Physio 1 - Week 2 PDF

WEEK 2 - PHYS 1 LEARNING OBJECTIVES Give examples of muscle function Describe the 4 specific muscle properties Describe the types of muscles and muscle fibers Describe the levels of organization in skeletal muscle Describe the importance of Sarcoplasmic reticulum, mitochondria, and T-tubules for the...

WEEK 2 - PHYS 1 LEARNING OBJECTIVES Give examples of muscle function Describe the 4 specific muscle properties Describe the types of muscles and muscle fibers Describe the levels of organization in skeletal muscle Describe the importance of Sarcoplasmic reticulum, mitochondria, and T-tubules for the skeletal muscle fiber Describe how resting membrane potentials are generated Describe the phases of an action potential and how they occur Describe the components of a neuromuscular junction Describe the roles of acetylcholine in the neuromuscular transmission Describe how neuromuscular transmission occurs Describe how Botulinic toxin and Organophsphate/Carbamate pesticides interact with neuromuscular transmission Describe Myasthenia Gravis and its influence on the neuromuscular junction Describe how the excitation-contraction coupling occurs Describe the role of T-tubules, Sarcoplasmic reticulum, and Ca 2+ in the initiation of muscle contraction Describe the constitution of thin and thick filaments Describe the “walk along theory” of muscle contraction Describe how muscle changes its strength of contraction Describe the length-tension relationship List the sources of energy for muscle contraction MUSCLE PHYSIOLOGY NERVE CELLS Functions Motor Neuron Locomotion Neuron whose cell body is located WITHIN the CNS and whose axon travel within peripheral nerves and synapse Respiration Digestion Parturition Blood and Lymph circulation Swallowing Generation of body heat Specific Properties with EFFECTOR ORGANS Sensory Neuron Send signal from the periphery to the interneuron Located WITHIN CNS Interneuron Connects sensory and motor neurons Contractibility: ability to shorten or control Excitability: ability to be stretched Elasticity: ability to return to original shape after being stretched Muscle Types Organelles of Muscle Cell Sarcoplasmic reticulum - specialized Endoplasmic reticulum ◦Regulates calcium storage, release and reuptake Mitochondria - runs parallel to the myofibrils and can be found in large numbers ◦Supplies myofibril with large amounts of ATP T-tubules - arranged transversely to myofibril ◦Allow plasma membrane of muscle fiber to carry depolarization of action potential to interior of the fiber Myoglobin - protein located primarily in the striated muscles of vertebrates ◦Only found in skeletal and cardiac muscle ◦Serves as local oxygen reservoir that can temporarily provide oxygen ◦Total amount depends on body weight, degree of muscle development, and myoglobin concentration SKELETAL MUSCLE ORGANIZATION Crucial for body movement Muscle Fiber Types Attached to bone by tendons Type 1 = Red Fibers Stimulated by MOTOR NERVE by VOLUNTARY CONTROL ◦Slow twitch = slow contracting and fatigue- Body movement is the result of the contraction of skeletal resistant fibers muscle across a moveable joint ◦Rich in mitochondria Level of Organization ◦Relies on OXIDATIVE METABOLISM Epimysium: sheath of connective tissue surrounding the ◦Muscles to maintain posture muscle Type 2 = White Fibers Perimysium: connective tissue extensions from the ◦Fast twitch = fast-contracting and more epimysium that surrounds each fascicle easily fatigable fibers Fascicle: a bundle or cluster of muscle fibers ◦Fewer mitochondria Endomysium: connective tissue extensions from the ◦Relies on GLYCOLYTIC METABOLISM perimysium that surrounds the muscle fibers and are attached ◦Type 2A = fast twitch while fatigue to the sarcolemma resistant Sarcolemma: thin membrane enclosing a skeletal muscle ‣ Mixture of oxidative-glycolytic fiber (cell) metabolism Muscle Fibers: have elongated shape and contain the basic ◦Type 2B = fast twitch and fast fatiguing contractile units ‣ Dependent on glycogen for energy Myofibrils: composed of a linear series of repeating sarcomeres ‣ Muscle designed for sprinting Just get Sarcomeres: basic contractile unit of striated muscle fibers ◦Found between Z lines (Z discs) Myofilaments: responsible for actual muscle contraction ◦Thin filament: actin, troponin, tropomyosin ‣ Troponin has affinity for Ca 2+ ◦Thick filament: myosin ‣ 2 globular heads that bind ATP and actin ◦Titin: filamentous elastic molecules ‣ One end attached to Z disc with other connected to myosin remember thewords longerasorganization getssmaller MEMBRANE POTENTIAL GENERATION Membrane Potential Difference in electrical potential between the interior and exterior of a biological cell Membranes alter the rate at which particles can diffuse and they do so selectively Diffusion potential: potential difference generated across a membrane when a charged solute (ion) diffuses down its concentration Membrane Potential Phases 1. Resting Phase: membrane is polarized before action potential begins (-70mV) 2. Threshold: minimal voltage change to trigger an action potential (-55mV) 3. Depolarization State: membrane becomes permeable to sodium ions A. Change in membrane potential causes Na+ voltage gated channels to open leading to the inside of the gradient Ionic differences are consequence of ◦Differential permeability of the membrane to the ions ◦Operation of a membrane pump K+ high concentration in CYTOSOL Na+ high concentration in EXTRACELLULAR FLUID Resting potential of nerve fibers is -70mV Factors Determining Resting Potential Diffusion of K+ through nerve cell membrane ◦Leak channels allow K+ to diffuse OUT of cell ◦K+ moves into cell as it is attracted to the negative charge from proteins Nerst Potential: diffusion potential level across a membrane that exactly opposes the membrane becoming positively charged 4. Repolarization State: re-establishment of normal negative resting potential A. Voltage gated K+ channels open to a greater degree than normal B. These channels are slow to open so they begin halfway through the depolarization process 5. Hyperpolarization State: combination of no more Na+ flowing into and K+ ions leaving the cell A. K+ channels are slow to close so membrane potential becomes more negative than resting 6. Refractory Period: prevents a new action potential from occurring in excitable fibers A. Absolute = time needed for Na+ channels to reverent from inactivated to resting B. Relative = Na+ channels are closed so action potential is inhibited but not blocked so strong enough net diffusion of a particular ion through the stimulus can shift membrane potential to threshold membrane Diffusion of Na+ through the nerve cell membrane voltagesateanatanannasaos wagesateartenanneisansonen ◦Leak channels allow Na+ to diffuse repolarization INTO cell repolarization ◦Membrane is less permeable to Na Na-K Pump ◦Transports 3 Na+ OUT and 2 K+ IN ◦ATPase function of the protein becomes activated after binding voltage gated manners open am voltage gated inresno matanannasonen wagegateanatananneissaactonorma Hyperpolarization amresting membrane voltage gated potential us restingstate retractor absolute period retractor relative NEUROMUSCULAR JUNCTION Components Motor Unit = motor neuron + muscle fibers ◦Small motor units = control movements that require precision ◦Large motor units = do not require precise movement, more about strength and force Each muscle fiber is only touched by ONE neuron Motor Endplate: modified area of the muscle fiber membrane at which a synapse occurs Chemical Synapses ◦Presynaptic side: terminal portion of the motor neuron ‣ Large number of synaptic vesicles ‣ Active zone: holds the vesicles in the inner surface of the terminal membrane ‣ SNARE proteins: specific proteins that hold the vesicles in the right place ‣ Mitochondria creates acetylcholine ‣ Acetylcholine is the neurotransmitter if the neuromuscular junction Stored in synaptic vesicles that line Neuromuscular Transmission When the action potential reaches the neuromuscular junction the wave of depolarization opens the voltage-gated calcium channels Influx of calcium to enter the PRESYNAPTIC TERMINAL Increase of calcium releases vesicles Vesicles move to the active zone, DOCK, FUSE, and RELEASE Acetylcholine from terminals Acetylcholine diffuses across the synaptic cleft and binds with NICOTINIC RECEPTORS ◦These are ligand gated ion channels Binding opens the channel allowing for Na+ to flow inside the cell creating a LOCAL DEPOLARIZATION in the muscle fiber membrane which triggers an actual action potential Acetylcholine is RAPIDLY removed from the synaptic cleft by ACETYLCHOLINESTERASE ◦Prevents continuous muscle re-excitation ◦Small amounts DIFFUSE out of the cleft and is no longer available up in rows in active zone side ◦Synaptic Cleft: narrow space between the presynaptic can presynaptic and postsynaptic membranes n ‣ Subneural clefts = numerous small folds of the muscle membrane greatly increases surface area ◦Postsynaptic side: muscle cell membrane that has specialized features that facilitate synaptic synaptic resides can synaptic an I receptors ‣ Junctional folds = folds aligned with the active zones of the presynaptic terminals with receptors at the mouth of the folds inesteras can.name 7 iaine Iconic receptor transmission ‣ Acetylcholine receptors = Nicotinic ca voltage gated side postsynaptic CLINICAL CORRELATION Botulism = SNARE proteins Destroys the binding proteins (SNARE) in vesicle docking and interferes with Acetylcholine release Causes FLACCID MUSCLE PARALYSIS which can lead to death Ingestion of neurotoxin produced by a gram-positive, rod shape, anaerobic bacteria usually from uncooked, spoiled food Organophosphate - irreversible Inactivates ACETYLCHOLINESTERASE leading to an excess of acetylcholine and overstimulation of Nicotinic receptors at the neuromuscular junctions Carbamate - reversible Inactivate ACETYLCHOLINESTERASE leading to an excess of acetylcholine and overstimulation of Nicotinic receptors at the neuromuscular junctions Myasthenia Gravis = acetylcholine receptors Abnormal reduction in acetylcholine receptors Exercise induced weakness Congenital = present from birth and becomes apparent between 6-9 weeks of age Acquired = autoimmune disease from IgG against acetylcholine receptors ◦Antibodies may bind directly to acetylcholine receptor blocking ion channel opening ◦Antibodies may increase the degradation rate of acetylcholine receptors, resulting in decreased concentration of receptors at the postsynaptic membrane EXCITATION-CONTRACTION COUPLING Process transforms the nerve impulse into muscle contraction Action potential in muscle fibers occur in SAME WAY described for nerve cells 1. End plate potential is generated at the NEUROMUSCULAR JUNCTION 2. Depolarization: generating and propagating an action potential A. Local depolarization spreads to adjacent areas of the sarcolemma opening voltage-gated channels B. Na+ diffuses into the cell following its electrochemical gradient 3. Repolarization: restoring the sarcolemma to its initial polarized state A. Na+ channels close and voltage-gate K+ channels open Action potentials on the sarcolemma spread in both directions along the length of the fiber but also to the interior of the cell along the transverse tubules (T-tubules) 1. Action potential propagates down T-tubules 2. DHPR senses membrane depolarization, opening RYR channel on Sarcoplasmic reticulum 3. RYR opens briefly and releases a pulse of Ca 2+ 4. Ca 2+ diffuses to myofilaments and binds to troponin 5. Ca 2+ causes tropomyosin to move away from myosin-binding sites 6. Myosin heads bind to ATP (low-energy configuration) where ATPase activity cleaves ATP —> ADP + Pi causing head to become “cocked” 7. Myosin heads bind to myosin binding sites creating a cross-bridge A. Myosin head bends towards the center of sarcomeres causing actin to slide towards M-line 8. Binding of new ATP causes detachment of myosin head from actin filament 9. Ca 2+ active transport pump removes Ca 2+ ions from the myofibrillar fluid after contraction occurs WALK ALONG THEORY tropomyosin t stropomyosin actin 4 j myosin am pop a ng sarcoplasmicreticulum n ttubule T sarcolemma i MUSCLE CONTRACTION Contraction Strength All-or-None Response: muscle fiber either contracts completely or not at all Strength Categories ◦Twitch: single contraction and relaxation cycle produced by an action potential within the muscle fiber itself ◦Summation: if another action potential comes before the complete reaction of a muscle twitch, then the next twitch will simply SUM onto the previous one ‣ Size principle: as more and larger motor units are activated, the force of muscle contraction becomes progressively stronger ‣ Frequency: at lower frequency stimulation, contractions occur one after another ‣ Total strength of contraction rises progressively with the increasing frequency ◦Tetanus - Tetanization: when the frequency reaches a critical level the successive contraction eventually becomes so rapid that they fuse together ‣ Whole muscle contraction appears to be completely smooth and continuous Muscle Length Muscle contraction STRENGTH is intimately related to muscle LENGTH Skeletal muscles operate with the greatest active tension when ENERGY SOURCES FOR MUSCLE CONTRACTION Phosphocreatine (Creatine Phosphate) Creatine produced from amino acids in the liver are phosphorylated in the muscle by the enzyme Creatine phosphokinase to produce phosphocreatine Carries a high energy phosphate bond similar to the bonds of ATP Used to reconstitute the ATP molecule Only a small amount in muscle Glycolysis - 2 ATP produced Enzymatic breakdown of carbohydrates as glucose and glycogen, then with the release of energy and the production of pyruvic acid and lactic acid Process can be done in the absence of oxygen Not as fast as oxidative metabolism + many end products - lactate Oxidative Metabolism 95% of energy used for contraction Combining O2 with the end products of glycolysis and with other sources of energy to produce ATP Short period of time = carbohydrates Long term activity = fatty acids close to an ideal length often their RESTING LENGTH If shortened or stretched, strength of contraction is diminished Tension = number of cross-bridge interactions = degree of overlap between thick and thin filaments Decreased length: overly contracts, high degree of overlap = Z-disc = ends of the sarcomere M Line = middle of the sarcomere decrease tension Increased length: little degree of interaction = decrease tension H Zone = only thick filaments I band = only thin filament Light band A band = thick and thin filament Dark band