muscles Flashcards

1
Q

general roles of skeletal muscle and structure?

A

voluntary movements of bones
inspiration and contraction of diaphragm
skeletal muscle ‘pump’ helps return venous blood to the heart

structure break down - muscle fascicle - muscle fibre - myofibril - sarcomeres

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2
Q

sarcomeres - what are the lines and bands and stuff?

A

they appear striated

z line at each end

I bind = just actin (the lighter one) - gets smaller as muscle contracts

A band = overlapping of actin and myosin, appears darkest

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3
Q

how is contraction initiated?

A

Motor neurons carry electrical impulse to the muscle.
AP causes release of ACh.
Depolarises sarcolemma, passes along T tubules and right to the sarcoplasmic reticulum.
Depolarises it and releases Ca2+ from stores

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4
Q

what are T tubules?

A

These are invaginations in the plasma membrane.
Form a triad with sarcoplasmic reticulum

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5
Q

how quick is contraction?

A

5 cycles of the whole thingy per head (myosin head)

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6
Q

explain how the contraction mechanism works

A

(Starting with the myosin bound to actin strongly) ATP binds to myosin head, reducing affinity of myosin head for the actin, breaking crossbridge.
Second ATP is hydrolysed for head straightening. The ADP and phosphate actually stay bound to the myosin heads, phosphorylation causes a conformational change, and the myosin head straightens out.
Then makes a weak link to actin = actin myosin cross bridge.
Phosphate is released from the myosin head, strengthening the cross bridge. Head bends, pulls it along = contraction. ADP is released, we’re back to a tight binding with a bent head

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7
Q

what is summation?

A

when action potentials in quick succession cause an increase in strength of contraction

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8
Q

what are the three kinds of muscle fibres (speed-wise) and their colour?

A

slow/type I = red due to myoglobin which stores oxygen, has a rich blood supply to provide this oxygen, slow levels of sustainable force like posture

fast oxidative/type IIa = middle man, typically more forceful so needs more ATP and has glycogen stores

fast glycolytic/type IIb = anaerobic so rely on glycolysis

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9
Q

neuromuscular junction? botox?

A

we kind of know this - nicotinic Ach receptors (LGICs) , let in Na+, activates Ca2+ voltage gated channels etc…

botox effects snares, preventing docking and therefore exocytosis of ACh, causing paralysis/muscle weakness

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10
Q

inhibitors?

A

literally at every possible point/step of muscle contraction

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11
Q

aerobic training is and does what?

A

aerobic - long distance running/swimming = sustained low level exercise, stimulating slow fibres

type IIx fibres may be converted into IIa

this increases resistance to fatigue, also causes changes in capillaries to improve blood suppy
no increase in strength

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12
Q

anaerobic training is and does what?

A

contraction of type IIa and IIb fast twitch muscle fibres like wright lifting

results in an increase in strength as more myofilaments are added to myofibrils to increase diameter of muscle fibres (not more muscle fibres just bigger ones)

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13
Q

energy delivery when we exercise - how fast is oxygen delivery and what does this mean for the beginning of exercise?

A

increase in O2 demand cannot be met immediately, it takes a few minutes for oxygen delivery and uptake to reach it’s maximum

this means in the earlier (2) minutes of exercise we rely on stored energy

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14
Q

what stored energy is sued in early exercise?

A

ATP and phosphocreatine stores - used up very quickly

must change to anaerobic glycolysis

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15
Q

what are the three immediate stores of energy that don’t last long?

A

ATP to ADP + Pi

ADP + PCr in presence of creatinine kinase makes ATP + creatinine

adenylate kinase ADP + ADP forms ATP and AMP

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16
Q

anaerobic phase of energy release - how of muscle fibres use glycogen stores? why is it inefficient?

A

anaerobic metabolism uses glycolysis

stored glycogen of 300-400g in muscle fibres

glycogenolysis produces glucose 1 phosphate, converted to glucose 6 phosphate and enters glycolysis

net 2 molecules of ATP is inefficient

17
Q

isseu with anaerobic glycolysis?

A

2 ATP is a low yield
pyruvate is converted to lactic acid which causes fatigue

18
Q

after a few minutes the aerobic phase beings - how is this better and what happens to the previously produced lactate

A

generates around 30 ATP
glucose is sourced from blood following glycogen break down in liver
lactate converted into pyruvate and enters ox. phosph

19
Q

in extended periods of exercise, what else can happen to lactate? what else can be used energy?

A

lactate and alanine can be used by the liver to generate more glucose

can be released from non-exercising muscles to redistribute glycogen stored

fat - non-muscle lipids are mobilised, made back into fatty acids and taken up by muscle, where triacylglycerol stores are broken down

20
Q

muscle fatigue - what is it?

A

a decline in force and velocity of muscle shortening

21
Q

what is
1) central fatigue
2) peripheral fatigue
3)high-frequency fatigue and low-frequency fatigue

A

1) central fatigue is a minor factor, and is possible to overcome
2) peripheral fatigue - at level of muscle fibre with various factors
3) high frequency fatigue is an alteration in the cell Na+/K+ balance, which effects membrane potential and reduces efficiency in generation of action potentials
happens more in the fast type II fibres

low frequency fatigue is reduced release of Ca2+, typically in type I slow fibres

22
Q

ATP depletion, lactic acid build up and glycogen depletion - what are they?

A

intense stimulation can cause large drops in ATP near the sites of cross-bridges

lactic acid build up can lead to cell acidification

glycogen depletion is exactly what it says