Unit 3 Flashcards
Skeletal Muscle
Attached to bones of the skeleton (controls body movement). Contract in response to signals from somatic motor neurons (can not initiate contractions on its own or by hormones). Has striations.
Cardiac Muscle
Found only in the heart (pump to move blood around the body). Striations.
Striated Muscle
Alternating light I bands and dark A bands. One pair of striations forms a sarcomere.
Muscle Fibre
A muscle cell.
Myosin
Contractile protein. A motor protein that consists of two coiled protein molecules (chains) that have two important parts (head and tail region) and is capable of converting chemical energy (ATP) into movement. These two regions are joined by a flexible hinge.
Actin
Contractile protein. Formed from two F-actin chains that are twisted together.
A Band
A region containing thick and thin filaments. The thick and thin filaments overlap at the outer edges of the A band. The center is occupied by thick filaments only. Anisotropic.
I Band
A region containing only thin filaments. A Z disc runs through the middle of an I band thus each half of the I ban is part of a different sarcomere. Isotropic.
M Line
A site of attachment for the thick filaments. The M line is the center of the sarcomere.
Contraction
When a muscle develops tension.
Sliding Filament Theory
At rest the ends of thick (myosin) and thin (actin) filaments overlap slightly within each sarcomere. Thick and thin filaments slide past each other with no change in the length of the filaments themselves. The thin (actin) filaments slide along the thick (myosin) filaments towards the M line of the sarcomere bringing the Z disks closer together resulting in a smaller I band and H band.
Troponin
Regulatory protein. Where Ca^2+ binds to.
Excitation-Contraction Coupling
The series of electrical and mechanical events in a muscle that leads to muscle contraction. Occurs through an action potential in the muscle membrane.
Transverse Tubules/T-Tubules
A series of branching tubes associated with the sarcoplasmic reticulum. The lumen is continuous with the ECF. It is closely associated with the terminal cisternae. Allows for rapid action potential diffusion into the muscle fibre.
ACh
Acetylcholine. Binds to nicotinic receptors on the motor end plate.
Acetylcholinesterase
Degrades ACh into acetic acid and choline.
Load
The demands/stressors.
Isotonic
A skeletal muscle contraction that creates force and moves a load. The load is usually constant and the muscle length changes.
Tetanus
A term for the state of a muscle when it reaches maximum force of contraction. Effects both slow and fast twitch muscles.
Complete/Fused Tetanus
Fast stimulation rate. Fibre does not have time to relax. No calcium exchange (muscle isn’t able to relax).
Incomplete/Unfused Tetanus
Slow stimulation rate. Fibre relaxes slightly between stimuli.
Fast Twitch Fibres
Two types. Type IIA which are oxidative-glycolytic fibres and Type IIX which are glycolytic fibres. Have a high threshold for stimulation (more neurons).
Calcium-Dependent Calcium Release
When the release of calcium from the SR is dependent on the concentration of calcium in the cytosol.
Myosin Light Chain Kinase (MLCK)
Phosphorylates myosin light chains.
Myosin Light Chain Phosphatase (MLCP)
Dephosphorylates myosin light chains.
Smooth Muscle
Primary muscle of internal organs and tubes ex. stomach, blood vessels, urinary bladder, and etc. Influences movement of materials through the body. No striations.
Tendon
Attaches skeletal muscle to bones by dense regular connective tissue (collagen).
Myofibril
The functional units of a skeletal muscle (proteins used for muscle contractions). Are contractile and elastic protein bundles. Occupy most of the space in a muscle fibre.
Thick Filament
Myosin (around 250 joined together, heads with heads and tails with tails).
Thin Filament
Actin, troponin, and tropomyosin.
Z Line
The site of attachment for thin filaments. One sarcomere is made of 2 Z discs and the filaments between them.
H Zone
Part of the A band. Is a region containing only thick filaments. The central region is lighter than the outer edges.
Crossbridge
The attachment of myosin to actin.
Relaxation
When the muscle is not contracting.
Myoglobin
An oxygen-carrying haeme protein.
Tropomyosin
Regulatory protein. Covers the binding sites for actin in skeletal muscle.
Neuromuscular Junction
The synapse between a somatic neuron and a skeletal muscle fiber.
EPP
End plate potential aka. skeletal muscle action potential.
Tension
Occurs when the muscle is contracting.
Isometric
A skeletal muscle contraction that creates force without movement. Muscle length is constant and the load is usually greater than the force that can be applied. Is done by the elastic elements (titin) stretching to take up force until they are fully stretched.
Summation
An increase in force generated by a muscle due to the repeated stimulation from action potentials that occur before the muscle has fully relaxed.
Phosphocreatine/Creatine Phosphate
A high energy phosphate molecule. It easily donates an inorganic phosphate to ADP to create ATP in a short amount of time but it is a limited supply.
Slow Twitch Fibres
Type I. Are oxidative fibres. Have a low threshold for stimulation (less neurons).
Calmodulin
A protein that activates MLCK.
Rigor State
When myosin is tightly bound to actin.
Sarcomere
A muscle cell (the basic contractile unit of a muscle fibre).
Calcium
An important ion in muscle contractions.
Skeletal Muscle Fibre Types
1) Slow Twitch Oxidative Fibers (Type I)
2) Fast Twitch Oxidative-Glycolytic Fibers (Type IIA)
3) Fast Twitch Glycolytic Fibers (Type IIB OR Type IIX)
Motor Unit
The basic unit of contraction in an intact skeletal muscle. Is composed of a group of muscle fibres of the same type (the number of fibres varies) and a somatic neuron that controls them. Contracts in an all-or-none fashion.
Recruitment
The force of contraction of a muscle is increased by using more motor units.
Muscle
Tissue specialized to convert biochemical reactions into mechanical work. Can only contract, cannot expand except when physically pulled by antagonistic muscle groups. Generate heat and contribute to body temperature homeostasis.
Muscle Functions
1) Motion
2) Force
Collagen
A protein arranged into cable-like fibers.
Epimysium
The outermost layer of a skeletal muscle fiber.
Fascicles
Bundles of muscle tissue covered by perimysium and bunches of fascicles are wrapped by the epimysium.
Perimysium
Covers fascicles (a connective tissue sheath).
Endomysium
Covers the muscle fibres.
Skeletal Muscle Structure
Outermost Layer
Epimysium
Perimysium
Fascicles
Endomysium
Muscle Fiber
Myofibril
Structure of a Muscle Fibre
1) Long, cylindrical cell.
2) Several hundred nuclei on the surface of the fibre.
3) Majority of space is taken up by the myofibrils.
4) Contains so many myofibrils that there is little room for other organelles.
5) Cytosol contains many glycogen granules (energy storage) and mitochondria (ATP synthesis).
Sarcolemma
The cell membrane of a muscle fibre.
Sarcoplasmic Reticulum (SR)
Specialized endoplasmic reticulum in muscle cells.
Terminal Cisternae
Concentrated portions of the sarcoplasmic reticulum. Is a sequester Ca^2+ (large [Ca^2+]).
Triad
One T-tubule with flanking terminal cisternae.
Sarcoplasm
The cytoplasm in a muscle cell.
Nebulin
Accessory protein. Aligns thin filament.
Titin
Accessory protein. Elastic protein that returns stretched muscle to a relaxed state. Helps maintain the health of the myofibril.
Contractile Proteins
Actin and myosin.
Regulatory Proteins
Troponin and tropomyosin.
Accessory Proteins
Nebulin and titin.
Filamentous
When G-actin (globular actin) subunits polymerize to form a chain of F-actin.
Muscle Tension
The force created by a contracting muscle whereas the load is a weight or force that opposes the contraction.
Sir Andrew Huxley and Rolf Niedeigerke (1954)
Observed that the length of the A band remains constant throughout muscle contraction. Came up with the sliding filament theory of contraction.
Excitation-Contraction Coupling Steps
1) ACh is released by the neuron into the synpatic cleft at the neuromuscular junction and binds to nicotinic cholinergic receptors on the motor end plate. The receptors are Na+/K+ channels.
2) The binding of ACh opens the channels. Both Na+ and K+ move across the membrane. ACh is removed by acetylcholinesterase. Na+ influx exceeds K+ efflux resulting in local depolarization occurring at the synapse called an end plate potential (EPP) aka an action potential.
3) The end plate potential (action potential) then moves down the T-tubule system. T-tubule membrane has dihydropyridine receptors (DHP receptors) which are L-type calcium channels (voltage-gated calcium channels). Depolarization changes the conformation of the DHP receptors. DHP receptors are mechanically linked to the Ca^2+ channels of the SR known as ryanodine receptors (RyR).
4) DHP receptors then changes RyR conformation which results in the opening of SR Ca^2+ channels (Ca^2+ leaves the SR). This increases cytosolic [Ca^2+].
5) Ca^2+ binds to troponin on the thin filament which moves tropomyosin into the on position revealing actin binding sites.
6) Myosin is now able to bind to actin and go through the crossbridge cycle.
CROSSBRIDGE CYCLE
1) Myosin head (only one) binds to actin at the actin binding site and forms a weak crossbridge.
2) The inorganic phosphate from a hydrolyzed ATP releases from myosin that causes the myosin head to pivot towards the centre of the sarcomere (power stroke). This pulls the thin filament towards the M line.
3) ADP releases from myosin resulting in myosin being tightly bound to actin (rigor state).
4) A new molecule of ATP attaches to the myosin head causing the crossbridge to detach. That molecule of ATP hydrolyzes and the cycle begins again until the binding sites on actin are blocked.
DHP Receptor
Dihydropyridine receptors.
RyR
Ryanodine receptors.
Skeletal Muscle Relaxation
Occurs when Ca^2+ is pumped back into SR by Ca^2+ ATPase. The decrease in [Ca^2+] in the cytosol causes troponin and Ca^2+ to unbind. The unbinding of Ca^2+ to troponin will shift tropomyosin into the off position and covers the binding site on the actin subunits of the thin filaments. Elastic elements (titin) pull filaments back to the relaxed position when myosin unbinds.
Hypertrophy
Myoblasts active and divide to repair tears in muscles resulting in muscle growth.
Creatine Kinase (CK)
Catalyzes the reaction of creatine phosphate and ADP to form ATP.
Twitch
A single contraction-relaxation cycle. The duration is determined by the rate of removal of Ca^2+ from the cytosol.
Latent Period
The short delay between the action potential and the beginning of the muscle tension. Overlaps with muscle fiber action potential (excitation-contraction coupling).
Oxidative Fibres
Usually appears red due to the presence of myoglobin. Are smaller than glycolytic fibres due to multiple mitochondria and are better vascularized (more blood vessels).
Muscle Tension Is Influenced By
1) The muscle type (fast twitch fibres can generate more tension).
2) The sarcomere length at the start of contraction.
Contraction of the Muscle Can Be Varied By
1) Changing the type of motor unit that is activated.
2) Changing the number of motor units that are active.
Single Unit Arrangement
Smooth muscle cells are coupled by gap junctions. It is not necessary to electrically stimulate each individual fibre (only one cell is required to receive the action potential). It is found on the walls of internal organs ex. blood vessels.
Multi-Unit Arrangement
Smooth muscle cells that don’t have gap junctions. Each individual muscle fibre is separately innervated (every cell needs to receive the action potential). Used for fine movement ex. iris of the eye and parts of reproductive organs.
Differences Between Smooth and Skeletal Muscle on Whole Muscle Level
1) Contraction of smooth muscle changes muscle shape not just length.
2) Smooth muscle develops tension (force) slowly.
3) Smooth muscle can maintain contraction longer without fatiguing. Important because some are contracted most of the time ex. internal bladder sphincter.
Differences Between Smooth and Skeletal Muscle on Cellular Level
1) Fibres are much smaller in smooth muscle than in skeletal muscle (about the same diameter as a single myofibril in a skeletal muscle fibre).
2) Actin and myosin are not arranged into sarcomeres thus no banding pattern (no striations).
3) Actin and myosin are arranged in long bundles diagonally around the periphery of the cell.
4) Actin is anchored at dense bodies. It is not attached to Z lines (there are no Z discs).
5) No T-tubules in sarcolemma and there is not much sarcoplasmic reticulum (SR).
6) Force of contraction is related to amount of Ca^2+ released.
Dense Bodies
Cell membrane structures in smooth muscle where actin is anchored.
Caveolae
Special vesicles in smooth muscle that are invaginations of the sarcolemma that are specialized for cell signalling.
Differences Between Smooth and Skeletal Muscle on Molecular Level
1) Less myosin per unit actin in smooth muscle than skeletal muscle.
2) Actin and myosin filaments are longer and overlap more in smooth muscle.
3) Myosin ATPase activity is much slower in smooth muscle.
4) Myosin heads are located along all parts of myosin molecule in smooth muscle.
5) There is no troponin in smooth muscle.
Ca^2+ Enters From Extracellular Fluid (ECF) Through
1) Voltage-gated Ca^2+ channels (open when cell depolarizes).
2) Stretch-activated channels (open when membrane is stretched).
3) Chemically-gated channels (open in response to hormones).
Smooth Muscle Contraction
1) Signal to initiate contraction (increase in cytosolic Ca^2+). Ca^2+ enters from extracellular fluid (ECF) and results in release of SR Ca^2+.
2) Ca^2+ binds to calmodulin (CaM) in the cytosol.
3) Ca^2+/CaM activates the enzyme myosin light chain kinase (MLCK).
4) MLCK activates myosin by phosphorylating the light chain of the myosin molecule in the head using energy and Pi from ATP. This ATP is used to activate the myosin through phosphorylation (not for crossbridge cycling).
5) The phosphorylated myosin (active) can now interact with actin and go through crossbridge cycling and allow contraction to occur in the smooth muscle cell (MLCK uses the Pi from ATP to activate myosin, turn it on, but additional ATP is needed to go through crossbridge cycling for contraction to occur).
Myosin is Not Phosphorylated
ATPase activity is blocked.
Myosin is Phosphorylated
ATPase activity is active.
Ca^2+-Na+ Anti-Port
Passively transports Ca^2+ out of the cell against the concentration gradient by taking advantage of Na+ entering with its concentration gradient (no ATP).
Ca^2+-ATPase
Actively transports Ca^2+ out of the cell (requires ATP).
Relaxation in Smooth Muscle
1) Ca^2+ is removed from the cytosol (goes back into the SR or leaves the cell).
2) Decrease in Ca^2+ levels in the cytosol causes Ca^2+ to unbind from calmodulin (inactivates MLCK).
Latch State
Used to describe how the dephosphorylation of myosin does not automatically relax the muscle. Tension is maintained (myosin remains bound to actin) but with minimal ATP consumption.
Myocardial Cells
Cardiac muscle cells. Majority are striated muscle (contractile fibres are organized into sarcomeres). Are much smaller than skeletal muscle cells with a single nucleus and with about 1/3 of the cell volume being occupied by mitochondria. The T-tubules are much larger and branched and the sarcoplasmic reticulum (SR) is smaller. Adjacent cells are joined by intercalated discs with desmosomes.
Autorhythmic/Pacemaker Cells
The 1% of cardiac muscle cells that are not involved in contraction. They are not striated (no sacromeres). They are involved in the electrical excitation of the heart and are known as the electrical conduction system of the heart. They initiate heartbeats and allow the electrical excitation to spread rapidly throughout the heart. They are connected to other cardiac cells via gap junctions.
Cardiac Muscle Contraction
Very Similar to Skeletal Muscles EXCEPT
1) Calcium enters through external Ca^2+ channels triggering calcium-induced calcium release from the SR (the SR calcium provides around 90% of that needed for contraction).
2) Ca^2+ leaves the cytosol via Na+/Ca^2+ antiport and Ca^2+-ATPase.
3) Exhibit graded (NOT all-or-none) contractions (the force generated is proportional to the number of active crossbridges). The number of active crossbridges is proportional to cytosolic [Ca^2+], therefore, the force generated is proportional to cytosolic [Ca^2+].
Factors Influencing Cardiac Muscle Contraction Force
1) Changes in [Ca^2+]
—> Regulated by epinephrine and norepinephrine (binds to and activates β1 adrenergic receptors (G Protein Couple Receptors) which activates cAMP second messenger signalling pathway that leads to):
——> Phosphorylation of voltage-gated Ca^2+ channels (increases the probability of the channel to open, increases [Ca^2+] in the cytosol).
——> Phosphorylation of phospholamban (leads to increase SR Ca^2+-ATPase activity, increases SR Ca^2+. Overall, results in a more forceful contraction and a shorter duration of contraction).
2) Sarcomere Length
—> Tension generated is proportional to length of muscle fibre (due to degree of overlap between actin and myosin).
—> Stretching a myocardial muscle cell may also allow more Ca^2+ to enter through cell membrane Ca^2+ channels, contributing to a more forceful next contraction.
Cardiac Muscle Action Potential
Phase 4 - Resting Membrane Potential (-90 mV).
Phase 0 - Depolarization (the AP opens voltage-gated Na+ channels causing a rapid increase in membrane Na+ permeability (close again)).
Phase 1 - Initial Repolarization (open fast K+ channels allow initial repolarization).
Phase 2 - The Plateau (initial depolarization triggers voltage-gated Ca^2+ channels to slowly open causing an increase in Ca^2+ permeability and the fast K+ channels close).
Phase 3 - Rapid Repolarization (the Ca^2+ channels close and the slow voltage-gated K+ channels open (triggered by the initial depolarization) and the resting stage ion permeability is restored (Phase 4)).
