Muscle Physiology Flashcards

1
Q

Structure of skeletal muscle

A

-made up of sarcomeres which make up muscle fibres.
- sacromeres are made up up actin,myosi,troponin,tropomyosin protein

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2
Q

Thin filaments

A

-made up of actin, troponin and tropomyosin

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3
Q

Thick filaments

A
  • made up of myosin
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4
Q

Cross-bridge cycling

A
  • controlled by action potentials
  • myosin heads binds via the actin-myosin binding site
  • mysosin pulls the actin filaments torwards the centre of the filaments, The power stroke is fueled by the hydolyses of ATP to ADP and phosphate which cause a conformational change to myosin head
    -ATP binds to myosin heads causing the dissociation of the actin-myosin complex
  • ATP is hydrolysed
  • a cross bridge forms and the myosin head bind to the new position on actin
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5
Q

Role of troponin c

A

Allows troponin to bind to calcium

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6
Q

Role of troponin T

A

Allows troponin to binds to tropomyosin

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7
Q

Role of troponin I

A

Allows troponin to bind to ATP

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8
Q

How is the cross-bridge cycle dependent on the Ca2+

A

-in a low calcium environment tropomyosin blocks the actin-myosin binding site
- in high calcium environments. Calcium binds to tropomyosin causing a conformational changing exposing the actin-myosin binding site

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9
Q

Role of transverse tubules

A
  • in the membrane of muscles
  • increases the surface area of the membrane
  • allows action potential to be be penetrated deeper in the meme table which allows to be closer to the sacroplasmic reticulum which has lots of stored calcium
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10
Q

Triad structure

A
  • has the T-tubule with sarcoplasmic reticulum on each side
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11
Q

The effect of action potential on muscle movements

A
  • signal transduction lead to action potential trigger in the muscle fibre
    -AP propagated down the sacromela and T-tubules
  • leads to the depolarisation of t-tubules sensed by Dihydropyridine receptors (DHPR) which are voltage-gated channels
  • caused the release of calcium by ryanodine receptors from the SR into the cytoplasm
    -initiated the cross-bridge cycling and contraction
    -CA2+ is pumped back into SR by SERCA terminating crossbridge cycling
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12
Q

Factors which influence the force of contraction

A
  • frequency of action potentials. The higher the frequency the higher the force in contraction
  • number and size of motor units activated. Can be increased with training and leads to higher force of contraction
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13
Q

what is meant by cardiac muscle is a syncytium

A
  • the heart is made up of two syncytium which are clusters of cardiomyocytes
    -allows electrical impulses to travel through the heart which is crucial for the synchronized contraction of the heart chambers (atria and ventricles), leading to the effective pumping of blood through the circulatory system
    -contains a gap junction which allows the propagation of action potentials from cell to cell
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14
Q

what is meant by absolute refractory period of the cardiac muscle

A

-nearly all the NA+ channels are in the inactivated state.

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15
Q

what is the relative refractionary period of the cardiac muscle

A
  • NA+ channels are recovering from inactivation and excitability returns towards normals a the number of channels in the inactivated state decreases
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16
Q

refactionary periods of cardiac muscle

A
  • they are longer compared to skeletal muscle because the long refractory period of cardiac muscle cells is a crucial adaptation to ensure the orderly and rhythmic contraction of the heart, preventing potential issues of overstimulation. This feature contributes to the stability and efficiency of the cardiac cycle.
17
Q

what is striated muscle?

A

-skeletal muscle and cardiac muscle= complicated structures

18
Q

difference between the mechanisms of contraction in cardiac muscle and in skeletal muscle

A

-skeletal muscles has mechanically coupled ryanodine receptors whereas in cardiac muscle they are ligand-gated and open as a result of increased calcium which then releases more calcium
-skeletal muscle have an all of nothing contraction whereas cardiac muscle is controlled by graded calcium meaning The more calcium available, the stronger the contraction therefore the heart can adapt to the body physiological needs

19
Q

frak-starling law of the heart

A
  • the amount of strech of the cardiac muscle determines the amount of force generated during contraction-more streach=more force
    -Stretching the muscle fibers enhances the sensitivity of the muscle to calcium ions.
20
Q

Beta one adrenoreceptors involement of the intropy of the heart

A

-When the sympathetic nervous system is activated, such as during the “fight or flight’ noradrenaline is released which binds to beta-1 adrenergic receptors on the surface of cardiac muscle cells.
- this activates adenylate cyclase in turn, catalyzes the conversion of AT to cAMP
- cAMP activates (PKA), an enzyme that phosphorylates various proteins involved in the contractile process. which increases calcium levels

21
Q

postive drugs for intropic pharmaceuticals

A
  • B-adrenoceptor aagonist e.g. adrenaline and noradrenalibe
22
Q

negative drugs for intropic pharmaeceuticals

A

-calcium channel blockers and B-adrenoreceptors antagonist

23
Q

Functions of smooth muscle

A
  • regulating blood pressure
    -hair standing on end-piloerection
24
Q

Smooth muscle composition

A
  • thin filaments are longer in smooth muscle so can contract and relax to a greater extent
  • shorter thick filaments
  • gap junction present for electrical and chemical communications
  • dense body’s they provide ridged filaments for the filaments to attach too
  • have abnormally high levels of NA+ and CA2+
25
Q

Action potential as a mechanism for contraction in smooth muscle

A
  • contraction are not highly dependent on membrane potentials therefore can be a diverse range of membrane potentials that can cause a concentration including no action potentials
26
Q

does smooth muscle have a sacroplasmic reticulum ?

A

-smooth muscle has a lack of sacraplasmic reticulum

27
Q

Contraction regulation of smooth muscle by calmodulin

A

-Ca2+ influx from extracellular sources
- Ca2+bind to calmodium forming a complex. This causes a conformational change of activates myosin light chain kinase (MLC)
- this converts ATP to ADP
-ADP attached to myosin heads and cross-cycling cycle begins

28
Q

Regulation of smooth muscle relaxation

A
  • stimulis activates cAMP or cGMP. this activates MLCP. myosin light chain phosphorylasewhich rremoves phosphate from the myosin heads
    -causes dissociation of actin-myosin interactions
29
Q

Pharmacological control of smooth muscle contraction

A

-stimulation of increased Ca2+
-agonist of ligand-gated channels
-increased sensitivity to ca2+ by manipulation of MLC-kinase and MLC-phosphate activity

30
Q

Pharmacological control of smooth muscle relaxation

A

-Reducing intracellular Ca2+- by using Calcium channel blockers (e.g. dihydropyridines such as nifedipine)
- Or Drugs and agonists of Gαs coupled receptors that activate potassium channels
- Inhibiting cross-bridge cycling- by Guanylyl cyclase activators (e.g. nitric oxide, nitrates)
- or cGMP phosphodiesterase inhibitors (e.g. sildenafil/Viagra