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biosci block 6 & 7 > Lecture 31. Muscle 2 > Flashcards

Lecture 31. Muscle 2 Flashcards

1
Q

When does muscle develop maximum tension?

A

when all myosin is aligned with actin filament and every myosin head can attach to actin

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2
Q

when does muscle develop no tension?

A

when the muscle is stretched out so that myosin and actin filaments do not overlap and myosin heads cannot bind to actin

OR

When the muscle is shortened so that all myosin and actin filaments are jammed together and it cannot generate tension( myosin pulls actin in opposite direction)

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3
Q

Why when the muscle is shortened it is harder to develop tension?

A

Myosin and actin overlap to the point, where myosin starts interacting with the wrong actin filament.

Cross-bridge cycle is happening but it is pulling in the wrong direction-> ineffective

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4
Q

Length-Tension relationship

A

During isometric muscle contraction
At the level of the sarcomere the maximum active force (tension
developed) is dependent on the degree of actin and myosin overlap

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5
Q

What is the optimum range for sarcomeres?

A

The maximal force between 2.0 – 2.2 µm
• A lengths >2.2 µm active forces decline as the extent of overlap between
filaments reduce, reducing the number of cross-bridges
• At lengths <2.0 µm filaments collide and interfere with each other reducing
force developed

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6
Q

What is the optimum range for sarcomeres?

A

The maximal force between 2.0 – 2.2 µm
• A lengths >2.2 µm active forces decline as the extent of overlap between
filaments reduce, reducing the number of cross-bridges
• At lengths <2.0 µm filaments collide and interfere with each other reducing
force developed

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7
Q

Elastic components of muscle

A
  • Internal( eg titin)
  • Externals( elastin in CT)
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8
Q

Passive vs active force in muscle

A

As muscle is stretched the connective
elements resist the stretch = passive force. No energy required

Active force- due to muscle contraction

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9
Q

Total tension is:

A

Total tension is the sum of the active tension
dependent on the sarcomere length and the passive tension

As the muscle is getting stretched passive tension contributes more to the total tension than active tension

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10
Q

When the muscle is stretched out what type of tension is it?

A

passive

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11
Q

Excitation contraction coupling

A

-Alpha motor neuron transmits a signal to the muscle fiber

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12
Q

Motor unit

A

A motor unit consists of a motor neuron and all the
muscle fibers it innervates.

One motor neuron can innervate multiple muscle cells at the same time

-> One AP in a nerve will cause contraction in more than 1 muscle fiber

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13
Q

Steps of muscle cell excitation

A
  1. Ach released into the neuromuscular junction
    AP travels down the motoneuron
    The AP at the synapse causes the opening of V-gated Ca2+ channels
    Ca2+ causes the neurotransmitter vesicles to merge with the membrane, causing them to release Acetylcholine in the synaptic cleft
  2. Activation of Ach receptors
    Binding of Ach to the receptors in the muscle causes opening of ligand-gated ion (Na+) channels-> Na+ moves into the cell-> depolarization of end-plate potential
  3. A muscle AP is triggered. If the threshold is reached -> V-gated Na+ channels open and AP is triggered. AP is propagated along sarcolemma into T-tubule
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14
Q

What is an area of high concentration of V-gate Ca2+ channels

A

In the synapse of a pre-synaptic neuron

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15
Q

When does the change from electrical signal to chemical signal happen?

A

when the neurotransmitter is released into the synapse

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16
Q

What channels propagate AP?

A

V-gated Na+ channels

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17
Q

why are the effects of Ach short-lasting?

A

It is quickly broken down

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18
Q

What breaks down Acetylcholine?

A

enzyme acetylcholine esterase

19
Q

AP in skeletal muscle

A
  • Slow depolarization at the start mostly due to the ligand-gated Na+ channels
  • Once the threshold is reached-V-gated Na+ channels open-AP
  • V-gated Na+ channels close, V-gated K+ channels open- repolarization
20
Q

How quick is AP in muscle cell?

A

1-2 msec

21
Q

Steps of muscle contraction

A
  • AP spreads along the sarcolemma and down T-tubule, triggering the opening of V-gated Ca2+ channels in SR→ release Ca2+
  • Ca2+ binds to troponin, moving tropomyosin of the binding site
  • Cross-bridge cycle
  • Ca2+ removed→ contraction ends
22
Q

Where are Calcium channels and their receptors located?

A

Ca2+ channels- Sarcoplasmic reticulum SR

Receptors for channels(Voltage sensors)- t-tubules

23
Q

How is Ca2+ removed after contraction?

A

Calcium is actively pumped back into the sarcoplasmic reticulum via Ca2+-ATPase pumps

24
Q

Sources of ATP for muscle metabolism

A
  1. Creatine phosphate
  2. Anaerobic glucolysis
  3. Aerobic metabolism
25
Q

Creatine phosphate

A

a spare phosphate in the muscle, that can bind to ADP to make ATP

26
Q

How quickly is creatine phosphate used up?

A

15 sec

27
Q

What is creatine phosphate good for?

A

Energy source

Good For quick jump, power lifting, quick and powerful movements

28
Q

Does creatine phosphate require oxygen for ATP production?

A

NO. Anaerobic

29
Q

How long is anaerobic glycolysis effective for?

A

Dominant system from about 10-30 sec of max effort

Can go up to max 120 sec(2 min)

30
Q

Is anaerobic glycolysis effective?

A

only 2 ATP per glucose→ not very effective

31
Q

What if the negative effect of anaerobic glycolysis?

A

Built-up of metabolites that change the ph and stop some processes that require a steady ph from happening

This limits its duration

32
Q

What would anaerobic metabolism be good for?

A

Sprinting

33
Q

Aerobic metabolism

A
  • Can get energy from multiple sources, not just glucose
  • Long lasting
  • Efficient. 32 ATP per glucose

BUT does not generate a lot of power- max 300 W

Requires oxygen

34
Q

Aerobic metabolism

A
  • Can get energy from multiple sources, not just glucose
  • Long lasting
  • Efficient. 32 ATP per glucose

BUT does not generate a lot of power- max 300 W

Requires oxygen

35
Q

VO2 max

A

measures the max oxygen consumption

More oxygen is used as the workload is increased

At the max point- no more Oxygen consumed, aerobic-to anaerobic

36
Q

How can muscle types vary among people?

A
  • genetics and lifestyle
  • Some people have more Type 1 or 2 muscle fibers

the ratio of 2 varies among individuals

37
Q

Type 1 and 2 muscle fibers

A

Type 1- slow twitch, rely on aerobic metabolism. More mitochondria and blood supply. Look redder

Type 2- fast-twitch. Anaerobic( eg weight lifting). Bigger. Higher SR pumping capacity

38
Q

Types of motor units

A

Type 1 (“slow twitch”):

• Units with neurons innervating the slow efficient aerobic cells (maintaining posture, walking)

Type 2 (“fast twitch”):

• Units with the neurons innervating the large fibres that fatigue rapidly but develop large forces (jumping, weight lifting)

39
Q

How can force be regulated?

A
  • Rate of stimulation of individual motor units
  • The number of motor units recruited
40
Q

How long is the muscle contraction?

A

50-200 msec

~100 times longer than AP

41
Q

tetanus

A

merging of twitches into a bigger signal

42
Q

Frequency modulation

A

Temporal summation

Increasing the number of AP and thus muscle twitches leads to tetanus and an increased contraction strength

-longer and more powerful contraction

43
Q

tetanus is caused by a bacteria( different from tetanus in contraction)

A
  • leads to a tetanic contraction in the whole body
  • need to give a relaxant and ventilate them
  • toxin produced by the bacteria leads to continuous AP down the motor neurons

→ lack of inhibition

-

44
Q

Regulating force by muscle fiber recruitment

A
  • typically start with small fibers( aerobic metabolism) and recruit more and more to generate more force( anaerobic)
  • changing voltage in one muscle fiber will not generate more force, but recruiting more fibers at the same time will
  • the first ones to be recruited are the most sensitive, the last ones are the lest sensitive
  • the bigger the voltage the more AP in different muscle cells the more muscle fibers are involved

biosci block 6 & 7 (8 decks)

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