of the fiber. Muscle Fibers (Form follows Function) Multiple nuclei against inside of plasma membrane – Due to fusion of multiple myoblasts during development Sarcolemma (muscle cell membrane) has tunnel-like in foldings or transverse (T) tubules that penetrate the cell – Carry electric current to cell interior Sarcoplasm (cytoplasm of muscle cell) contains: 1. Myofibrils (bundles of parallel protein microfilaments called myofilaments) 2. Glycogen for stored energy & myoglobin binding oxygen Sarcoplasmic reticulum (specialized endoplasmic reticulum of muscle cells) is series of interconnected, storage sacs called terminal cisternae – Stores Calcium!!!! The Muscle Fiber Sarcolemma Mitochondrion Myofibril Dark A band Light I band Nucleus (b) Diagram of part of a muscle fiber showing the myofibrils. One myofibril is extended from the cut end of the fiber. Sarcomere Smallest contractile unit (functional unit) of a muscle fiber Thin (actin) filament Z disc H zone Z disc Thick (myosin) I band A band I band M line filament Sarcomere Sarcomere Z disc M line Z disc Thin (actin) filament Elastic (titin) filaments Thick (myosin) filament Muscle Proteins 4 muscle proteins in 2 groups 1. Contractile proteins (do the work of contraction): 1)Myosin: thick filament 2)Actin: thin filament 2. Regulatory proteins (regulate contraction): 3)Troponin 4)Tropomyosin –Act like a switch that starts & stops shortening of muscle cell –Calcium released into sarcoplasm binds to troponin, activating contraction –Troponin moves the tropomyosin off the actin active sites 3 types of Muscle Filaments (1): 1. Thick Filaments (15 nm dia) Made of 200 to 500 myosin molecules (protein) – 2 entwined polypeptides (golf clubs) Arranged in a bundle with heads (cross bridges) directed outward in a spiral array around the bundled tails – Central area is a bare zone with no heads 3 types of Muscle Filaments (2): 2. Thin Filaments (7 nm dia): Two intertwined strands of fibrous (F) actin – Strands are made of subunits called globular (G) actin with an active site Groove holds tropomyosin molecules One troponin molecule stuck to each tropomyosin – Binds calcium!!!! 3 types of Muscle Filaments (3): 3. Elastic Filaments: Springy protein called titin (connectin) – Connects thick filament to Z disc structure 3 Functions: 1. Keep thick & thin filaments aligned with each other 2. Resist overstretching 3. Help the cell recoil to its resting length (elasticity) Overlap of Thick & Thin Filaments Striations and Sarcomeres Please note that due to differing operating systems, some animations will not appear until the presentation is viewed in Presentation Mode (Slide Show view). You may see blank slides in the “Normal” or “Slide Sorter” views. All animations will appear after viewing in Presentation Mode and playing each animation. Most animations will require the latest version of the Flash Player, which is available at http:// get.adobe.com/flashplayer. Striations = Organization of Filaments Dark A bands (regions) alternating with lighter I bands (regions) – A = anisotrophic and I = isotropic stand for the way these regions affect polarized light A band is thick filament region (myosin) – Lighter, central H band area I A I contains no thin filaments (actin) H I band is thin filament region – Bisected by Z disc protein called connectin, anchoring elastic & thin filaments – From one Z disc (Z line) to the next is a sarcomere Thin filament Z Line Thick filament Relaxed versus Contracted Sarcomere Muscle cells shorten because their individual sarcomeres shorten – Pulls Z discs closer together – Pulls on sarcolemma Note: neither thick nor thin filaments change length Their overlap changes as sarcomeres shorten Animation: Sliding filaments Sliding Filament Theory Sliding Filament Theory Video 1 https://www.youtube.com/watch?v=BVcgO4p88AA Video 2 https://www.youtube.com/watch?v=Ktv-CaOt6UQ Nerve-Muscle Relationships Skeletal muscle must be stimulated by a nerve or it will not contract (paralyzed) Cell bodies of motor neurons are in brainstem or spinal cord Axons of somatic motor neurons are called somatic motor fibers – Each branches, on average, into 200 terminal branches that supply one muscle fiber each Each motor neuron and all the muscle fibers it innervates are called a motor unit Motor Units Motor Unit = A motor neuron & muscle fibers it innervates – Dispersed throughout the muscle – When contract together causes weak contraction over wide area – Provides ability to sustain long-term contraction as motor units take turns resting (postural control) Number of muscle fibers/nerve fiber 1. Fine Control: Few muscle fibers per nerve fiber Eye muscles 2. Strength control: Gastrocnemius muscle has 1000 fibers per nerve fiber Neuromuscular Junction Myelinated axon Action of motor neuron potential (AP) Axon terminal of Nucleus neuromuscular junction Sarcolemma of the muscle fiber Ca2+ Synaptic vesicle Ca2+ containing ACh Mitochondrion Synaptic Axon terminal of motor neuron cleft Fusing synaptic vesicles Neuromuscular Junction - LM Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Motor nerve fibers Neuromuscular junction Muscle fibers Figure 11.7a (a) 100 µm Victor B. Eichler 33 Neuromuscular Junctions (Synapse) Synapse =region where a nerve fiber makes a functional connection with its target cell (neuromuscular junction, NMJ) Neurotransmitter released from nerve fiber stimulates muscle cell – Acetylcholine (ACh) Components of synapse: 1. Synaptic knob is swollen end of nerve fiber (contains ACh) 2. Motor end plate is specialized region of muscle cell surface a) Has ACh receptors that bind ACh released from nerve b) Acetylcholinesterase breaks down ACh and causes relaxation 3. Synaptic cleft = tiny gap between nerve and muscle cells 4. Schwann cell envelopes & isolates NMJ The Neuromuscular Junction Motor End Plate Muscle Contraction & Relaxation Four actions involved in this process 1. Excitation: action potentials in the nerve cause action potentials in muscle fiber 2. Excitation-contraction coupling: action potentials on the sarcolemma activate myofilaments (actin and myosin) 3. Contraction: shortening of muscle fiber or formation of tension 4. Relaxation: is return of fiber to its resting length 1. Excitation of a Muscle Fiber (from nerve cell) (on muscle cell) 1. Excitation (steps 1 & 2) Nerve signal stimulates voltage-gated calcium channels – Cause release of vesicles containing ACh = ACh release 1. Excitation (steps 3 & 4) ACh binds to receptors on surface of muscle cells: – Opens acetylcholine receptor that lets Na+ enter and K+ exit the cell – Causes action potential at the end-plate called end-plate potential (EPP) 1. Excitation (step 5) End-plate potential opens nearby voltage-gated channels in plasma membrane producing an action potential in the muscle fiber itself Animation: NMJ Electrically Excitable Cells (muscle & nerve) Plasma membrane is polarized or charged – Resting membrane potential (high Na+ outside of cell, high K+ inside) – Charge across the membrane is membrane potential Inside is slightly more negative (-90 mV) Membrane potential of muscle and nerve cells changes in response to stimulation – Na+ rushes into cell and K+ out of cell – Causes quick up-and-down change in membrane potential called the action potential – Action potential then travels along the membrane (sarcolemma) of the muscle cell Self propogates – nerve impulse Na+ channels close, K+ channels Depolarization open due to Na+ entry Repolarization due to K+ exit Na+ channels open Threshold K+ channels close 2. Excitation-Contraction Coupling 2. Excitation-Contraction Coupling(steps 6&7) Action potential spreads over sarcolemma and enters the T tubules (carry action potential into middle of muscle) 1. Voltage-gated channels open in T tubules causing calcium gates to open in SR (sarcoplasmic reticulum) 2. Calcium stored in SR rushes into muscle cell 2. Excitation-Contraction Coupling(steps 8&9) Ca2+, released by SR, binds to troponin Troponin-tropomyosin complex changes shape and exposes active sites on actin Animation: ECC 3. Contraction (steps 10 & 11) Cross-bridge formation: 1. Myosin ATPase in myosin head hydrolyzes an ATP molecule, activating the head and “cocking” it in an extended position 2. It binds to an active site on actin forming cross-bridge 3. Contraction (steps 12 & 13) 3. Power stroke = myosin head releases ADP & phosphate as it flexes pulling the thin filament 12. Power Stroke; 4. More ATP binds (necessary sliding of thin to break cross-bridge) filament over thick repeating step 1 and pulling the thin filament along Half of the heads remain attached to a thin filament, preventing slippage Thin and thick filaments do not become shorter, just slide past each other (sliding filament theory) Animation: Cross-bridge cycle https://www.youtube.com/watch?v=BVcgO4p88AA https://www.youtube.com/watch?v=NfEJUPnqxk0 4. Relaxation (steps 14 & 15) Nerve stimulation ceases and acetylcholinesterase removes ACh from receptors so stimulation of the muscle cell ceases 4. Relaxation (step 16) Active transport pumps calcium from sarcoplasm (cytoplasm of muscle cell) back into SR where it binds to calsequestrin – Active transport requires energy of ATP, so relaxation uses ATP as well as muscle contraction 4. Relaxation (steps 17 & 18) Loss of calcium from sarcoplasm results in troponin- tropomyosin complex moving over the active sites which stops the production or maintenance of tension Muscle fiber returns to its resting length due to stretching of series-elastic components and contraction of antagonistic muscles Video https://www.youtube.com/watch?v=BVcgO4p88AA Neuromuscular Toxins & Paralysis Pesticides contain cholinesterase inhibitors that bind to acetylcholinesterase & prevent it from degrading ACh – Spastic paralysis & possible suffocation – Minor startle response can cause death Flaccid paralysis with limp muscles unable to contract caused by curare that blocks action of Ach Major life-threatening consequences come from effects on respiratory muscles – Voluntary skeletal muscles – Can lead to respiratory arrest Botulism – type of food poisoning caused by a neuromuscular toxin secreted by the bacterium Clostridium botulinum – blocks release of ACh causing flaccid paralysis – Botox Cosmetic injections for wrinkle removal Rigor Mortis Stiffening of the body beginning 3 to 4 hours after death -- peaks at 12 hours after death & diminishes over next 48 to 60 hours Results from increase Cytosolic calcium: 1. Sarcoplasmic reticulum deteriorates releasing calcium 2. Sarcoplasm deteriorates letting in extracellular calcium Activates myosin-actin cross bridging & muscle contracts – Muscle relaxation requires ATP, but ATP is no longer produced after death, muscle can not relax Fibers remain contracted until myofilaments decay Isometric & Isotonic Contractions Contraction does not always mean shortening Isometric muscle contraction – Develops tension without changing length Isotonic muscle contraction – Tension development while shortening = concentric – Tension development while lengthening = eccentric Energy Needs of Muscle Muscles need ATP to contract (and relax): An exercising muscle uses about 10 million ATP molecules/second/cell Depending on length and intensity of exercise, ATP comes from 3 sources: 1. Phosphagen system: Pi groups transferred to ADP 1) Creatine kinase : Pi from creatine Phosphate to ADP to produce ATP 2) Myokinase: Pi from one ADP to another ADP 2. Aerobic respiration 2 ways to produce ATP 3. Anaerobic respiration Muscle Immediate Energy Needs In a short, intense exercise (100 m dash), oxygen need is supplied by myoglobin Most ATP demand is met by transferring Pi from other molecules (phosphagen system) 1. Myokinase transfers Pi groups from one ADP to another, converting the latter to ATP Enough power for 1 minute brisk walk or 6 seconds of sprinting 2. Creatine kinase obtains Pi groups from creatine phosphate and donates them to ADP to make ATP Muscle Short-Term Energy Needs Anaerobic Respiration Once phosphagen system is exhausted, anaerobic fermentation takes over: – Glycolysis uses glucose from blood and stored glycogen to generate ATP anaerobically (without oxygen) Byproduct is lactic acid Produces ATP for 30-40 seconds of maximum activity – While playing basketball or running around baseball diamonds Muscle Long-Term Energy Needs Aerobic Respiration After 40 seconds of exercise, respiratory & cardiovascular systems kick into high gear and “catch up” to deliver enough oxygen for aerobic respiration – Oxygen consumption rate increases for first 3-4 minutes and then levels off to a steady state – ATP production keeps pace with demand (36 ATP molecules per glucose) Limits are set by depletion of glycogen & blood glucose, loss of fluid and electrolytes through sweating Energy Needs of Muscle Prolonged-duration Short-duration exercise exercise ATP stored in ATP is formed Glycogen stored in muscles is broken ATP is generated by muscles is from creatine down to glucose, which is oxidized to breakdown of several used first. Phosphate generate ATP. nutrient energy fuels by and ADP. aerobic pathway. This pathway uses oxygen released from myoglobin or delivered in the blood by hemoglobin. When it ends, the oxygen deficit is paid back. Fatigue Fatigue is progressive weakness & loss of contractility from prolonged use of muscles. Causes: 1. Glycogen is consumed: ATP synthesis declines 2. ATP shortage causes sodium-potassium pumps to fail to maintain membrane potential & excitability 3. Accumulation of lactic acid lowers pH of sarcoplasm inhibiting enzyme function 4. Accumulation of extracellular K+ lowers the membrane potential & excitability 5. Motor nerve fibers use up their acetylcholine Slow- and Fast-Twitch Fibers Not all muscle fibers are metabolically alike, but all fibers of a single motor unit are similar. 2 Main Types: 1. Slow-twitch fibers (oxidative)- type I or red (SO) – Adapted for aerobic respiration – Resistant to fatigue – More capillaries, mitochondria and myoglobin – Soleus & postural muscles 2. Fast-twitch fibers (glycolytic - anaerobic) – type II (white) (FG) – Enriched with phosphagen & glycogen-lactic acid systems – More prone to fatigue – Extraocular eye muscles, gastrocnemius and biceps brachii Strength and Conditioning Can’t change the number of muscle cells, so how does conditioning help: Increase strength of contraction: – Muscle size and fascicle arrangement – Size of motor units and motor unit recruitment – Frequency of stimulations, length of muscle at start of contraction and fatigue Resistance training (weight lifting) – Stimulates cell enlargement due to synthesis of more myofilaments -- some cell splitting may occur Endurance training (aerobic exercise) – Produces an increase in mitochondria, glycogen & density of capillaries