Skeletal Muscle Flashcards
Describe the highly structured organization of skeletal muscle and explain the
“striated” appearance of skeletal muscle. Describe the connective tissue layers and
the relationships between these connective tissue investments and the capillaries,
muscle fibers, and proprioceptors.
Fascicles of muscle with fibers in it (epimysium->perimysium->endomysium), sarcolemma surrounds fibers, myofibril in fibers and sarcomeres in those that have myofilaments
Striation from myofilament arrangement, dark is mostly myosin and light band is all actin
Distinguish the different skeletal muscle fiber types including differences in size,
force production, mitochondrial density, capillary density, and recruitment order.
Extrafusal, large diameter and long length, multinucleated, peripheral nuclei, striated, can contract
Type I – slow smallest, fatigue resistant, small
Type IIx – fast, glycolytic, fatigable, largest
Type IIa – fast glycolytic and oxidative, not as fatiguable, medium speed
Type is dictated by myosin isoform, mosaic form across it (mixed)
Describe the function of and identify the location of the sarcolemma, t-tubules,
sarcoplasmic reticulum, and triad.
Sarcolemma surrounds fiber, has T tubules that let AP conduct along the fiber and into T tubule into cell, they have a special voltage receptor
Myofibrils in muscle fiber, cylinders in there, T tubules interface each of them with sarcoplasmic reticulum with Ca there, triad is 2SR + T tubule with SR having Ca channel (RyR) and T tubule having voltage sensor (DHSR)
- Explain the importance and location of the myofilaments, Z disk and M line, A-band
and I-band and force translating proteins – desmin, dystrophin, and titin. Be able to
relate these structures to the sliding filament mechanism of contraction.
Sarcomere is smallest contractile unit within myofibril, stacked end to end, Z line or disk defines the ends with M line in middle, myofilaments in sarcomere are contractile protein so has actin (thin, 2 together, troponin-tropomyosin where Ca comes in and blocks myosin, binds myosin when contracting) and myosin (thick, ATPase) overlapping each other
A band is myosin and actin, I band is only actin
Actin and myosin contact it is cross bridge, Ca comes in
Low Ca no cross bridge no contact
Anchoring proteins – titin M line to Z line
Structural protein – for force, dystrophin/desmin/costameres, towards sarcolemma
Describe the sliding filament mechanism of contraction and the stages of the cross-
bridge cycle in terms of ATP hydrolysis, calcium regulation, and movement and
attachment of the heads of myosin. Explain the role of calcium in regulating cross-
bridge formation including where it is stored and released.
Stages of cross bridge cycle, trying to pull actin towards M line
1. Myosin setting – ATP required to cock the myosin head
2. Cross bridge formation – need Ca
3. Power stroke – ATP required for myosin to pull actin
4. Attachment – ATP needed for myosin to let go
5. Release – no ATP then cannot release, RIGOR
Describe the three types of contraction describing what happens at the level of the
sarcomere and give examples or each type. Describe and graph the length-tension
relationship for isometric contractions and the elements that contribute to passive
and active force.
Isometric – same length put produce force
Concentric – shorten muscle
Eccentric – lengthen muscle
Initial length impacts force, active force is actin/myosin overlap, passive force is stretching muscle from elastic elements, total force is both together
Describe a motor unit and the distribution of fibers within a motor unit across the
muscle. Describe the activation of skeletal muscle within the context of a motor unit.
Describe the two neural mechanisms for modulation of muscle (and motor unit)
contraction force and explain the principal of orderly recruitment.
Somatic nervous system controls skeletal muscles, alpha motor neurons innervate, needed for muscle cell survival
One motor unit innervates multiple fibers, each fiber innervated by one motor unit, number of them depends on the size of the muscle, fine motor control small fibers/motor neurons (Type I), motor unit control many fibers and larger neurons (Type II), range within most muscles
Spread activation throughout the muscle belly
Neuromuscular junction – nerve terminal and muscle fiber with area in between, one AP at each NMJ and propagate AP along sarcolemma
Temporal summation – increasing force by sending motor neuron AP more frequently, no additional muscle, tetanus is short interval fused action Spatial summation – increasing total active motor units to have more force, sum tension of motor units, we can do this because were not always using all of our motor units These are in an all or nothing fashion Henneman size principal is gradual increase in motor unit recruitment, recruit small first, then bring on larger ones that can fatigue after
Explain the general location, function, and innervation of the muscle proprioceptors,
muscle spindle and Golgi tendon organ.
Spindle detects length change, intrafusal fibers within capsule, for myotatic stretch reflex
Golgi tendon organ – nerve endings in end of muscle fibers, responds to change in tension, response counters force in antagonist muscle
Excitation contraction coupling with motor nerve and sarcolemma spread, depends on somatic nervous system
Record at sarcolemma, motor end plate, and action potential site
AP gets to terminal, opens voltage gated Ca channel, vesicles migrate and Ach diffuses to motor end plate, activates nicotinic receptors, Na spreads, sarcolemma AP happens and spreads in sarcolemma
Contraction coupling – AP propagate and depolarizes t-tubules and changes confirmation of voltage sensor to change RYR and open Ca channel which travels to myofilaments and starts cross bridge contraction until SERCA pump stops Ca and muscle relaxes
Distinguish how the following drugs or diseases that alter receptor binding, ion
channels, enzyme activity, or structural proteins will affect muscle contraction and
performance. Describe what aspects of excitation contraction coupling are affected
and whether tension developed, motor neuron action potentials and/or muscle
action potentials are affected. Do this for lidocaine, myasthenia gravis, muscular
dystrophy, Lambert-Eaton Myasthenia Syndrome, Brody’s disease, Botox and
botulism, and malignant hyperthermia.
Botox – administer, targets Ach release to stop it, normal AP at terminal, block at end plate potential, no muscle fiber AP/Ca release/no cross bridge/no force
Lidocaine – block the AP in the nerve, no AP at terminal so everything is blocked
Myasthenia gravis –
Muscular dystrophy -
Malignant hypothermia – happens with inhaled anesthetics, RYR forced open so tons of Ca, SERCA pump can’t keep up so get more cross bridge and more force, tachycardia, no electrical signal (no AP)
Describe the skeletal muscle clinical presentation and known causes of the
following: fibromyalgia, myasthenia gravis, dystonia, amyotrophic lateral sclerosis,
muscular dystrophy (Duchenne’s and Becker’s).
Duchenne – no dystrophin, X linked
Becker – compromised dystrophin
Limb Girdle – mutated sarcoglycans
Congenital – mutated desmin
Define myalgia, rhabdomyolysis, myoglobinuria, and myotonia. Describe the causes
of elevated blood levels of creatine kinase. Describe the danger of rhabdomyolysis
and the symptoms associated with it.
Myalgia – muscle pain
Rhabomyolysis – tearing apart of skeletal muscle
Myglobinuria – leakage of proteins due to muscle weakness
Myotonia – prolonged contraction
Creatine kinase – leaks out with cell membrane damaged, elevated during MI
