Week 4 Flashcards

1
Q

Muscles cannot contract on their own, they need input from the ________ to send signals to the muscle.

A

nervous system

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2
Q

Where do motor units connect with muscles

A

Neurotransmitter junction

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3
Q

What is the synaptic cleft

A

It is where all the neurotransmitter diffuses in order to produce a contraction

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4
Q

How does an action potential travel from the CNS to the muscle fibre

A

1.CNS sends an action potential to the muscle fibre via the axon,
2. Potential arrives via the axon terminal which will depolarize the plasma membrane. This opens calcium channels, which produces calcium ions into the axon terminals.
3. This calcium binds to proteins.
4. Synaptic vesicles then release acetylcholine. This diffuses across the synaptic cleft to the motor end plate, binding to nicotinic receptors.
5. This binding of acetylcholine opens an ion channel. Na+ can pass through these channels, creating local depolarization of the motor end plate.
6. The muscle fibre action potential is then initiated.

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5
Q

What is the latent period

A

After the action potential, there is a latent period before the tension in the muscle fibre begins to increase

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6
Q

Relationship between muscle fibre action potential and the muscle contraction

A

Action potential creates tension in the muscle.
It is over before the signs of muscular contraction begins

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7
Q

What is the contraction time

A

Time from the beginning of tension development (at the end of the latent period) to the peak tension

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8
Q

How does calcium aid the sliding filament model

A

Calcium binds to troponin, which will uncover the binding sites of the actin filament and will help for actin to form a cross bridge with myosin to generate force.

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9
Q

Difference between a relaxed and active muscle in the sliding filament model

A

In a relaxed muscle, there is low calcium, cross bridge cannot form as tropomyosin is covering the binding site (held back by troponin)
In an active muscle, there is high Calcium. Ca2+ binds to troponin. Tropomyosin moves away from cross bridge binding site. Actin binds to cross bridge

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10
Q

Difference between a relaxed and active muscle in the sliding filament model

A

In a relaxed muscle, there is low calcium, cross bridge cannot form as tropomyosin is covering the binding site (held back by troponin)
In an active muscle, there is high Calcium. Ca2+ binds to troponin. Tropomyosin moves away from cross bridge binding site. Actin binds to cross bridge

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11
Q

Summary of the sliding filament model PART 1 - Calcium, troponin, tropomyosin

A

The formation of a cross bridge is initiated when calcium ions released from the sarcoplasmic reticulum bind to troponin. This causes troponin to change shape. Tropomyosin moves away from the myosin binding site on actin allowing the myosin head to bind actin to form a cross bridge.

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12
Q

Summary of sliding filament model PART 2 - myosin, ATP, hydrolysis

A

The myosin head must be activated before a cross bridge cycle can begin. This occurs when ATP binds to the myosin head and is hydrolysed to ADP and inorganic phosphate. The energy liberated from the hydrolysis of ATP activates the myosin head.

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13
Q

Summary of the sliding filament model PART 3 - the contraction

A

The activated myosin head binds to actin, forming a cross bridge. Inorganic phosphate is released.
ADP is released and the myosin head pivot sliding the myofilament towards the centre of the sarcomere. When another ATP binds to the myosin head, the length between the myosin head and actin weakens, and the myosin head detaches. ATP is hydrolysed to ADP and inorganic phosphate. The energy released during hydrolysis reactivates the myosin head for cycle to start again.

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14
Q

Difference between tension and load in a muscle

A

Tension is the force that a muscle exerts on the joint when it is contracting
Load is the force that is exerted on a muscle by an object

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15
Q

Muscle tension must _____ the load in order for the muscle fibres to shorten, and therefore move the object that is responsible for the load.

A

Exceed

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16
Q

Concentric contractions in relation to tension and load

A

Tension > load

17
Q

Eccentric contractions in relation to tension and load

A

Load > tension

18
Q

In a shortening contraction, an increasing load causes

A

The latent period to increase
The duration of the twitch to become shorter
The velocity of shortening to slow down (gradient to decrease)

19
Q

In the absence of a load, a shortening contraction reaches its ________________

A

maximum shortening velocity

20
Q

Difference between an unfused tetanus and a fused tetanus

A

Unfused = the muscle fibre has time to partially relax before the next stimulation. Oscillation
Fused = muscle fibre has no time to relax between stimulations. The development of tension is continuous.

21
Q

Tension in a slow oxidiative muscle fibre

A

Tension is low but can be maintained for a long time

22
Q

Tension in te type 2a, fast oxidative muscle fibre

A

Tension in the muscle begins high, but slows over a period

23
Q

Tension in the type 2x fast glycolytic muscle fibre

A

Fibre produces lots of tension quickly, but that quickly drops

24
Q

Techniques to determine fibre type

A

Colour of fibre – type I fibres are more red in colour due to more capillaries and mitochondria due to their oxidative capacity
Muscle biopsy – use of a needle to cut a piece of muscle – puts untder microscope and able to see the MFTs.

25
Q

Spikes and discharge frequencies

A

When you record an action potential, we call it a spike. Multiple spikes are called discharges. If the frequency of discharges increases, the force produced by a muscle increases

26
Q

Main mechanisms in which motor units can generate more force is by

A

An increase in discharge rate and also increasing motor unit recruitment

27
Q

Hypertrophy v hyperplasia

A

Hypertrophy is an increase in the size of the muscle fibres
Hyperplasia is an increase in the number of muscle fibres

28
Q

Ananbolism

A

the rate of muscle protein synthesis > muscle protein breakdown = muscle gain

29
Q

Catabolism

A

the rate of muscle protein breakdown > muscle protein synthesis = muscle loss