Physiology Skeletal Muscle Contraction Bone Epimysium Perimysium Tendon

Physiology Skeletal Muscle Contraction

Bone Epimysium Perimysium Tendon Endomysium Muscle fiber in middle of a fascicle Blood vessel Perimysium wrapping a fascicle Endomysium (between individual muscle fibers) Muscle fiber Fascicle Perimysium © 2013 Pearson Education, Inc.

Skeletal Muscle: Attachments Attach in at least two places ◦ Insertion – movable bone ◦ Origin – immovable (less movable) bone Attachments direct or indirect ◦ Direct—epimysium fused to periosteum of bone or perichondrium of cartilage ◦ Indirect—connective tissue wrappings extend beyond muscle as ropelike tendon or sheetlike aponeurosis © 2013 Pearson Education, Inc.

Microscopic Anatomy of A Skeletal Muscle Fiber Long, cylindrical cell ◦ 10 to 100 µm in diameter; up to 30 cm long Multiple peripheral nuclei Sarcolemma = plasma membrane Sarcoplasm = cytoplasm ◦ Glycosomes for glycogen storage, myoglobin for O 2 storage Modified structures: myofibrils, sarcoplasmic reticulum, and T © 2013 Pearson Education, Inc.

Myofibrils Densely packed, rodlike elements ~80% of cell volume Contain sarcomeres - contractile units ◦ Sarcomeres contain myofilaments Exhibit striations - perfectly aligned repeating series of dark A bands and light I bands © 2013 Pearson Education, Inc.

Diagram of part of a muscle fiber showing the myofibrils. One myofibril extends from the cut end of the fiber. Sarcolemma Mitochondrion Myofibril Dark A band Light Nucleus I band © 2013 Pearson Education, Inc.

Striations H zone: lighter region in midsection of dark A band where filaments do not overlap M line: line of protein myomesin bisects H zone Z disc (line): coin-shaped sheet of proteins on midline of light I band that anchors thin filaments and connects myofibrils to one another Thick filaments: run entire length of an A band Thin filaments: run length of I band partway into A band © 2013 Pearson Education, Inc. Sarcomere: region between two

Connective Tissue Endomysium ◦ 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

Thin (actin) filament Small part of one myofibril enlarged to show the myofilaments responsible for the banding pattern. Thick Each sarcomere extends from one Z (myosin) filament disc to the next. Z disc I band H zone Z disc I band A band Sarcomere © 2013 Pearson Education, Inc. M line

Thin (actin) filament Small part of one myofibril enlarged to show the myofilaments responsible for the banding pattern. Thick Each sarcomere extends from one Z (myosin) filament disc to the next. Z disc I band H zone Z disc I band A band Sarcomere © 2013 Pearson Education, Inc. M line

Sarcomere Repeating Patterns within the myofibrils Myofibrils ◦ Proteins within the myofibers ◦ Myosin ◦ Actin

Muscle Anatomy Sarcolemma ◦ Muscle fiber cell membrane Myofibrils ◦ Highly organized bundles of contractile and elastic proteins ◦ Carries out the work of contraction

Myofibrils = Contractile Organelles of Myofiber Contain 6 types of protein: l l l Actin Myosin Tropomyosin Troponin Titin Nebulin Contractile Regulatory Accessory

Titin and Nebulin l Titin: biggest protein known (25, 000 aa); elastic! l l l Stabilizes position of contractile filaments Return to relaxed location Nebulin: inelastic giant protein l Alignment of A & M

Structure of Myofibril Elastic filament ◦ Composed of protein titin ◦ Holds thick filaments in place; helps recoil after stretch; resists excessive stretching Dystrophin ◦ Links thin filaments to proteins of sarcolemma Nebulin, myomesin, C proteins bind filaments or sarcomeres together; maintain alignment © 2013 Pearson Education, Inc.

Changes in a Sarcomere during Contraction

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

Role of calcium Tropomyosin Troponin complex • Troponin and Tropomyosin bind to actin block the actin – myosin binding sites • Troponin is a calcium binding protein

When Troponin binds calcium it moves Tropomyosin away from the actin-myosin binding site Ca Ca

Actin Thin Filament ◦ Attached to Z-lines Globular ◦ ◦ protein 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

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

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

Regulation of Contraction by Troponin and Tropomyosin q Tropomyosin blocks myosin binding site (weak binding possible but no powerstroke) q Troponin controls position of tropomyosin and has Ca 2+ binding site q Ca 2+ present: binding of A & M q Ca 2+ absent: relaxation

Sarcoplasmic Reticulum (SR) Network of smooth endoplasmic reticulum surrounding each myofibril ◦ Most run longitudinally Pairs of terminal cisternae form perpendicular cross channels Functions in regulation of intracellular Ca 2+ levels ◦ Stores and releases Ca 2+ © 2013 Pearson Education, Inc.

T Tubules Continuations of sarcolemma Lumen continuous with extracellular space Increase muscle fiber's surface area Penetrate cell's interior at each A band–I band junction Associate with paired terminal cisterns to form triads that encircle each sarcomere © 2013 Pearson Education, Inc.

Muscle Anatomy Sarcoplasmic Reticulum ◦ 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

Where does Calcium come from? l l 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

T-Tubules Rapidly moves action potentials that originate at the neuromuscular junction on the cell surface

Motor nerve Membrane depolarization or APs carried deep into the muscle by Ttubules T-tubule + Neurotransmitter receptors SR

SR Ryanodine Receptor T-tubule My SR myoplasm Dihydropyridine receptor

Ca++ SR Ca++ pump Myoplasm (intracellular) _ +_ + _ _ +_ + + _ + _+ _+ + T-tubule (extracellular)

Actin filament Binding sites Strong binding Weak binding Myosin head group S 2 link Stretching of the link generates tension Myosin filament

Why do thin filaments move? Net force Equal and opposite force on thick filament

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

What if we don’t have this? ATP X Actin + myosin Actomyosin complex Rigor mortis

Causes of Fatigue Central Fatigue ◦ Subjective feelings of tiredness ◦ Arises in the CNS ◦ Psychological fatigue precedes physiological fatigue in the muscles Subjective feelings of tiredness Low p. H may cause fatigue

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

Oxidative only Oxidative or glycolytic Muscle Fiber Classification

Muscle Adaptation to Exercise Endurance training: l More & bigger mitochondria l More enzymes for aerobic respiration Resistance training: l More actin & myosin proteins & more sarcomeres l l More myoglobin no hypertrophy More myofibrils muscle hypertrophy

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

Skeletal Muscle Types Slow-twitch Muscle Fibers (Type I) ◦ Red ◦ High Myoglobin levels ◦ Slow to Fatigue

Contractions Isometric Contractions ◦ Creates force without movement Isotonic Contractions ◦ Moves loads

Slide 1 1 Fully relaxed sarcomere of a muscle fiber H A Z I

1 Fully relaxed sarcomere of a muscle fiber Z I H © 2013 Pearson

Slide 3 2 Fully contracted sarcomere of a muscle fiber Z I Z A

Slide 4 1 Fully relaxed sarcomere of a muscle fiber H A Z I

Action potential (AP) arrives at axon terminal at neuromuscular junction ACh released; binds to receptors on sarcolemma Phase 1 Motor neuron stimulates muscle fiber (see Figure 9. 8). Ion permeability of sarcolemma changes Local change in membrane voltage (depolarization) occurs Local depolarization (end plate potential) ignites AP in sarcolemma AP travels across the entire sarcolemma AP travels along T tubules Phase 2: Excitation-contraction coupling occurs (see Figures 9. 9 and 9. 11). SR releases Ca 2+; Ca 2+ binds to troponin; myosin-binding sites (active sites) on actin exposed Myosin heads bind to actin; contraction begins © 2013 Pearson Education, Inc.

Slide 1 Open Na+ channel Closed K+ channel Na+ ACh-containing synaptic vesicle Ca 2+ − − − − + + + + − − K+ Axon terminal of neuromuscular junction Synaptic cleft − − − + + Action potential 2 Depolarization: Generating and propagating an action potential (AP). The local depolarization current spreads to adjacent areas of the sarcolemma. This opens voltage-gated sodium channels there, so Na+ enters following its electrochemical gradient and initiates the AP. The AP is propagated as its local depolarization wave spreads to adjacent areas of the sarcolemma, opening voltage-gated channels there. Again Na+ diffuses into the cell following its electrochemical gradient. Wave of depolarization Closed Na+ channel 1 An end plate potential is generated at the neuromuscular junction (see Figure 9. 8). Open K+ channel Na+ + + + + − − − + + + + + − − − − K+ © 2013 3 Repolarization: Restoring the sarcolemma to its initial polarized state (negative inside, positive outside). Repolarization occurs as Na+ channels close (inactivate) and voltage-gated K+ channels open. Because K+ concentration is substantially higher inside the cell Pearson Education, + than in the extracellular Inc. fluid, K diffuses rapidly out of the muscle fiber.

Slide 2 ACh-containing synaptic vesicle Ca 2+ Axon terminal of neuromuscular junction Synaptic cleft Wave of depolarization 1 An end plate potential is generated at the neuromuscular junction (see Figure 9. 8). © 2013 Pearson Education, Inc.

Slide 3 Open Na+ channel Closed K+ channel Na+ ACh-containing synaptic vesicle Ca 2+ − − − − + + + + − − K+ Axon terminal of neuromuscular junction Synaptic cleft − − − + + Action potential 2 Depolarization: Generating and propagating an action potential (AP). The local depolarization current spreads to adjacent areas of the sarcolemma. This opens voltage-gated sodium channels there, so Na+ enters following its electrochemical gradient and initiates the AP. The AP is propagated as its local depolarization wave spreads to adjacent areas of the sarcolemma, opening voltage-gated channels there. Again Na+ diffuses into the cell following its electrochemical gradient. Wave of depolarization 1 An end plate potential is generated at the neuromuscular junction (see Figure 9. 8). © 2013 Pearson Education, Inc.

Slide 4 Open Na+ channel Closed K+ channel Na+ ACh-containing synaptic vesicle Ca 2+ − − − − + + + + − − K+ Axon terminal of neuromuscular junction Synaptic cleft − − − + + Action potential 2 Depolarization: Generating and propagating an action potential (AP). The local depolarization current spreads to adjacent areas of the sarcolemma. This opens voltage-gated sodium channels there, so Na+ enters following its electrochemical gradient and initiates the AP. The AP is propagated as its local depolarization wave spreads to adjacent areas of the sarcolemma, opening voltage-gated channels there. Again Na+ diffuses into the cell following its electrochemical gradient. Wave of depolarization Closed Na+ channel 1 An end plate potential is generated at the neuromuscular junction (see Figure 9. 8). Open K+ channel Na+ + + + + − − − + + + + + − − − − K+ © 2013 3 Repolarization: Restoring the sarcolemma to its initial polarized state (negative inside, positive outside). Repolarization occurs as Na+ channels close (inactivate) and voltage-gated K+ channels open. Because K+ concentration is substantially higher inside the cell Pearson Education, + than in the extracellular Inc. fluid, K diffuses rapidly out of the muscle fiber.

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

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

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

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

Events at Neuromuscular Junction Converts a chemical signal from a somatic motor neuron into an electrical signal in the muscle fiber

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

Slide 1 Myelinated axon of motor neuron Action potential (AP) Axon terminal of neuromuscular junction Sarcolemma of the muscle fiber 1 Action potential arrives at axon terminal of motor neuron. Synaptic vesicle containing ACh 2 Voltage-gated Ca 2+ channels open. Ca 2+ enters the axon terminal moving down its electochemical gradient. Axon terminal of motor neuron Fusing synaptic vesicles 3 Ca 2+ entry causes ACh (a neurotransmitter) to be released by exocytosis. ACh 4 ACh diffuses across the synaptic cleft and binds to its receptors on the sarcolemma. 5 ACh binding opens ion channels in the receptors that allow simultaneous passage of Na+ into the muscle fiber and K+ out of the muscle fiber. More Na+ ions enter than K+ ions exit, which produces a local change in the membrane potential called the end plate potential. 6 ACh effects are terminated by its breakdown in the synaptic © 2013 cleft by acetylcholinesterase and diffusion away from the junction. Synaptic cleft Junctional folds of sarcolemma Sarcoplasm of muscle fiber Postsynaptic membrane ion channel opens; ions pass. ACh Degraded ACh Acetylcho. Pearson Education, linesterase Inc. Ion channel closes; ions cannot pass.

Slide 2 1 Action potential arrives at axon terminal of motor neuron. Synaptic vesicle containing ACh Axon terminal of motor neuron Synaptic cleft Fusing synaptic vesiclesa ACh Junctional folds of sarcolemma Sarcoplasm of muscle fiber © 2013 Pearson Education, Inc.

Slide 3 1 Action potential arrives at axon terminal of motor neuron. 2 Voltage-gated Ca 2+ channels open. Ca 2+ enters the axon terminal moving down its electochemical gradient. Synaptic vesicle containing ACh Axon terminal of motor neuron Synaptic cleft Fusing synaptic vesiclesa ACh Junctional folds of sarcolemma Sarcoplasm of muscle fiber © 2013 Pearson Education, Inc.

Slide 4 1 Action potential arrives at axon terminal of motor neuron. 2 Voltage-gated Ca 2+ channels open. Ca 2+ enters the axon terminal moving down its electochemical gradient. 3 Ca 2+ entry causes ACh (a neurotransmitter) to be released by exocytosis. Synaptic vesicle containing ACh Axon terminal of motor neuron Synaptic cleft Fusing synaptic vesiclesa ACh Junctional folds of sarcolemma Sarcoplasm of muscle fiber © 2013 Pearson Education, Inc.

Slide 5 1 Action potential arrives at axon terminal of motor neuron. 2 Voltage-gated Ca 2+ channels open. Ca 2+ enters the axon terminal moving down its electochemical gradient. 3 Ca 2+ entry causes ACh (a neurotransmitter) to be released by exocytosis. Synaptic vesicle containing ACh Axon terminal of motor neuron Synaptic cleft Fusing synaptic vesiclesa ACh 4 ACh diffuses across the synaptic cleft and binds to its receptors on the sarcolemma. Junctional folds of sarcolemma Sarcoplasm of muscle fiber © 2013 Pearson Education, Inc.

Slide 6 5 ACh binding opens ion channels in the receptors that allow simultaneous passage of Na+ into the muscle fiber and K+ out of the muscle fiber. More Na+ ions enter than K+ ions exit, which produces a local change in the membrane potential called the end plate potential. Postsynaptic membrane ion channel opens; © 2013 Pearson Education, ions pass. Inc.

Slide 7 6 ACh effects are terminated by its breakdown in the synaptic cleft by acetylcholinesterase and diffusion away from the junction. ACh Degraded ACh Acetylcholinesterase Ion channel closes; © 2013 Pearson Education, ions cannot pass. Inc.

Slide 8 Myelinated axon of motor neuron Action potential (AP) Axon terminal of neuromuscular junction Sarcolemma of the muscle fiber 1 Action potential arrives at axon terminal of motor neuron. Synaptic vesicle containing ACh 2 Voltage-gated Ca 2+ channels open. Ca 2+ enters the axon terminal moving down its electochemical gradient. Axon terminal of motor neuron Fusing synaptic vesicles 3 Ca 2+ entry causes ACh (a neurotransmitter) to be released by exocytosis. ACh 4 ACh diffuses across the synaptic cleft and binds to its receptors on the sarcolemma. 5 ACh binding opens ion channels in the receptors that allow simultaneous passage of Na+ into the muscle fiber and K+ out of the muscle fiber. More Na+ ions enter than K+ ions exit, which produces a local change in the membrane potential called the end plate potential. 6 ACh effects are terminated by its breakdown in the synaptic © 2013 cleft by acetylcholinesterase and diffusion away from the junction. Synaptic cleft Junctional folds of sarcolemma Sarcoplasm of muscle fiber Postsynaptic membrane ion channel opens; ions pass. ACh Degraded ACh Acetylcho. Pearson Education, linesterase Inc. Ion channel closes; ions cannot pass.

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

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

Excitation-Contraction Coupling The process where muscle action potentials initiate calcium signals that in turn activates a contractionrelaxation cycle

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 Ca 2+ release from sarcoplasmic reticulum Ca 2+ binds to troponin

Slide 1 Actin Ca 2+ Thin filament Myosin cross bridge Thick filament Myosin 1 Cross bridge formation. Energized myosin head attaches to an actin myofilament, forming a cross bridge. ATP hydrolysis 4 Cocking of the myosin head. As ATP is hydrolyzed to ADP and Pi, the myosin head returns to its prestroke high-energy, or “cocked, ” position. * *This cycle will continue as long as ATP is available and Ca 2+ is bound to troponin. 2 The power (working) stroke. ADP and Pi are released and the myosin head pivots and bends, changing to its bent low-energy state. As a result it pulls the actin filament toward the M line. In the absence of ATP, myosin heads will not detach, causing rigor mortis. 3 Cross bridge detachment. After ATP attaches to myosin, the link between myosin © 2013 Pearson Education, and actin weakens, and the myosin head detaches (the cross bridge “breaks”). Inc.

Slide 2 Actin Myosin cross bridge Thin filament Thick filament Myosin 1 Cross bridge formation. Energized myosin head attaches to an actin myofilament, forming a cross bridge. © 2013 Pearson Education, Inc.

Slide 3 2 The power (working) stroke. ADP and Pi are released and the myosin head pivots and bends, changing to its bent low-energy state. As a result it pulls the actin filament toward the M line. © 2013 Pearson Education, Inc.

Slide 4 3 Cross bridge detachment. After ATP attaches to myosin, the link between

Slide 5 ATP hydrolysis 4 Cocking of the myosin head. *This cycle will continue as long as ATP is available and Ca 2+ is bound to troponin. As ATP is hydrolyzed to ADP and Pi, the myosin head returns to its prestroke high-energy, or “cocked, ” position. * © 2013 Pearson Education, Inc.

Slide 6 Actin Ca 2+ Thin filament Myosin cross bridge Thick filament Myosin 1 Cross bridge formation. Energized myosin head attaches to an actin myofilament, forming a cross bridge. ATP hydrolysis 4 Cocking of the myosin head. As ATP is hydrolyzed to ADP and Pi, the myosin head returns to its prestroke high-energy, or “cocked, ” position. * *This cycle will continue as long as ATP is available and Ca 2+ is bound to troponin. © 2013 2 The power (working) stroke. ADP and Pi are released and the myosin head pivots and bends, changing to its bent low-energy state. As a result it pulls the actin filament toward the M line. In the absence of ATP, myosin heads will not detach, causing rigor mortis. 3 Cross bridge detachment. After ATP attaches to myosin, the link between myosin Pearson and. Education, actin weakens, and the myosin head detaches (the. Inc. cross bridge “breaks”).

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

Destruction of Acetylcholine ACh effects quickly terminated by enzyme acetylcholinesterase in synaptic cleft ◦ Breaks down ACh to acetic acid and choline ◦ Prevents continued muscle fiber contraction in absence of additional stimulation © 2013 Pearson Education, Inc.

Events in Generation of an Action Potential Repolarization – restoring electrical conditions of RMP ◦ Na+ channels close and voltage-gated K+ channels open ◦ K+ efflux rapidly restores resting polarity ◦ Fiber cannot be stimulated - in refractory period until repolarization complete ◦ Ionic conditions of resting state restored by Na+-K+ pump © 2013 Pearson Education, Inc.

Nicotinic Cholinergic Receptors

DHP (dihydropyridine) receptors open Ca 2+ channels in t-tubules Intracytosolic [Ca 2+] Contraction Ca 2+ re-uptake into SR Relaxation

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

Summary of events 1. 2. 3. 4. Synaptic Depolarization of the plasma membrane is carried into the muscle by TTubules 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

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

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

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?

What produces a muscle cramp? How is Potassium related to muscle cramps? ◦ Look up Hypokalemia and Hyperkalemia

Muscle Contraction and ATP Supply Phosphocreatine ◦ Backup energy source ◦ Quick energy used up in approx. 15 minutes

During skeletal muscle contraction the binding of the myosin head to G-actin occurs at which step? Cross bridge B. Power stroke C. Working stroke D. Force stroke A.

During the cross bridge the myosin head is in the ____ configuration. Low energy B. High energy C. Medium energy D. Power energy A.

Name the connective tissue layer that surrounds a fascicle in skeletal muscle. A. B. C. D. E. Endomysium Epimysium Perimyseum Tendon Epicardium

Name the functional unit of skeletal muscle. Sarcolemma B. Saroplasmic Reticulum C. Sarcomere D. Myosin A.

The thick filament is also referred to as A. B. C. D. E. Actin Myosin Tropomyosin Troponin C G Actin

Which protein in G-Actin is responsible for blocking the bind site of myosin? A. Tropomyosin B. Troponin C C. Sarcoplasmic Reticulum D. Sarcolemma

During skeletal muscle contraction Calcium is stored in the A. B. C. D. E. Sarcolemma Sarcomere Sarcoplasmic Reticulum Golgi Apparatus Transverse Tubules

The build-up of potassium in the _______ causes the resting membrane potential of skeletal muscle to depolarize. A. B. C. D. Sarcolemma Sarcoplasmic reticulum Transverse tubule Tropomyosin

Which enzyme is located on the myosin head? A. B. C. D. E. ATP synthase ATP reductase Phophodiesterase Oxidase

During cross bridge formation myosin will bind to ____. A. B. C. D. Troponin C Tropomyosin G-Actin Myosin

The phenomenon of rigor mortis is a direct result of A. The breaking of myosin bonds by ATP B. The breaking of actin bonds by ATP C. The inability of the myosin cross bridges to combine with single amino acids D. The loss of ATP in dead muscle cells