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102 Cards in this Set
- Front
- Back
Characteristics of muscle tissue |
Excitability - response to stimulus Contractility - shorten/generate force Extensibility - passively stretch over wide range Elasticity - passively stretch, some recoil |
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Fascicle |
Bundle of parallel muscle fibers, length of the entire muscle |
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Nuclueation of skeletal muscle |
multinucleated, under sarcolemma, peripherally located |
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Sarcoplasm |
intracellular fluid |
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Myofibrils |
tube like structures filling muscle cells |
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Striations |
repeating pattern of striations along each myofibril |
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Myofilaments - types |
Thick filaments - myosin, anchored to z-line by titan Thin filaments - actin, anchored to z-line |
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Composition of z-line |
Nebulin |
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Sliding filament MOA |
overlapped thin & thick filaments. crossbridge binds to actin-triggers power stoke (thin fil. pulled toward thick fil.) ADP and Pi released, new ATP attaches-crossbridge releases. crossbridge/power stroke occurs asynchronously |
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Myosin |
tail and 3 heads-cross bridges each crossbridge has 2 actin binding sites and myosin ATPase |
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Actin |
G-actin, bunch of G-actin strung together, called actin helix |
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2 regulatory proteins on actin
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Tropomyosin - rod-shaped portein covering myosin binding sites (1 per each 7 g-actin)
Troponin - 1 troponin per tropomyosin |
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excitation-contraction coupling |
sequence of events starting with AP in sarcoma and ending in crossbridge activity |
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neuromuscular junction (NMJ) |
synapse of somatic motor neuron on skeletal muscle. ACh always excitatory, at the center of skeletal muscle |
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motor end plate |
portion of the sarcolemma just after the axon terminal, contains N1 receptors with gated cation channels |
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end plate potential
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depolarization when ACh binds to cation channels (N1 receptor), EPP will spread, conducted decrementally spreading to adjacent sarcolemma, single EPP pushing it to threshold causing AP
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sarcoplasmic reticulum |
series of loose connective sacs that surrounds each myofibril, stores calcium when not being stimulated, release Ca++ upon stimulation, reuptake of Ca++ via active transport |
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transverse tubules
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invaginations of sarcolemma that occur at regular intervals along the entire length of sarcolemma, function is to rapidly conduct AP to the inteior of cell, lumens are filled with ISF
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ryanodine receptor |
voltage gated calcium channel located on SR |
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function of calcium |
internal trigger that allow contraction to occur (any muscle), binds to troponin, pulls tropomyosin out of blocking position, Ca++ stays bound as long as concentration remains elevated ~skeletal muscle - response to 1 AP there is enough Ca++ to saturate all troponins, all cross bridges can participate (not in cardiac/smooth) |
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skeletal muscle resting membrane potential |
-90mV |
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Botulism |
bacterium releases toxin that blocks release of ACh producing flaccid paralysis |
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Black widow venom |
massive release of ACh, spasms and convulsions |
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depolarizing neuromuscular blocking agents
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N1 agonist
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myasthenia gravis |
autoimmune dz that destroys N1 receptors at MEP, treated with cholinesterase inhibitors |
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Motor unit |
single motor neuron and all muscle fibers it controls, # of muscles are highly variable. activity is all or none, muscles have variety of large and small motor units |
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contraction |
generation of tension within a muscle by crossbridge activity |
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external muscle tension |
tension exerted by contracting muscle on an object |
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load |
force exerted by the object on the muscle, after it is stimulated to contract |
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external muscle tension>afterload |
muscle shortenes |
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external muscle tension<afterload
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no shortening occurs
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isometric |
muscle develops tension but does not shorten or lengthen |
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isotonic |
muscle changes length while the afterload on the muscle remains constant (constant tension) |
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Concentric contractions Lengthening contractions |
Muscle shortens Unsupported load on muscle is greater than tension generated. muscle lengthened inspite of force generated by crossbridging |
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muscle twitch |
mechanical response to a single AP |
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latent period |
period between excitation and the development of tension. includes time needed to release Ca++ from SR, move tropomyosin, cycle crossbridges, and the influence of series elastic component |
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Can muscle AP be summated |
not really, each AP results in twitch. Wave summation results in unfused tetanus-slight increase in external tension d/t series elastic component take-up. fused tetanus occurs from rapid APs causing contraction to max or fatigue |
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series elastic component |
transmission of muscle tension to bone. internal tension generated by muscle to load must be transferred through connective tissue. Greatest contribution to latent period |
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length tension curve (at tetanic contraction) |
relationship between inital resting length of striated muscle and how much tension it can develop when stimulated at tetanic frequency |
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preload |
resting length of the muscle prior to its stimulation |
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optimal preload |
explained by sliding filament mechanism of contraction, perfect overlap of thin/thick filaments so each crossbridge is in reach of thin filament |
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load-velocity relationship ~Large afterload? |
velocity of muscle shorting is inversely related to afterload of muscle ~takes longer for internal tension to become greater than external tension |
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factors determining muscle tension |
tension of each fiber - AP frequency, fiber length, diameter Number of active fibers - per motor unit and # of motor units |
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3 ways muscle can form ATP |
-phosphorylation of ADP by creatine phosphate -oxidative phosphorylation of ADP - mitochondria -phosphorylation of ADP - glycolytic paththway |
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what mechanisms of ADP phosphorylatino is used in short, high intensity exercise? |
Creatine phosphate, 1 step chemical rxn, avg. stores last 10-15 sec. 1 CP= 1 ATP, 1 creatine (byproduct) |
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Other anaerobic pathway of ADP phosphorylation |
anaerobic glycolysis, glucose from glycogen converted into pyruvic acid/ATP. 1 Glucose=2 ATP, 1 pyruvic acid-->lactic acid ~60sec until fatigue |
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Aerobic pathway |
Nutrients: Pyruvate (from glycolysis), FFA, AA, glucose - requires O2 32 ATP produced, CO2, H2o byproducts of glucose metabolism ~hours until fatigue |
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Muscle fiber type characteristics |
Twitch characteristics Amount of tension developed related to diameter Resistance to fatigue |
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Twitch characteristics for fast/slow twitch |
Fast twitch develop peak tension sooner-related to myosin ATPase activity (ATP can be split faster) as well as calcium kinetics-rate Ca++ can be released from SR |
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tension characteristics fast/slow |
slow fibers - smaller diameter, less sarcomeres fast fibers - larger diameter, more sarcomeres, pale color, fatigue easier |
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resistance to fatigue |
slow twitch less fatigue, d/t diameter and ATP production |
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Types of muscle fibers |
slow oxidative, fast oxidative, fast glycolytic fibers |
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Describe slow oxidative fibers |
oxidative phosphorylation: High mitochondria, capillaries, myoglobin content. Low: glycolytic enzyme activity and glycogen content, myosin ATPase acitivty, contraction velocity. Small fiber diameter, motor unit size |
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Describe fast oxidative fibers |
Oxidative phosphorylation. High: mitochondria, capillaries, myoglobin. Intermediate glycolytic enzyme activity and glycogen stores. High myosin ATPase activity, fast contraction, intermediate motor unit size |
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Describe fast glycolytic fibers |
glycolysis, few mitochondria, capillaries, low myoglobin(white color). high: glycolytic activity/stores, fatigue rate, myosin ATPase activity, contraction velocity. large fiber diameter |
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VO2 max |
Determines respiratory fitness, factors in capacity for ATP production via oxidative phosphorylation, influenced by CV and respiratory systems as well |
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What determines fiber type distribution among different people? |
Genetics Motor neuron innervating the muscle |
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Mechanisms/types of muscle fatigue |
synaptic fatigue Conduction fatigue (K+ buildup) Lactic acid - H+-->decreased enzyme act. inhibition of crossbridge cycling -ADP buildup CNS mechanisms: change in internal environment-feedback info to CNS Depletion of glycogen- hypoglycemia |
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2 theories of increased muscle mass |
hypertrophy - existing cells get larger hyperplasia - increased # of cells (from satellite cells-undifferentiated myogenic cells) |
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innervation to skeletal muscle |
somatic motor neurons, alpha & gamma |
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Where do somatic motor neurons originate? |
(lower motor neuron) ventral horn of spinal cord and cranial nerve motor nuclei of the brainstem Always excitatory - EPP-AP-contraction |
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Motor unit |
basic unit of contraction, one motor neuron plus muscle cells it innervates |
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Upper motor neuron |
contain in the descending tracts (corticospinal and extrapyramidal) and synapse on lower motor neuron, can be inhibitory or excitatory |
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motor neuron pools |
motor neuron cell body groups, a group is composed of multiple neuron cell bodies fro neurons that innervate a specific muscle, extend over several spinal cord segments |
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What determines which motor units in a given muscle are activated during contraction? |
Not all are activated in most muscle contractions. Activation is based on size of motor unit, fiber type of motor unit, size of motor neuron, excitability of motor neuron - ease of which it can be pushed to threshold |
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Recruitment is based on size principle, what is this principle? |
muscle fibers of a given motor unit are of the same fiber type, slow oxidative are more excitable due to shorter distance to axon hillock, EPSPs have less distance to travel, less chance of decrement. Require a larger stimulus for larger motor units to get activated |
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what controls activity to alpha motor neurons? |
thousands of synaptic inputs (EPSP/IPSP) all integrated in the spinal cord |
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What are the sources of input to an alpha motor neuron? |
Higher CNS- -excitatory or inhibitory upper motor neurons (motor cortex-corticospinal tracts and extrapyramidal tracts) Somatosensory afferents - pain, nociceptive Muscles afferents - spindles, golgi tendons |
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Myotatic reflex |
basic mechanism of skeletal muscle tone present in all skeletal muscle, resistance to a muscle offers to being stretched or lengthened, necessary to maintain posture, counter gravity |
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What are the sensory receptors of the myotatic reflex? |
Muscle spindle - responsible for monitoring muscle length and rate of change of muscle length |
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Anatomy of muscle spindle? |
Extrafusal muscle fibers(normal muscle cells) innervated by a-motor neurons Spindle muscle fibers - parallel-monitor rate of change -contractile end gamma motor neuron -primary afferent fiber (grp I) sitmulus is stretch, interprets rate of AP -secondary afferent fibers (grp I) stimulus is stretch, interprets length |
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How do muscle spindle work? |
at baseline spindle will fire at a certain frequency and brain interprets this as muscle length -stretched spindles - fire AP at higher rate -contract spindles -AP stops firing, only a-stim, no gamma -2* fibers provide info re: absolute length of fiber -1* fibers provide info re: rate of change |
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What would intrafusal fibers need to be stimulated by efferent gamma motor neurons? What is the called? |
when muscle shortenens, spindles go slack--> decreased AP firing (but we need feedback)--> intrafusal fibers are also contracted to allow central region to provide info about musc length Alpha-gamma co-activation |
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What is reciprocal inhibition in relation to reflexes? |
Coordinates agonist/antagonist muscles. excitatory stim to quad muscle, inhibitory stim to hamstrings in patellar tendon reflex |
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golgi tendon organ - anatomy |
located in tendons (connection of muscle to bone) |
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Golgi tendon physiology |
monitors tension exerted by the muscle, series arrangement allows monitoring of tension compared to spindles. w/ passive stretch, golgi tendon fire APs-->relax muscle, tension decreases. muscle contraction>stimulus than passive stretch |
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Inverse myotatic reflex |
-deep tendon reflex - golgi reflex -seen w/ hypertonic limb (SCI) -myotatic reflex is hyperactive, lots of resistance to passive stretch -w/ passive stretch-->more tense, golgi activated --> through interneuron muscle inhibited-->relax. (clapsed knife reflex) -may contribute to smooth onset/termination of contraction needed for walking |
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Flexor-withdrawl reflex |
-SC mediated, Protective -stimulus activates pain receptors (1st order aff.) through interneurons activate motor neurons of flexor and inhibit extensors |
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crossed extensor reflex |
with pain stimulus in lower extremity, opposite leg extensors must activate/flexors inactivate--keeps body from falling |
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spasticity following SCI |
refex arcs are intact, but higher order inhibition is blocked |
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pathophys of Polio |
virus kills lower motor neurons, produces flaccid paralysis, usually confined to a few motor neuron pools |
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ALS mechanisim |
attacks upper and lower motor neurons controlling skeletal muscles, gradually weaken and atrophy |
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basic characteristics of SM |
non-striated, single central nucleus, walls of hollow organs, involuntary (ANS and hormones), often has underlying tone, can be stretched and still generate tension, can replicate(mitosis), underdeveloped SR, no T-tubules, no troponin, tropomyosin present-but no blocking position |
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Internal structure of SM cells |
Thin filament attached to dense body with thick filament between Dense bodies - attachment for thin & intermediate filaments(structural component) |
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Mechanism of contraction of SM - sliding filament mechanism |
thick/thin filament interact - myosin ATPase on crossbridges has low activity |
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ECC |
Pi of myosin x-bridge to bind to actin regulation at level of thick filament stimulus increases Ca++ conc. (CICR) Ca++ binds to calmodulin myosin light-chain kinase binds to Ca++(activation)-->Pi to x-bridge-->binds to thin fil--> power stroke-->ADP/Pi released, new ATP attaches myosin light-chain phosphatase - cleaves phosphate-x-bridge can no longer interact with thin filament |
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where does Ca++ for ECC come from(SM)? |
Enters ECF through voltage regulated channels, chemically gated channels SR is poorly developed, AP travels down sarcolemma, can trigger release of Ca++ from SR through 2nd messenger |
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SM contraction all or none? |
no, graded response to amount of available Ca++ |
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How does SM cell remove CA++ from sarcoplasm? |
primary active transport pumps in sarcolemma resequester Ca++ to SR |
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What regulates entry and removal from the SR of SM cells |
+spontaneous elecitral activity in plasma membrane +/- NT of ANS +/- hormones +/- local factors release d/t changes in chem composition + stretch |
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How can SM cells generate AP spontaneously? |
depolarization - Ca++ entry through volt. gated Ca++ channels rhythmic changes in membrane potential can result in rhythmic pattern of AP-pacemaker potentials - leaking CA++ and Na+ channels and decreased K+ leaking out of cell |
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Describe specific characteristics of GI SM |
resting membrane potential varies over time amplitude modulated by enteric nervous system SNS decreases amplitude PSNS increases amplitude |
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Describe single unit smooth muscle cells |
found in walls of hollow organs SM cells contract and relax as single unti d/t they are linked w/ gap junctions innervated by ANS, hormones, chemical enviornments |
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Describe multiunit SM cells |
found in skin, eyes Very dependent on ANS, no pacemaker activity |
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Cardiac Muscle characteristics |
branched single nucleus, striated, woven end to end with intercalated discs high capillary density, mitochondrial density Sarcomeres - thin & thick filaments SR not as well developed as skeletal musc. T-tubules - larger than skeletal musc same sliding filament mechanism as skeletal Heart beat=twitch |
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is there enough Ca++ at rest to saturate all troponins in cardiac muscle cells? |
no, increased Ca++=incrased contractility - more x-bridge cycling |
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Describe cardiac musc AP |
100x longer than skeletal phase 4 - resting membrane -90mV (more permeable to K+ than Na+) Phase 0 - large rapid depol. -->30mV (Na+ gates) Phase 1 - small repol - Na+ out, K+ in Phase 2 - plateau - L-type Ca++ channels open Phase 3 - L-type Ca++ close, volt gated K+ channels open(K+ exits) repolarizing |
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What is calcium induced calcium release (CICR)? |
Ca++ enering from volt gated Ca++ channels in sarcolemma will bind to receptors on SR and cause it to release more Ca++ (1* stimulus for Ca++ release-95%) |
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How is Ca++ increased with sympathetic B1 stimulation? |
Gprotein-activates adenyl cyclase, increased cAMP, incr protein kinase-->phosphorylation of: -L-type Ca++channels, incr CICR -phospholambin - incr SR Ca++ pump, increasing reuptake of Ca++ and speed of relaxation(diastole) -troponin I -- increased removal of Ca++ increased speed of relaxation Gprotein acts directly on L-type Ca++ channels, incr Ca++influx, incr contractility |
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Caridac glycosides |
inhibit Na/K pump, increase intracellular [Na+] which decreases rate of Na/Ca exchanger (2* active transport Na+ in Ca out) results in more Ca++ intracellular/stored in SR, more CICR |
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Is summation possible in cardiac muscle? |
No, mechanical response is as long as the electrical response, nothing left to summate d/t longer AP |
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During single heart beat are all cardiac cells turned on or is it similar to skeletal muscle where only the necessary amount for the required contraction is stimulate? |
In cardiac contraction, all cardiac cells are contracting, however not all x-bridges are contracting at any one time. also # of x-bridges active dependent on [Ca++] |