PROG for CHMBCH
PROG for CHMBCH BCH 5886
Popular in Course
verified elite notetaker
verified elite notetaker
Test Prep (MCAT, SAT...)
verified elite notetaker
verified elite notetaker
verified elite notetaker
Popular in Biochemistry and Molecular Biology
This 12 page Class Notes was uploaded by Ms. Riley Hansen on Thursday September 17, 2015. The Class Notes belongs to BCH 5886 at Florida State University taught by Timothy Cross in Fall. Since its upload, it has received 42 views. For similar materials see /class/205659/bch-5886-florida-state-university in Biochemistry and Molecular Biology at Florida State University.
Reviews for PROG for CHMBCH
Report this Material
What is Karma?
Karma is the currency of StudySoup.
You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!
Date Created: 09/17/15
ExercisePhysiology Test 3 Structural Aspects of Skeletal Muscle 3 Know what general proteins that comprise the thick and thin filaments i Thick Filament Proteins 1 Iquot S 5quot NS 9 5 Myosin contractile protein that splits ATP and is responsible for the llpower strokequot of the myosin head CProtein structural protein that holds the myosin tails in a correct spatial arrangement may hold H protein of an adjacent thick filament at an even distance during force generation may also control the number of myosin molecules in a thick filament MQrotein helps hold the thick filament in place part of Mline Myomesin provides strong anchoring point for the protein Titin M provides ATP from phosphocreatine located proximal to the myosin heads part of the Mline o actin attaches actin filaments together at the Zdisk Desmin vimentin synemin link Zdisks of adjacent myofibrils together Spectral and dystroghin have structural and functional roles as sarcolemma proteins m Helps keep the thick filament centered between the two Z Iines during contraction by linking them ii Thin Filament Proteins Iquot S Actin main contractile protein interacting with myosin during excitationcontraction coupling Tropomyosin Regulatory ropelike protein that extends over the entire length of Factin Under resting conditions it blocks the myosin binding sites on actin Troponin Found in every 7 h Gactin along the thin filament Three subunits Tnl inhibitory subunit inhibits movement of tropomyosin by positioning tropomyosin on the actin binding site 2 TnT tropomyosinbinding subunit binds loosely onto tropomyosin to prevent it from moving off of actin 3 TnC calcium binding subunit contains four binding sites for calcium two of them have high affinity and at rest Mg2 binds to them Two of the binding sites have low affinity for CaZ and they are empty at rest Cardiac muscle only has 3 total ions Activation when the intracellular calcium level rises to a critical level four calcium ions bind to the TnC thereby causing the entire subunit configuration to change TnT then binds tightly to tropomyosin and the entire troponin protein physically moves tropomyosin to expose the myosinbinding sites on actin Once the myosinbinding site is exposed Sl subfragment of myosin can insert creating cross bridge b Know what the sarcolemma and sarcoplasm are i The sarcolemma surrounds the muscle fiber beneath the endomysium and encloses the fiber s cellular contents It is comprised of both the plasma and basement membranes The basement membrane is the outermost covering collection of glycoproteins and collagen network that is freely permeable to proteins solutes and other metabolites The plasma membrane is the true cell boundary that is found just beneath the basement membrane The plasma membrane is made up of a lipid bilayer and is much more selective to ions solutes and substrates Functions Maintains the proper acidbase balance allowing it to contract repeatedly during exercise Involved in propagating an action potential that will lead to muscle contraction conducts wave of depolarization over each muscle fiber Transports metabolites from the blood in the capillaries to the center cytosol of the muscle fiber Serves as an elaborate region of functional folds at the neuromuscularjunction Contains caveolae which provide additional length during fiber stretching allows lengthening to occur without damaging the plasma membrane Insulates the fibers ii The sarcoplasm interior of the plasma membrane rich in soluble proteins myofilaments and true myonuclei as well as highenergy intermediates ATP PC substrates glycogen and lipids enzymes of metabolism mitochondrial proteins ribosomes for protein synthesis cytosolic proteins and so on c Know what the ttubules and sarcoplasmic reticulum are Sarcoplasmic reticulum network of tubular channels and vesicles that provide the structural integrity to the cell Allows for the depolarization waves to spread rapidly from outer cell to inner cell Stores calcium ions TTubule system found within the SR provides for the spreading of depolarization waves contains pumps that take up calcium from the fiber s sarcoplasm creating a calcium gradient between the SRhigher and the sarcoplasm surrounding the filaments lower d What is a sarcomere and what are its boundaries A sarcomere is the strongest contractile unit of a skeletal myofiber The sarcomere length is the distance from one Zdisk to the next optimal length25 pm The optimal length is directly proportional to the capacity for force generation doesn t have high force capacity if it s too small or too large lengthtension relationship Aband dark band band isotropic band Hzone central region of the Aband where there is no thick and thin filament overlap Hzone is bisected by the Mline Mline composed of proteins that keep the sarcomere in proper spatial orientation as it lengthens and shortens Z disks most dense e Functional importance of muscle ber to muscle length ratio The ratio of different muscle type fibers will dictate the function of the muscle Long muscle fibers will produce a higher active muscle range because there are more sarcomeres in series it would have the same peak force as a short muscle fiber Additionally fiber length increases the muscle s absolute maximum contractile velocity and a longer range before muscle action is depleted Shorter fiber to muscle ratios correlate to muscles used for contractile force Longer fiber to muscle ratios correlate to muscles used for speed Ex Medial gastrocnemius calf vs Sartorius muscle hamstring vs eye 1 Medial Gastronemius length of about 250mm with fiber lengths of 35mm 15 of muscle length The muscle fiber makes up a small percent of the muscle and it correlates to a high force capacity This is why calf muscles are used in exercises like jumping 2 Sartorius Muscle length of about 500 mm with fiber lengths of 450mm 90 of muscle length Increased muscle fiber length in long muscles correlates to increased velocity 3 ntraocular muscles of eye 12mm fine movements that don t require a lot of force f How do endurance and resistance training affect the size of a muscle ber and why is the this case in terms of diffusion of oxygen and other nutrients to the center ofthe muscle Endurance 1 Slow Twitch fiber size will either remain the same or increase which will allow for a significantly higher oxidative capacity either way Higher oxidative capacity will allow more oxygen to be diffused to the muscle center and would therefore allow for more efficient energy usage 2 Fast Twitch Fiber size will not change and therefore oxygen diffusion wouldn t be affected by this factor Resistance 1 Slow Twitch The size of fibers would increase which would allow for more efficient oxygen diffusion and oxidative capacity 2 Fast Twitch The most significant fiber size increase occurs with these fibers The actual contractile proteins increase in size which allows for more available muscle for contraction g Know the difference between muscle fiber types I IIA IIX in terms of myosin ATPase activity shortening velocity mitochondrial and capillary density cross section area and in general what sport and activities fast IIA IIX and slow I fibers support Also know general rates of fatigue of each fiber Type slowtwitcthed Myosin ATPase is the slowest in these fibers which causes the shortening velocity to be slower as well This basically means Type fibers contract slowly Mitochondrial and capillary densities are very high in these fibers which allow them to have high oxidative capacity Cross sectional area is small so its contractile force is small The oxidative capacity of Type fibers allows oxygen to be readily available to the muscle cells which makes them ideal for longterm aerobicendurance activities Their high oxidative capacity also makes them very fatigue resistant which accounts for why marathon runners can run so long Type IIA fastoxidativeglycolyticzpink Myosin ATPase is moderately fast which causes the shortening velocity to be moderately fast This means Type a fibers contract moderately fast and produce moderately strong forces Type a have high mitochondrial and intermediate capillary density which allows them to have a high oxidative capacity in addition to their high glycolyitic capacity These fibers fatigue quickly Cross sectional area is moderately large These fibers are mostly used in aerobic and anaerobic exercise activities that require power strength and endurance Type X fastglycolyticlwhite Myosin ATPase is very fast which causes the shortening velocity to be very fast fastest contractility The mitochondrial and capillary densities are very low which means these fibers rely on anaerobic conditions Cross sectional area is the largest which means it can produce the most force These fibers are mostly used in anaerobic activities like weight training where resting intervals can be applied due to the high fatigue rate associated with this type h Know any exerciseinduced adaptations Endurance 1 Slow Twitch fiber size oxidative capacity glycogen content fat oxidation capillary density and blood flow during exercise all increase These adaptations account for the ability for endurance trained individuals to better utilize oxygen for the muscle cells Glycogen content and fat oxidation increase so that the muscle cells can produce a constant flow of energy which accounts for low fatigue rates of these fiber types More blood can flow through the body during exercise because the muscles require higher oxygen demands which can be accounted for by an increase in capillary number 2 Fast Twitch The only muscle factors that change are oxidative capacity glycogen content and fat oxidation These changes allow the normally predominantly glycolytic fasttwitch fibers to be more energy efficient With prolonoged aerobic training fast twitch muscle fibers can become almost as fatigue resistant Resistance 1 Slow Twitch The size of fibers and anaerobic capacity will increase with strength training allowing more force to be generated This would allow these fibers to be able to function more without the presence of oxygen 2 Fast Twitch The size increases significantly with some increase in anaerobic capacity allowing more force to be generated This would allow these fibers to be able to function more without the presence of oxygen Muscular Contraction a What mineral is the key to muscular contraction Calcium is key to muscular contraction It is stored in the Sarcoplasmic Reticulum SR and is released into the cell after the action potential arrives at sensors Know the role of troponin and tropomyosin in muscular contraction Troponin is a 3subunit regulating protein that changes conformation when four Ca ions bind to it THC Once changed TnT subunit then binds to tropomyosin Tropomyosin which usually covers myosinbinding sites on actin at rest is then physically moved by Troponin so that the myosin head is free to insert This allows for crossbridge formation At rest the inhibiting subunit of troponin prevents tropomyosin from moving off of the myosinbinding site on actin so that crossbridge formation cannot form c Describe the chemical and mechanical steps in crossbridge cycle and explain how the crossbridge cycle results in shortening ofthe muscle sliding lament hypothesis and Hypothetical scheme of crossbridge cycle etc i Chemicallmechanicalsteps 1 In resting state actin and energized myosin ADP Pi cannot interact because of the blocking effect of tropomyosin regulated by troponin Upon release of calcium from the SR energized myosin binds to actin 2 Tension is developed and movement quotpower strokequot occurs with the release of ADP and Pi as energy This leaves the myosin head open for binding 3 Dissociation of actin and myosin requires the presence of ATP to bind to the myosin head so that it can pump calcium back into the SR 4 ATP is then hydrolyzed and myosin returns to its energized resting state ii Sliding filament model The thick and thin filaments move in relation to each other without changing length resulting in change in sarcomere and therefore muscle length The myosin crossbridges cyclically attach rotate and detatch from the actin filaments with energy from ATP hydrolysis providing the motor to drive fiber shortening The sarcomere s zones and bands change producing a force at the Z band The Hzones disappear and the lband becomes very narrow as the sarcomere shortens A band stays the same d Principles theories and relationsihips eg Size principle lengthtension relationship and etc i Size Principle As muscle force requirements increase motor neurons are recruited with progressively larger axons expressing a recruitment order to produce muscle action The selective recruitment and firing pattern of fast twitch and slowtwitch motor units that control stabilizing regions provide the mechanism to produce the desired coordinated response Slowtwitch motor units with lower thresholds for activation are recruited during lightmoderate effort jogging cycling swimming More rapid powerful movements activate first type Ila and then type llx weight lifting Type I9 type lla type llb Lengthtension relationship The tension developed is proportional to the degree of overlap between actin and myosin filaments and hence to the number of active crossbridges The optimum length of the sarcomere 222 pm corresponds to the greatest overlap and the highest active tension When the muscle fiber is stretched further than this optimal length there was no overlap between the myosin and actin filaments so no active tension was developed beyond 375pm 2 When the sarcomere length was shorter 167pm thin filaments from opposite ends of the sarcomere interfere with each other When the sarcomere length is decreased to the length of the thick filament there is no developed force ForceVelocity the velocity of muscle contraction is inversely proportional to the load Large forces cannot be exerted in very rapid movements The greatest velocities are attained under conditions of low loading This occurs because the force generated by the muscle depends on the total number of crossbridges attached before the power stroke As velocity increases the filaments slide past each other faster and faster so the filaments are attached to each other for less time This causes the force to decrease Conversely as velocity decreases the filaments slide past each other at a slower rate and allow for more crossbridge attachments This generates a greater force when the power stroke occurs 1 2 Type fibers have a lower velocity and force when compared with Type II fibers Training can increase both velocity and force Force greater e Know excitationcontraction EC coupling be able to describe the sequences involved in ECcoupling muscle contraction from release of ACH from the motor neuron all the way until relaxation i Features 1 2 ii Seguences 1 Iquot S P Equot 9 EC coupling is the process of converting an electrical stimulus Action Potential to mechanical response contraction Fundamental to muscle physiology can be dysregulated in many disease conditions An action potential originates in the CNS and travels to a dmotor neuron which then transmits the AP down its own axon The AP then activates voltagedependent Ca2 channels on the axon and Calcium rushes in The increase in calcium causes synaptic vesicles containing the ACh to fuse with the plasma membrane at the active zone The vesicles then release ACh into the synaptic cleft via exocytosis and ACh diffuses across the synapse It then binds to and activates nicotinic ACh receptor on the motor end plate 1 Half of the ACh molecules are hydrolyzed by acetylcholinesterase Binding of ACh to d subunit of ACh receptor opens the cation gated chanel and allows Na rush in and K to trickle out The muscle fiber membrane then becomes more positively charged triggering an AP The AP spreads through the muscle fiber s network of Ttubules depolarizing the inner portion of the muscle fiber This stimulates Ca2 release Calcium binds to Troponin C subunit which then activates it to bind to tropomyosin which moves the blocking effect off of the myosinbinding site on actin Myosin is then able to bind to the actin filament and release its power stroke to shorten the sarcomere These contraction steps repeat as long as ATP is available and Ca2 is available in the thin filament Relaxation The myosin ceases binding to the thin filament and the contractions come to a halt Meanwhile Ca2 is actively pumped back in the SR to maintain sarcoplasmic calcium concentrations The active pumping of calcium ions back into the SR creates a deficiency in the fluid around the myofibrils When calcium concentrations become depleted tropomyosin changes conformation so that it can block the binding site on actin again Duration and intensity of active state depend on calcium concentrations around the contractile filaments f The mechanical coupling hypothesis 1 Release of calcium from SR during ECcoupling is known to be a result of coordinated functional interaction of muscle surface membrane calcium channels DHPRs with SR calcium release channels RyR1s in skeletal muscle 2 Arrival of AP activates a voltage sensor DHPR on the external membrane by changing the conformation of it Dispositions the 4 subunits of DHPR that link to 4 subunits of RyRs This causes the opening of 4 subunits of Rle thereby resulting in a release of Ca into the cytosol of the skeletal muscle 1 DHPR voltagedependent calcium channel found in the T tubules of muscles associates with RyRs of the SR to induce calcium release and thus muscle contraction RyRs Ryanodine receptros SR Cab release channel that is essential for muscle contraction activation occurs by coupling to the DHP channel Binding of ryanodine modifies the RyR1 s conductance and gating by causing a partial opening state at low concentration and a fully closed channel at high concentration triggering one will trigger all RyR1 receptors 3 By triggering one RyR1 channel it could activate all associated RyR1 channels in a junction Coordinated activation would ensure the speed of skeletal muscle contraction Correlates to the allornone twitch in skeletal muscle g Actions of Calcium ions in skeletal muscle and its calcium pumps i Functions of calcium ions 1 Initiating the contractile process in muscle fibers 2 Acting as a second messenger releasing ACh from motor nerve terminals 3 ln damaged plasmalemma calcium ions will flow down their electrochemical gradient and disrupt the structure and function of the cytoplasmic contents ii Calcium Pumps2 both move calcium ions against large gradients both are stimulated by the presence of Mg2 ions both require hydrolysis of ATP for energy which has the ability to transport 2 Cab ions across the membrane 1 Surface membrane pump 5MP larger than SRP requires Cazcalmodulin binding site in order for the pump to be activated 2 Sarcoplasmic reticulum pump SRP responds to Cab ions directly 1 5 Each pump has a low capacity for transporting ions thus a high density of pumps in the SR membrane is necessary to bring down calcium concentration in the cytosol quickly With each cycle of pump 2 Ca ions are transported into the SR in exchange for 2 K ions Unequal exchange causes the cytosol near the SR to become increasingly negative When the Cabenters the SR they are detached from the pump by Cap binding proteins high affinity ATPase enzyme and low affinity calsequestrin SR CaZATPase SERCA primarily responsible for muscle relaxation by transporting cytosolic calcium into the lumen of the SR coupled to to ATP hydrolysis soforms SERCA1 and SERCAZ SERCA1 found in type II muscle fibers SERCAZ found in type muscle fibers h Exercise and ECcoupling 39 Exercise induced Sudden Cardiac Arrest intracellular calcium cycling in normal heart relies on an intricate interplay of cardiac calsequestrin with the proteins of the RyRZ channel complex and that disruption of these interactions can lead to cardiac arrhythmia Study showing that an evident increase in the mRNA and protein expression of DHPR in a study following a 15week low intensity aerobic exercise program no changed levels of RyR1 9 more abundant demand for DHPR after muscle activity increases Ecc exercise downhill running resulted in ultrastructural changes in the arrangement of Ttubules and the disruption of triads 1 Increase in the of longitudinal segments of the Ttubule network 2 Changes in the direction and disposition of the triads Endocrine System and Muscle Growth a What are satellite cells role in muscle growth i Properties 1 Satellite cells are located in between the basement and plasma membranes and act as adult myoblasts for hypertrophy and regeneration 2 They are normally dormant but can be activated when muscle repairregeneration is required 3 Chemotaxic properties they can migrate from one location to another area of higher need within a muscle fiber and then can develop a new muscle fiber Multinucleic 200300 nucleimm of fiber length Very prominent in early life 4070 of nuclei are satellite cells Decrease drastically as we age ii Purposes 1 Growth and development of muscle 2 Adaptive capacity of skeletal muscle to various forms of training or disuse 3 Recovery from exerciseinduced traumatic injury or neuromuscular disease b Know the mechanisms of satellite cell activation Normally dormant must be induced to proliferate differentiate and fuse to growingregenerating myofiber Activated when myofibers hypertrophy in experiment models of functional loading stretch Exercise activates satellite cells which migrate to damaged area proliferate the area creating new myonuclei Factors Promoting 1 IGFl insulinlike growth factor produced inside muscle cell when its damaged or stressed IGFl mRNA increased over a 16 wk period of resistance training more with younger subjects 5quot 4 5 Mechanogrowth factor MGF loadsensitive loadinduced expression decreases with age Increased over a 16 wk period of resistance training after first week Cyclin D1 modulates progression through 61 in the cell cycle Expression increases with mechanical load in humans and rodents Cyclin Bl Myogenic Regulatory factors MRFs iii Factors inhibiting 1 Myostatin inhibits muscle growthdevelopment by blunting proliferationdifferentiation of myogenic precursor cells May act by up regulating cdk inhibitors cell cycle inhibition Highly expressed in HIV patients muscle wasting Results can occur with quotWhippetsquot and quotsuper babies P27kip basal expression higher in older satellite cells 2 P21dquot c What is the myonuclear domain theory i As a muscle cell increases in size it becomes increasingly difficult for a single nucleus to govern the entire cell To adapt the muscle fiber must add more nuclei to keep up with the increased cell size This is accounted for by satellite cells d Know what the general optimal exercise prescription is for hypertrophy and strength and briefly explain why these prescriptions work i Prescriptions 1 Iquot Hypertrophy The goal here is to increase muscle growth by using higher loads in higher volumes This could be done by using higher reps 812 with lower resting periods The muscle increases in size when there is an increase in muscular tension which signals proteins to activate genes to stimulate protein synthesis and satellite cell proliferation Overload training increases the size of individual muscle fibers which causes overall cell growth Fasttwitch fibers are weight lifters are about 45 larger than fibers of healthy endurance athletessedentary individuals Metabolic characteristics of specific fibers undergo modification within 48 weeks of target resistance training Hypertrophy is independent of aging Strength training The goal is to increase maximal strength and neural function increase in motor unit capacity You could do this by lifting close to maximal load for a 15 repetition range with longer rest periods You increase strength by increasing load not repetitions The muscle strengthens when trained near its current maximal force generating capacity Progressiveresistance weight training Isometric training and isokinetic training are the three common exercise systems used to train muscles to become stronger Based on muscle concentric shortening eccentric lengthening and isometric static muscle actions The recommendations for most middleaged and older adults focus on maintaining muscle and bone mass and muscular strength and muscular endurance to enhance the overall health ii The muscle is capable of these actions because of 4 factors 1 Speci city the underlying attributes of a skill are specific to that skill and generally have low transfer The greatest gains will occur by performing the specific task you want to be improved 2 Accommodation the response of a biological object to a given stimulus decreases over time If you do the same thing each workout your body will stop adapting 3 Overload principle adaptation only takes place if the magnitude of training load is above habitual level Most basic way would be to increase the weight that you lift 4 Variety your body needs variety to adapt either qualitatively or quantitatively IV Muscular Diseases and Conditions a Know the general etiology of muscular dystrophy i Group of genetic hereditary muscle diseases that cause progressive muscle weakness Characterized by progressive skeletal muscle wasting weakness defects in muscle proteins and death of muscle cells and tissue 1 Symptoms mostly affects children Poor balance Frequent falls Walking difficulty Drooping eyelids Affects on cardiac and smooth muscle cells heartorgan dysfunction 2 9 diseases Duchenne Becker Limb girdle congenital fascioscapulohumeral myotonic oculopharyngeal distal and Emery Dreifuss NIH 1 Duchene Muscular Dystrophy DMD 13300 births Caused by mutations in the gene which encodes dystrophin causing it to be absent Onsets at age 26 Dystropin vital part of a protein complex that anchors the sarcomere to the myofibril membrane keeping the muscle integrity Acts as an anchor protein for the actin filament Lack of dystropin causes contraction induced injury in their muscles because they go into degeneration rapidly The degenerated muscles are replaced by connective tissue which virtually has no function Can affect young males due to its Xlinked recessive inheritance pattern 23 come from mother 13 caused by mutations in the genes of the egg or embryo Symptoms affects pelvis upper arms and upper legs Involves all voluntary muscles no cure survival beyond 20 is rare 2 Becker s Muscular Dystrophy BMD 118430 births Dystrophin is of abnormal weight and shape onset 216 years Symptoms are less severe than DMD survive until middle age WPF N Eventually those with MD lose the ability to breathe because the diaphragm is a skeletal muscle that gets replaced with connective tissue 3 Diagnosis muscle biopsy DNA blood test physical examinationmedical history loss of muscle mass 4 Treatment No specific treatment inactivity can worsen the disease Daily physical therapy and orthopedic instruments may be helpful Muscle weakness may be attenuated by regular low intensity exercise Exercise recommendations Studies addressing physical training were successfully carried out in mice with MD Researchers were able to define thresholds and intensity frequency and duration to minimize the dystrophic process and improve muscle function This was possible because they were able to define the disease and exercise response mechanisms Human testing has not been carried out because the disease and exercise response mechanisms are undefined and the risk for exacerbating the dystrophic process is too high b Know the general etiology and exercise treatment for sarcopenia Definition Sarcopenia refers to the degenerative loss of skeletal muscle mass and strength associated with aging This leads to multiple problems regarding everyday lifestyle and functions related to mobility Trends 1 The general trend is a decrease in the size of type II fibers both type a and type le and an increase in type fibers to compensate for this loss This correlates to elderly people losing power and velocity of muscular contractility this correlates to why elderly people move slower and are more susceptible to fallrelated injuries When the elderly person falls they don t have the power to respond quickly enough 2 Another trend seen is a grouping affect of type muscle fibers This is necessary because neurons tend to die with old age since they aren t being used In order to accommodate for this the type muscle fibers group together so that they can be innervated by the same motor unit This produces more synchronous muscle velocities which help with a smoother mobility Elderly people without this feature can become very shaky because their muscle fibers are all contracting at different velocities 3 Another trend lies between males and females Elderly females are the most drastically affected by sacropenia This could have to do with different muscle mass ratios between males and females which aging seems to magnify Young males contain the optimal muscle fiber content iii Exercise treatment 1 LoadMediated Myofiber Hypertrophy there was a slight increase in Type II muscle fibers for the elderly male population with 16 weeks of loadmediated hypertrophy training 2 Endurance Crosssectional areas of fibers for elderly sprinters changed mostly in the content of type llx muscle fibers The concentration of type muscle fibers increased to compensate for this type llx fiber loss iv Application people are recommended to stay active and trained so that when aging occurs less type II muscle fibers are lost and they are able to use power functions of their muscles This would help reduce the physical dangers of aging individuals
Are you sure you want to buy this material for
You're already Subscribed!
Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'