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BMS150 test 2 > skeletal muscle II (wk9) > Flashcards

skeletal muscle II (wk9) Flashcards

1
Q

what does myosin bind to form a cross bridge

A

g actin

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2
Q

what are the 3 tropoins and what do they bind to to expose the myosin binding site of g actin

A

§ When calcium binds to Troponin C, The troponin complex undergoes a conformational change and Troponin T “pulls” tropomyosin and Troponin I off of the myosin-binding site of G-actin subunits

§ Myosin is now able to bind to G-actin and form a cross bridge

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3
Q

4 steps of the cross bridge cycle

A
  1. ATP hydrolysis
    2.cross bridge formation
  2. power stroke
  3. detachment of myosin from actin
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4
Q

when myosin is bound to ATP what affinity does it have for actin

A

low; so no cross bridge form

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5
Q

how does myosin turn ATP into ADP + Pi

A

intrinsic ATPase ; myosin head hydrolysis

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6
Q

what is a power stroke

A

The cross bridge generates force as myosin neck rotates toward center or sarcomere
w
* Actin and myosin filaments slide post one another
* Z lines get closer together, shortening the sarcomere & generating force

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7
Q

what gets closer together to shorten the sarcomere and generate force

A

z line

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8
Q

how does myosin detach from actin

A

ATP binds myosinw

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9
Q

what happens if no ATP to bind myosin so that it can detach from actin

A

rigor mortis

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10
Q

why does sarcomere length matter

A

The amount of actin and myosin filament overlap determines the tension that is developed by a contracting muscle.

need some overlap to have tension and contract

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11
Q

isotonic vs isometric

which is force > load and load > force

A

isometric: load>force

isotonic: force> load

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12
Q

isotonic vs isometric which one does the muscle length shorten and which one doesnt change length

A

isometric- no change

isotonic- shortens

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13
Q

how do muscles relax

A

When the sarcolemma is no longer depolarized, the L-type calcium channels no longer trigger release of calcium from the SR through the ryanodine receptor

§ L-type channels return to their resting membrane potential state

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14
Q

where does calcium get re sequestered into

A

SR

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15
Q

how does calcium go back into SR in muscle relaxation

A

SERCA

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16
Q

what binds calcium in the SR to sequester it and keep it there in muscle relaxation

A

calsequestrin and calreticulin

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17
Q

where does cross bridge and muscle contraction take place

A

cytosol

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18
Q

where to put calcium for muscle relation

A

out of cytosol; mainly into SR but some into ECF

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19
Q

what is the fuel storage for type I vs type II muscle fibers

A

I- fat

II- glycogen

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19
Q

how does exercise effect slow vs fast twitch muscls

A

hard to change proportions in body but can change size of individual muscle fibers w particular training

lots of it is genetics

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20
Q

what activity is type I used for

A

low force, endurance ie. marathon

21
Q

what activity is type II used for

A

high force, quick fatigue i.e. sprint

22
Q

contraction time for type I vs II

A

I- slow

II- quick

23
Q

size of motor neuron/ nerve fibers for type I vs II

A

I- small
II- large

24
Q

oxidative vs oxidative glycolytic vs glycolytic

A

type I - O
type IIA- OG
type IIB- G

25
Q

what can be found more in type I slow fibers

A

capillaries (w oxygen), mitochondria, myoglobin

26
Q

what can be found more in type II fast fibers

A

SR (Ca2+), glycolytic enzymesw

27
Q

what are the 3 metabolic systems responsible for recycling AMP and ADP back into ATP to provide a continuous supply of ATP in muscle fibers

A

§ 1. Phosphagen system
§ 2. Glycogen Lactic acid system
§ 3. Aerobic system

28
Q

phosphagen system; which bond has lots of energy

A

High energy phosphate bond of phosphocreatine has more energy than the bond of ATP

29
Q

what 2 things make up phosphagen system

A

phosphocreatine and ATP

30
Q

what time length is the phosphagen system used for

A

8 to 10 seconds of maximal power

31
Q

glycolysis steps

A

glycose - 2 pyruvate - 2 ATPf

32
Q

enough vs not enough oxygen

A

enough; oxidative phosphorylation (aerobic)

not enough is lactic acid

33
Q

what do type IIB fibers do with minimal mitochondria

A

lactic acid;; insufficient oxygens

34
Q

after pyruvate if insufficient oxygen

A

latin acid (via lactate dehydrogenase) which diffuses out of muscles into, ISF, blood and make NAD+

35
Q

how long does the glycogen lactic acid system work for

A

1.3-1.6 minutes

36
Q

how does aerobic system work

A
  • In presence of oxygen, pyruvate is broken down into carbon dioxide, water and energy via citric acid cycle and ETC
    § As long as nutrients in the body last, the aerobic system can be used for unlimited duration
37
Q

what is cori cycle purpose and what is gain/loss of ATP

A

net loss of A4 ATP
propose; get lactate out of muscle and ATP in from liver

38
Q

how to replenish energy system and ATP

A

Energy systems must be replenished

§ Phosphocreatine can be used to replenishes levels of
ATP

§ Glycogen-lactic acid system replenishes both phosphocreatine and ATP

§ Oxidative metabolism can replenish all systems: ATP, phosphocreatine and glycogen-lactic acid system
* Additional oxygen is needed – “oxygen debt”

  • Glycogen levels must be replenished
39
Q

oxygen debt

A

after exercise breath lots

40
Q

what is muscle strength determined by

A

size

i.e. put a lot of force on tendon and could rupture or avulse it

41
Q

how is muscle power measured

A

Measure of the amount of work that the muscle can perform in a given period of time

42
Q

muscle endurance

A

via CARBS

Depends on nutritive support for the muscle
* Amount of glycogen that has been stored in the muscle
prior to the period of exercise
§ High CHO diet stores more glycogen in muscles than mixed diet or high fat diet
* Also greatly depends on the type & size of muscle fibre that is predominant in the muscle under investigation

43
Q

mechanisms of skeletal muscle remodeling- growth

A

hypertrophy, hyperplasia, legthening

44
Q

hypertrophy

A

increase muscle fibre size by adding more myosin and actin

45
Q

hyperplasia

A

increase # of fibers

46
Q

lengthening

A

add new sarcomeres to ends of fibers

47
Q

hypertrophy vs hyperplasia vs lengthiening

A

Hypertrophy (common, weeks)
-Caused by near maximal force development (eg. weight lifting)
Increase in actin and myosin
Myofibrils split

  • Hyperplasia (rare)
    – Formation of new muscle fibers
    – Can occur with endurance training
  • Hypertrophy and hyperplasia
    – Increased force generation
    – No change in shortening capacity or velocity of contraction
  • Lengthening (normal)
    – Occurs with normal growth
    – No change in force development
    – Increased shortening capacity
    – Increased contraction velocity
48
Q

muscle atrophy

A

§ Muscle no longer receives contractile signals required to
maintain normal muscle size

§ Causes of muscle atrophy * Denervation/neuropathy * Tenotomy
* Sedentary lifestyle
* Plaster cast
* Space flight (micro-gravity)

49
Q

acute vs chronic muscle atrophy

A

§ Acute/subacute
* Degeneration of contractile
proteins
* Decrease max force of contraction
* Decrease velocity of contraction
* If contractile signals return, full return to function can occur in as little as 3 months
§ Eg. Nerve supply grows back,

§ Functional return of the muscle decreases, with no return of function after 1 to 2 year
§ In final stages, muscle fibers are destroyed.
* Number of sarcomeres/fibre will often be lost, resulting in a shortening of the muscle + fibrosis à contracture
* Fiber are replaced by fibrous and fatty tissue with little contractile proteins

BMS150 test 2 (18 decks)

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