Muscle Physiology- Keagan Flashcards by Isabelle Lux

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

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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

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Gap junctions between cells in skeletal vs cardiac muscles

Skeletal- absent
Cardiac- present- AP can travel from cell to cell

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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

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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

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The only adequate stimulus for skeletal muscle is __

Nervous impulse

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Each muscle fiber is a single ____ cell

Multi nucleaated

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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

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Desmin

Rod/ column looking thing that holds Z line to sarcolemma

Myofibrillar myopathies

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Dystrophin

Poly peptide chain/rope looking thing
Holds thick filaments to proteins within sarcolemma

Duchennes muscular dystrophy

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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

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What enzymes aid in Ach synthesis and degradation

CAT (choline acetyltransferase)- synthesizes (choline+ acetyl CoA= Ach)
ACE (acetylcholinesterase)- degrades (Ach= choline + acetate)

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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

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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

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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

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How does botulinum toxicity affect action potentials

Botulinum toxicity inhibits the release of Ach from presynaptic nerve

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Organic Phosphates poisoning

Organophosphate pesticide blocks ACE which prevents Ach breakdown

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Myorelaxants

Cause myorelaxation by blocking the NMJ

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What is a Twitch and its phases

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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

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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)

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Antibodies destroy VG Ca channels in presynaptic nerve

Decreases Ca influx= decrease Ach release

Failure of neuromuscular transmission and muscle weakness

Malignant Hyperthermia

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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

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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

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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

Muscle Physiology- Keagan Flashcards

(46 cards)