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Midterm

Biology 339 – Midterm #2.docx

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Department
Biology
Course Code
BIOL 339
Professor
Chris Moyes

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Biology 339 – Midterm #2 Notes Muscles I  What are the main Cytoskeletal elements in Eukaryotes o Fibers and tubules  Microtubules, intermediate filaments and actin  Actin filaments: long chain of monomers of actin o Motor Proteins  Kinesin, dynein and myosin  Motor Proteins o It is the head of the protein that is responsible to binding onto things o Uses ATP to move o Myosin and Kinesin are evolutionarily similar  Myosin and dynein walk along the same microtubules o Motor domain breaks down ATP to facilitate movement o There are many different types of Mysosin  3 types I, II, V  Actin and Myosin in Muscle o How does Myosin V walk?  Duty cycle  At anytime one or other head is going to be bound  If one isn’t bound, the myosin would fall off  Works on vesicles, tail end binds on the vesicle and it walks along  2 arms working in monkey bar motion have to hold on at all times o How does Myosin I walk?  It walks along actin filaments and is a coordinated motion of many myosin I that all work independently but always have some holding on  Grabs on with one arm o Structural differences in Actin and Myosin  Actin  General features of muscle actin (alpha) are very similar to cytoskeletal actin (beta)  Myosin  Myosin II  dimmer of two myosin molecules  Organized into a heterohexamer of 2 myosin II (heavy chains) and 4 myosin (light chains) o 2 essential and 2 regulatory  also assosciated proteins  MLC Kinase, MLC phosphatase o Functional Differences in Muscle Actin and Myosin  Actin  Actin filaments (thin filaments) are organized into stable arrays (no dynamic action or treadmilling)  Actin stays stuck to a Z-disk plate which has 6 thin filaments attached around a thick filament  Myosin  Arranged in thick filaments  Myosin hexamers (thick filaments) organized into 2 stable bouquets, arranged tail-to-tail  Arranged in the center of the thin filaments  Individual muscle myosins have: o Shorter unitary displacement  step size o Short duty cycle  proportion of time spent on actin  Muscle needing transport vesicles have myosin V and I o These are critical for building muscles  Myosin II is mainly used to build contractile muscles  Muscle contraction – when relaxed can slide actin filaments and move back to the arrangement  Myosin is going to reach up to find an actin to pull on  Individual myosin motor protein is only attached 5% of the time because it needs to be able to pull on actin o It wouldn’t slide if it only stayed on!  Myosin V  long step sizes, holds on majority of the time  Myosin II  short step sizes, holds on minimal time  Basic Structure of Striated Muscle o Has alternating I bands and A bands where the I bands are the locotion of the Z-disks and the A bands have a space to allow contraction o One sarcomere is Z-disk to Z-disk  Or I band to I band o Titin  Makes sure thick filament stays in the middle o Structural Pro’s  Make sure it stays the same length/in the same place o CapZ  End of actin filament and interacts with the Z-disk o Sarcomere  Z-disk to Z-disk, form a myofibril  Cell has a collection of these arranged in the cell membrane o A contraction at the cellular level leads to a shape change of the cell o Difference between Myofibres and Cardiomyocytes  Cariomyocytes are single celled  Myofibres are much bigger by incorporating lots of individual cells together  lots of nuclei o Tension relationship between Sarcomere length and force  Venus Return  Heart grows in volume, as a result stretching pulls myofibres apart  Then fibres snap back at the maximum tension force to pump the blood  As heart volume increases = contractile force gets stronger  Classes of Vertebrate Muscle Types o Allow fine tuning of contractile properties:  Degree of shortening  though not all muscles shorten  Rate of shortening  fast twitch vs. slow twitch  Frequency of contraction  single vs. rapid cycling  Maintenance of contraction tonic vs. twitch  Endurance  ability to continue activity o Can make a muscle that contracts very fast but it wastes energy  Trade-offs come about by the way which muscles are built o Twitch muscles contract when necessary, but tonic muscles contract all the time o Most common muscle classes are Smooth and Striated muscle  Striated can be cardiac or skeletal  Regulation of Striated Muscle o Actinomyosin ATPase  Actin can bind onto myosin and cause myosin to release the actin  ATP binds onto myosin  Everytime there is a mechanical event  chemical response  And vice versa  Myosin Release  Causes a structural change so it can reach out and extend  ATP is hydrolyzed and then as soon as it releases; phosphate causes power stroke o Pulls myosin forward  ATP is released and then waits for the next cycle  Excitation-Contraction Coupling – EC coupling o At rest myosin cannot bind actin o Depolarization of muscle cell membrane o Propogatoin of depolarization o Influx of calcium ions o De-inhibition of actinomyosin o Reversal/Relaxation  Excitation in Skeletal muscle o In neurogenic muscle a motor neuron releases neurotransmitter to activate muscle at motor end plate o This is an all or none phenomenon  muscles in body do different degrees of contraction  All being regulated by the same muscle – within a cell, different nerves are used though  Regulated by nerves, when we contract – nerves send the signal o A wave of depolarization moves over the sarcolemma  Transverse tubules are invaginations of sarcolemma that allow depolarization to penetrate deep into the muscle interior  Depolarization has to happen very fast if you want the muscle to contract  T-tubules take the cell membrane and push it deep within in the cell  bringing it in close proximity to the sarcoplasmic reticulum  Depolarization causes the release of Calcium  Cardiac vs. Skeletal Muscle o Abundance of t-tubules influence delay between initiating depolarizing event and activation of the muscle o Cardiac muscle has fewer sarcoplasmic reticulum then that of skeletal muscle  skeletal muscle has more ability to store calcium  Excitation in Cardiac and Smooth Muscle o Faster action potential in skeletal muscle allows repeated contractions o Longer action potential in cardiac creates refractory period o Contracting and relaxing  Prevent that rhythm from getting screwed up  Twitch muscle – really fast when needed and then able to relax o Skeletal Muscle  Depolarizing event  Acetylcholine binds and opens sodium channels ultimately leading to calcium channels opens thus firing the action potential  Hyperpolarization blurp  Induce another excitation after that excitation you get another depolarization, therefore more sodium and calcium being released  larger contractions o Cardiac Muscle  Channels are organized so that it stays depolarized  Cannot depolarize again right after  not until it reaches a repolarized state can another excitable action occur  Cannot contract again before it is fully relaxed  Important for the intrinsic rhythm of the heart o Both cardiac and skeletal muscle contract when intracellular Ca2+ levels rise  The trigger for the increase and the source of sarcoplasmic Ca2+ differ  Calcium binding, calcium channels and ATP hydrolysis drive calcium against the gradient o EC-Coupling in Cardiac Cells  Lots of calcium outside the cell  Sarcolemma opens  calcium channels open  Calcium induced, calcium release 1) Depolarization of the plasma membrane of the sarcolemma opens DHPR which allows calcium into the cell 2) Elevated calcium triggers the opening of RyR (ryanodine receptor) on the Sarcoplasmic reticulum allowing calcium to escape. Elevated cytoplasmic Ca2+ triggers actinomyosin ATPase 3) After repolarization, ion pumps begin returning Ca2+ to resting locations, outside the cell and in the sarcolemma o EC-Coupling in Skeletal cells o Channels are physically connected 1) Excitation  depolarization of plasma membrane opens DHPR  Ca2+ enters, changes DHPR structure trigger the opening of ryanodine receptor 2) Calcium is released and the RyR opening allows Ca2+ to escape the sarcoplasmic reticulum  elevated cytoplasmic Ca2+ levels trigger actinomyosin ATPase 3) Relaxation, repolarization ion pumps being returning CA2+ to resting locations outside and in the sarcoplasmic reticulum o Faster  faster action potentials  Process of Excitation o Contractions start with an increase in Ca2+  Calcium binds to TnC  troponin complex  Weakening the actin interaction  Tropomyosin move into the actin groove  Actin: myosin cross-bridge cycling o Relaxation  Ca2+ pumped across Sarcolemma into Sarcoplasmic reticulum  Ca released by TnC which strengthens the actin interaction and returns it to inhibitory position  Smooth Muscle o Smooth muscle is not striated  lack sarcolemma o Dense bodies  way to organize thick and thin filaments  All over the place o No t-tubules  allow things to go fast in striated muscle  Therefore, things happen slow o Control of contractility is exerted at both thick and thin filaments o Many cell regulators and hormones alter contractility o Ca-sensitive and Ca-independent pathways  although no troponin o Muscles can contract without change in calcium  although it works better with presence of calcium o No tropomyosin complex in smooth muscle  Calcium will bind onto calmodulin instead o Smooth muscle is very complex and has variable sensitivity to calcium  Muscle Diversity o Many stimuli for changing striated muscle in individuals  Embryonic development gives fiber types  Activity-based responses change fiber types o These changes involve switching of isoforms of contractile proteins, motor neuron properties, proteins in EC coupling, and metabolic support  The changes/differences allow muscle specialization within an individual  Muscle Recruitment o Red Muscle  Used for low intensity movements  Myoglobin  used for oxygen storage and facilitated diffusion  Mitochondria contain a lot of iron  making it red  Redness is all about oxygen  Efficient and used for long periods of time o White Muscle  Responsible for burst muscle  excitation  Mimicks what a nerve would do  Arranged in a way that there are enough capillary around to ensure enough oxygen is available o What differs amongst these muscle types?  Metabolism  Bioenergetics  Oxidative phosphoralation or glycolysis  Oxygen delivery  Myofibrils  Sarcomere arrangement  series or parallel  Myosin properties: ATPase rate  fast to slow  Excitation and EC Coupling  Motor neurons, Sarcolemma Na channels, t-tubules  Calcium channels, terminal cisternae, parvalbumin  Glycolysis and Oxidative Phophoralation o Glycolysis  Doesn’t need oxygen  isn’t limited to oxygen delivery  High rate of ATP production rate  Use only 2/3 glucose  and use glucose  No oxygen dependance  Used for short, fast bursts o Oxidative Phosphoralation  Has a slower rate of ATP production  Have a slower efficiency for ATP use  Need fats and a variety of fuels  Dependant on oxygen  Best suited for long term, steady state exercise activity  Changing Capillarity o Low oxygen (poor delivery, extra use) causes capillary lining (endothelium) to become hypoxic o Endothelium triggers hypoxia inducible factor (HIF) pathways, which cause secretion of VEGF o VEGF stimulates growth of capillaries  angiogenesis o More VEGF=more capillaries  therefore more oxygen uptake and transfer  Force Development and Muscle Design o Series of tradeoffs  How fast you can contract and the force you can generate  Trade off between velocity and force o For a given muscle, maximal force generation occurs with a minimal shortening o Myosin differ in their contraction kinetics o Sarcomeres arranged in series are good at shortening  Used for quickness o Sarcomeres arranged in parallel are good at force generations  Used for strength  Myosin Isoform Diversity o Every animal has a large repertoire of myosin genes  Myosin I and V are important in vesicle transport  Myosin II is central to muscle o Every animal has a repertoire of myosin II genes  Differ in ATPase rate and force generation  Muscles can change which isoform they express o Getting from place to place  myosin I and V  Compare muscles specialized for long term and short term activities o Differences in birds  Hummingbirds  highest mitochondria content, high capillarity  Geese  lots of glycolysis  lots of modified hemoglobin frequency, have different myosins o Differences in fish  Many often use muscle to maintain their shape  Tunas swim 20, 30, 40 miles per day  Bird Flight Muscle o Hummingbirds have the highest wing beat frequency among vertebrates o Hovering requires generating lift on both up and down stroke o Both flight muscles are well developed o The muscles that hover for hummingbirds is red muscle  Insect Flight Muscle o To beat faster than hummingbirds, some insects require different modes of EC coupling  asynchronous flight muscles  Calcium moves in, activates and then moves out o Have 2 different muscles operating at different times  One brings wing up, the other brings wing down  relax when the opposite one is doing its thing  Heater Organs o Have adapted in many different species  deepwater fish have heater muscle around their eyes o Tuna have internalized red muscle that keeps their body warmer  High Frequency muscle in Sonic Organs o Many species make noise by contracting muscles at high frequencies  Locomotion o Locomotion is more than just muscle activity o It requires integration of multiple physiological systems  It requires muscle, skeletal and blood vessel systems to all coordinate together  Neural Control of Muscle o Complex movements are coordinated by central pattern generators  An area within the CNS that controls the timing of muscle contractions o Have brain tell motor neurons when its time to stimulate specific tissues o Activation of specific motor neurons permits recruitment of fibers at different speeds  Example of Muscle changes in Salmon o Salmon must travel a long distance, upstream without food o Need to integrate muscle biology with digestive physiology o In the beginning they have lots of fat and as they move up fat will decrease and protein takes over o By the end glycogen is the most prominent  as it migrates up it has to give up this idea locomotion and think about building a nest  Antagonistic Muscles o Movement requires muscles to be arranged antagonistic to each other o The set of muscles controlling a movement comprise a locomotor module  Bicep contracts to flex the arm  Tricep contracts to extend the arm o Antagonistic muscles do the opposite things  different muscles for up and down movement that help to move wings  Musculoskeletal System o Not homologous structures but have the same function  Endoskeleton and exoskeleton o Lions are much larger than cheetahs and both are specialized for strength or speed  The cheetah has an arm muscle that is attached closer to the join that causes a long and fast response  Cheetah is good at running fast  Lion has an arm muscle that is located further away from the joint  makes it good at contracting with great force  Biomechanics o Convergence between physiology and physics o Deals with the concepts of force, work and power o Allows you to translate between different ways of expressing the energetic costs of movement o Animals tend to design muscles that optimize power rather than force o Isometric contraction  High Force, no Velocity of shortening  low power o Isotonic contraction  With little weight: low force, h
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