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

skeletal muscle II (wk9) Flashcards

(50 cards)

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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

Study These Flashcards
A

low force, endurance ie. marathon

21
Q

what activity is type II used for

Study These Flashcards
A

high force, quick fatigue i.e. sprint

22
Q

contraction time for type I vs II

Study These Flashcards
A

I- slow

II- quick

23
Q

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

Study These Flashcards
A

I- small
II- large

24
oxidative vs oxidative glycolytic vs glycolytic
type I - O type IIA- OG type IIB- G
25
what can be found more in type I slow fibers
capillaries (w oxygen), mitochondria, myoglobin
26
what can be found more in type II fast fibers
SR (Ca2+), glycolytic enzymesw
27
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
§ 1. Phosphagen system § 2. Glycogen Lactic acid system § 3. Aerobic system
28
phosphagen system; which bond has lots of energy
High energy phosphate bond of phosphocreatine has more energy than the bond of ATP
29
what 2 things make up phosphagen system
phosphocreatine and ATP
30
what time length is the phosphagen system used for
8 to 10 seconds of maximal power
31
glycolysis steps
glycose - 2 pyruvate - 2 ATPf
32
enough vs not enough oxygen
enough; oxidative phosphorylation (aerobic) not enough is lactic acid
33
what do type IIB fibers do with minimal mitochondria
lactic acid;; insufficient oxygens
34
after pyruvate if insufficient oxygen
latin acid (via lactate dehydrogenase) which diffuses out of muscles into, ISF, blood and make NAD+
35
how long does the glycogen lactic acid system work for
1.3-1.6 minutes
36
how does aerobic system work
* 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
what is cori cycle purpose and what is gain/loss of ATP
net loss of A4 ATP propose; get lactate out of muscle and ATP in from liver
38
how to replenish energy system and ATP
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
oxygen debt
after exercise breath lots
40
what is muscle strength determined by
size i.e. put a lot of force on tendon and could rupture or avulse it
41
how is muscle power measured
Measure of the amount of work that the muscle can perform in a given period of time
42
muscle endurance
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
mechanisms of skeletal muscle remodeling- growth
hypertrophy, hyperplasia, legthening
44
hypertrophy
increase muscle fibre size by adding more myosin and actin
45
hyperplasia
increase # of fibers
46
lengthening
add new sarcomeres to ends of fibers
47
hypertrophy vs hyperplasia vs lengthiening
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
muscle atrophy
§ 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
acute vs chronic muscle atrophy
§ 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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