KIN 3306 1nd Edition Lecture 5 Outline of Last Lecture I. Test InformationII. Extra Credit InformationIII. Top HatIV. Short Answer Question SamplesV. Essay Question SamplesOutline of Current Lecture I. OverviewII. Structure of MuscleIII. Structure of a Muscle FiberIV. Components of a Muscle FiberV. Components of a MyofibrilVI. Components of a SarcomereVII. MyosinVIII. ActinIX. Actin and Myosin StructureX. Muscle ContractionXI. Phases of Muscle ContractionXII. Resting Membrane PotentialThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.XIII. Action PotentialXIV. Excitation-Contraction CouplingXV. Motor UnitXVI. Neuromuscular JunctionXVII. Sliding Filament TheoryXVIII. Energy for ContractionXIX. Muscle RelaxationXX. Fiber Type CharacteristicsXXI. Bergstrom Muscle Biopsy NeedleXXII. Muscle HistochemistryXXIII. Fiber Type and PerformanceXXIV. Other Factors Which Influence Muscle ForceXXV. Force – Length RelationshipXXVI. Muscle Fatigue during ExerciseXXVII. Summary of Muscle FibersCurrent LectureI. Overviewa. Muscle Contractionb. Muscle Fiber Typesc. Fiber Type and Athletic Performanced. Muscle Fatigue during Exercisee. SarcopeniaII. Structure of Musclea.III. Structure of a Muscle Fibera.b. Muscle Fiber = Muscle Cellc. Myofibrils are the smallest piecesIV. Components of a Muscle Fibera. Plasmalemma – plasma membranei. Attach to tendonsii. Folds for stretchingiii. Junctional foldsiv. Transport in and out of cellb. Sarcoplasm – cytosol/cytoplasmi. Gelatin-like substanceii. Storage site for glycogen, myoglobin, and other proteins/mineral/fats, organellesc. Transverse Tubulesi. Run laterally through muscle fiberii. Path for nerve impulsesiii. Path in and out of muscle fiberd. Sarcoplasmic Reticulumi. Runs parallel to muscle fiberii. Calcium storageV. Components of a Myofibrila.b. We can break down myofibrils into sarcomeres. The sarcomere is what is physically contracting to allow our muscles to contractVI. Components of a Sarcomerea. Sarcomere – basic contractile unit of a myofibrili. I-Bandii. A-Bandiii. H-Zoneiv. M-Line v. Z-Discb. Sarcomere includes two types of protein filamentsi. Thick Filament – Myosinii. Thin Filament – Actinc. Alignment of the thick and thin filaments is what give muscle its striationsVII. Myosina. Comprises 2/3 of skeletal muscle proteinb. Two protein strands twisted togetherc. Globular heads (myosin crossbridges)d. Titin filaments stabilize myosini. Titin is the light line that connects to the z disc. Titin is not considered to be a part of the thick filament but after the muscle contracts, titin will puteverything back in starting position to maintain the resting position.VIII. Actina. Thin filaments are composed of 3 proteinsi. Actin: globular proteins form strandsii. Tropomyosin: twists around actin strandiii. Troponin: bound at intervals to actinb. Anchored to Z-Diskc.d. Tropomyosin’s purpose is to block myosin binding sites on actin. This way, in resting conditions, myosin cant binde. When Ca2+ is bound to troponin, it will then move TropomyosinIX. Actin and Myosin Structurea.X. Muscle Contractiona. Muscles are divided into motor units comprised of:i. Alpha-motor neuronii. Muscle fibersb. In summary: Muscle contraction begins with a neural impulse. Muscles are voluntary. All of our muscles are divided into motor units – one motor neuron that touches/innervates several muscle fibersXI. Phases of Muscle Contractiona. Action Potential/Calcium Releaseb. Calcium-Troponin Binding; Tropomyosin Shifc. Actin-Myosin Bindingd. Myosin Power Stroke/ATP Bindinge. In summary: AP leads to calcium release. Troponin moves Tropomyosin so actin and myosin can bind. The power stroke is the movement of myosin to contract the sarcomere. Then, ATP is used to fuel muscle contraction.XII. Resting Membrane Potentiala. RMP = -70mVb. Caused by uneven separation of charged ions inside (K+) and outside (Na+) the cellc. More ions outside the cell than insided. Membrane more permeable to K+e. Sodium-Potassium Pumps maintain imbalancei. 3 Na+ outii. 2 K+ inf. In summary: AP is an electrical/nerve impulse. The RMP is the charge of a musclefiber cell at rest. The reason it has a charge is because of the ion distribution. There are less ions inside the cell versus outside of the cell. The ions we’re talking about are K and Na. To maintain this negative charge of -70mV, we have a Na/K pump. K leaks a little bit in and out of the cell. An AP is a disruption of this restingcharge that propagates an electrical impulse into the cell.XIII. Action Potentiala.b. In summary: The initial stimulus comes from neurotransmitters (in muscles, the neurotransmitter is Ach). This stimulus initiates the AP. Repolarization is when K runs out. In the dip after #7, this is called hyperpolarization – because the K gatesare not tightly regulated so they stay open a little longer than they need to so K will get out a bit more.c. In summary: AP is always the same magnitude. What can make AP strong or less strong is summation and recruitment. Summation is if you have several APhappening quick, all of them work together and generate one big contraction. Recruitment is where more muscle fibers are recruited and so more motor units are recruited.d. Make sure to know what is happening at each phase and what an AP is doing TQ*XIV. Excitation-Contraction Couplinga. Action potential travels to sarcoplasmic reticulum, causes release of calcium into sarcoplasmb. Calcium binds to troponin on thin filamentc. Troponin moves Tropomyosin, revealing myosin binding sites on actind. Myosin cross bridges bind to actine. In summary: AP goes into the T Tubules and so this is when we get the initiation of the muscle contraction. Once the AP comes through, the SR releases calcium so calcium will be freely available.XV. Motor Unita.XVI. Neuromuscular Junctiona.b. In summary: They do not actually touch. The neuron sits in a fold within the plasmalemma. As AP goes down, there is a neurotransmitter that carries thesignal from the neuron to the muscle fiber since they’re not physically touching. As it gets to the end, the neurotransmitter is released into the space (synaptic cleft), the Ach binds to plasmalemma, and this is the initial signal that starts the AP so it can get over the -55 threshold.c. In summary: It goes from electrical signal  chemical signal  then reinitiates the electrical signal that