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97 Cards in this Set
- Front
- Back
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muscle tissue is divided into.. |
skeltetal muscle tissue cardiac muscle tissue smooth muscle tissue |
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SKELETAL MUSCLE TISSUE |
-ATTACHED TO THE SKELETAL SYSTEM -ALLOW US TO MOVE -VOLUNTART CONTROL |
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SKELETAL MUSCLE TISSUE: |
-MUSCLE TISSUE -CONNECTIVE TISSUES -NERVES -BLOOD VESSELS |
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ORGANIZATION OF CONNECTIVE TISSUE: |
MUSCLES OF THREE LAYERS OF CONNECTIVE TISSUES: 1. EPIMYSIUM..DENSE IRREG. CT 2. PERIMYSIUM.. DENSE REGULAR FIBROUS CT 3. ENDOMYSIUUM .. AREOLAR CT |
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EPIMYSIUM..OUTER CT LAYER |
-exterior dense irreg. ct with collagen fibers - connected to deep& superficial fascias (tissue between myos-) -seperates muscle from surrounding tissues |
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ENDOMYSIUM.. fine areolar CT |
-Surrounds indivitual muscle cells (muscle fibers) - contains capillaries and nerve fibers contacting muscle cells -contains stem cells that repair damage
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PERIMYSIUM..fibrous ct |
-surrounds muscle fiber bundles called fascicles -contains blood vessel and nerve supply to these fascicles |
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ORGANIZATION OF CONNECTIVE TISSUE |
- to form connective tissue attachment to bone matrix: DIRECT to periostium or INDIRECT as a tendon or APONEUROSIS |
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ORGANIZATION OF MUSCLES: BLOOD VESSELS/ NERVES |
- muscles have an extensive vascular systen that: - supply large amount of oxygen -supply nutrients -carry away wastes SKELETAL MUSCLES ARE VOLUNTARY MUSCLES, CONTROLLED BY NERVES OF THE CENTRAL NERVOUS SYSTEM |
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SKELETAL MUSCLE CELLS |
-develop through the fusion of embryonic mesodermal cells called MYOBLAST-stem cells similiar to messenchymal cells in CT -very large multi nucleated |
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SARCOLEMMA/ TRANSVERSE TUBULES |
-sarcolemma= cell membrane of muscle fiber -surrounds the SARCOPLASM -change in transmembrane potential causes contractions to begin commencing myo movement |
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MYOFIBRILS |
-myofibril= bundles of protein filament MYOFILAMENTS *MYOFILAMENTS ARE RESPONSIBLE FOR MUSCLE CONTRACTION* 2 main types of myofilaments -THIN FILAMENT=ACTIN -THICK=MYSOSIN |
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TRANSVERSE TUBULES (T TUBULES) |
- transmit action potential -allow muscle fibers to contract simultaneously through T TUBULES -Connect sarcolemma to the rest of the muscle fiber to transport action potential ACTION POTENTIAL= T TUBLES |
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SARCOPLASMIC RETICULUM |
-surrounds myofibrils - helps transmit action potential to myofibril - forms chambers (terminal cisternae) attached to T tubules from the surface Sarcolemma |
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SARCOPLASMIC RETICULUM.. TRIAD |
TRIAD... -formed from one T Tuble and 2 terminal cisternae |
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CISTERNAE |
-concentrated Ca2+ storage from -releases Ca2+ back into the sarcoplasm and into the sarcomeres units to begin muscle contraction |
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SARCOMERES = MUSCLE CONTRACTION |
-* contractile funtional unit of muscle* - structural units/ sections of myofibrils -form visible patterns within myofibrils ( creating striped/ striated pattern within myofibrils -ALTERNATING DARK THICK FILAMENTS (A BANDS) and LIGHT, THIN FILAMENTS (I BANDS) Dark=thick=MYOSIN Light=thin=ACTIN
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SARCOMERES A BANDS: |
- contains an M LINE at the center of the A band -midline of the sarcomere |
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H ZONES .. sarcomeres |
-H zone
-lighter zone around the M line -has thick filaments but no thin filaments |
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ZONE OF OVERLAP |
- WHERE THICK AND RHIN FILAMENTS OVERLAP |
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Sarcomeres I BANDS (LIGHTER) |
- Z lines at the center of the I bands - at two ends of the sarcomere |
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TITIN |
TITIN.. -strands of protein - reach from tips of thick filaments to the Z line -stabilize filments |
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6 PROTEIN FILAMENTS THAT MAKE UP MYOFIBRILS: |
1. MYOSIN: THICK FILAMENTS 2. F ACTIN:THIN FILAMENTS w/ an active site ( G actin) which binds myosin site 3. NEBULIN: (thin)n keeps F Actin filaments together 4. Tropomyosin(thin) : keeps actin and myosin apart during muscle contractions 5. troponin: (thin) binds tropomycin strand to the active G actin site controlled by Ca+ ion presence 6. Titin: stabilize actin and myosin |
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TROPOMYOSIN |
-Double stranded -prevents actin/ myosin interaction |
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TROPONIN |
- binds tropomyosin to G-actin -controlled by Ca2+ |
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INITIATING CONTRACTION: |
- Ca2+ binds receptor on TROPONIN molecule - TROPONIN - TROPMYOSIN complex position changes - allows the exposure of G actin site on F actin to Occur |
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THICK FILAMENTS |
- contain titin strands that recoil after stretching - MYOSIN MOLECULE APPEARANCE: -tail -binds to other myosin molecules Head -made of two globular protein subunits -reaches to thin filament |
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MYOSIN ACTION |
-during contraction, myosin heads interact with actin filaments forming cross bridges -causing a pivot, producing sliding action/motion |
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SLIDING FILAMENTS AND MUSCLE CONTRACTION |
SLIDING FILAMENTS- - thin filaments of sarcomere slide toward the M line, alongside thick filaments -the width of the A zone stays the same - Z lines move closer together |
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SKELETAL MUSCLE CONTRACTION: |
process of contraction initiated by - neural stimulation of sarcolemma -causes exicitation -coupling at the sarcomere unit -MUSCLE FIBER CONTRACTION -interaction of thick and thin filaments -tension production occurs |
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CONTROL OF SKELETAL MUSCLE ACTIVITY |
-neuromuscular junction: - special intercellualr connection between the nervous systen and skeletal muscle fiber -controls calcium ion release into the sarcoplasm |
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EXITATION -CONTRACTION / COUPLING |
- ACTION POTENTIAL at sarcolemma reaches a TRIAD -causing a releasing of Ca2+ - Triggers a contraction - Requires myosin heads to be in "cocked" position -head is loaded by ATP energy |
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CONTRACTION CYCLE: |
1. contraction cycle begins 2. active- site exposure 3. cross-bridge formation 4. myosin head pivoting 5. cross bridge detachment 6. myosin reactivation |
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FIBER SHORTENING |
-sarcomeres shorten, muscle pulls together, producing tension -muscle shortening can occur at both ends of the muscle, or at only one end of the muscle - |
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RELAXATION |
-Contraction Durati0on prior to relation Depends on: -duration of neural stimulus (how long) - number of free calcium ions in sarcoplasm -availability of ATP |
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RELAXATION |
-ca2+ concentrations fall -ca2+ detaches from troponin -Active sites are recovered by tropomyosin |
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RIGOR MORTIS |
-runs of out ATP -calcium build up |
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Skeletal muscle fibers... |
shorten as thin filaments slide between thick filaments |
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Free ca2+ trigger... |
contraction |
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Sarcoplasmic Reticulum |
releases Ca2+ when a motor neuron stimulates the muscle fiber |
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Relaxation and return to resting length are.. |
passive |
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TENSION PRODUCTION |
- As a whole a muscle fiber is either contracted or relaxed Depends on.... - the number of pivoting cross-bridges - fibers resting length at the time of stimulation -the frequency of stimulation |
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TENSION PRODUCTION BY MUSCLE FIBERS.. |
-Length tension relationships are determined by- -number of pivoting cross bridges-which depends on - the amount of overlap between thick and thin fibers -The optimum overlap produces greatest amount of tension -Too much or too little reduces efficiency ** resting length is 75% to 130% optimal length |
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TENSION PRODUCTION BY MUSCLE FIBERS |
- The frequency of stimulation -single neural stimulation produces - a single contraction known as a TWITCH -Lasts about 7-100msec -sustained muscular contractions -require many repeated stimuli |
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TENSION PRODUCTION BY MUSCLE FIBERS TWITCHES |
- 1. Latent Period- action potential move through sarcolemma causing Ca2+ release 2. contration phase: calcium ions binds -tensions build to a peak 3. Relaxation phase: Ca2+ levels fall -active sites are covered and tension falls to resting levels |
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TREPPE |
- stair-step increase in twitch tension - repeated stimulations immidietly after relaxation phase - stimulus frequency CAUSES A SERIES OF CONTRACTIONS WITH INCREASING TENSION |
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WAVE SUMMATION |
-increasing tension or summation of twitches -repeated stimulations before the end of relaxation phase - causes increasing tension or summation of twitches |
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INCOMPLETE TETANUS |
-twiches reach maximum tension and there is a brief period of rest -rapid stimulation continues and muscle is not allowed to relax for a length of time |
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COMPLETE TETANUS |
- if stimulation frequency is high enough, muscle never begins to relax, and is in continuous contraction |
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TENSION PRODUCTION DEPENDS ON 3 FACTORS |
1. INTERNAL TENSION: produced by muscle fibers 2. EXTERNAL TENSION: Exerted by muscle fibers on elastic extracellular fibers 3. TOTAL NUMBER OF MUSCLE FIBERS STIMULATED |
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MOTOR UNITS IN SKELETAL MUSCLE |
- contain hundreds of muscle fibers -contract at the same time - controlled by a single motor neuron |
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RECRUITMENT |
- Recruitment: (multiple motor unit summation) - smooth motion and increasing tension are produced by slowly increasing the size or number of motor units stimulated MAXIMUM TENSION: "SPASM/ CHARLIE HORSE" - achieved when all motor units reach tetanus - |
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SUSTAINED TENSION |
-less than maximum tension -allows motor units rest in rotation |
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MUSCLE TONE : |
- normal tension and firmnes of a muscle at rest - muscle units actively maintain body position without motion -increasing muscle tone increases metabolic energy used even at rest |
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ISOTONIC CONTRACTION |
- skeletal muscle changes length -resulting in motion -muscle tension>load (resistance) -muscle shortens (concentric contraction) - if muscle tension (resistance) -muscle lenghtens (eccentric contraction) |
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MOTOR UNITS AND TENSION PRODUCTION |
-Contraction are classified based on pattern of tension production ISOTONIC ISOMETRIC |
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ISOMETRIC |
-skeletal muscle develops tension , but is prevented from changing length -ISO= SAME, METRIC =MEASURE |
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LOAD AND SPEED OF CONTRACTION |
-are inversely related -heavier the load (resistance) on a muscle -the longer it takes for the shortening to begin -the less the muscle will shorten |
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MUSCLE RELAXATION AND THE RETURN TO RESTING LENGTH |
- gravity -can take the place opposing muscle contraction to return to a muscle to its resting state |
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MUSCLE RELAXATION AND TO RETURN TO RESTING LENGTH |
1. Elastic Forces- affect return to resting - pull of elastic elements(tendons and ligaments) 2. Opposing muscle contractions- affects return to resting -reverse the direction of the original motion -are the work of opposing skeletal muscle pairs ex: lifting a weight would have a contraction which would oppose the opposite side |
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ATP PROVIDES ENERGY FOR MUSCLE CONTRACTION |
-sustained muscle contraction uses a lot of ATP energy -muscles store enough energy to start contraction - muscle fibers must manufacture more ATP as needed |
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ATP/ CP RESERVES |
- Adenosine Triphosphate (ADP) - the active energy molecule -CREATINE PHOSPHATE - the storage molecule for excess ATP energy in resting muscle |
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ENERGY RECHARGES ADP TO ATP |
- using enzyme creatine kinase (CK) -when CP is used up, other mechanisms generate ATP ADP-->ATP
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AEROBIC MECHANISM |
-Primary energy source of resting muscles -breaks down fatty acids - produces 34 ATP molecules per glucose molecule |
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GLYCOLYSIS |
- primary energy source for peak muscular activity -produces two ATP molecules per molecule of glucose -breaks down glucose from glycogen stored in skeletal muscles |
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ATP GENERATION |
- Cells produce ATP in two ways: 1. Aerobic metabolism: fatty acids in the mitochondria 2. Anaerobic glycolysis: in the cytoplasm **breaks down sugar- ADP |
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ENERGY TO POWER CONTRACTIONS |
- skeletal muscles at rest metabolize fatty acids and store glycogen - During light activity, muscles generate ATP through Anearobic breakdown of carbohydrates, lipids, or amino acids - At peak activity, energy provided by anearobic reactions that generate lactic acid as a byproduct |
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RECOVERY PERIOD |
-The time required after exertion for muscles to return to normal - Oxygen becomes available --pull in muscles - Mitochondrial activity resumes |
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MUSCLE FATIGUE |
- When muscles can no longer perform a required activity, they are fatigued -Results of Muscle Fatigue -depletion of metabolic reserves - damage to saroclemma & sarcoplasmic reticulum -low PH (lactic acid)-"cramps" - Muscle exhaustion/pain |
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LACTIC ACID REMOVAL AND RECYCLING AFTER PEAK PERFORMANCE |
The Cori Cycle : -the removal and recycling of lactic acid by the liver - liver converts lactate to pyruvate which then converts to glucose -Glucose is released to recharge muscle glycogen reserves |
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OXYGEN DEBT |
After exercise or other exertion: - the body needs more oxygen than usual to normalize metabolic activities -resulting in heavy breathing -also called EXCESS POSTEXERCISE OXYGEN CONSUMPTION (EPOC) |
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HORMONES AND MUSCLE METABOLISM (4 OUTSIDE FACTORS AFFECTING ENERGY ANY MUSCLE ACTIVITY ) |
1) Growth Hormone 2) Testosterone 3) Thyroid Hormones 4) Epinephrine..aka adrenaline |
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HEAT PRODUCTION AND LOSS |
-Active muscle produce heat -Up to 70% of muscle energy can be lost as heat, raising body temperature |
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MUSCLE PERFORMANCE |
FORCE: - The maximum amount of tension produced ENDURANCE - the amount of time an activity can be sustained -Force and Endurance depend on: -The types of muscle fibers being utilized - Physical conditioning of the body and myos |
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THREE MAJOR TYPES OF SKELETAL MUSCLE FIBERS: |
1) Fast Fibers 2) Slow Fibers 3) Intermediate Fibers |
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SLOW FIBERS |
- Are slow to contract, slow to fatigue -small diameter, more mitochondria - Have high oxygen supply -Contain myoglobin (red pigment, binds oxygen) EX: Red meat - Chicken legs from walking all day |
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FAST FIBERS |
"White Meat" -contract very quickly - large diameter, large glyocgen reserves, few mitochondria -have strong contraction/ fatigue quickly -less myoglobin - EX: weight lifters |
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INTERMEDIATE FIBERS |
"mixed between both" -mid-sized -low myoglobin -more capillaries than fast fibers, slower to fatigue EX: being in good shape |
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MUSCLE PERFORMANCE AND THE DISTRIBUTION OF MUSCLE FIBERS |
White muscles: -mostly fast fibers -pale( chicken breast) Red muscles: -mosly slow fibers -dark (chicken legs) Most human muscles -mixed fibers -pink |
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MUSCLE HYPERTROPHY (exercise/ wt lifting) |
Muscle growth from heavy training: - increases diameter of muscle fibers -increases number of myofibrils (actin/myosin) - increases mitochondria, glycogen reserves |
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MUSCLE ATROPHY |
Lack of muscle activity reduces muscles size, tone and power |
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PHYSICAL CONDITIONING |
-Improves both power and endurance ANAEROBIC ACTIVITIES: (50-meter dash/ wt lifting) -use fast fibers - fatigue quickly with strenous activity IMPROVED BY: -frequent, brief, intensive workouts -Causes hypertrophy |
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IMPORTANCE OF EXERCISE |
-What you dont use you lose.. -muscle tone indicates base activity in motor units of skeletal muscles -muscles become flaccid when inactive for days or even weeks -muscle fibers break down proteins, become smaller and weaker - with prolonged inactivity, fibrous tissue may replace muscle fibers |
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PHYSICAL CONDITIONING: |
-Improves both power and endurance -Aerobic Activities: (prolonged activity) -supported by mitochondria -requires oxygen and nutrients IMPROVES: -Endurance by training fast fibers to be more like intermediate fibers -cardiovascular performance |
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CARDIAC MUSCLE TISSUE |
-Cardiac muscle cells are striated and found only in the heart -Striations are similiar to that of skeletal muscle because the internal arrangement of myofilaments are similiar |
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CARDIAC MUSCLE TISSUE CHARACTERISTICS: |
-unlike skeletal muscle, Cardiac muscle cells (cardiocytes): -are small -single nucleus -short, wide T tubules -no triads -Have SR with no terminal cisternae-do not store Ca - Are aerobic (high myoglobin, mitchondria) - have intercalated discs |
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INTERCALATED DISC |
-Coordination of cardiocytes -because intercalated disc link heart cells mechanically, chemically, and electrically, the heart functions like a single, fused mass of cells |
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INTERCALATED DISCS |
-Are specialized contact points between cardiocytes -join cell membranes of adjacent cardiocytes (gap junctions, desmosomes) - Functions of intercalated Discs: -maintain structure -enhance molecular and electrical connections -conducts action potentials |
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FUNCTIONAL CHARACTERISTICS OF CARDIAC MUSCLE TISSUE: |
-Automaticity: -contraction without neural stimulation -controlled by pacemaker cells Variable contraction tension: - controlled by nervous system Extended contraction time: - ten times as long as skeletal muscle Prevention of wave summation and tetanic contractions by cell membranes -long refractory time |
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SMOOTH MUSCLE IN BODY SYSTEMS |
-Forms around tissues: -in integumentary system an arrector pili muscle causes "goose bumps" In blood vessels/ airways: -regulates blood pressure/ airflow In reproductive and glandular systems: -produces movement In digestive and urinary systems -forms sphincters "door, enter/exit" EX Anal -produces contractions |
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STRUCTURAL CHARACTERISTICS OF SMOOTH MUSCLE |
-non striated tissue -different internal organization of actin and myosin -different functional characteristics |
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CHARACTERISTICS OF SMOOTH MUSCLE CELLS |
- long, slender, spindle shaped -single, central nucleus - no T Tubules, myofibrils, or sarcomeres - no tendons or aponeuroses - have scattered myosin fibers -myosin fibers have more heads per thick filament -have thin filaments attached to dense bodies -dense bodies transmit contractions from cell to cell |
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FUNCTIONAL CHARACTERISTICS OF SMOOTH MUSCLE |
1) Excitation: contraction coupling 2) length: tension relationships 3) control of contractions 4) smooth muscle tone |
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LENGTH- TENSION RELATIONSHIPS |
-thick and thin filaments are scattered -resting length not related to tension development -functions over a wide range of lengths (plasticity) |
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EXCITATION- CONTRACTION COUPLING |
- Free Ca2+ in cytoplasm triggers contracction -Ca2+binds with calmodulin -In the sarcoplasm - activates myosin light-chain kinase - Enzyme breaks down to ATP initiates contraction |
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CONTROL OF CONTRACTIONS |
-Multiunit Smooth muscle cells: -connected to motor neurons Visceral smooth cells: -not connected to motor neurons..involuntary - rhythmic cycles of activity controlled by pacemaker cells |
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SMOOTH MUSCLE TONE |
-Maintains normal levels of activity -modified by neural, hormonal, or chemical factors |
