TEST #2 - Lecture notes Exam 2 PDF

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Anatomy & Physiology 3/19/18 Exam #2 Functions of Muscles Movement Stability Control or openings and passageways (sphincters) Heat production Glycemic Control (Muscles store glucose) Types of Muscle Skeletal - Striated - Strong contractions - Fatigues easily - Voluntary - Usually attached to bones - Myofiber is long (up to 30 cm) Smooth - No striations - Forms within organs and viscera - Fatigue resistant Cardiac - Striated - Fatigue resistant Characteristics of Muscle Fibers Striations - result from precise organization of myosin and actin - Alternating A-bands (dark) and I-bands(light) - Uniform reflection of polarized light - Z discs provides anchorage for thin and elastic filaments (bisects I band) I band: “I” isotropic (light) A band: “A” anisotropic (dark) H band: middle of A band, thick filament only (not as dark) M line: middle of H band Sarcomere - Segment from z disc to z disc - Functional contractile unit of muscle fiber ~ muscles shorten because their individual sarcomeres shorten

~ neither thick nor thin filaments change length during shortening, only the amount of overlap changes Sarcolemma - plasma membrane of muscle fiber Sarcoplasm - Cytoplasm of muscle fiber - Myofibrils: long protein cords that occupy sarcoplasm - Glycogen: Carb stored to provide energy for exercise - Myoglobin: Oxygen -binding protein that allows for oxygen storage in muscle cells - Mitochondria packed into spaces between myofibrils Myoblasts - stem cells that fused to form each muscle fiber early in development Satellite Cells: unspecialized myoblasts remaining between the muscle fiber and endomysium (regeneration of damaged muscle) Sarcoplasmic Reticulum - smooth ER that forms a network around each myofibril - Terminal cisterns - dilated end-sacs of SR which cross the muscle fiber form one side to another - Acts as calcium reservoir - releases calcium through channels to activate contraction T-Tubules - transverse tubular infoldings of sarcolemma which penetrate through the cells and emerge on other side Triad - t tubule and two terminal cistern associated with it Myofilaments Thick filaments made of several myosin molecules - Two chain intertwined to form shaft like tail - Double globular head - Heads directed outward in a helical array around the bundle Thin filaments Fibrous (F) actin: two intertwined strands - String of globular (G) actin subunits which with an active site that can bind to head of myosin molecule Tropomyosin molecules: - Each blocking six or seven active sites of G actin subunits Troponin Molecule - Small calcium binding protein on each tropomyosin molecule Elastic Filaments Titin: huge, springy protein - Run through core of thick filament and anchor it to the Z disc and M line - Help stabilize and position the thick filament - Prevent overstretching and provide recoil

Contractile Proteins - Myosin and actin bind repeatedly and rapidly to make the muscle contract Regulatory proteins - Tropomyosin and troponin act like a switch that determines when fiber can and cannot contract Myofibril - Bundle of protein myofilaments with muscle fiber - Fill up cytoplasm - Surrounded by sarcoplasmic reticulum and mitochondria - Has banded striated appearance due to overlap of protein myofilaments Contraction - Contraction is activated by release of calcium into the sarcoplasm - The calcium then binds to the troponin - Troponin then changes shape and move tropomyosin off the active sites on the actin Dystrophin - Clinically important protein - Links actin in outermost myofilament to membrane proteins that link to the endomysium - Transfers forces of muscle contraction to connective tissue and then the tendon - “Muscular dystrophy” - genetic defect in dystrophin Connective Tissues and Compartments Endomysium - Thin sleeve of loose connective tissue around each fiber - Allows room for capillaries and nerves - Chemical environment for nerves Perimysium - Thicker layer of connective tissue that wraps around fascicles - Carries nerves, blood vessels and stretch receptors Fascicles - Bundles of muscle fibers wrapped together Epimysium - Fibrous sheath around whole muscle - Outer surface becomes fascia, inner surface projections become perimysium Fascia - Sheet of connective tissue that separates neighboring muscles from each other and subcutaneous tissue

Muscles and Fascicle Orientation Fusiform muscles - thick in the middle and tapered at the end Parallel Muscles - uniform width and parallel fascicles Triangular (convergent) muscles - broad at one end and narrow at the other Circular muscles (sphincters) - form rings around the body of the openings Pennate Muscles - feather shaped Unipennate - fascicles approach tendon from one side Bipennate - fascicles approach tendon from both sides Multipennate - bunches of feathers converge to single point Muscle Compartments Group of functionally related muscles enclosed by fascia Intermuscular Septa - very thick fascia that separate compartments from each other Compartment Syndrome - Blood flow to compartment is obstructed by pressure - Nerves can regenerate after pressure is relieved by muscle damage is permanents - “Ischemia” (poor blood flow) Indirect Attachment to Bone - Some muscles don’t attach directly to the bone but the fascia or tendon of another muscle of on collagen fibers of dermis Tendons - connect muscle to bone Aponeurosis - tendon is broad and flat Retinaculum - connective tissue band that tendons form separate muscles and pass under Direct (fleshy) Attachment - Little seperate between muscle and bone - Muscle emerge directly from bone Origin - stationary, Insertion - moving Intrinsic Muscle - entirely contained within a region (hand) Extrinsic muscle - acts on designated region but has one attachment somewhere else Function of Groups of Muscles Action - effect of muscle to produce or prevent movement Prime Mover (agonist) - muscle that produces most force during particular joint action

Synergist - muscle that aids prime mover Antagonist - opposes the prime mover or prevents excessive movement Fixator - muscle that prevents movement of bone Muscle Innervation - Innervation - identity of a nerve that stimulates Spinal nerve - arise from spinal cord, innervate muscles below the neck Cranial nerve - arise from base of brain Muscle - Nerve Relationship - Skeletal muscle never contracts unless stimulated by nerve - If nerve connections are severed a muscle becomes paralyzed “Denervation atrophy” - shrinking or paralyzed muscle when nerve is disconnected Somatic Motor Neurons - Cell bodies in brainstem and spinal cord - Serve the skeletal muscle Somatic Motor Fibers - Axons that lead to skeletal muscle - Each nerve fiber branches out to num of muscle fibers - Each fiber is supplied by only one motor neuron Motor Unit - One nerve fiber and all the muscle fibers innervated by it Muscle fibers of one motor unit: - Dispersed throughout the muscle - Contract in unison - Produce weak contraction over wide area - Provide ability to sustain long-term contraction ~ Effective contraction usually involves several motor units at once (average motor unit contains 200 muscle fibers) Small motor unit - fine degree of control - Hand and eye muscles Large motor unit - more strength than control - Powerful contraction supplied by large motor units of hundreds of fibers (Gastrocnemius) - has 1000 muscle fibers per neuron Neuromuscular Junction - when target cell is a muscle fiber Synapse - point were nerve fiber meets its target cell - Each terminal branch within the NMJ forms separate synapse with the muscle fiber

Axon terminal - swollen end of nerve fiber - Contains synaptic vesicles with acetylcholine (ACh) Synaptic Cleft - gap between axon terminal and sarcolemma Schwann cell - envelope and isolates the NMJ Action of NMJ - Nerve impulse causes synaptic vesicles to undergo exocytosis which releases ACh into synaptic cleft - Muscle Cell has millions of ACh receptors which are proteins incorporated into its membrane - Junctional folds of sarcolemma under the axon terminal increases the surface area of ACh receptors Basal Lamina - thin layer of collagen and glycoprotein which separates the schwann cell and muscle cell from surrounding tissues - It contains acetylcholinesterase (AChE) which breaks down Ach,  allowing for relaxation Electrically Excitable Cells - muscle fibers and neurons that are electrically excitable Electrophysiology - study of electrical activity of cells Voltage (electrical potential) - a difference in electrical charge from one point to another - The difference in potential between the ICF and ECF Unstimulated (resting) Cell - Sodium potassium pump maintains more anions (negatively charged) on the inside of the membrane than on the outside, this causes the plasma membrane to be more negatively charged by comparison to its outer surface - Resting membrane potential (RMP) of the plasma membrane is around (-90 mV) in skeletal muscle cells) Excess sodium ions (NA+) in the extracellular fluid (ECF) Excess Potassium ions (K+) in the intracellular fluid (ICF) Stimulated (active) Muscle Fiber Action Potential - Quick up and down voltage shift (Depolarization and repolarization) Phase #1 - Na+ ion gate open in plasma membrane Phase #2 - Na+ flows into the cell down its electrochemical gradient Phase #3 - Na + gates close and K+ gates open Phase #4 - K+ rushes out of the cell partly repelled by the positive sodium charge and party because of its concentration gradient Phase #5 - Loss of positive potassium ions turns the membrane negative again (repolarization)

The Action protein perpetuates itself down the length of the cell membrane Impulse - An action potential at one point causes another one to happen immediately in front of it which then triggers one even further along and so forth

Behavior of Skeletal Muscle Fibers Four major phases of contraction and relaxation Excitation - process where nerve action potentials lead to muscle action potentials Excitation-contraction coupling - events that link the action potentials on the sarcolemma to activation of the myofilaments and therefore preparing them to contract Contraction - When muscle fiber develops tension and shortens Relaxation - When stimulation ends a muscle fiber relaxes and returns to its resting length Excitation of a Muscle Fiber 1. A nerve signal arrives at the axon terminal and stimulates a voltage-regulated Ca2+ gates to open - Calcium ions enter the axon terminal 2. Ca2+ stimulates exocytosis of synaptic vesicles which release ACh into synaptic cleft 3. ACh diffuses across the synaptic cleft and binds to receptor proteins on the sarcolemma - The ACh receptors are ligand-gated ion channels that must bind two ACh molecules in order to open 4. When the channel opens, NA+ flows into the cell and K= flows out - The sarcolemma reverses polarity from -90 mV to +75 mV and then falls back to a level close to the RMP as K+ exits This rapid fluctuation in membrane voltage at motor end plate is end-plate potential (EPP) 5. Areas of sarcolemma adjacent to the NMJ have voltage-gated ion channels that open in response to EPP - This allows NA+ to flow in and K+ to go out - generating action potential - The muscle fiber is now excited and the potential can be passed along the sarcolemma

Excitation-contraction coupling 6. A wave of action potentials spreads from the end plate in all directions - It hen enters the T tubules, continuing down them into the cell interior 7. Action potentials open voltage-gated ion channels in the T tubules - These gates are linked to calcium channels in the terminal cisternae of the sarcoplasmic reticulum (SR) - When the channels in the SR are open, Ca2+ is able to diffuse out of the SR and into the cytosol which is down its concentration gradient 8. Calcium binds to the troponin of the thin filaments 9. The troponin-tropomyosin complex changes shape, exposing the active sites on the actin filaments and making them available for binding to myosin heads Contraction 10. Myosin ATPase hydrolyzes ATP that is bound to the myosin head and turns it into ADP and Phosphate (Pi) - The energy released activates the head which “cocks: into extended high-energy position 11. With ADP and phosphate still bound, the activated myosin head binds to an exposed active site on the thin filament, forming a cross-bridge 12. Myosin releases the ADP and Pi and flexes into a bent, low-energy position - It also tugs the thin filament along with it - this is called a power stroke 13. Upon binding to another ATP myosin releases the actin - It is now prepared to repeat the process by hydrolyzing the ATP and recocking (the recovery stroke ) - It will then attach to a new active site farther down the thin filament When One myosin releases an actin, many other heads on the same thick filament are still bound to the acton the thin filament - SO it doesn’t slide back The cycle of power and recovery strokes is repeated many time by each myosin head, at a rate of about five strokes per second, and each stroke consumes one molecule of ATP

Relaxation 14. Nerve signals stop arriving the neuromuscular junction (NMJ) so the synaptic knob stops releasing ACh 15. As ACh dissociates from the receptor, AChE breaks it down - The axon terminal reabsorbs the fragments but now there is no additional ACH to replace it 16. During excitation and contraction, the SR simultaneously releases and reabsorbs Ca2+ - When the nerve stops firing, Ca2+ release ceases and only its reabsorption continues - The Ca2+ in the SR binds to a protein called calsequestrin and is stored until stimulation occurs again 17. The level of free calcium in the cytosol decreases since Ca2+ dissociates from troponin and is reabsorbed but not replaced 18. Tropomyosin moves back into position, blocking the active sites of the actin filament and preventing myosin binding A muscle returns to its resting length with the aid of two forces - The contraction of an antagonist muscle lengthens it (E.g. contraction of the triceps brachii stretches the biceps brachii) The pull of gravity on the body part can also return it to its resting length Neuromuscular Toxins and Paralysis - Toxins interfering with synaptic function can paralyze muscles - Some pesticides contain cholinesterase inhibitors - Bind to acetylcholinesterase and prevent it from degrading Ach - Spastic paralysis: continual contraction of the muscles Flaccid Paralysis - a state in which the muscles are limp and cannot contract - Curare (a plant poison) competes with ACh for receptor sites but does not stimulate the muscles Botulism - type of food poisoning caused by neuromuscular toxin secreted by the bacterium Clostridium botulinum

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Blocks release of ACh causing flaccid paralysis Botox cosmetic injections used for wrinkle removal

Length-Tension Relationship The amount of tension generated by a muscle depends on how stretched or shortened it was before stimulation - If overly shortened before stimulated, a weak contraction results as thick filaments just hit against the z discs - If too stretched before stimulated, a weak contraction results as minimal overlap between thick and thin filaments results in minimal cross-bridge formation - Optimum resting length  produces greatest force when muscle contracts - The nervous system maintains muscle tone (partial contraction) to ensure that resting muscles are near this length Rigor Mortis Rigor mortis - hardening of muscles and stiffening of body beginning 3 to 4 hours after death - Deteriorating sarcoplasmic reticulum releases Ca+2 - Deteriorating sarcolemma allows Ca+ 2 to enter cytosol - Ca+2 activates myosin-actin cross bridging - Muscle contracts but cannot relax Muscles relaxation requires ATP but there is no ATP after death - Fibers remain contracted until myofilaments begin to decay Rigor mortis peaks about 12 hours after death then diminishes over the next 48 to 60 hours Myogram - a chart of the timing and strength of a muscle’s contraction Threshold - minimum voltage necessary to generate an action potential in the muscle fiber and produces a contraction Twitch - a quick cycle of contraction and relaxation when stimulus is at threshold or higher Muscle Twitch Latent period - very brief delay between stimulus and contraction

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Time required for excitation, excitation - contraction coupling, and tensing of elastic components of muscle (generating internal tension)

Contraction phase - time when muscle generates external tensions - Force generated can overcome the load and cause movement Relaxation phase - time when tension declines to baseline - SR reabsorbs Ca2+ myosin releases actin and tension decreases - Takes longer than contraction Entire twitch duration varies between 7 and 100 ms Contraction Strength of Twitches - With subthreshold stimuli - no contraction at all - At threshold intensity and above - twitch produced - Even if the same voltage is delivered, different stimuli cause twitches varying in strength Due TO: - The muscles starting length influences tension generation - Muscles fatigue after continual use - Warmer muscle’s enzymes work more quickly - Muscle cells hydration level influences cross-bridge formation - Increasing the frequency of stimulus delivery increases tension output Muscles must contract with variable strength for different tasks Stimulating the nerve with higher voltages produces stronger contractions - Higher voltages excite more nerve fibers which stimulate more motor unit to contract Recruitment or multiple motor unit (MMU) summation is  the process of bringing more motor units into play with stronger stimuli - Recruitment occurs according to the size principle: weak stimuli (low voltage) recruit small units while strong stimuli recruit small and large units for powerful movements Low frequency stimuli produce identical twitches Higher frequency stimuli produce temporal (wave) summation - Each new twitch rides on the previous one generating higher tension - Only partial relaxation between stimuli result in fluttering incomplete tetanus Unnaturally high stimulus frequencies cause steady, contraction called complete (fused) tetanus

Tetanus - Maximum tension in the muscle fiber - Most ATP is being used at once - Tension will eventually crash and cause muscle fatigue Isometric Contraction - Muscle produces internal tension but external resistance causes it to stay the same length - Can be a prelude to movement when tension is absorbed by elastic component of muscle - important in postural muscle function and antagonistic muscle joint stabilization -

Kohnstamm phenomenon - involuntary muscle contraction after a long voluntary isometric contraction

Isotonic Contraction - Muscle changes in length with no change in tension - Concentric contraction: muscles shortens as it maintains tension (ex. slowly lifting weight) - Eccentric contraction: muscle lengthens as it maintains tension (ex slowly lowering weight) At the beginning of contraction - isometric phase - Muscle tension rises but muscle does not shorten When tension overcomes resistance of the load - Tension levels off Muscle begins to shorten and move the load-isotonic phase Cardiac and Smooth Muscle Cardiac and smooth muscle share certain properties - Their cells are myocytes - not as long and fibrous as skeletal muscles - they have one nucleus - They are involuntary - They receive innervation from the autonomic nervous system (not from somatic motor neurons) Properties of cardiac muscle - Contracts with regular rhythm

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Works in sleep or wakefulness - without fail - and without conscious attention Highly resistant to fatigue Muscle cells of a given chamber must contract in unison Contractions must last long enough to expel blood

Characteristic of Cardiac Muscle Cells - Striated like skeletal muscle but cardiomyocytes are shorter and thicker - Sarcoplasmic reticulum is less developed by T tubules are larger and admit from the extracellular fluid - Cardiomyocyte is joined to other cells by intercalated discs Appear as thick, dark lines in stained tissue sections Electrical gap junctions allow cardiomyocyte to stimulate neighbors Ther...