Quiz 5 (Section 2 Quiz 2) Flashcards
which of the following are true statements about cross-bridge cycling?
-the power stroke propels the actin filaments towards the center of the sarcomere
-ATP hydrolysis is the source of energy that cock the myosin head to prepare for the power stroke.
which of the following are properties of slow muscle fibers (Type 1)?
-muscles with a large proportion of slow muscle fibers have functions which require sustained muscle contractions
-slow muscle fibers rely primarily on oxidative metabolism for energy generation.
which of the following are ways to increase the force produced by a muscle?
-recruitment of a greater number of muscle fibers
-recruitment of larger motor units
-increasing the frequency of muscle contraction
-fober hypertrophy through resistance trianing
which of the following are true statements about acetlycholine (ACh)?
acetylcholine is the neurotransmitter responsible for sending signals across the neuromuscular junction.
muscle action potentials:
-can travel down the T-tubules into the center of the muscle cell
-are an all-or-none phenomenon
which of the following are true statements about excitation-contraction coupling?
-an end plate potential is formed when sodium ions enter the muscle cell through ACh-gated ion channels
-opening of the ryanodine-receptor channel (RyR) is triggered by the conformational change of the dihydropyridline receptor (DHPR)
-calcium ions bind to troponin to expose the mysoin-binding sites on actin
muscle contraction =
sacromere shortening
mysoin
thick filament
protein that is the main contractile machinery for sacromere shortening
actin
thin filament
protein that myosin “walks” along during sacromere shortening
myosin heads:
pivot on their hinges during contraction. [balls]
myosin tails:
wraps together with other tails to form the body of the thick filament [cocks]
ATP binding site
the myosin heads act as a ATPase enzyme and converts ATP to ADP to release energy for contraction
Actin binding site
the myosin heads bind and unbind to actin during contraction
tropomyosin:
protein wrapped spirally around the F-acting (double helix filament structure)
Troponin:
complexes of 3 protein subunits attatched intermittently to tropomyosin. regulatory protein can shift the position of the tropomyosin relative to the F actin
when muscle is at rest
the tropomyosin blocks the myosin binding sites on each of the G actin
each troponin has a binding site for calcium ions
describe muscle contraction:
- the tropomyosin and troponin block the myosin binding sites on the actin.
- the calcium ions bind to the troponin and the troponin-tropomyosin shift to expose the myosin binding sites.
- ADP attaches and contracts the muscle
sarcoplasmic reticulum:
-specialized reticulum in muscle fibers
-similar to smooth endoplasmic reticulum in other cells
-stores calcium ions in high concentration
-releases calcium into sarcoplasm in response to muscle action potential
when myosin walks along actin it:
brings the Z disks closer to the M line. this is sarcomere shortening which shortens the overall muscle/is muscle contraction
cross bridge cycling will continue until:
-muscle cell runs out of ATP
-low calcium ion concentration causes tropomyosin to once again block cross bridge formation
-load on the muscle becomes too great for further pulling to occur
-ends of myosin filament hit the z disk
work:
performed when a muscle moves a load.
W = L * D
work output = load * distance of movement
energy:
-comes from chemical reactions in muscle cells
-is transferred from the muscle to the external load to lift or move it
uses of energy in the muscle:
primary use: ATP is necessary for cross bridge cycling to generate contractile force
-ATP to pump calcium ions from the sarcoplasm into the sarcoplasmic reticulum after the contraction is over
-ATP to run the Na+/K+ pumps to maintain ionic concentration gradients for muscle action potentials
sources of energy for contraction:
-Free ATP in the muscle cells (very low concentration). only sustains for 1-2 seconds
-phosphocreatinine: low concentration, cleaved to release energy for bionding phosphate ion onto ADP to reconstitute ATP, can sustain for 5-8 seconds
-glycolysis: breakdown of glycogen stored in muscle cells. used to reconstitue both ATP from ADP and phosphocreatinine after it was depleted too. occurs in absence of oxygen. leads to build up of byproducts (pyruvic and lactic acid). can susatin for 1 min.
-ocidative metabolism: combines oxygen with cellular foodstuffs. used to reconstitute ATP and phosphocreatinine. sustain for many hours. responsible for more than 95% of energy used by the muscles fpr long term contraction.
velocity of contarction is maximal when
there is no load on the muscle
as load on the muscle increases,
volocity of contrtaction decreases. net force available to shorten muscle is reduced
when muscle load increases to the maximum muscle force,
no shortening occurs, velocity is zero.
muscles vary in:
-size/length (1mm-50cm)
-muscle fiber diameter (10-80 micrometers)
-contraction energetics
-contraction time course
slow fibers (type 1, red muscle):
-small fibers
-innervated by smaller neurons
-more extensive blood supply
-higher numbers of mitochondria
-more reliance on oxidative metabolism
-large amounts of myoglobin
-reddish appearance
fast fibers (type 2, white muscle):
-large fibers
-extensive sarcoplasmic reticulum for rapid Ca+2 release
-less extensive blood supply
-fewer mitochondria
-large amounts of glycolytic enzymes to support glycolysis; oxidative metabolism is secondary
-low myoglobin gives whitish appearance
motor neurons:
innervate muscle cells.
-cell body: in the spinal cord
-axon: extends through the peripheral nerve to the muscle target. the axon branches to terminate on several muscle fibers (cells)
motor unit:
a single motor neuron and all the muscle fibers it innervates.
-the motor unit functions together as a group
-number of muscle fibers per motor unit varies: on average 80-100 per unit, small muscles with precise control have 2-3 per unit, and large muscles with coarse control have several hundred muscle fibers per unit
muscle twitch:
muscle contraction generated by a single action potential
force summation:
adding together individual twitch contractions to increase the intensity of overall muscle contraction. multiple fiber summation and frequency summation.
multiple fiber summation:
increasing muscle force by increasing the number of motor units contracting simultaneously.
size principal
-smaller motor units are recruited first by the central nervous system.
-larger and larger motor units are recruited successively
force production
large motor units produce more force than smaller units. small increments of force during weak contraction.
large increments in force during strong contraction.
frequency summation:
increasing muscle force by increasing the frequency of contraction. low frequency: muscle contraction fully relaxes between individual twitches. as frequency increases, the new contraction happens before the preceding contraction is fully relaxed. total strength of contraction rises.
tentanization:
the process through which successive muscle contractions fuse together, such that the overall contractions become smooth and continuous. results in tetany or tetanic contraction. tetanus frequency = 35-50 Hz
muscles can change in:
diameters, lengths, strength, vascular supplies, proportions of muscle fiber types
muscle hypertrophy:
an increase of the total mass of a muscle.
-almost always due to fiber hypertrophy(increase in the number of myosin and actin filaments, causing enlargement of the muscle cells). sometimes results in the splitting of myofibrils to form new myofibrils
hyperplasia of muscle fibers:
an increase in the number of muscle fibers within a muscle.
-occurs through linear splitting of previously enlarged muscle fibers.
-rare, only in response to extreme muscle force genration
when a muscle is stretched to greater than normal length:
new sarcomeres are added to the ends of the myofibrils
when a muscle is continually shortened below normal length:
sarcomeres at the ends of the myofibrils disappear
muscle atrophy:
decrease of the total mass of the muscle.
-occurs when the muscle remains unused for many weeks
-rate of degradation of contractile proteins is greater than rate of replacement
denervation atrophy:
muscle atrophy that occurs when a muscle loses its nerve supply. if it is repaired quickly, can return to muscle function within months. is muscle remains denervated for >1 year, can never restore the muscle function. these muscle fibers are destroyed and replaced with fibrous tissue.
neuromuscular transmission:
how the signal travels from the motor neuron to the muscle cell
excitation-contraction coupling
how changes in muscle fiber membrane potential lead to muscle contraction
motor neural pathway:
motor cortex -> medulla oblongata -> CNS pathway -> spinal cord segment -> muscle fibers
motor unit:
a single motor neuron and all the muscle fibers it innervates. functions together as a group. motor neurons and cel bodies in the spinal cord and axons in the peripheral nerves. after entering the muscle belly, the neuron branches to terminate on several muscle fibers (from three to several hundred)
neuromuscular junction
where each nerve makes a special synapse with the muscle fiber. junction between the motor neuron and the muscle cell.
-has the synaptic space/ cleft: space between the cel membranes 20-30 nm.
-sub neural clefts: increase surface area for neurotransmitter to act midpoint of the muscle fiber.
synapse:
structure that enables signal transmission from one neuron to the next, or from a neuron to a target cell, typically through the use of chemical messengers (neurotransmitters)
how does a signal travel:
pre-synaptic neuron -> post synaptic neuron/cell/organ
motor end plate:
portion of the muscle fiber that receives neural input and generates muscle action potentials leading to muscle contraction.
synaptic transmission:
process by which one neuron communicates with another or with a muscle cell.
-involves conversion of an electrical signal into a chemical signal then back to an electrical signal: 1. electrical signal 1 (neural action potentials), 2. chemical signal (neurotransmitters), 3. electrical signal 2 (muscle action potential)
acetylcholine
the neurotransmitter which travels from the motor neuron, across the synapse, to excite the muscle fiber membrane.
steps for acetylcholine:
- ACh is synthesized and stored
- ACh is released by the pre-synaptic motor neuron and travels through synapse
- ACh binds to receptors on post-synaptic muscle fiber
- ACh binding leads to muscle action potential, followed by muscle contraction
- ACh is degraded to remove it from the synapse
where is acetylcholine made?
in the axon terminals
acetylcholine secretion by nerve terminals:
- axon potential travels down neuron to axon terminal
- axon depolarization opens voltage-gated Ca+2 channels
- Ca+2 ions enter cell
- Ca+2 ions trigger a kinase cascade that leads to fusion of ACh vesicles with the presynaptic membrane. the ACh vesicles dock at release sites and duse with plasma membrane
- ACh is released into synapse through exocytosis
- ACh diffuses across the synaptic cleft toward the muscle cell membrane.
where does acetylcholine bind?
to acetlycholine receptor on acetylcholine-gated ion channels on muscle cell. leads to conformational change that opens the channel.
what does acetylcholine do?
allows a lot of Na+ ions to enter into the sarcoplasm. any positively charged ions flow in the cell but more sodium than any other ion. leads to depolarization of the muscle fiber membrane.
end plate potential= local potential:
local potential is the graded potential. small local changes in membrane potential due to a stimulus. can vary in amplitude. can trigger an action potential if it surpasses a sufficient threshold. action potential will propagate across muscle membrane. local potential is different to action potential
acetylcholinesterase:
enzyme that rapidly destroys ACh in the synapse. it splits ACh into acetate ion and choline. the choline is reabsorbed into the neural terminal for recycling.
ACh recycling:
formation of new vesicles happens at the axon terminal
transverse tubules (t-tubules):
internal extensions of the plasma membrane that run transverse to (across) myofibrils. open to the exterior of the cell. allow action potential to spread into center of cell
sarcoplasmic reticulum:
stores Ca+2 ions that are composed of terminal cisternae and longitudinal tubules
terminal cisternae:
large chambers that store Ca+2 ions in high concentration, immediately adjacent to T-tubules
longitudinal tubules:
long tubules that surround all surfaces of the myofibrils
how to t-tubules and sarcoplasmic reticulum run?
adjacent to one another at triads
dihydropyridine (DHP) receptors:
voltage sensitive receptors within t-tubules. triggered by action potentials traveling in the t-tubule
ryanodine receptor channels (RyR):
channels in the membrane of the sarcoplasmic reticulum. calcium release channels. triggered to open by activation of DHPR. release Ca+2 into sarcoplasm, leading to contractoin
excitation-contraction coupling:
process through which an action potential triggers muscle contraction.
- ACh binds to receptors on muscle cell, leading to end plate potential
- end plate potential triggers action potential
- action potential travels across plasma membrane and into t-tubule
- voltage change sensed by DHP receptor
- conformational change of DHP receptor leads to opening of RyR in sarcoplasmic reticulum
- sarcoplasmic reticulum releases Ca+2 ions into sarcoplasm
- Ca+2 binds to troponin which leads to actin myosin binding and cross bridge cycling
calcium ions must be removed from the sarcoplasm to stop muscle contraction
sarcoplasmic reticulum Ca+2 -ATPase (SERCA)
continually active calcium pump in walls of sarcoplasmic reticulum. moves Ca+2 from sarcoplasmic reticulum against its concentration gradient
calsequestrin
calcium binding protein inside sarcoplasmic reticulum which can bind and store calcium
