Muscle Physiology- Keagan Flashcards
How is cytosolic calcium removed in skeletal muscles and cardiac muscles
Skeletal muscle- SERCA only
Cardiac muscles- SERCA and Na/Ca exchanger
SERCA= sarco-endoplasmic reticulum Calcium ATPase
Magnitude of Calcium release in skeletal muscle vs cardiac muscle
Ca induced Ca release from sarcoplasmic reticulum in both
Skeletal muscle- magnitude of SR calcium release can not be altered
Cardiac muscle- magnitude ca be altered
Gap junctions between cells in skeletal vs cardiac muscles
Skeletal- absent
Cardiac- present- AP can travel from cell to cell
Skeletal muscle functions
Move skeleton
Posture/maintenence
Soft tissue support/internal organ protection
Respiration/voluntary control of digestive and urinary tracks
Body temp regulation
Properties:
Excitability
Contractability
Elasticity
What is a motor unit
Alpha motor neuron and all the muscle fibers that supplies it
Postural muscles w tonic contractions= thousands of muscle fibers in motor unit
Smaller muscles/quick response= 1-10 muscle fibers
Lesion of motor unit= paralysis/atrophy
The only adequate stimulus for skeletal muscle is __
Nervous impulse
Each muscle fiber is a single ____ cell
Multi nucleaated
Three components of actin and what they do
Actin- two strands
Tropomyosin- cover myosin binding sites on actin
Troponin- Ca regulator- detects Ca and will tell tropomyosin to leave
Desmin
Rod/ column looking thing that holds Z line to sarcolemma
Myofibrillar myopathies
Dystrophin
Poly peptide chain/rope looking thing
Holds thick filaments to proteins within sarcolemma
Duchennes muscular dystrophy
Titin
Disease?
Thick filament to Z line
stabilize the thick filament, center it between the thin filaments, prevent overstretching of the sarcomere, and to recoil the sarcomere like a spring after it is stretched.
Dilated cardiomyopathy
What enzymes aid in Ach synthesis and degradation
CAT (choline acetyltransferase)- synthesizes (choline+ acetyl CoA= Ach)
ACE (acetylcholinesterase)- degrades (Ach= choline + acetate)
Explain what prevents and allows neurotrasmitter exocytosis
Before AP- presynaptic vesicle is filled with NT docks- exocytosis impossible
Ca enters= synaptoagmin (regulatory protein/Ca regulator) changes positioning
This change forces the fusion of vesicles to cell membranes= exocytosis
Myasthenia Gravis
chronic autoimmune disorder
weakness and rapid fatigue of voluntary muscles.
Immune system creates antibodies that block, destroy or alter Ach receptors= less muscle contraction
Tensilon test
Tests for Myasthenia Gravis
- injects Tinsilon (acetylcholinesterase inhibitor) that doesnt break down Ach in NMJ
-this increases Ach in NMJ
If muscle strength improves=positive for myasthenia Gravis
How does botulinum toxicity affect action potentials
Botulinum toxicity inhibits the release of Ach from presynaptic nerve
Organic Phosphates poisoning
Organophosphate pesticide blocks ACE which prevents Ach breakdown
Myorelaxants
Cause myorelaxation by blocking the NMJ
What is a Twitch and its phases
Twitch- muscle contraction caused by single AP
1. Latent period- excitation- contraction/no tension
2. Period of contraction- x bridges are forming- tension rises/muscle shortens
3. Period of relaxation- calcium return to SR, tension decrease/ muscle length to normal
Stages of excitation contractions coupling
- AP spreads along sarcolemma and inside T-tubules
- Dihydropyridine receptors (voltage sensors) open VG Ca channels (Ryanodine receptors)
- Ca released into sarcoplasm from cisterns
- Ca binds to C-subunit of troponin
- Myosin binding site son actin are uncovered= ready to contract
Eaton-lambert myasthenia (ELM)
Antibodies destroy VG Ca channels in presynaptic nerve
Decreases Ca influx= decrease Ach release
Failure of neuromuscular transmission and muscle weakness
Malignant Hyperthermia
Genetic defect of ryanodine receptor (aids in release of Ca into sarcoplasm)
Causes sustained muscle contractions, excessive O2 consumption and CO2 production, acidosis, hyperthermia
Huxley-Hanson theory
Myofibrils contracted due to contraction of a lot of sarcomeres
Length of actin and myosin don’t change
Contraction is due to actin filamanets sliding along myosin filaments
Proces requires ATP
What is rigor mortis
The state of muscle rigidity that develops after death
Muscle fibers depleted of ATP= no relaxation
Almost all myosin heads fixed to actin
Metabolic myopathies are a group of genetic disorders that compromise ____
ATP production
Total Tension= __ + __
Passive Tension + Active Tension
Passive- force generated due to stretch without contraction
Active- force generated by sliding of microfilaments proportional to number of active cross-bridges
What creates a plateau in the level of force from a muscle
Max number of cross bridges
What is Tetanus- complete and incomplete
Tetanus- result of summation of many contractions occurring in rapid succession- effects of previous contractions are still remaining before next occurs
Incomplete- stimulation is reduced- results in jerky contraction-relaxation of cycles (wavy)
Complete- sustained muscle contraction (straight)
Clostridium tetanus
Toxin clostridium tetanus blocks release of inhibitory NTs (GABA/glycine) by Renshaw Cells
Results in repetitive stimulation of motor neurons= increased intracellular calcium= sustained muscle contraction= TETANUS
Ex. Lock jaw
Isometric muscle contraction
No change in length/ no movement
Isotonic
Movement of muscle and joint- change in length of muscle
Structural peculiarities of smooth muscle
No sarcomeres
No T-tubules- but small caveoli
Not well developed SR (high dependence of ECF calcium
1/5 myosin of skeletal muscle
Longer myosin
Single unit v multi unit
Applies to smooth muscle
Single unit- cells connected by gap jxns- muscle contracts as one whole unit (Uterus, bladder)
Multi unit- each muscle cells behaves as separate cell- fast response to stimuli (muscles of iris)
Cholecytokinin stimulates contraction of __
Gall bladder
Vasopressin and Angiotensin II stimulate contraction of __
Blood vessels
Sildenafil enhances effect of ___ in ___
Enhances effect of nitric oxide (NO) in corpus cavernosum
Nervous supply to smooth muscles
-supplied by __
- nervous endings form, __
-NT released into __
- supplied by PNS/SNS
-no synapses-nerve endings form varicosities
-NTs released into extracellular fluid
AP spreads to other cells along gap jxns
Smooth muscle differences in excitability
Threshold is lower
AP amplitude is lower/longer
Depolarization opens up VG calcium channels, Ca influx slows repolarization
Automaticity
The ability of cell to generate AP without any external stimuli
Smooth muscle slowly permeable to Na= depolarization w/o AP
Smooth muscle Actin and myosin differences
-thin filament doesn’t have troponin
-myosin binding sites are always ready
-myosin heads are inactive at rest
Excitation-contraction coupling in smooth muscle- how do differences Ca channels open
From extracellular space:
-VG Ca channel- open change in membrane potential
-ligand-gated- NT binding opens
-mechanical sensitive Ca channel- open in response to stretch stimulus
From SR
- chemical stimuli (NT, hormone,drug) bind to receptor on cell membrane—> cause intracellular formation of IP3–> IP3 bind to sarcoplasmic receptors to stimulate Ca release
-Ca-induced calcium release- Ca from outside comes in and opens intracellular Ca channel
Cross-bridge cycling- smooth muscle
thick filament regulation
Cytoplasmic Ca bind to calmodulin (CaM)-
Ca-calmodulin complex binds to myosin light chain kinase (MLCK) and activates it
Active MLCK catalyzes phosphorylation of myosin light chain on myosin head
This causes conformational change that enables myosin to bind to actin
Limiting factor that causes SM X-bridge to be slow
ATPase is slow
To stop cycle, the head must be dephosphorylated
The latch phenomenon
If myosin head is inactive (dephosphorylated) while attached- cycle is finished VERY SLOWLY
-keeps smooth muscle partially contracted for low ATP cost
Allow smooth muscle to stay contracted for long time
Why is the range length greater in smooth muscle?
Thick filaments are longer that skeletal muscle and force can be developed over greater range of stretched lengths
Why is maximum force greater at optimum length in smooth muscle?
Because passive tension is much greater at optimal length
Smooth muscle forms hollow structures with a lot of connective tissue which gives it higher passive force
