muscles Flashcards

1
Q

1a) What is the role of ATP in myofibril contraction?

A

(Reaction with ATP) breaks/allows binding of myosin to actin/ actinomyosin bridge; Provides energy to move myosin head;

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2
Q

1c )The mice that were not able to produce creatine were homozygous for a recessive allele of a gene. Mice that are heterozygous for this allele are able to produce forces similar to those of normal mice that are homozygous for the dominant allele of the same gene.
Explain why the heterozygous mice can produce forces similar to those of normal mice.

A

(Heterozygous) have one dominant/normal allele (for creatine production);
(This) leads to production of enough/normal amount of creatine;

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3
Q

2a )Describe the roles of calcium ions and ATP in the contraction of a myofibril.

A
  • Calcium ions diffuse into myofibrils from (sarcoplasmic) reticulum;
    -Calcium ions) cause movement of tropomyosin (on actin);
    -(This movement causes) exposure of the binding sites on the actin; Myosin heads attach to binding sites on actin;
    -Hydrolysis of ATP (on myosin heads) causes myosin heads to bend;
    (-Bending) pulling actin molecules;
    -Attachment of a new ATP molecule to each myosin head causes myosin heads to detach (from actin sites).
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4
Q

2(b) ATP is an energy source used in many cell processes. Give two ways in which ATP is a suitable energy source for cells to use.

A

.
1 .Releases relatively small amount of energy / little energy lost as heat;

  1. Releases energy instantaneously;
  2. Phosphorylates other compounds, making them more reactive;
  3. Can be rapidly re-synthesised;
  4. Is not lost from / does not leave cells.
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5
Q

3a)Mitochondrial disease (MD) often causes muscle weakness (lines 1–3). Use your knowledge of respiration and muscle contraction to suggest explanations for this effect of MD.

A
  1. Less force generated because fewer actin and myosin interactions in muscle;
  2. Fatigue caused by lactate from anaerobic respiration.
    1-Reduction in ATP production by aerobic respiration;
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6
Q

c)Suggest how the change in the anticodon of a tRNA leads to MD

A

Change to tRNA leads to wrong amino acid being incorporated into protein; Tertiary structure (of protein) changed;
Protein required for oxidative phosphorylation / the Krebs cycle, so less / no
ATP made.

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7
Q

(d) If someone has MD, the concentration of lactate in their blood after exercise is usually much higher than normal (lines 15–17). Suggest why.

A

Mitochondria / aerobic respiration not producing much / any ATP;
(With MD) increased use of ATP supplied by increase in anaerobic respiration; More lactate produced and leaves muscle by (facilitated) diffusion.

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8
Q

5a)Both slow and fast muscle fibres contain ATPase.
Explain why.

A

Muscle) contraction requires energy / ATP;
Splitting / breakdown / hydrolysis of ATP;
3. Use of ATP by myosin.

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9
Q

5(b) The tissue in the diagram came from muscle with a high proportion of brown-staining fibres. Was the tissue removed from slow or fast skeletal muscle?
Explain your answer.

A

Fast because (lots of) ATPase allows rapid hydrolysis of ATP
or
Slow because (lots of) ATPase allows rapid synthesis of ATP.

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10
Q

5c)The muscle tissue in the diagram had been stained for viewing with a microscope.
What is the evidence that it had been stained for viewing with an optical (light) microscope? Explain your answer.

A

1.
Need light to see colour / brown / yellow;

  1. Cannot see colour / brown / yellow with electrons / an electron microscope;
  2. No organelles are visible.
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11
Q

7 In which type of athlete would the sports scientist expect to find muscle fibres with the highest number of mitochondria?
-Explain the reason for your choice of athlete.

A

(Group) 5 / marathon runners.
5 / marathon runners) have highest percentage of slow fibres;

  1. (Slow fibres) use aerobic respiration / aerobic respiration occurs in mitochondria;
  2. (Slow fibres) best for endurance / long periods of exercise / to avoid fatigue.
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12
Q

7b The leg muscles of long-distance cyclists are usually larger than the leg muscles of non-athletes.
Suggest why.

A

No (overall) change in number of fibres;

Increase in diameter of fibres;

(Due to) training / exercise;

(Long-distance) cyclists have more / higher percentage of slow fibres (than fast)

low fibres of wider diameter than fast fibres; (Long-distance) cyclists have more mitochondria; (Long-distance) cyclists have more capillaries (in muscles).

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13
Q

7c A reader of the sports scientist’s results stated that ‘the results show that regular weightlifting changes your proportion of slow and fast skeletal muscle fibres.’

A

Weightlifting favoured by / weightlifters have a high proportion of fast / low proportion of slow fibres

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14
Q

8(a) What is the role of phosphocreatine (PC) in providing energy during muscle contraction

A

(Phosphocreatine) provides phosphate / phosphorylates;

To make ATP;

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15
Q

8b ) There is a lot of variation in the time taken for PC to be re-formed in people of a very similar age.
Suggest one reason for this variation.

A

Genetic differences;
Level of fitness / amount of regular exercise done / mass of muscle;
Sex;
Ethnicity
Metabolic rate;
Number of fast / slow muscle fibres

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15
Q

9 (a) Describe the part played by each of the following in myofibril contraction.
(i) Tropomyosin
myosin

A

Moves out of the way when calcium ions bind;
Allowing myosin to bind (to actin) / crossbridge formation;

16
Q

9b he high glycogen content of fast muscle fibres

the number of capillaries supplying slow muscle fibres.

A

(Glycogen broken down) gives (lots of) glucose for glycolysis / anaerobic respiration;

Glycolysis / anaerobic respiration not very efficient / only yields 2 ATP per glucose;

17
Q

10c
(c) People who have McArdle’s disease produce less ATP than healthy people. As a result, they are not able to maintain strong muscle contraction during exercise. Use your knowledge of the sliding filament theory to suggest why.

A
  1. Attachment / cross bridges between actin and myosin;
    Accept the role of ADP in attachment
  2. ‘Power stroke’ / movement of myosin heads / pulling of actin;
    Not just ‘filaments slide’ as given in the question stem
  3. Detachment of myosin heads;
  4. Myosin heads move back / to original position / ‘recovery stroke’
18
Q

11bi You could use an optical microscope and a slide of stained muscle tissue to find the diameter of one of the muscle fibres. Explain how.

A

Measure with graticule / eyepiece scale;
Calibrate against something of known size:

19
Q

bii A student found the mean diameter for the slow muscle fibres in a section. Give two precautions that she should have taken when sampling the fibres. Give a reason for each precaution.

A

Equivalent measurements taken;
At random to avoid bias / avoid choice of particular fibres;
Large number to be representative / minimise effect of extremes / of anomalies;

20
Q

(12d) People with mitochondrial disease have mitochondria that do not function properly.

Some people with mitochondrial disease can only exercise for a short time. Explain why a person with mitochondrial disease can only exercise for a short time.

A

(Mitochondria) use aerobic respiration;

Mitochondria produce ATP / release energy required for muscles (to contract);

21
Q

Explain what caused the decrease in length in I band and h zone

A

filaments in I / thin filaments / actin filaments slide in between myosin / thick filament; thin filaments enter H zone / meet in middle of A band / pull Z lines closer

22
Q

14a Labelled antibodies and an electron microscope can be used to produce images locating proteins on the surface of organelles, but cannot be used to observe cross muscle cells. Explain why.

A
  1. e.m. gives high resolution due to short wavelength of electrons;
  2. antibodies attach specifically to target proteins;
  3. gold particles are electron dense;
  4. electrons must pass through a vacuum so material must be dead / fixed for e.m.; 5. cross-bridge cycling requires living cells / metabolism / named aspect-e.g. ATP synthesis;
23
Q

16 ii Explain the role of calcium ions and ATP in bringing about contraction of a muscle fibre.
Calcium ions
atp

A

Bind to troponin;
Remove blocking action of tropomyosin / expose myosin binding sites

ATP:
Allows myosin to detach from actin / to break cross bridge;
[allow attach and detach]
Releases energy to recock / swivel / activate myosin head / drive power stroke;

24
Q

16bi An action potential is generated at the cell body of the motor neurone. Explain how this action potential passes along the motor neurone to the neuromuscular junction.

A

Depolarisation of axon membrane / influx of Na establishes local
currents;

Change permeability to Na / open Na gates of adjoining region;

Adjoining region depolarises / influx of Na ;

25
Q

16bii (ii) When the action potential arrives at the neuromuscular junction, it results in the secretion of acetylcholine into the synaptic cleft. Explain how.

A

Depolarisation of (presynaptic) membrane;
Ca channels open / increased permeability to Ca causing influx of Ca ;
Vesicles move towards / fuse with presynaptic membrane;

26
Q

16cii (ii) Explain why explosive exercises, such as sprinting and weightlifting, will be more affected by this muscle loss than aerobic exercises, such as jogging.

A

Fast fibres used (in explosive exercise);

27
Q

17bi
Describe how calcium ions cause the myofibril to start contracting.

A

Ca binds to [part of] the actin / troponin;
this causes tropomyosin to be displaced;
uncovers [myosin] binding sites [on actin] / allows actin to bind;

28
Q

17bii Describe the events that occur within a myofibril which enable it to contract.

A

myosin heads bind to actin / cross bridge formation / actomyosin formed;
myosin heads / crossbridges swivel / ratchet mechanism; causing actin to slide relative to myosin;
energy provided by hydrolysis of ATP;

29
Q

17 d Recent research has shown that the difference in fibre types is due in part to the presence of different forms of the protein myosin with different molecular shapes.
Explain how a new form of myosin with different properties could have been produced as a result of mutation.

A

change in base sequence in DNA / addition / deletion / substitution of a base in DNA of the gene which codes for myosin;
change in amino acid sequence / primary structure;
causes a different tertiary structure;
which alters the binding properties of myosin;

30
Q

18(b)
Cross-channel swimmers may suffer from muscle fatigue during which the
mechanism is disrupted. One factor thought to contribute to muscle fatigue is a decrease in the availability of calcium ions within muscle fibres. Explain how a decrease in the availability of calcium ions could disrupt the contraction mechanism in muscles.

A

cannot interact with / move tropomyosin from binding sites on actin;

myosin(heads) do not bind / actinomyosin not formed; does not activate ATPase / energy not released from ATP;

31
Q

19bi Explain the importance of ATPase during muscle contraction.

A

breaks down ATP yielding energy;
used to form / break actomyosin bridges;

32
Q

21c Describe the role of calcium ions in the contraction of a sarcomere.

A

interact with / move / touch tropomyosin;

to reveal binding sites on actin;

allowing myosin (heads) to bind / touch actin / actinomyosin formed; activate ATPase / energy released from ATP;

33
Q

22 Acetylcholine is the neurotransmitter at neuromuscular junctions.
(c) Describe how the release of acetylcholine into a neuromuscular junction causes the cell membrane of a muscle fibre to depolarise.

A

movement by diffusion;
binding to receptors on (post-synaptic) membrane;
causing sodium channels to open / sodium ions to move in to muscle (cell);

34
Q

22
(d) Use your knowledge of the processes occurring at a neuromuscular junction to explain each of the following.
(i) The cobra is a very poisonous snake. The molecular structure of cobra toxin is similar to the molecular structure of acetylcholine. The toxin permanently prevents muscle contraction.

A

toxin binds to / competes for / blocks the acetylcholine receptors; acetylcholine can not depolarise the membrane / the toxin does not cause depolarisation;

35
Q

22ii (ii) The insecticide DFP combines with the active site of the enzyme acetylcholinesterase. The muscles stay contracted until the insecticide is lost from the neuromuscular junction.

A

acetylcholinesterase is unable to breakdown acetylcholine; acetylcholine still available to depolarise the membrane / generate action potentials in the membrane;

36
Q

23b
Surgeons sometimes use a drug called pancuronium to stop muscles contracting during an operation.
Pancuronium binds to acetylcholine receptors on muscle fibres.
Pancuronium causes muscle paralysis. Explain how.

A

(b)
(Pancuronium) not removed from receptor by ACh-esterase / not broken down by ACh-esterase;
(Pancuronium) prevents ACh from binding / blocks receptor site;
+ ACh(normally)causesopeningofNa channels/causesaction
potential in muscle fibre;

(Pancuronium) prevents influx of Ca ions (to start contraction);
(Pancuronium) prevents unblocking of binding sites on actin;

37
Q

24 (b) Explain what leads to the differences in appearance between the relaxed myofibril and the contracted myofibril.

A

When contracted:
Thick & thin filaments/myosin & actin overlap more;
Interaction between myosin heads & actin / cross-links form;
Movement of myosin head;
Thin filaments / actin moved along thick filaments / myosin;
Movement of thin filaments / actin pulls Z-lines closer together;
Displacement of tropomyosin to allow interaction;
2+ Role of Ca ;
Role of ATP