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Skeletal Muscular Contraction
Physiology Skeletal Muscular Contraction
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http://www. youtube. com/watch
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Connective Tissue Endomysium Perimysium Epimysium
Surrounds each muscle fiber (cell) Attaches to Z-lines in each sarcomere Perimysium Surrounds bundles (fascicles) of muscle fibers Attaches to endomysium Epimysium Attaches to the Perimysium Continuous with tendon
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Sarcomere Repeating Patterns within the myofibrils Myofibrils
Proteins within the myofibers Myosin Actin
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Muscle Anatomy Sarcolemma Myofibrils Muscle fiber cell membrane
Highly organized bundles of contractile and elastic proteins Carries out the work of contraction
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Contain 6 types of protein:
Myofibrils = Contractile Organelles of Myofiber Contain 6 types of protein: Actin Myosin Tropomyosin Troponin Titin Nebulin Contractile Regulatory Accessory
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Titin and Nebulin Titin: biggest protein known (25,000 aa); elastic!
Stabilizes position of contractile filaments Return to relaxed location Nebulin: inelastic giant protein Alignment of A & M
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Changes in a Sarcomere during Contraction
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Myosin Myo- muscle Motor protein of the myofibril Thick filament
Attaches to the M-line Heads point towards Z-lines Myosin heads are clustered at the ends of the filament Myosin tails are bundled together
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Actin Thin Filament Globular protein Attached to Z-lines G-Actin
Has binding site for myosin head Forms a Cross-Bridge when myosin binds to G-actin Five Actin proteins surround the myosin in 3-D pattern
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Actin filament Binding sites Strong Weak binding binding
Myosin head group S2 link Stretching of the link generates tension Myosin filament
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Equal and opposite force
Why do thin filaments move? Net force Net force Equal and opposite force on thick filament
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Actin Tropomyosin Protein that covers over the myosin binding site on G-Actin Myosin head can’t bind to G-Actin, muscle relaxes If the binding site on G-Actin is uncovered by removing Tropomyosin then myosin and actin bind, muscle contracts
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Actin Troponin C Protein attached to Tropomyosin
When Troponin C changes shape it pulls on Tropomyosin Calcium binding to Troponin C causes this protein to change shape Tropomyosin moves and uncovers the binding site on G-Actin, so Actin and Myosin can bind Contraction
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Regulation of Contraction by Troponin and Tropomyosin
Tropomyosin blocks myosin binding site (weak binding possible but no powerstroke) Troponin controls position of tropomyosin and has Ca2+ binding site Ca2+ present: binding of A & M Ca2+ absent: relaxation
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Muscle Anatomy Sarcoplasmic Reticulum Terminal Cisternae
Modified endoplasmic reticulum Wraps around each myofibril like a piece of lace Stores Calcium Terminal Cisternae Longitudinal tubules Transverse tubules (T-tubules) Triad-two flanking terminal cisternae and one t-tubule T-tubules are continuous with cell membrane
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Role of calcium Troponin and Tropomyosin bind to actin
Troponin complex Troponin and Tropomyosin bind to actin block the actin – myosin binding sites Troponin is a calcium binding protein
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When Troponin binds calcium it moves Tropomyosin away from the actin-myosin binding site
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Where does Calcium come from?
Intracellular storage called Sarcoplasmic Reticulum Surround each myofibril of the whole muscle Contains high concentration of calcium Transverse Tubules connects plasma membrane to deep inside muscle
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T-Tubules Rapidly moves action potentials that originate at the neuromuscular junction on the cell surface
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Membrane depolarization or APs carried deep into the muscle by T-tubules
Motor nerve T-tubule + Neurotransmitter receptors SR
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My SR Ryanodine Receptor Dihydropyridine receptor T-tubule SR myoplasm
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_ + _ + + + + _ _ + _ + _ + _ + _ + + Ca++ Ca++ Ca++ SR Ca++ pump
Myoplasm (intracellular) _ _ _ _ + _ + + + _ + + _ _ + _ + T-tubule (extracellular) _ + _ + _ + +
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Sliding Filament Theory
When myosin binds to the binding site on G-actin muscular contraction occurs. The more myosin that bind to G-actin the greater the force of contraction Calcium must be present
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Sliding Filament Theory
Cross Bridge Myosin in the High Energy Configuration binds to G-Actin ADP + Pi are bonded to the myosin head when the cross bridge forms Power Stroke When the myosin and actin bind the myosin head changes shape Myosin pulls the actin and pulls on the Z-line Sarcomere shortens ADP+Pi no longer binds to myosin head
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Sliding Filament Theory
ATP binds to the myosin head Myosin changes to its Low Energy Confirmation In the Low Energy Confirmation Myosin breaks its bonds with Actin Rigor Mortis Lack of ATP Build up of Lactic Acid
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Sliding Filament Theory
ATPase ATP is hydrolyzed to ADP + Pi ATPase is on the myosin head Myosin changes shape back to its High Energy Confirmation
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Sliding Filament Theory
Some Myosin heads detach from Actin while other heads continue to keep their attachments No slipping of the Z-lines Contraction is held in place
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What if we don’t have this?
ATP X Actin + myosin Actomyosin complex Rigor mortis
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Events at Neuromuscular Junction
Converts a chemical signal from a somatic motor neuron into an electrical signal in the muscle fiber
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Events at Neuromuscular Junction
Acetylcholine (Ach) is released from the somatic motor neuron Ach initiates an action potential in the muscle fiber The muscle action potential triggers calcium release from the sarcoplasmic reticulum Calcium combines with troponin C and initiates contractions
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Events at Neuromuscular Junction
Ach binds to cholinergic receptors on the motor end plate Na+ channels open Na+ influx exceeds K+ efflux across the membrane End-Plate Potential (EPP) EPP reaches threshold and initiates a muscle action potential
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Events at Neuromuscular Junction
Action Potentials move down the membrane K+ builds up in the t-tubules Depolarization occurs Calcium gates on the SR opens Calcium diffuses into the cytoplasm of the cell
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Excitation-Contraction Coupling
The process where muscle action potentials initiate calcium signals that in turn activates a contraction-relaxation cycle
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Initiation of Contraction
Excitation-Contraction Coupling explains how you get from AP in axon to contraction in sarcomere ACh released from somatic motor neuron at the Motor End Plate AP in sarcolemma and T-Tubules Ca2+ release from sarcoplasmic reticulum Ca2+ binds to troponin
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Net Na+ entry creates EPSP AP to T-tubules
Details of E/C Coupling Nicotinic cholinergic receptors on motor end plate = Na+ /K+ channels Net Na+ entry creates EPSP AP to T-tubules DHP (dihydropyridine) receptors in T-tubules sense depolarization
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Nicotinic Cholinergic Receptors
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DHP (dihydropyridine) receptors open Ca2+ channels in t-tubules
Intracytosolic [Ca2+] Contraction Ca2+ re-uptake into SR Relaxation
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Excitation-Contraction Coupling
High cytosolic Calcium levels binds to Troponin C Tropomyosin moves to the “on” position and contraction occurs Calcium-ATPase pumps Calcium back into the SR The more myosin heads that binds to actin to stronger the force of contraction
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Summary of events Synaptic Depolarization of the plasma membrane is carried into the muscle by T-Tubules Conformational change of dihydropyridine receptor directly opens the ryanodine receptor calcium channel Calcium flows into myoplasm where it binds troponin Calcium pumped back into SR
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Neuromuscular Junction
The more terminal boutons to attach to myofibers the greater the control of the muscle. Recruitment The greater the number of terminal boutons attached to myofibers there is more fine control of the muscle
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Excitation-Contraction Coupling
Twitch A single contraction-relaxation cycle in a skeletal muscle fiber A single action potential in a muscle fiber Latent Period Between the muscle action potential Time required for excitation-contraction coupling to take place
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Is There Truth In Advertising?
Is the banana company telling the truth when they claim that bananas being high in Potassium actually prevents or relieves muscle cramps? If so, how does this increase in Potassium relieve muscle cramps? If not, why not and how do we actually relieve muscle cramps?
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Muscle Contraction and ATP Supply
Phosphocreatine Backup energy source Quick energy used up in approx. 15 minutes
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Causes of Fatigue Central Fatigue Subjective feelings of tiredness
Arises in the CNS Psychological fatigue precedes physiological fatigue in the muscles Low pH may cause fatigue
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Muscle Fiber Classification
Oxidative only Oxidative or glycolytic Muscle Fiber Classification
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Muscle Adaptation to Exercise
Endurance training: More & bigger mitochondria More enzymes for aerobic respiration More myoglobin no hypertrophy Resistance training: More actin & myosin proteins & more sarcomeres More myofibrils muscle hypertrophy
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Causes of Fatigue Peripheral Fatigue
Arises between the neuromuscular junction and the contractile elements of the muscle Ach depletion, neuromuscular junction receptor loss Myasthenia Gravis
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Skeletal Muscle Types Fast-twitch muscle fibers (type II) White Fibers
Low Myoglobin Develops tension two to three times faster than slow-twitch fibers Splits ATP more rapidly to complete contraction faster Fatigues quickly
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Skeletal Muscle Types Slow-twitch Muscle Fibers (Type I) Red
High Myoglobin levels Slow to Fatigue
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Contractions Isometric Contractions Isotonic Contractions
Creates force without movement Isotonic Contractions Moves loads
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