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Nervous System > Muscle physiology > Flashcards

Muscle physiology Flashcards

1
Q

What triggers the contraction of skeletal muscle?

A

An action potential

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2
Q

Function of skeletal muscle

A

Attach bone via tendons to allow movement

Form the tongue and exert contractile forces via investments in connective tissue

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3
Q

What does the amount of force exerted depend upon?

A
  • number of active muscle fibres
  • frequency of stimulation
  • rate at which muscle shortens
  • initial resting length of muscle
  • cross sectional area of muscle
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4
Q

How + why do motor units vary in size?

A

Less muscles supplied by one motor neurone to allow for a finer degree of control, such as extra-ocular muscle of eye

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5
Q

Maximal stimulus definition

A

Stimulus that is sufficient to activate all the fibres in a muscle

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6
Q

What happens to the muscle during contraction?

A
  1. Action potential passes along its length
  2. contractile response- consists of an initial phase of acceleration where the tension in the muscle increases until it equals the load to which it is attached
  3. At first the muscle shortens rapidly and then the rate of shortening begins to decrease
  4. Muscle relaxes and the tension it exerts falls to zero
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7
Q

Why does the muscle contraction last longer than the AP?

A

cycle of lengthening and shortening takes a lot longer, whereas an AP is rapid

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8
Q

Explain twitch summation

A

A twitch is a brief contract caused by the muscle.

If the twitches occur very shortly after another, then there is an increase in tension.

Tension in the tendons, already formed from the first contractions cannot decay between the twitches.

Also, calcium released has not got time to be reabsorbed by the sarcoplasmic reticulum, so more troponin binds to it.

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9
Q

Tetany explained

A

Many twitches in very quick succession which forms a sustained muscle contraction.

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10
Q

Two different forms of tetany explained

A

Non-fused- muscle fibres do not completely relax before the next stimulus because they are being stimulated at a fast rate

fused- contracting tension remains constant I’m a steady state

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11
Q

Where is tetany normal?

A

allow muscle tone and maintain posture

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12
Q

stages of cross-bridge cycling and sliding filament theory

A
  1. AP travels through the T tubules and depolarises the motor unit
  2. The depolarisation triggers voltage gated calcium channels to open, causing calcium to move down their electrochemical gradient into the intracellular fluid.
  3. calcium binds to the troponin molecule, causing tropomyosin to undergo a conformational change and releasing the myosin binding site on actin
  4. The bulbous myosin head then binds to actin to form a cross bridge
  5. ATP binds to myosin head group causing it to dissociate from actin
  6. hydrolysis of ATP provides energy for the myosin head group to change angle
  7. myosin with bound ADP then binds to actin and the cycle repeats
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13
Q

What is the sliding filament theory?

A

Thick and thin filaments slide past each other to allow muscle contraction

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14
Q

What happens to the organisation of the sarcomere?

A

A band remains the same, I band shortens, M line remains the same, H band shortens, distance between Z lines (sarcomeres) decreases

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15
Q

Cross bridge cycling definition

A

the association and dissociation of actin and myosin

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16
Q

Length-tension relationship

A

At rest- maximal overlap, able to contract

When stretched, less overlap between actin and myosin, so less cross bridges leading to a decline in the muscle’s ability to contract

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17
Q

3 roles of sarcoplasmic reticulum

A

calcium storage, release and absorption

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18
Q

Explain calcium storage

A

Calsequestrin protein located in SR which binds to around 50 calcium ions, allowing more calcium ions to bind as it prevents the disruption of ion gradients and pH

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19
Q

Explain briefly calcium release

A

Calcium spark occurs- ions released through a ryanodine receptor

20
Q

Explain briefly calcium absorption

A

Contains SERCA ATPase which pump calcium back into the SR

21
Q

Excitation contraction coupling definition

A

The process by which a muscle action potential triggers a contraction

22
Q

Explain ECC in skeletal muscle

A
  1. Wave of depolarisation spreads through T tubules
  2. This triggers calcium ions to enter the cell through L type channels located in the cell membrane.
  3. The L type channel is mechanically coupled with the RyR, thus causes it to undergo a conformational change and release calcium from the sarcoplasmic reticulum.
23
Q

What binds calsequestrin to SR membrane?

A

Triadin and Junctin

24
Q

How is contraction terminated?

A

motor neurones stop releasing ACh so less calcium becomes released. L type DHPR channels shut. SERCA pumps out calcium.

troponin binds to tropomyosin again and the muscle relaxes

25
Q

How does SERCA work?

A

Phospholamban protein bound to SERCA- inactivated

when phospholamban is phosphorylated by PKA SERCA becomes inactivated, pumping calcium ions from the cytosol to the lumen of the SR

26
Q

heterogeneity definition

A

A material that is non uniform in composition

27
Q

Two different forms of cardiac muscle cell

A

sino- Atrial and ventricular myocytes

28
Q

How is an action potential formed in the Sino-atrial cells?

A
  1. non-selective cation channel is slowly activated when the membrane potential becomes more negative than -50mV
  2. This is caused by the outward flow of potassium ions during repolarisation
  3. This results in a net inward current called the funny current that progressively becomes less negative
  4. the resulting slow depolarisation activates a calcium current which sums that funny current until an action potential is triggered
  5. rise in calcium permeability results in a reversal in charge
29
Q

Action potential at atrial and ventricular myocytes

A

determined mainly by permeability to potassium ions

  1. upstroke of action potential caused by an increase in sodium ion diffusion
  2. slowly activating calcium channels open, leading to plateau phase during depolarisation
  3. initial rapid phase of repolarisation due to the shutting of sodium channels
30
Q

Explain ECC in cardiac muscle

A
  1. wave of depolarisation in dyad causes L type voltage gated channels on the sarcolemma to open
  2. the resulting calcium influx activates the RyR calcium release channels found on the cisternae of the sarcoplasmic reticulum
31
Q

What is this process called?

A

calcium induced calcium release

32
Q

What causes the relaxation of cardiac myocytes?

A

Calcium ions pumped from sarcoplasm either into the SR or out of cells

into sarcoplasm via SERCA

out of cells using sodium calcium exchanger. one calcium ion for every 3 sodium

33
Q

Explain the Frank-Starling mechanism

A

Based on the link between the initial length of myocardial fibres and the force generated by contraction.

There is an optimal length between sarcomeres at which the tension in the muscle fibre is greatest, resulting in the greatest force of contraction.

34
Q

Where is smooth muscle located?

A

gastrointestinal tract- sphincters
urinary tract- ureters, bladder and urethra
genital system, vascular and lymphatic, eye- iris and ciliary muscle
hair follicles

35
Q

Two forms of activity in smooth muscle explained

A

myogenic- single unit, can contract regularly without input from a motor neurone

neurogenic- multi unit- contractions must be initiated by the autonomic nervous system

36
Q

Role of action potential + how it spreads

A

Smooth muscle becomes depolarised due to the influx of calcium and sodium cells. Action potential passes through cells via gap junctions in single unit.

37
Q

ECC stages

A
  1. muscle becomes depolarised
  2. voltage gated calcium channels in membrane opened (L type) allowing calcium to flow into the cell
  3. some CICR through Ryanodine receptors present on sarcoplasmic reticulum
38
Q

How does calcium initiate contraction?

A
  1. 4 calcium ions bind to calmodulin protein
  2. the calcium-calmodulin complex activates an enzyme called myosin light chain kinase
  3. MLCK phosphorylates the regulatory region on the myosin light chains, which changes conformation
  4. allows myosin head to then bind to actin and undergo cross bridge recycling
39
Q

Why are smooth muscle contractions slow?

A

Slow hydrolysis of ATP

‘latch state’ occurs when proteins are bound together to conserve energy

40
Q

How else is intracellular calcium increased in endothelium?

A
  1. adrenaline binds to alpha 1- adrenergic receptor
  2. GqPCR then contains alpha sub unit with a bound GTP that binds to PLC enzyme
  3. PLC then becomes activated and converts PIP2 into DAG and IP3
  4. IP3 then binds to a ligand gated calcium channel which increases intracellular calcium
41
Q

What two nucleotides inhibit contraction?

A

cAMP and cGMP

42
Q

How are they produced and why do they inhibit contraction?

A
  1. Adenylate and guanylate cyclase produce cGMP and cAMP
  2. The two kinases phosphorylate a number of proteins
  3. inhibit L type channels, IP3 receptors and stimulate SECA, increase myosin light chain phosphatase which inactivates the enzyme.
43
Q

What two molecules inhibit myosin light chain phosphatase? + explain

A

Protein kinase C- phosphorylates myosin, so acts competitively

Rho-Kinase- phosphorylate myosin and phosphorylates the myosin binding sub unit on the enzyme, thus inactivation

44
Q

What else can stimulate contraction in smooth muscle?

A

hormones and locally produced compounds such as acetylcholine

45
Q

Excitatory and inhibitory innervation of smooth muscle explained

A

Gs GPCR- alpha subunit stimulates a response- inositol triphosphate pathway - may produce cAMP which inhibits myosin light chain kinase

Gi- GPCR- alpha subunit may stimulate response, by blocking production of cAMO

Nervous System (9 decks)

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