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Ch. 9 muscle

anatomy and physiology of muscle

Diseases related to muscle physiology Sarcopenia- age related loss of muscle Diabetes (1 and 2)- skeletal muscle removes glucose from blood Cardiovascular disease- heart; Cardiac hypertrophy deals with cardiac muscle; Coronary artery disease deals with smooth muscle
Basic muscle function turns chemical energy into mechanical force
Functional characteristics of muscle 1.Excitability or irritability 2. Contractibility 3.Extensibility 4.Elasticity
Excitability or irritability the ability to receive and respond to stimuli (depolarization)
Contractibility the ability to shorten forcibly
Extensibility the ability to be stretched or extended
Elasticity The ability to recoil and resume the original resting length
3 types of muscle 1.Skeletal-striated and multi-nucleated; voluntary 2.Cardiac- striated and multi-nucleated; involuntary 3.Smooth- not striated and single nuclei for each cell; involuntary
Skeletal muscle multiple nuclei; regular banding patterns that are organized by contractile proteins
Skeletal muscle development muscle arises from the mesoderm; myoblast; multi-nucleated myotube; myofiber
Myoblast muscle cell, fused together
multi-nucleated myotube myoblasts fused together no longer have mitotic abilities; instead we alter size (weight lifting) by adding or subtracting nuclei by adding satellite cells (cells floating outside myotube)
Myofiber smalles complete contractile system; activated when nerve hits myotube but if nerve fails to make contact the myotube will wither and die
Structure of skeletal muscle 1.Epimysium 2.Fascicle 3.Fibers 4.Myofibril 5.Sarcomere 6.Perimysium 7.Endomysium 8.Sarcolemma
Epimysium Layer of connective tissue outside muscle that covers the entire thing; dense irregular connective tissue
Fascicle a bundle of muscle fibers wrapped in perimysium; contains smaller bundles of muscle fibers
Perimysium A layer of connective tissue that wraps muscle fibers into bundles or fascicles; dense irregular tissue
Fibers Formed by the fusion of myoblasts; a long, cylinder, multi-nucleated cell; nuclei is under sarcolemma and has other cell organelles like mitochondria; each fiber is wrapped in endomyseum
Endomysium Areolar connective tissue; layer of connective tissue that surrounds muscle fibers
Sarcolemma The plasma membrane of a muscle cell (muscle fiber)
Myofibril The basic unit of a muscle; Where contraction takes place; a long strand of sarcomeres; found in the skeletal muscle fibers; held together in a long chain by proteins and organized into myofiliments
Sarcomere Smallest functional unit of skeletal muscle; Shortens for muscle contraction; runs Z-disc to Z-disc; composed to thick filaments-Myosin and thin filaments- Actin (slide past each other to contract)
Overview of skeletal muscle contraction Myosin binds to actin to shorten; myosin heads work with receptor proteins of actin
Muscle striations made by sarcomeres; striations consist of A-bands, I-bands, M-lines, and H-zones
A-band Anisotropic- light does not pass through due to high concentration of protein; Dark area
I-band Isotropic- light can pass through due to less protein; light area
M-line Dark band in the center of the sarcomere; consists of proteins that anchor thick filaments to the center of the sarcomere
H-zones Light bands that are located on either side of the M-line
I-band (blue circles) 6 actin form a circle; thin filaments (actin) molecules only
H-zone (red circles) Thick filaments (myosin) molecules only
M-line (red circles connected) proteins connect thick filaments (myosin) only; do not connect think filaments at all
A-band (blue and red circles) thick and then filaments (actin and myosin); 6 thin filaments for every thick filament
Thick filaments (myosin) structure Globular myosin head- binds to actin; tails- are intertwined that interact with other myosin subunits and regulate motor activity; neck- acts as a lever (hinges to change shape)
Thin filaments (actin) structure long chains made of actin molecules (twisted); each actin has a myosin binding site; protein strands run through actin filament called tropomyosin; yellow proteins called troponin
Tropomyosin Protein strands; blocks myosin binding site on actin and prevents contraction
Troponin complex Yellow proteins complexes that contain 3 proteins; inhibit tropomyosin to allow binding and contraction when and action potential is created
T-Tubules Part of the plasma membrane of the sarcolemma; studded with calcium channels for depolarization; run transversely through muscle fibers
Sarcoplasmic Reticulum Located on either side of the T-tubules; Stores (muscle relaxation), releases (muscle contraction), and sequesters calcium
Terminal cisterna Site where T-tubule tells sarcoplasmic reticulum to release calcium for contraction; large sac-like structure
Triad T-tubules, Terminal cisterna, and sarcoplasmic reticulum
Voluntary control A neuron must tell the muscle what to do
Cardiac muscle specialized striated muscle; involuntary
Development of cardiac muscle Cardiomyocyte- located in walls of heart; generate electrical impulses of the heart; single or multi-nucleated
Contraction of cardiac muscle Automaticity- spontaneous contraction Syncytium- single cell function and 1 (gap junction) because cells meet end to end; allows contractions to work together
Neural control of cardiac muscle Autonomic nervous system- parasympathetic (relax) and sympathetic (stimulate) no neural muscular junction
Cardiac muscle functional structures Sarcomere- T-tubules, SR, Mitochondria Intercolated disks with gap junctions
Sliding filament theory during contraction the thin filaments slide past the thick filaments to they overlap; When sarcomere is contracted I-bands are gone and Z-discs are pulled to the center of the sarcomere
Cross-bridge cycling 4 steps; when actin bind to myosin we have a cross-bridge; Cycling- going back and forth between strong and weak bonds
Step 1 Cross-bridge cycling Myosin binds to actin forming a cross-bridge
Step 2 Cross-bridge cycling Phosphate falls off and myosin bends forward which draws thin filaments towards center of the sarcomere and ADP falls off
Step 3 Cross-bridge cycling ATP binds to myosin and disassociates or weakens bond between actin and myosin
Step 4 Cross bridge cycling Myosin will change ATP to ADP and phosphate and re-cocks the myosin head
Role of calcium in contraction Calcium binds to troponin C; Troponin then triggers tropomyosin to move
Neuron muscular junction Site where the neuron makes contact with the muscle
Buton (neurotransmitter) Releases vessicles containing ACH (acetylcholine) into the synaptic cleft; ACH binds to receptors on Na and K channels; ACH opens channels in the cleft which causes membrane potential which initiates and raises membrane potential
After acetylcholine is used... It is broken down and leaves the cleft
Action potential When a membrane depolarizes and repolarizes; membrane can depolarize and recover in 4ms
Threshold a point you must reach or exceed for something to occur; all or none; when threshold is met or exceeded sodium channels will open
Depolarization Na channels will be signaled to open and sodium will rush in the cell; the membrane potential will become positive; this action moves down the sarcolema
Repolarization When a section of the membrane has a positive potential the potassium channels will open allowing the membrane to be polarized again; this also moves down the sarcolema right behind the depolarization
After Depolarization/repolarization The channels close and Na (out) and K (in) are pumped back to the appropriate sides of the membrane through sodium potassium pumps
Resting membrane potential -90
depolarization and the triad signal to depolarize can travel down T-tubules by the Na channels; this process signals sarcoplasmic reticulum through receptors; the SR then releases Ca to bind to troponin ect.
End plate potential The rise in membrane potential of the cleft; gets to about -40 or -50 which meets threshold requirements and causes depolarization
When acetylcholine stops and membrane potential is positive... channels open and membrane repolarizes
Twitch muscle contraction stimulated by a single stimulus
3 periods of a twitch 1.Latent period 2.Contraction period 3. Relaxation period
Latent period Beginning; everything up to myosin binding to actin
Contraction period Middle; Myosin binds to actin; takes about 30ms to peak
Relaxation period End; decreasing amount of tension
Slow vs fast twitch twitch characteristics come from the metabolic properties of myofibrils; no difference in latent period
Fast twitch Very quick to peak in the contraction period and very quick to fatigue
Slow twitch Slower to peak in contraction period and slower to fatigue
Gastrocnemius (fast twitch); quick to peak and quick to relax
Soleus (slow twitch); longer to peak and longer to relax
Graded muscle responses (i.e. tension production) 1.Frequency stimulation 2.Amount of motor neurons activated
Frequency stimulation crude; before the first contraction can relax we have a second contraction on top of the first; causes more force with the same muscle- energy is reserved and more Ca is being released to cause more reactions; can continue till max cross-bridges formed
motor neuron control each fiber is controlled by a specific motor neuron but one motor neuron can be responsible for controlling 40-200 fibers
Amount of motor neurons activated (size principle); as stimulus voltage increases the amount of fibers activated increases and higher the tension; high contraction force by increasing # of motor units contracting; smallest to largest
Smallest to largest small units used for small tasks and vice versa; we can regulate force by regulating the motor neurons activated
Length tension relationship optimal sarcomere length; too much contraction; too much stretching
Optimal sarcomere length max number of cross bridges are formed
Over contracted If we contract the sarcomere by too much the thin filaments will over lap and it will block binding sites so tension and # of cross-bridges will decrease; can continue to shorten until no more cross-bridges can be formed
Over stretched If we extend the sarcomere by to much then tension and number of cross bridges will decrease as actin and myosin separate; will continue until no cross-bridges can be formed
Smooth muscle Involuntary; not striated; single nucleated cells; found in the lining of most organs
Development in smooth muscle Layers of cells can have different shapes- no cell phenotype; single, central nuclei;synchronous contractions due to cellular junctions; lacks organization; No sarcomere
Neural control in smooth muscle Autonomic nervous system- parasympathetic, and sympathetic; no defined nerve ending plates
Contraction types of smooth muscle 1.Phasic contraction- single unit (gastrointestinal) 2.Tonic contraction- multiunit (blood vessels)
Layers of cells longitudinal and circular layers of cells; they contract at different times; cells have gap junctions that tell the cells around them to contract
Autonomic nervous system Norepineprine is released by a varicosity of an autonomic nerve fiber and can cause numerous muscles to contract (involuntary)
Varicosity bulbous swelling of innervating nerves; release neurotransmitters into wide synaptic clefts called diffuse junctions
Intermediate filaments cytoskeletal structure, helps give the cell characteristics like twisting while shortening
Caveolae (poorly developed SR); receptor mediated, concentrates calcium, helps to take calcium from outside the cell to make up for poor SR
Thin to thick filament ratio (smooth muscle) 1 thick filament to every 13 thin filaments
Filaments in Smooth muscle actin and myosin are not organized in sarcomeres; no troponin or tropomyosin
E-C coupling Calcium is released into cell and binds to calmodulin; kinase phosphorilates myosin; the more phosphate groups the more contractions
Calmodulin enzyme that phosphorilates kinase
Single unit contraction single-unit muscle (visceral muscle); contracts rhythmically as a unit via gap junctions; may have spontaneous action potentials; arranged in opposing sheets to exhibit stress-relaxation response; (ex. gut contractions)
peristalsis alternating contractions and relaxations of smooth muscle that mix and squeeze substances through the lumen (ex. stomach)
Mulit-unit Rare gap junctions; infrequent spontaneous depolarizations; structurally independent muscle fibers; a rich nerve supply, may form motor units; graded contractions (ex. airways, blood vessels, arrector pili, internal eye)
Stress relaxation response smooth muscle can expand due to a stimulus and if the expansion is held for long enough the muscle will then relax and allow more room for more tension all while keeping its ability to contract
hyperplasia increase in the number of cells which may result in an increase of that organ; smooth muscles used this to undergo mitosis and increase number (only muscle that can divide)
Atherosclerosis heart disease
Hyperplasia (estrogen and the uterus) at puberty estrogen stimulates the synthesis of more smooth muscle which allows uterus to grow to adult size; also happens during pregnancy to accommodate the increasing size of the baby
Created by: Rootb



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