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3A Musculoskeletal System > 3.1 Muscle Contraction > Flashcards

3.1 Muscle Contraction Flashcards

(48 cards)

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1
Q

Muscles are made of many …?

A

Muscle fasciculus

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2
Q

Muscle fasciculi are made of many …?

A

Muscle fibres

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3
Q

Muscle fibres are made of many …?

A

Myofibrils

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4
Q

Which of these is a muscle cell
-muscle fasciculus
-muscle fibre
-myofibril
-myofilament
-whole muscle

A

Muscle fibre

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5
Q

What is the membrane of a muscle fibre

A

Sarcolemma

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6
Q

What is a neuromuscular junction

A

Where one nerve innervates many muscle fibres

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7
Q

What neurotransmitter is released at the neuromuscular junction for skeletal muscle

A

Acetlycholine

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8
Q

What type of receptors are on the sarcolemma at the neuromuscular junction

A

Ionotropic nicotinic receptors

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9
Q

Where in the muscle fibres are Ca ions stored

A

Sarcoplasmic Reticulum

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10
Q

What is the first stage following the generation of an action potential in the sarcolemma

A

The AP propagates along the sarcolemma and down the T tubules

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11
Q

What are T tubules

A

Transverse tubules are extensions of the sarcolemma that descend into the muscle cell’s interior

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12
Q

What is caused once an action potential reaches the T tubules

A

Ca ions are released from the terminal cisternae of the sarcoplasmic reticulum

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13
Q

Describe the structures in place at the meeting between the T tubule and sarcoplasmic reticulum in skeletal muscle

A

A DHPR (dihydropyridine receptor) is on the T tubule membrane. A RYR (ryanodine receptor) is on the sarcoplasmic reticulum membrane. The DHPR and RYR are electromechanically coupled

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14
Q

Describe the mechanism of Ca release from the sarcoplasmic reticulum in skeletal muscle

A

The voltage from the action potential causes a conformational change in the DHPR. This causes the DHPR to mechanically pull on the RYR. The RYR then opens and Ca from the terminal cisternae comes out of the sarcoplasmic reticulum and into the sarcoplasm.

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15
Q

What type of receptor is a DHPR

A

An L type (stays open for a long time) voltage gated calcium channel.

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16
Q

How are Ca stored in the sarcoplasmic reticulum

A

The calsequestrin protein binds to the Ca ions and holds them in place in the terminal cisternae of the sarcoplasmic reticulum

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17
Q

How does the release of calcium ions into the sarcoplasm then allow for the actin/myosin cross bridge cycling

A

Calcium ions bind to troponin, causing the troponin to have a conformational change. The troponin can then move the tropomyosin out of the way, this then exposes the actin active sites for the myosin to bind to.

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18
Q

Describe how the actin myosin cross bridge cycle allows for muscle contraction and relaxation

A
  • ATP is hydrolysed so the myosin head is in a high energy state
    -the myosin head then forms cross bridge attachments to the active sites of the actin filaments
  • the ADP and Pi are released and the myosin head pivots and pulls back, this pulls the actin filaments towards the m line, known as the working stroke
  • new ATP binds to the myosin head which detaches the myosin from its cross link with the actin
    -the ATP is hydrolysed and the myosin head cocks, the process starts again
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19
Q

Why does rigor mortis occur after death

A

Because there is no ATP to break the actin/myosin cross bridge, hence the muscle stays contracted (before the muscle fibres start to deteriorate)

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20
Q

What happens in the sarcoplasm after the action potential finishes

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A

The calcium is removed by active transport back into the sarcoplasmic reticulum, this is done via the SERCA protein pump. Once the calcium is back in the sarcoplasmic reticulum, sarcalumenin attracts the calcium back to the calsequestrin in the terminal cisternae. Without calcium in the sarcoplasm, tropomyosin can go back to blocking the actin active site and the muscles can relax.

21
Q

What nerve type innervates skeletal muscle

Study These Flashcards
A

alpha motor neurons

22
Q

Give 4 ways that skeletal muscle contraction force can be regulated

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A

-temporal summation
-spatial summation
-starting sarcomere length
-reflex arcs

23
Q

How is muscle contraction force regulated by spatial summation

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A

Via muscle fibre recruitment, determining how many muscle fibres (from different motor units) are going to be sent the message to contract

24
Q

How is muscle contraction force regulated by temporal summation

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A

Temporal summation is when a second action potential is sent before the muscle has time to fully relax after the first. This causes tetany

25
What is the difference between fused and unfused tetanus
Unfused tetanus is when the muscles relax slightly after every temporal signal, but fused tetanus is when even more signals are sent, so the muscles just remain tensed
26
How is muscle contraction force affected by the starting lengths of the sarcomeres
When sarcomeres are too long at starting length, there is less cross over between the actin and the myosin. Also, when sarcomeres are too short at starting length, there is not much space the myosin can pull the actin along. In both cases not as much force can be generated by the actin being pulled along.
27
Give key features of cardiac muscle contraction
-all the cells are joined by gap junctions, so the signal is shared by all the cells and the tissue functions as an electrical syncytium -cardiac muscle cells are smaller than skeletal muscle cells -thick and thin filaments in the myofibrils are organised in a similar way to in skeletal -has lots of mitochondria -has more connective tissue and less sarcoplasmic reticulum than skeletal muscle -T tubule position differs to that of skeletal muscle -the action potential in cardiac muscle lasts much longer than that in skeletal muscle
28
What is the main difference between the initiation of contraction in cardiac muscle vs in skeletal muscle.
In cardiac muscle, extracellular calcium is required. This allows for calcium induced calcium release
29
What is the difference in the coupling between DHPR and RYR in cardiac vs in skeletal.
In skeletal muscle, the coupling is electromechanical but in cardiac muscle, the coupling is electrochemical.
30
Describe the process of calcium induced calcium release in cardiac muscle
As action potentials reach the T tubule, it opens the DHPR (as they are voltage gated), external 'trigger' calcium can them enter the DHPR. The trigger calcium then binds to the RYR on the sarcoplasmic reticulum. This causes the RYR to open and the calcium to exit into the sarcoplasm.
31
Does more calcium enter the sarcoplasm in skeletal or cardiac muscle?
Cardiac
32
In cardiac muscle, how is a Ca concentration gradient restored following contraction
- a 3Na+/1Ca2+ antiporter (secondary active transport) - a sarcolemmal Ca2+ pump (primary active transport) - a SERCA pump
33
Why cant a SERCA pump alone be used to restore Ca concentration gradient in cardiac muscle following contraction
If the only mechanism was SERCA bringing Ca back into the sarcoplasmic reticulum, then more and more Ca would go in each time (as external Ca is entering the sarcoplasm). Hence other methods are also used
34
Why is summation not an option for cardiac muscle.
spatial - due to the electrical syncytium nature, no more muscle cells can be recruited temporal - as we need heart cells to relax fully, any tetany would be lethal
35
What is the alternative to a neuromuscular junction in cardiac muscle
The sinoatrial node undergoing spontaneous depolarisation to act as a pacemaker for the heart.
36
Give 3 ways that cardiac muscle contraction force can be regulated
-cytosolic calcium concentration -stretch of cells -Bowditch Effect
37
Explain how cytosolic calcium concentration can regulate cardiac muscle contraction force
A greater cytosolic calcium concentration will cause more actin active sites to be exposed more actin myosin cross linking and a greater force of contraction
38
Explain how stretch of cardiac muscle cells can regulate cardiac muscle contraction force
When a cell is stretched, its calcium sensitivity increased. Hence for the same amount of calcium, there is a greater contraction force. But this only works up to a point of stretch.
39
Describe the Bowditch effect and explain how it regulates cardiac contraction force
The Bowditch effect is when, as heart rate increases, contraction force increases. This is because as heart rate increases, more action potentials are generated so more so sodium enters the muscle cells. Hence, with a higher sodium concentration, the activity of the sodium/calcium antiporter is reduced. Therefore more of the Ca in the sarcoplasm has to be taken up by the SERCA into the sarcoplasmic reticulum. So then more Ca is released from the sarcoplasmic reticulum during contraction thus increasing contraction force.
40
What is the negative Bowditch effect and what is it a hall mark of.
The negative bowditch effect is when there is no increase in sarcoplasmic reticulum Ca levels following increased heart rate (the Bowditch effect is not happening). This indicates heart failure, as there is less expression of the SERCA proteins
41
What are the main features of smooth muscle in comparison with skeletal and cardiac
-there is no striation, instead the actin and myosin can interact not in straight lines and the muscle can contract in different directions -there are many different types of smooth muscle cells that have different contraction patterns -contraction is regulated by myosin, instead of actin for skeletal and cardiac
42
Describe the difference between single unit smooth muscle and multi unit smooth muscle
Multi unit is found in large blood vessels, airways and cillliary muscles and is made up of discrete units. Each unit needs to be separately innervated by autonomic nerves. Single unit, is the majority and is found everywhere else. The cells are joined together by gap junctions allowing for coordinated contractions as one unit.
43
Describe the difference between tonic smooth muscle and phasic smooth muscle
Phasic smooth muscle has rhythmic activity and corresponds to single unit smooth muscles such as in the GI or urinary tract. Tonic smooth muscle is continuously active and corresponds to multi unit smooth muscle such as vascular or respiratory.
44
Give some key smooth muscle structures
-gap junctions for communication -adherens junctions for mechanical linkage -caveolae which are the T tubule equivalents -a sarcoplasmic reticulum with calcium channels such as RYR, InsP3 gated and SERCA
45
Briefly explain smooth muscle contraction.
Although there is no striation, the filaments still have an order. Compared with striated muscle, there is more actin but less myosin. Groups of the filaments are connected to dense bodies and the cytoskeleton transmits force throughout the cell. The contraction cycles are slower than in striated muscle but can generate more force
46
Briefly describe the smooth muscle actin/myosin cross bridge cycling
-4 calcium ions bind to calmodulin, the Ca/calmodulin complex activates MLC (myosin light chain) kinase -MLCK then phosphorylates myosin so it can interact with actin -following contraction, MLC phosphatase then allows for relaxation
47
What is the main regulator of smooth muscle contraction and give examples of how it can be effected.
Ca concentration e.g by Nerves Hormones Pacemaker activity Drugs
48
Give 3 ways the Ca2+ can be increased in smooth muscle to cause contraction?
-direct entry of Ca into sarcoplasm via ligand channels and voltage gated channels -calcium induced calcium release from the sarcoplasmic reticulum -the IP3-CERCA pathway

3A Musculoskeletal System (6 decks)

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