Exam 6 PART 1 Flashcards
Muscle Tissue
- Nearly half of body’s mass
- Can transform chemical energy (ATP) into directed mechanical energy, which is capable of exerting force
Types of Muscle Tissue
•Terminologies: Myo, mys, and sarco are prefixes for muscle
–Example: sarcoplasm: muscle cell cytoplasm
•Three types of muscle tissue
–Skeletal
–Cardiac
–Smooth
•Only skeletal and smooth muscle cells are elongated and referred to as muscle fibers
•Skeletal muscle
–Skeletal muscle tissue is packaged into skeletal muscles - organs that are attached to bones and skin
–Skeletal muscle fibers are longest of all muscle and have striations (stripes)
–Voluntary muscle - consciously controlled
–Contract rapidly; tire easily; powerful
–Requires innervation to contract
•Cardiac muscle
–Cardiac muscle tissue is found only in heart
•Makes up bulk of heart walls
–Striated
–Involuntary: cannot be controlled consciously
•Can contract on its own, but nervous system can increase rate
•Smooth muscle
–Smooth muscle tissue: found in walls of hollow organs
•Examples: stomach, urinary bladder, and airways
–Not striated
–Involuntary: cannot be controlled consciously
Can contract on its own without nervous system stimulation
•All muscles share four main characteristics:
–Excitability (responsiveness): ability to receive and respond to stimuli
–Contractility: ability to shorten forcibly when stimulated
–Extensibility: ability to be stretched
–Elasticity: ability to recoil to resting length
•Four important functions
1.Produce movement: responsible for all locomotion and manipulation
•Example: walking, digesting, pumping blood
- Maintain posture and body position
- Stabilize joints
- Generate heat as they contract
•Additional functions
–Protect organs, form valves, control pupil size, cause “goosebumps”
Skeletal muscle is an organ made up of different tissues with three features:
nerve and blood supply, connective tissue sheaths, and attachments
Nerve and Blood Supply
•Each muscle receives a nerve, artery, and veins
–Consciously controlled skeletal muscle has nerves supplying every fiber to control activity
•Contracting muscle fibers require huge amounts of oxygen and nutrients
–Also need waste products removed quickl
Connective Tissue Sheaths
- Each skeletal muscle, as well as each muscle fiber, is covered in connective tissue
- Support cells and reinforce whole muscle
- Sheaths from external to internal:
–Epimysium: surrounding entire muscle
–Perimysium: surrounding fascicles (groups of muscle fibers)
–Endomysium: surrounding each muscle fiber
Attachments
- Muscles span joints and attach to bones
- Muscles attach to bone in at least two places
–Insertion: attachment to movable bone
–Origin: attachment to immovable or less movable bone
•Attachments can be direct or indirect
–Direct (fleshy): epimysium fused to periosteum of bone or perichondrium of cartilage
–Indirect: connective tissue wrappings extend beyond muscle as ropelike tendon or sheetlike aponeurosis
•Skeletal muscle fibers are
long, cylindrical cells that contain multiple nuclei
Sarcolemma and Sarcoplasm
- Sarcolemma: muscle fiber plasma membrane
- Sarcoplasm: muscle fiber cytoplasm
Skeletal Muscle fibers contain
- many glycosomes for glycogen storage, as well as myoglobin for O2 storage
- Modified organelles: Myofibrils, Sarcoplasmic reticulum, T tubules
Myofibrils
•densely packed, rodlike elements
–Single muscle fiber can contain 1000s
–Accounts for ~80% of muscle cell volume
•Myofibril features
–Striations
–Sarcomeres
–Myofilaments
–Molecular composition of myofilaments
Striations:
•stripes formed from repeating series of dark and light bands along length of each myofibril
–A bands: dark regions
•H zone: lighter region in middle of dark A band
–M line: line of protein (myomesin) that bisects H zone vertically
–I bands: lighter regions
•Z disc (line): coin-shaped sheet of proteins on midline of light I band
Sarcomere
–Smallest contractile unit (functional unit) of muscle fiber
–Contains A band with half of an I band at each end
•Consists of area between Z discs
–Individual sarcomeres align end to end along myofibril, like boxcars of train
•Myofilaments
–Orderly arrangement of actin and myosin myofilaments within sarcomere
–Actin myofilaments: thin filaments
- Extend across I band and partway in A band
- Anchored to Z discs
–Myosin myofilaments: thick filaments
•Extend length of A band
Connected at M line
•Molecular composition of myofilaments
Thick Filaments
composed of protein myosin made up of two heavy chains that form the tail, and four light chains that form the two globular heads
- Myosin heads contain binding sites for ATP and actin
- During contraction, heads link thick and thin filaments together, forming cross bridges
•Molecular composition of myofilaments
–Thin filaments:
–Thin filaments: composed of fibrous protein actin
•Actin is polypeptide made up of G actin (globular) subunits
–G actin subunits bears active sites for myosin head attachment during contraction
•G actin subunits link together to form long, fibrous F actin (filamentous)
•Two F actin strands twist together to form a thin filament
–Tropomyosin and troponin: regulatory proteins bound to actin
•Molecular composition of myofilaments
–Other proteins help form the structure of the myofibril
•Elastic filament: composed of protein titin
–Holds thick filaments in place; helps recoil after stretch; resists excessive stretching
•Dystrophin
–Links thin filaments to proteins of sarcolemma
•Nebulin, myomesin, C proteins bind filaments or sarcomeres together
–Maintain alignment of sarcomere
Sarcoplasmic reticulum:
•network of smooth endoplasmic reticulum tubules surrounding each myofibril
–Most run longitudinally
–Terminal cisterns form perpendicular cross channels
–SR functions in regulation of intracellular Ca2+ levels
Stores and releases Ca2+
•T tubules
–Tube formed by protrusion of sarcolemma deep into cell interior
- Increase muscle fiber’s surface area greatly
- Lumen continuous with extracellular space
- Allow electrical nerve transmissions to reach deep into interior of each muscle fiber
–Tubules penetrate cell’s interior at each A–I band junction between terminal cisterns
•Triad: area formed from terminal cistern of one sarcomere, T tubule, and terminal cistern of neighboring sarcomere
•Triad relationships
–T tubule and SR cistern contains integral membrane proteins that protrude into intermembrane space (space between tubule and muscle fiber sarcolemma)
- Tubule proteins act as voltage sensors that change shape in response to an electrical current
- SR integral proteins control opening of calcium channels in SR cisterns
–When an electrical impulse passes by, T tubule proteins change shape, causing SR proteins to change shape, causing release of calcium into cytoplasm
Contraction:
- the activation of cross bridges to generate force
- Does not necessarily shorten muscles
- Shortening occurs when tension generated by cross bridges on thin filaments exceeds forces opposing shortening
- Contraction ends when cross bridges become inactive
Sliding filament model of contraction
•states that during contraction, thin filaments slide past thick filaments, causing actin and myosin to overlap more
–Neither thick nor thin filaments change length, just overlap more
- In the relaxed state, thin and thick filaments overlap only slightly at ends of A band
- When nervous system stimulates a muscle fiber, myosin heads are allowed to bind to actin, forming cross bridges, which cause sliding (contraction) process to begin
- Cross bridge attachments form and break several times, each time pulling thin filaments a little closer toward center of sarcome in a ratcheting action
–Causes shortening of muscle fiber
- Z discs are pulled toward M line
- I bands shorten
- Z discs become closer
- H zones disappear
- A bands move closer to each other
•Four steps must occur for skeletal muscle to contract:
- Nerve stimulation
- Action potential, an electrical current, must
be generated in sarcolemma - Action potential must be propagated along
sarcolemma - Intracellular Ca2+ levels must rise briefly
- Steps 1 and 2 occur at neuromuscular junction
- Steps 3 and 4 link electrical signals to contraction, so referred to as excitation-contraction coupling
The Nerve Stimulus and Events at the Neuromuscular Junction
- Skeletal muscles are stimulated by somatic motor neurons
- Axons (long, threadlike extensions of motor neurons) travel from central nervous system to skeletal muscle
- Each axon divides into many branches as it enters muscle
- Axon branches end on muscle fiber, forming neuromuscular junction (NMJ) or motor end plate
–Each muscle fiber has one neuromuscular junction with one motor neuron
- Axon terminal (end of axon) and muscle fiber are separated by gel-filled space called synaptic cleft
- Stored within axon terminals are membrane-bound synaptic vesicles
–Synaptic vesicles contain neurotransmitter acetylcholine (ACh)
- Infoldings of sarcolemma, called junctional folds, contain millions of ACh receptors
- NMJ consists of axon terminals, synaptic cleft, and junctional folds
•Events at the neuromuscular junction
–Nerve impulse arrives at axon terminal, causing ACh to be released into synaptic cleft
–ACh diffuses across cleft and binds with receptors on sarcolemma
–ACh binding leads to electrical events that ultimately generate an action potential through muscle fiber
–ACh is quickly broken down by enzyme acetylcholinesterase, which stops contractions
myasthenia gravis
–disease characterized by drooping upper eyelids, difficulty swallowing and talking, and generalized muscle weakness
–Involves shortage of ACh receptors because person’s ACh receptors are attacked by own antibodies
–Suggests this is an autoimmune disease
Generation of an Action Potential Across the Sarcolemma
•Resting sarcolemma is polarized, meaning a voltage difference exists across the membrane
–Inside of cell is negative compared to outside
–Na+ and Ca2+ are high outside the cell and K+ is high inside the cell
•An action potential is caused by changes in electrical charges
•Action potentials occur in three steps
- End plate potential
- Depolarization
- Repolarization
- End plate potential
–ACh released from motor neuron binds to ACh receptors on sarcolemma
–Causes chemically gated ion channels (ligands) on sarcolemma to open
–Na+ diffuses into muscle fiber down its electrochemical gradient
•Some K+ diffuses outward, but not much
–Because Na+ diffuses in, interior of sarcolemma becomes less negative (more positive)
–This results in local depolarization called end plate potential
- Depolarization:
generation and propagation
of an action potential (AP)
–If end plate potential causes enough increase in membrane voltage to reach critical level called threshold, voltage-gated Na+ channels in membrane will open
–Large influx of Na+ through channels into cell triggers AP that is unstoppable and will lead to muscle fiber contraction
–AP spreads across sarcolemma from one voltage-gated Na+ channel to next one in adjacent areas, causing that area to depolarize
- Repolarization:
restoration of resting conditions
–Na+ voltage-gated channels close, and voltage-gated K+ channels open
–K+ efflux out of cell rapidly brings cell back to initial resting membrane voltage
Refractory period:
–muscle fiber cannot be stimulated for a specific amount of time, until repolarization is complete
–Ionic conditions of resting state are restored by Na+-K+ pump
•Na+ that came into cell is pumped back out, and K+ that flowed outside is pumped back into cell
Excitation-contraction (E-C) coupling:
- events that transmit AP along sarcolemma (excitation) are coupled to sliding of myofilaments (contraction)
- AP is propagated along sarcolemma and down into T tubules, where voltage-sensitive proteins in tubules stimulate Ca2+ release from SR
–Ca2+ release leads to contraction
•AP is brief and ends before contraction is seen
Channels Involved in Initiating Muscle Contraction
- Nerve impulse travels down axon of motor neuron
- When impulse reaches axon terminal, voltage-gated calcium channels open, and Ca2+ enters axon terminal
- Ca2+ influx causes synaptic vesicle to exocytose ACh into synaptic cleft
- ACh binds to receptors on sarcolemma, causing chemically gated Na+-K+ channels to open and initiate an end plate potential
- When threshold is reached, voltage-gated Na+ channels open, initiating an AP
- Voltage-sensitive proteins in T tubules change shape, causing SR calcium release channels to release Ca2+ into the cytosol
•At low intracellular Ca2+ concentration
–Tropomyosin blocks active sites on actin
–Myosin heads cannot attach to actin
–Muscle fiber remains relaxed
At higher intracellular Ca2+ concentrations
- Ca2+ binds to troponin
- Troponin changes shape and moves tropomyosin away from myosin-binding sites
- Myosin head is then allowed to bind to actin, forming cross bridge
Cycling is initiated
- causing sarcomere shortening and muscle contraction
- When nervous stimulation ceases, Ca2+ is pumped back into SR, and contraction ends
•Four steps of the cross bridge cycle
- Cross bridge formation: high-energy myosin head attaches to actin thin filament active site
- Power (working) stroke: myosin head pivots and pulls thin filament toward M line
- Cross bridge detachment: ATP attaches to myosin head, causing cross bridge to detach
- Cocking of myosin head: energy from hydrolysis of ATP “cocks” myosin head into high-energy state
•This energy will be used for power stroke in next cross bridge cycle
•Rigor mortis
–3–4 hours after death, muscles begin to stiffen
•Peak rigidity occurs about 12 hours postmortem
–Intracellular calcium levels increase because ATP is no longer being synthesized, so calcium cannot be pumped back into SR
•Results in cross bridge formation
–ATP is also needed for cross bridge detachment
•Results in myosin head staying bound to actin, causing constant state of contraction
–Muscles stay contracted until muscle proteins break down, causing myosin to release
