Chapter 9 Muscular Flashcards
(83 cards)
1
Q
function of muscle
A
transform chemical energy (ATP) to directed mechanical energy to exert force
2
Q
types of muscle tissue
A
skeletal, cardiac, smooth
3
Q
prefixes for muscle
A
myo, mys, sarco
4
Q
skeletal muscle
A
organs attached to bones and skin; elongated cells called muscle fibers are striated; voluntary; contract rapidly, tire easily, powerful; require nervous system stimulation
5
Q
cardiac muscle
A
only in heart, bulk of heart walls; striated; can contract without nervous system stimulation; involuntary
6
Q
smooth muscle
A
in walls of hollow organs; not striated; can contract without nervous system stimulation; involuntary; usually in two layers (longitudinal and circular)
7
Q
excitibility
A
ability to receive and respond to stimuli
8
Q
contractility
A
ability to shorten forcibly when stimulated
9
Q
extensibility
A
ability to be stretched
10
Q
elasticity
A
ability to recoil to resting length
11
Q
connective tissue sheaths
A
support cells, reinforce whole muscle; layers–epimysium, perimysium, endomysium
12
Q
epimysium
A
dense irregular connective tissue surrounding entire muscle, may blend with fascia
13
Q
perimysium
A
fibrous connective tissue surrounding fascicles
14
Q
fasciles
A
groups of muscle fibers
15
Q
endomysium
A
fine areolar connective tissue surrounding each muscle fiber
16
Q
skeletal muscle attachments
A
attach in two places–insertion (movable bone) and origin (immovable bone); attachments are direct (epimysium fused to periosteum of bone or perichondrium of cartilage) or indirect (connective tissue wrappings extend beyond muscle as ropelike tendon or sheetlike aponeurosis
17
Q
anatomy of muscle fiber
A
long cylindrical cell 10-100 nanometers in diameter and up to 30 cm long; multiple peripheral nuclei; scarcolemma; scarcoplasm; modified structures include myofibrils, sarcoplasmic reticulum and t tubles
18
Q
sarcoplasm
A
cytoplasm of skeletal muscles; contains glycosomes for glycogen storage and myoglobin for oxygen storage
19
Q
sarcolemma
A
plasma membrane of skeletal muscles
20
Q
myofibrils
A
densely packed, rod-like elements that make up 80% of cell volume; contain sarcomeres (contractile units); exhibit striations of perfectly aligned repeating series of dark a bands and light i bands
21
Q
h zone
A
lighter region in midsection of dark A band where filaments do not overlap
22
Q
m line
A
line of protein myomesin bisects H zone
23
Q
z disk
A
coin-shaped sheet of proteins on midline of light I band that anchors thin filaments and connects myofibrils to one another
24
Q
thick filaments
A
run entire length of an A band
25
thin filaments
run length of I band and partway into A band
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scarcomere
region between two successive z disks' smallest contractile unit of muscle fiber; align along myofibril; contains A band with half I band at each end; composed of thick and thin myofilaments made of contractile proteins
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myofibril banding pattern
orderly arrangement of actin and myosin myofilaments within sarcomere.
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actin myofilaments
thin filaments which extend across i band and partway in a band; anchored to z discs
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myosin myofilaments
thick filaments which extend length of a band and connect at m lines
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ultrastructure of thick filament
composed of protein myosin; each composed of 2 heavy and 4 light polypeptide chains; myosin tails contain 2 interwoven heavy polypeptide chains; myosin heads contain 2 smaller light polypeptide chains that act as crossbridges during contraction (binding sites for actin of thin filiments, binding sites for ATP, ATPase enzymes)
31
sarcoplasmic reticulum
(SR) network of smooth endoplasmic reticulum surrounding each myofibril; most run longitudinally, pairs of terminal cisternae form perpendicular cross channels; functions in regulation of intracellular Ca2 levels (stores and releases Ca2)
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t tubules
continuations of sarcolemma; lumen continuous with extracellular space; increase muscle fiber's surface area; penetrate cell's interior at each A band-I band junction; associated with paired terminal cisterns to form triads that encircle each carcomere
33
triad relationships
t tubules conduct impulses deep into muscle fiber in every sarcomere; integral proteins protrude into intermembrane space from t tubule and SR cistern membranes and act as voltage sensors; SR foot proteins are gated channels that regulate Ca2+ release from SR cisterns
34
sliding filament contraction
during contraction, thin filaments slide past thick filaments increasing actin and myosin overlap; myosin heads bind to actin and sliding begins; cross bridges form and break several times, racheting thin filaments toward center of sarcomere; muscle fiber shortens and pulls z discs toward m line (i bands shorten, z discs move closer, h zones disappear, a bands move closer)
35
muscular activation
nervous stimulation generates action potential in sarcolemma
36
muscular contraction events
skeletal muscles stimulated by somatic motor neurons; axons of motor neurons travel from central nervous system via nerves to skeletal muscle; each axon forms several branches as it enters muscle; each axon ending forms neuromuscular junction with single muscle fiber (usually one per muscle)
37
steps ACh release
1) action potential arrives at axon terminal of motor neuron; 2) voltage-gated ca2+ channels open and ca2+ enters axon terminal moving down electochemical gradient; 3) ca2+ causes ACh to be released by exocytosis; 4)ACh diffuses across synaptic cleft and binds to receptors on sarcolemma; 5) ACh binding opens ion channels allowing simultaneous passage of Na+ into mucscle fiber and K+ ions out. More K+ exit which produces end plate potential; 6) ACh effects are terminated by breaking in synaptic cleft by acetylcholinesterase and diffuses away from junction; ion channel closes.
38
nmj
neuromuscular junction; situated midway along length of muscle fiber; axon terminal and muscle fiber separated by gel-filled space called synaptic cleft; synaptic vesicles of axon terminal contain acetylcholine (ACh); junctional folds of sarcolemma contain ACh receptors
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events at nmj
nerve impulse arrives at axon terminal and ACh released into synaptic cleft; ACh diffuses across cleft and binds with receptors on sarcolemma; electrical events generate action potential
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destruction of ACh
ACh effects quickly terminated by enzyme acetylcholinesterase in synaptic cleft; breaks down ACh to acetic acid and choline; prevents continued muscle fiber contraction in absence of additional stimulus
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generation of action potential
resting sarcolemma is polarized (voltage across membrane); action potential caused by changes in electrical charges; occurs in three steps: end plate potential, depolarization, repolarization
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end plate potential
local depolarization; ACh binding opens ligand-gated ion channels; simultaneous diffusion of Na+ (inward) and K+ (outward); more Na+ diffuses in so interior of sarcolmma becomes less negative; end plate potential achieved.
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depolarization
generation and propagation of an action potential; end plate potential spreads to adjacent membrane areas; voltage-gated Na+ channels open; Na+ influx decreases membrane voltage toward threshold; if threshold reached, action potential initiated; once initiated is unstoppable; created muscle contraction
44
repolarization
restoring electrical conditions of resting membrane potential; Na+ channels close and voltage-gated K+ channesl open; K+ efflux rapidly restores resting polarity; fiber cannot be simulated and in refractory period until repolarization complete; ionic conditions of resting state restored by Na+-K+ pump
45
excitation-contraction coupling events
AP propagated along sarcomere to t tubles; voltage-sensitive proteins stimulate Ca2+ release from SR; calcium binds to troponin and removes the blocking action of tropomyosin exposing binding sites for myosin on thin filaments; myosin binding to actin forms cross bridges and contraction begins; e-c coupling now ends
46
cross bridge cycle
energized myosin head attaches to an actin myofilament forming a cross bridge; ADP and P are released and the myosin head pivots and bends changing to its bent low-energy state and as a result pulls the actin filaments toward the m line (power stroke); after ATP attaches to myosin, the link between myosin and actin weakens and myosin head detaches and cross bridge detaches; ATP is hydrolyzed to ADP and P and mysoin head returns to prestroke high-energy (cocked) position
47
rigor mortis
3-4 hours after death occurs, muscles begin to stiffen with weak rigidity at 12 hours post mortem. Dying cells take in calcium and form cross bridges, but there is no ATP generated to break the cross bridges
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isometric contraction
no shortening; muscle tension increases but does not exceed load
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isotonic contraction
muscle shortens because muscle tension exceeds load; either concentric or eccentric contractions
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concentric contraction
muscle shortens and does work
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eccentric contraction
muscle generates forces as it lengthens
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motor unit
motor neuron and all (four to several hundred) muscle fibers it supplies. smaller number of motor units = fine control; muscle fibers from motor unit spread throughout muscle so single motor unit causes weak contraction of entire muscle; motor units in muscle usually contract asynchonously to help prevent fatigue
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muscle twitch
motor unit's response to a single action potential of its motor neuron; simplest contraction observable in lab
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phases of muscle twitch
latent: events of excitation-contraction coupling, no muscle tension;
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contraction:
cross bridge formation, tension increases;
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relaxation:
Ca2+ reentry into SR, tension declines to zero;
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contracts faster than it relaxes
https://o.quizlet.com/i/qJXZH4je\_UOsqhkDSBn9Ag.jpg
58
muscle tone
constant, slightly contracted state of all muscles due to spinal reflexes; keeps muscles firm, health and ready to respond
59
muscle metabolism
ATP only source of energy used directly for contractile activities; available stores of ATP depleted in 4-6 seconds; ATP regenerated by direct phosphorylation of ADP by creatine phosphate (CP), anaerobic pathway, or aerobic respiration
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anaerobic pathway
glycolysis (glycose degraded to 2 pyruvic acid molecules); at 70% of maximum contractile activity, pyruvic acid converted to lactic acid; lactic acid diffuses into blood stream, used as fuel by liver, kidneys and heart, converted back into pyruvic acid or glucose by liver; only yields 5% as much ATP as aerobic respiration, but produces ATP 2 1/2 times faster
61
aerobic pathway
produces 95% of ATP during rest and light to moderate exercise; a series of chemical reactions that require oxygen; occurs in mitochondira; fueled by stored glycogen, blood borne glucose, pyruvic acid from glycolosis, free fatty acids
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aerobic endurance
length of time muscles contract using aerobic pathways
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anaerobic threshold
point at which muscle metabolism converts to anaerobic
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force of muscle contraction
force of contraction depends on number of cross bridges attached which is affected by the number of muscle fibers stimulated, relative size of fibers, frequency of stimulation, degree of muscle stretch
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velocity and duration of contracton
influenced by muscle fiber type, load, recruitment
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muscle fiber types
classified according to speed of contraction and metabolic pathways for ATP synthesis: slow oxidative, fast oxidative, fast glycolytic
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oxidative fibers
muscles that use aerobic pathways
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glycolytic fibers
muscles that use anaerobic glycolysis
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disuse atrophy
result of immobilization, muscle strength declines 5% per day; without neural stimulation muscles atrophy to 1/4 of initial size; fibrous connective tissue replaces lost muscle tissue and rehabilitation is impossible
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microscopic structure of smooth muscles
spindle shaped fibers, one nucleus, no striations; lacks connective tissue sheaths, endomysium only; SR less developed than in skeletal muscle; caveolae of sarcolemma sequester Ca2+; no sarcomeres, myofribrils, or t tubles
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caveolae
pouch like infoldings of sarcolemma of smooth muscle tissue
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longitudinal layer
smooth muscle layer with fibers parallel to long axis of organ; contractions dilate and shorten muscles
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circular layer
smooth muscle layer with fibers parallel in circumference of organ; contractions constrict lumens and elongates organ
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peristalis
alternating contractions and relaxations of smooth muscle layers that mix and squeeze substances through lumen of hollow organs
75
contractions of smooth muscle
slow, synchronized contractions; cells electrically coupled by gap junctions and action potentials are transmitted from fiber to fiber; some cells self-excitatory (depolarize without stimuli) and act as pacemakers for sheets of muscle; slow to contract and relax, but maintains for prolonged periods with low energy cost, myofilaments may latch together to save energy; relaxation requires Ca2+ detachment from colmuodulin, active transport of Ca2+ into SR and ECF, dephosphorylations of myosin to reduce myosin ATPase activity
76
regulation of contraction
by nerves, hormones, or local chemical changes
77
neural regulation
nuerotransmitter binding increases Ca2+ in sarcoplasm; either graded (local) potential or action potential; response depends on neurotransmitter released band type of receptor molecules
78
hormone/local chemical regulation
some smooth muscle cells have no nerve supply and depolarize spontaneously or in response to chemical stimuli that bind G protein-links receptors; some respond to both neural and chemical stimuli; chemical factors include CO2 and pH
79
stress-relaxation response
responds to stretch only briefly, then adapts to new length; retains ability to contract on demand; enables organs such as stomach and bladder to temporarily store contents
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length and tension changes
can contract when between half and twice its resting length
81
hyperplasia
smooth muscle cells can divide and increase in number; for example, estrogen effects on uterus at puberty and during pregnancy
82
muscular dystrophy
Duchenne muscular dystrophy (DMD): most common and severe type; inherited; sex-liked, carried by females and expressed in males as lack of dystrophin (cytoplasmic protein that stabilizes sarcolemma); fragile sarcolemma tears, increasing C2+ entry which damages contractile fibers and makes cells inflamed which drops muscle mass; victims become clumsy and fall frequently and usually die of respiratory failure in 20s; no cure; prednisone improves muscle strength and function; myoblast transfer therapy disappointing; coaxing dystrophic muscles to produce more utrophin (protein similar to dystrophin) successful in mice; viral gene therapy and infusion of stem cells with correct dystrophin genes show promise
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aerobic pathway
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