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The Muscular System Chapter 7 The Muscular System Chapter 7
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There are four characteristics associated with muscle tissue: Excitability Contractility Extensibility Elasticity
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The characteristics of muscle tissue enable it to perform some important functions, including: Movement Maintaining posture Supporting soft tissues within body cavities Protection Maintaining body temperature
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Types of muscle tissue: Skeletal Cardiac Smooth (Visceral)
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Skeletal muscle tissue Associated with & attached to the skeleton Under our conscious (voluntary) control Cells are long, cylindrical & multinucleate Microscopically the tissue appears striated
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Cardiac muscle tissue Makes up myocardium of heart Unconsciously (involuntarily) controlled Microscopically appears striated Cells are short, branching & have a single nucleus Cells connect to each other at intercalated discs
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Smooth (visceral) muscle tissue Makes up walls of organs & blood vessels Tissue is non-striated & involuntary Cells are short, spindle-shaped & have a single nucleus Tissue is extremely extensible, while still retaining ability to contract
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Anatomy of skeletal muscles Skeletal muscle fiber (cell) Muscle Fascicle Surrounded by perimysium Surrounded by endomysium endomysium perimysium Skeletal muscle Surrounded by epimysium epimysium tendon
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Microanatomy of a Muscle Fiber (cell)
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Microanatomy of a Muscle Fiber (Cell) sarcolemma transverse (T) tubules sarcoplasmic reticulum terminal cisternae myofibril thin myofilament thick myofilament triad mitochondria nuclei myoglobin
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Muscle fiber myofibril Thin filamentsThick filaments Thin myofilament Myosin molecule of thick myofilament sarcomere Z-line
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Thin Myofilament (myosin binding site) Z-line (Z-disc)
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Thick myofilament ( has ATP & actin binding site) M-line
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Sarcomere Z line A band H zone I band Zone of overlap M line Zone of overlap Thin myofilaments Thick myofilaments
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Mechanism involved in muscle cell contraction Occurs at molecular level Myosin heads attach to actin molecules (at binding (active) site) Myosin “pulls” on actin, causing thin myofilaments to slide across thick myofilaments, towards the center of the sarcomere Sliding Filament Theory Sarcomere in muscle cell at rest
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As sarcomeres shorten, myofibril shortens. As myofibrils shorten, so does muscle fiber (cell) Once a muscle fiber begins to contract, it will contract maximally This is known as the “all or none” principle
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Physiology of skeletal muscle contraction Skeletal muscles require stimulation from the nervous system in order to contract Motor neurons are the cells that cause muscle fibers to contract cell body dendrites axon Synaptic terminals (synaptic end bulbs) telodendria axon hillock motor neuron End bulbs contain vesicles filled with Acetylcholine (Ach)
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telodendria Synaptic terminal (end bulb) Neuromuscular junction Synaptic vessicles containing ACh Motor end plate of sarcolemma Synaptic cleft Neuromuscular junction
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Overview of Events at the neuromuscular junction An action potential (AP), an electrical impulse, travels down the axon of the motor neuron to the end bulbs (synaptic terminals) The AP causes the synaptic vesicles to fuse with the end bulb membrane, resulting in the release of Acetylcholine (ACh) into the synaptic cleft ACh diffuses across the synaptic cleft & binds to ACh receptors on the motor end plate The binding of ACh to its receptors causes a new AP to be generated along the muscle cell membrane Immediately after it binds to its receptors, Ach will be broken down by Acetylcholinesterase (AChE) – an enzyme present in the synaptic cleft
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Figure 7-4(b-c) 2 of 5 Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings Synaptic cleft Arrival of an action potential at the synaptic terminal Sarcolemma of motor end plate Arriving action potential Vesicles ACh AChE molecules ACh receptor site Action potential Synaptic terminal Axon Sarcolemma Muscle fiber An action potential (AP), an electrical impulse, flows down the axon of the motor neuron to the end bulbs (synaptic terminals)
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Figure 7-4(b-c) 3 of 5 Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings Synaptic cleft Vesicles in the synaptic terminal fuse with the neuronal membrane and dump their contents into the synaptic cleft. Release of acetylcholine Arrival of an action potential at the synaptic terminal Sarcolemma of motor end plate Arriving action potential Vesicles ACh AChE molecules ACh receptor site Action potential Synaptic terminal Axon Sarcolemma Muscle fiber The AP causes the synaptic vesicles to fuse with the end bulb membrane, resulting in the exocytosis of Acetylcholine (ACh) molecules into the synaptic cleft
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Figure 7-4(b-c) 4 of 5 Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings Synaptic cleft Vesicles in the synaptic terminal fuse with the neuronal membrane and dump their contents into the synaptic cleft. The binding of ACh to the receptors increases the membrane permeability to sodium ions. Sodium ions then rush into the cell. ACh binding at the motor and plate Release of acetylcholine Arrival of an action potential at the synaptic terminal Sarcolemma of motor end plate Arriving action potential Vesicles ACh AChE molecules ACh receptor site Action potential Synaptic terminal Axon Sarcolemma Muscle fiber Na + ACh diffuses across the synaptic cleft & binds to ACh receptors on the motor end plate
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The binding of ACh to its receptors causes a new AP to begin on the muscle cell sarcolemma (“excitation”) Immediately after it binds to its receptors, ACh will be broken down by Acetylcholinesterase (AChE) – an enzyme present in the synaptic cleft
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Physiology of Skeletal Muscle Contraction Once an action potential (AP) is generated at the motor end plate it will spread like an electrical current along the sarcolemma of the muscle fiber The AP will also spread into the T-tubules, exciting the terminal cisternae of the sarcoplasmic reticula This will cause Calcium (Ca +2 ) gates in the SR to open, allowing Ca +2 to diffuse into the sarcoplasm
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Resting sarcomere Myosin head Active-site exposure Troponin Actin Tropomyosin ADP P + P + P + Active site Sarcoplasm Ca 2+ ADP P + Calcium will bind to troponin (on the thin myofilament), causing troponin to change its shape. This then pulls tropomyosin away from the active sites (myosin binding sites) of actin molecules. Physiology of skeletal muscle contraction – events at the myofilaments
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Resting sarcomere Myosin head Active-site exposure Cross-bridge formation Troponin Actin Tropomyosin ADP P + P + P + Active site Sarcoplasm Ca 2+ ADP P + + P Ca 2+ ADP + P Ca 2+ Myosin heads are “energized” though conversion of ATP ADP + PO 4 3- at the ATP binding site (energy is absorbed into myosin heads as phosphate bond breaks) Once the active sites on actin molecules are exposed, the energized myosin heads hook into actin forming cross-bridges Physiology of skeletal muscle contraction – events at the myofilaments
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Resting sarcomere Myosin head Active-site exposure Cross-bridge formation Pivoting of myosin head Troponin Actin Tropomyosin ADP P + P + P + Active site Sarcoplasm Ca 2+ ADP P + + P Ca 2+ ADP + P Ca 2+ ADP + P Ca 2+ ADP + P Using the absorbed energy, the attached myosin heads bend and pivot, pulling the thin filament toward the center of the sarcomere (“power stroke”) The ADP & phosphate group are released from the myosin head, and a new molecule of ATP attaches to the head Physiology of skeletal muscle contraction – events at the myofilaments
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Resting sarcomere Myosin head Active-site exposure Cross bridge detachment Cross-bridge formation Pivoting of myosin head Troponin Actin Tropomyosin ADP P + P + P + Active site Sarcoplasm Ca 2+ ADP P + + P Ca 2+ ADP + P Ca 2+ ADP + P Ca 2+ ADP + P Ca 2+ ATP Ca 2+ As the new molecule of ATP binds to the myosin head, the cross bridge must detach from the actin strand The myosin head will get re-energized as the ATP ADP+P As long as the active sites are still exposed, the myosin head can bind again to the next active site Physiology of skeletal muscle contraction – events at the myofilaments
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Resting sarcomere Myosin head Myosin reactivation Active-site exposure Cross bridge detachment Cross-bridge formation Pivoting of myosin head Troponin Actin Tropomyosin ADP P + P + P + Active site Sarcoplasm Ca 2+ ADP P + + P Ca 2+ ADP + P Ca 2+ ADP + P Ca 2+ ADP + P Ca 2+ ATP Ca 2+ ADP P + + P http://www.youtube.com/watch?v=CepeYFvqmk4http://www.youtube.com/watch?v=CepeYFvqmk4 - animation http://www.youtube.com/watch?v=kvMFdNw35L0http://www.youtube.com/watch?v=kvMFdNw35L0 – animation with Taylor Swift song Physiology of skeletal muscle contraction – events at the myofilaments
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Physiology of Skeletal Muscle Contraction If there are no longer APs generated on the motor neuron, no more ACh will be released AChE will remove ACh from the motor end plate, and AP transmission on the muscle fiber will end Ca +2 gates in the SR will close & Ca +2 will be actively transported back into the SR With Ca +2 removed from the sarcoplasm (& from troponin), tropomyosin will re-cover the active sites of actin No more cross-bridge interactions can form Thin myofilaments slide back to their resting state (“elasticity”) Table 7-1
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These physiological processes describe what happen at the cellular level – how skeletal muscle fibers contract But what about at the organ level? How do skeletal muscles (like your biceps brachii) contract to create useful movement?
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Skeletal muscles are made up of thousands of muscle fibers A single motor neuron may directly control a few fibers within a muscle, or hundreds to thousands of muscle fibers All of the muscle fibers controlled by a single motor neuron constitute a motor unit
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The size of the motor unit determines how fine the control of movement can be – small motor units precise control (e.g. eye muscles large motor units gross control (e.g. leg muscles)
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Recruitment is the ability to activate more motor units as more force (tension) needs to be generated There are always some motor units active, even when at rest. This creates a resting tension known as muscle tone, which helps stabilize bones & joints, & prevents atrophy Hypertrophy – “stressing” a muscle (i.e. exercise) causes more myofilaments/myofibrils to be produced within muscle fibers; allows for more “cross bridges” resulting in more force (strength) as well as larger size
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Anatomy of the Muscular System Origin Muscle attachment that remains fixed Insertion Muscle attachment that moves Action What joint movement a muscle produces i.e. flexion, extension, abduction, etc.
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For muscles to create a movement, they can only pull, not push Muscles in the body rarely work alone, & are usually arranged in functional groups surrounding a joint A muscle that contracts to create the desired action is known as an agonist or prime mover A muscle that helps the agonist is a synergist A muscle that opposes the action of the agonist, therefore undoing the desired action is an antagonist
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Skeletal muscle movements at joints Flexion/extension Abduction/adduction Rotation – left/right; internal(medial)/external(lateral) pronation/supination Elevation/depression Protraction/retraction Dorsiflexion/plantarflexion Inversion/eversion
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Naming of skeletal muscles
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An Overview of the Major Skeletal Muscles Figure 7-11(a)
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An Overview of the Major Skeletal Muscles Figure 7-11(b)
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