Skeletal, smooth (and cardiac) muscle 1&2 Flashcards

1
Q

Describe the structure of skeletal muscle.

A

Skeletal muscle cells are merged together to form skeletal muscle fibres. They are called “multinucleate”.
The nuclei in skeletal muscles are pushed out to the side of the cells (fibres) due to the large amount of contractile proteins within the cells.
They are very very long fibres.
Skeletal muscle fibres have striations and are organised in a highly ordered manner.
Within a skeletal muscle fibre, there are small myofibrils which have the “striped” striations.

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2
Q

Compare the process of muscle formation (in utero) .vs. after injury or tear.

A

When in utero, the muscle is formed from mononucleate myoblasts, which increase the fibre size of the muscle during growth.
Myoblasts do not replace cells if damaged.

Satellite cells differentiate to form new muscle fibres after injury or tear.
We have a limited supply of satellite cells.
The neighbouring areas of damaged muscle undergo hypertrophy to compensate.
Muscle will never fully recover.

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3
Q

Define “the sarcomere”.

A

The sarcomere is the basic repeating (contractile) component of skeletal muscle.
It is contained on a myofibril, within Z-lines and consists of thin (actin) filaments and thick (myosin) filaments interacting together.
There is also a protein named titin which is responsible for stabilising myosin between actin.

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4
Q

Describe the “sliding filament” theory.

A

This theory implies that actin and myosin filaments slide over each other in a controlled way, to make the Z- lines of the sarcomere become closer together.
This is explained by the binding of the cross bridge heads of the myosin to the binding-sites on the actin.
Once bound, the heads on the myosin flip and pull the sarcomere into a more contracted pattern.

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5
Q

Describe the myosin cross bridge.

A

Has:
Actin binding sites
ATP binding sites (responsible for the energy required to flip the cross bridges.
Light chains in the head.
= large capacity for contraction.

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6
Q

Describe the importance of the ATP binding sites on the myosin cross bridge heads.

A

The binding of ATP to the myosin cross bridge head allows for the charging up of the cross bridge, ready to pull and move, and contract the muscle.
The energy from ATP is derived from its hydrolysis to ADP and Pi.
Once the contraction has happened, the muscle can only return to its relaxed state once new ATP has bound.

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7
Q

Describe the events of the cross bridge cycle.

A

1 - The cross bridge binds to actin, this is possible through the hydrolysis of ATP from previously, this causes the [Ca2+] to rise.
2 - The cross bridge then moves, pulling the myosin closer to the Z-line (so muscle is contracted) POWER STROKE. At this point ADP and Pi are released from the cross
bridge head.
3 - ATP binds to myosin causing the cross-bridge to detach from actin.
4 - Hydrolysis of ATP energizes the cross bridge, actin is separate from myosin and myosin is conjoined with ADP and Pi. Muscle is relaxed.

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8
Q

Describe troponin and tropomyosin as regulators of muscle contraction.

A

Tropomyosin partially covers the myosin binding site, and it is held in this blocking position by troponin.
= cooperative block.
If calcium binds to troponin, this alters the conformation of troponin and so tropomyosin is pulled away from myosin, allowing actin to bind (contraction).
For the blockage of sites again (relaxation), remove calcium.

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9
Q

Describe the ultrastructure of a skeletal muscle fibre.

A

Between each myofibril there is a mesh network of tubing called the sarcoplasmic reticulum. This is the main storage facility for Calcium.
Another structure within muscle fibres is the transverse tubules that are conduction systems responsible for reaching deep within muscle cells to conduct signals.
There is also a large amount of mitochondria, which is responsible for the generation of ATP within muscles.
(also rich supply of blood from many blood vessels within muscle fibres, that provides oxygen and transmits waste materials).

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10
Q

Describe the process of excitation-contraction coupling.

A

1 - Muscle action potential is propagated along the muscle cell membrane by voltage gated ion channels, through the transverse tubules and deep within the cell.
2 - Calcium released from lateral sac out of sarcoplasmic reticulum into cytoplasm of the cell
3 - Calcium binding to troponin removes blocking tropomyosin.
4 - Cross bridge moves = power stroke.
5 - Calcium taken up, and pumped out of cellular environment by Calcium ATPases, (after contraction).
6 - Calcium removal from troponin restores tropomyosin blocking action.

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11
Q

Describe how calcium is released from the lateral sac of the sarcoplasmic reticulum.

A

A calcium channel receptor called DHP senses the electrical depolarisation of the membrane of the transverse tubules and allows a trickle of calcium to exit the transverse tubules and enter the cell. This small amount of calcium in the cell is enough to trigger Ryanodine receptors that are close by to cause a mass wave of calcium into the cell.
This causes an AMPLIFIED SIGNAL.

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12
Q

Define a motor unit.

A

A motor unit is within large pieces of muscle.
Motor units are the combination of motor neurons and muscle fibres.
The muscle fibres within a unit may be scattered throughout muscle.
Allows for the scattering of innervation throughout a large piece of muscle.E

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13
Q

Define “tension” and “load” of a muscle.

A

Tension is the force exerted and generated by the muscle is the tension.
Load is the force exerted on muscle.

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14
Q

Define an isometric contraction.

A

Contraction with constant length.

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15
Q

Define an isotonic contraction.

A

Contraction with shortening length.
Also called concentric contraction.

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16
Q

Define a lengthening contraction.

A

Contraction with increasing length.

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17
Q

Define the “latent period”.

A

The latent period is the time before excitation-contraction starts.
It has more calcium and generates tension in the muscle.

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18
Q

Describe the contraction time.

A

The contraction time occurs between the start of tension and the time where we have peak tension.
Contraction time depends on [Calcium]/.

19
Q

Describe tetanus.

A

Tetanus occurs when the contraction of muscles builds up (from summation of lots of action potentials).
This can cause very long contractions that last until the muscle gets tired and has to relax to function properly.

20
Q

Describe fatigue.

A

Fatigue is essentially repeated muscle stim.
It depends on the fibre type, length of contraction and the fitness of the individual.

21
Q

Describe fatigue, as a protective mechanism.

A

Fatigue is how the muscle prevents itself from using up vast amounts of ATP (which would subsequently cause rigor).
AP’s still fire while in fatigue, therefore we can stop responding to neurons

22
Q

Describe the factors causing fatigue from high intensity, short term exercise.

A

Conduction failure due to potassium concentration increase (outside of cell), causing depolarisation, which means there is a loss of control and we are unable to regulate ion concentration.
Lactic acid concentration in muscles increases (generated as by product of energy metabolism) - this acidifies proteins, proteins lose function.
Rise in ADP and Pi, inhibits cross bridge cycle as there is a lower probability that ATP can occupy binding sites on myosin and this delays myosin detachment from actin filaments.

23
Q

Describe fatigue when exercising for long term, lower intensity.

A

Start to lose muscle glycogen
Blood glucose lowers
Dehydration

24
Q

Describe central command fatigue.

A

This is when the cerebral cortex cannot excite motor neurons.
No “will to win”.

25
Q

Describe oxidative skeletal muscle fibres.

A

Oxidative fibres have lots of mitochondria for oxidative phosphorylation.
Oxidative fibres contain myoglobin which is a buffer used for short term store of oxygen, it is required for the large oxygen delivery to the fibres.
The fibres are red in colour and have small diameters (to lower diffusion distance).
There is more vascularisation to deliver more oxygen and nutrients.

26
Q

Describe glycolytic skeletal muscle fibres.

A

These have few mitochondria.
Have a lower blood supply.
They have more glycolytic enzymes and glycogen.
The fibres are white in colour with large diameters.
(there is no myoglobin).

27
Q

Describe the result of anaerobic exercise (in muscle).

A

Anaerobic exercise is any type of exercise that doesn’t rely on use of oxygen, for example weightlifting.
Hypertrophy from anaerobic exercise causes an increase in muscle fibre diameter, and an increase in glycolysis.

28
Q

Describe the result of aerobic exercise (in muscle).

A

Aerobic muscle is exercise that relies on oxygen, hypertrophy from aerobic exercise causes an increase in mitochondria, vascularisation and muscle fibre diameter.

29
Q

Describe type 1 muscle fibres.

A

These are slow oxidative fibres, that can resist fatigue as they are required for longer contraction.

30
Q

Describe type 2a muscle fibres.

A

These are fast oxidative fibres, they have an intermediate resist to fatigue.

31
Q

Describe type 2b muscle fibres.

A

These are fast glycolytic fibres, they fatigue quickly as glycolysis is not efficient as it is easy to run out of energy.

32
Q

Describe 2 ways in which atrophy can occur.

A

By destruction of a nerve or the neuromuscular junction could lead to denervation atrophy.
Not using a muscle could lead to disuse atrophy.
Atrophy is the opposite of hypertrophy, and it is when muscle mass decreases.

33
Q

Describe the structure of smooth muscle.

A

Smooth muscle has no striations, and is spindle shaped.
It is mononucleate and divides throughout life.
Thick and thin filaments present.
The filaments are arranged diagonally across cells, they are anchored to cell membranes and cell structures by dense bodies (the equivalent of Z lines).

34
Q

Describe the appearance of smooth muscle when relaxed and contracted.

A

When smooth muscle is relaxed, the muscle appears thin, and the filaments aren’t overlapping.
When smooth muscle is contracted, the filaments are overlapping but in a much more disorganised manner than in skeletal muscle. Seems to bulge out over the fibres.

35
Q

Describe the process of contraction in smooth muscle (cross bridge cycle).

A

There is an increase in calcium concentration,
Calcium binds Calmodulin
The calcium-calmodulin complex binds to myosin light chain kinase (this enzyme is what regulates contraction).
The kinase phosphorylates myosin x bridges with ATP.
These phosphorylated X-bridges bind to actin filaments, which leads to eventual…
CONTRACTION AND TENSION.

36
Q

Describe the process of smooth muscle relaxation.

A

After persistent stimulation the calcium concentration increases.
The phosphorylated X-bridges may be dephosphorylated when still bound to actin,
They are dephosphorylated by myosin light chain phosphatase.
This decreases the rate of ATP-splitting,
Which then slows the X-bridge cycle.
This means tension can be maintained for a long time with low ATP consumption.

37
Q

Describe how smooth muscle retains its base line tone.

A

Blood vessel walls need to remain open for long periods, this requires a low level of contraction in smooth muscle. There is some calcium released which keeps contraction.
The base line tone is essentially a constant basal tone.
= constant trickle of calcium

38
Q

Describe the factors affecting contractile activity.

A

Contractile activity is affected by a dynamic balance of the following:
- Spontaneous electrical activity in muscle membranes = pacemaker activity.
- Autonomic neurotransmitters from varicosities.
- Hormones (e.g. oxytocin)
- Local factors (paracrine agents, pH, O2, osmolarity, ions, NO)
- Strech

39
Q

Describe the structure of single unit smooth muscle.

A

(GIT, uterus, small blood vessels)
- many cells linked by gap junctions
- signals travel between cells
- contract synchronously
- may contain pacemaker cells
- stretch evokes contraction

40
Q

Describe the sarcoplasmic reticulum of smooth muscle cells.

A

There are less sarcoplasmic reticulum present in smooth muscle compared to skeletal.
There are no Transverse tubules and there is a random arrangement.

41
Q

Describe how smooth muscle cells obtain Calcium ions from the outside of the cell.

A

Through VACC’s - voltage-activated calcium channels.
Calcium ions are removed from the cytosol by pumping back into the sarcoplasmic reticulum and out of the cell by calcium ATPase (slower process than be skeletal muscle).

42
Q

List the factors that affect contractile activity (dynamic balance of…).

A
  • Spontaneous electrical activity in muscle membranes (pacemaker activity)
  • Autonomic neurotransmitters from varicosities.
  • Hormones (e.g. oxytocin)
  • Local factors (paracrine agents, pH, O2, osmolarity, ions, NO)
  • Stretch (any muscle that is stretched will contract to compensate.
43
Q

Describe “single unit” smooth muscle.

A

Single unit smooth muscle (GIT, uterus, small blood vessels)
- many cells linked by gap junctions
- signals travel between cells
- contract synchronously
- may contain pacemaker cells
- stretch evokes contraction

44
Q

Describe “multiunit” smooth muscle.

A

Multiunit (airways, large arteries, veins).
- few or no gap junctions
- richly innervated by ANS
- don’t respond to stretch