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Ch. 9 muscle
anatomy and physiology of muscle
| Question | Answer |
|---|---|
| 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 |
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