Muscle Flashcards
What Ca2+ pours into when a signal initiated in CNS triggers an AP (can increase in frequency if nerve impulse’s does) in alpha motor neuron that opens the voltage-gated Ca2+ channel
Presynaptic nerve terminal (bouton)
Where Ca2+ pours into when increased Ca2+ triggers exocytosis of stored vesicles containing ACh
Synaptic cleft
Where Ca2+ pours into when increased Ca2+ triggers exocytosis of stored vesicles containing ACh
Synaptic cleft
Once ACh attaches to it, this acts as a ligand-gated nonselective cation channel that allows Na+ & K+ to pass through and depolarizes the postsynaptic membrane
Nicotinic ACh receptor
The resulting local depolarization that spreads to the nearby plasma membrane and triggers a muscle AP which propagates down the T-tubules and causes contraction
End-plate potential (EPP)
This enzyme rapidly hydrolyzes ACh to acetate & choline in the basal lamina
AChE
Transports choline into the presynaptic terminal where choline is then used as a substrate for new ACh synthesis
Choline acetyltransferase
When excess ACh is released for triggering muscle AP to ensure that the muscle AP will always be triggered when the nerve AP reaches the presynaptic terminal
Safety factor
Where a muscle AP is generated on the sarcolemma by the nerve AP transmission of chain events
Motor end plate (neuromuscular junction)
Propagates along the cell surface and reaches deeper inside the myofiber via invaginations of sarcolemma called T-tubules (transverse-tubules) and opens voltage-gated NA+ channel in it linked to Ca2+ channels in terminal cistern
Muscle AP
Propagates along the cell surface and reaches deeper inside the myofiber via invaginations of sarcolemma called T-tubules (transverse-tubules)
Muscle AP
Part of the sarcoplasmic reticulum (SR), it flanks each side of a T-tubule (this is a triad)
Terminal cisternae
Voltage-gated L-type Ca2+ channels activated when the T-tubule is depolarized and allows extracellular Ca2+ to enter the sarcoplasm
DHPRs (dihydropyridine receptors)
A Ca2+ channel on the SR membrane opened mechanically by an open DHPRs and allowing large amounts of Ca2+ stored in the SR to enter the sarcoplasm, increase Ca2+, & initiate muscle contraction. Thus, skeletal muscle won’t need to rely on extracellular Ca2+
-in terminal cisterna
Ryanodine receptor (RYR)
Troponin T - binds to tropomyosin
Troponin I - binds to actin inhibiting contraction
Troponin C - binds to Ca2+ acting as the regulatory element of Troponin complex
Troponin
Has 6 protein subunits, 2 myosin heavy chains form a long helical ‘tail’ and 2 globular ‘heads’.Tail points toward the center of sarcomere to form the M line while the head points to the ends to form the Z disk.
Myosin
A very large protein that links the thick myofilament to the Z disks, contributing to the strength & elasticity of the sarcomere.
Titin
Actin filaments insert into the Z disk by binding to this
Alpha actinin
A specialized plasma membrane region where intermediate filament protein linked Z disks are between. It contains integrin membrane proteins that bind to extracellular matrix proteins (laminin, fibronectin).
Costamere
A thick filament that doesn’t change in width throughout the contractile cycle when the sarcomere shortens
A band
A non-overlapping region of thin filament that narrows when the sarcomere shortens
I band
Non-overlapping region of thick filament that narrows when the sarcomere shortens
H zone
Thick and thin filaments slide past each other when sarcomere shortens, pulling the 2 adjacent Z lines closer
Sliding filament theory/ model
Hydrolyzes the new ATP and cocks the head
Myosin ATPase
A pump using one molecule of ATP to transport 2 Ca2+ molecules into the SR lumen and is the main Ca2+ reduction mechanism distributed throughout the SR membrane.
Sarcoplasmic & endoplasmic reticulum Ca2+ ATPase (SERCA)
Helps buffer Ca2+ in the SR which allows a large amount of Ca2+ to be stored inside the SR.
Ca2+ binding proteins (calsequestrin)
2 transporters on the sarcolemma that are the 2nd mechanism to reduce Ca2+
Na/ Ca2+ exchanger & plasma membrane Ca2+ ATPase
Caused by stretching of various structural elements of the muscle
Passive tension
Occurs during the increase (to a certain point) of tension of a muscle due to the shortening of sarcomere while the muscle length is fixed (muscle length variation = contraction force variation)
Isometric contraction
Causes the length of the whole muscle to change while the tension of the muscle stays the same
Isotonic contraction
The length at which the maximum force is generated, length beyond this point decreases the contraction force
Optimal length
When sarcomere length gets too long and the thick & thin filaments are no longer overlapped, preventing crossbridge formation to occur (insignificant compared to cardiac muscle preload)
Length-tension relationship (preload)
How fast a muscle shortens at zero load which depends on the rate of crossbridge cycling (depending on the muscle being white or red)
Maximum velocity (y-intercept)
The load at which the shortening velocity is at its lowest and cause isometric contraction (zero muscle shortening)
Maximum load (X-intercept = initial length)
A contraction at loads higher than the maximum load while muscle lengthens
Eccentric contraction
Contraction that starts before the muscle fully relaxes from previous contraction
Tetanus
When the muscle has a chance to relax before being stimulated to contract further while in a complete tetanus, the muscle never relaxes until the stimulation ends
Incomplete tetanus
Frequency summation, temporal summation, or summation from incomplete tetanus
AP frequency change
A Method for changing the force of muscle contraction where more motor neurons are stimulated to participate in the contraction by sending APs to muscle fibers they innervate when more force is needed.
Recruitment
The smaller motor units will be recruited 1st before larger motor units are recruited when more force is needed (spatial summation)
Size principle
Muscles lengthen by adding more sarcomere in series, which increases their length and allows them to shorten more and with a faster velocity
Growth
Increase the # of myofibrils in each muscle cell parallel and increase the maximum force that the muscle can achieve without affecting shortening length or velocity
Hypertrophy
Increase the # of myofiber in each muscle in parallel and increase the maximum force that the muscle can achieve without affecting shortening length or velocity
Hyperplasia
Parallel running mechanorecptors located in the muscle that sense the length and the rate of stretching (triggers AP) of the muscle
Muscle spindles
Senses the tension of the muscles in the tendons of muscles and sends the information to the brain. It’s involved in Bisynaptic reflex arc (Inverse myotatic reflex) that prevents muscle injury by inhibiting the contraction of that muscle. This can also be seen in a reflex seen in some patients called clasp-knife reflex.
Golgi tendon organs (GTOs)
Random contractions of the muscle fibers occurring when ACh from presynaptic terminals of the damaged nerve is released
Fasciculation
Develops several days after as a result of hypersensitivity to ACh (denervation hypersensitivity) due to the spreading of AChR from motor end plate throughout the membrane and manifests as contractions of the muscle.
Fibrillation
Caused by denervation of an affected muscle. Can be reversed if reinnervation occurs within a few months. If reinnervation doesn’t occur the muscle will be replaced by adipose & fibrous tissues (contracture).
Atrophy
Picking up EMG (not pathognomonic) using 2 electrodes to detect electrical potential differences.
Compound muscle action potential
A pathway for ATP synthesis in muscle cells that uses creatinine phosphate (cp) by converting between cp and ATP. It’s reversible.
Phosphagen system
Catalyzes the short conversion of CP to ATP
Creatine kinase
Glucose + 2ATP -> 6CO2 + 6H2O + 40ATP
Oxidative phosphorylation
Decline in muscle contraction and speed due to changes in the CNS that is related to motor control
Central fatigue
Decline in muscle contraction strength and speed due to abnormal transmission of motor command from the motor neuron to the muscle that could be a defect in the motor nerve or the neuromuscular junction
Neuromuscular fatigue
Decline in muscle contraction strength and speed due to something inside the muscle itself such as accumulation of metabolites, depleted SR Ca2+ store, diminished energy substrates
Muscular fatigue
Contains myosin ATPase that hydrolyzes ATP at a fast speed
White fiber (quick burst of power)
Fast oxidative fiber that’s not very susceptible to fatigue but can contract with a faster speed and stronger contraction than type I fibers, utilizing larger motor neurons forming larger motor units.
Type IIa (postural stability)
Fast glycolytic fiber that’s very susceptible to fatigue but can contract with a faster speed and stronger contraction than type I fibers, utilizing larger motor neurons forming larger motor units.
Type IIb (postural stability)
Actin is anchored by it instead of Z discs located in both the cytoplasm and the plasma membrane.
Dense bodies
Small invaginations of the plasma membrane that serve as the equivalent of T-tubules
Caveolae
A series of swelling where neurons synapse onto smooth muscle cells at multiple sites
Varicosities
Contract independently of its neighbors due to the lack of electrical connection via gap junction. They need neurons that provide fine control to the iris, the ciliary muscles, the vas deferens & the piloerector muscles.
Multiunit smooth muscle
Electronically coupled myocytes coupled via gap junctions to perform functional syncytium by the diffusion of ions (and depolarization) for coordinated but less specific contraction of the urinary bladder and GI
Unitary smooth muscle
Maintain a level of contractile force for sphincters, airways, and blood vessels
Tonic smooth muscles
Contract rhythmically or transiently upon stimulation for the GI, urinary bladder, & uterine wall
Phasic smooth muscle
Can be simple spike, post plateau spike, or slow wave and it’s depolarization relies on Ca2+ current (slower) instead of Na+
Smooth muscle APs
Post stretch-causing initial contraction gradual relaxation
Stress relaxation
Step1 it enters through voltage-gated channels on the membrane
Extracellular Ca2+
Step2 it’s released by the binding of Ca2+ RYR (ryanodine receptor), Ca2+ induced Ca2+ release
Sarcoplasmic Ca2+
Step3 it’s released from SR by inositol triphosphate (IP3), why the muscle can contract without a change in membrane potential.
2nd messenger-mediated Ca2+
Site on the myosin molecule
Smooth muscle regulatory site
A Ca2+ binding molecule in the cytoplasm that’s closely related to Troponin C that increases when 4 Ca2+ bind to it
Calmodulin
It binds to and activates an enzyme called myosin light-chain kinase (MLCK)
Ca2+-calmodulin complex (CaCM)
Phosporylates the regulatory light chin on the neck of myosin which causes confirmational change of the myosin molecule and increases its ATPase activity, allowing it to form crossbridge and the concentration to occur (slow rate myosin ATPase activity)
Myosin light-chain kinase (MLCK)
Enzyme required for muscle relaxation by dephosphorylation of the regulatory light chain of myosin
Myosin light-chain phosphatase (MLCP)
Can sustain tonic muscle at a high level of tension while keeping the energy expenditure low
Latch state
