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MSK exam 1 > metabolic profile of muscles > Flashcards

metabolic profile of muscles Flashcards

1
Q

skeletal muscle fascinating facts

A 
largest single tissue type in body
25% at birth
40% young adult
30% old age
consumes 30% O2 at rest
>90%  O2 at maximum exertion
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2
Q

types of skeletal muscle fibers

A

type I slow oxidative
type IIa fast oxidative glycolytic
type IIb fast glycolytic

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3
Q

type I slow oxidative

A

red fibers
produce most ATP aerobically
slow to fatigue
maintain prolonged low-intensity contractions

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4
Q

type IIb fast glycolytic

A

white fibers
produce most ATP by anaerobic glycolysis
fatigue rapidly
employ in rapid powerful contractions over short periods

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5
Q

type IIa fast oxidative-glycolytic

A

red fibers, intermediate in character, can produce ATP by both methods

prevalent in muscles involved in regular movement, present in most if not all human muscles

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6
Q

contraction velocity of skeletal muscle fibers

A

type I-slow
type IIa-fast
type IIb-fast

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7
Q

contraction duration of skeletal muscle fibers

A

type I-long
tpye IIa-short
type IIb-short

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8
Q

myosin-ATPase activity of skeletal muscle fibers

A

type I-low
type IIa-high
type IIb-high

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9
Q

energy utilization of skeletal muscle fibers

A

type I-low
type IIa-high
type IIb-high

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10
Q

fatigue resistance of skeletal muscle fibers

A

type I-high
type IIa-intermediate
type IIb-low

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11
Q

myoglobin content of skeletal muscle fibers

A

type I-high
type IIa-intermediate
type IIb-low

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12
Q

oxidative capacity of skeletal muscle fibers

A

type I-high
type IIa-high
type IIb-low

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13
Q

mitochondria of skeletal muscle fibers

A

type I-high
type IIa-high
type IIb-low

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14
Q

capillaries of skeletal muscle fibers

A

type I-many
type IIa-many
type IIb-few

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15
Q

glycolytic capacity of skeletal muscle fibers

A

type I-low
type IIa-intermediate
type IIb-high

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16
Q

glycogen content of skeletal muscle fibers

A

type I-low
type IIa-intermediate
type IIb-high

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17
Q

triacylglycerol content of skeletal muscle fibers

A

type I-high
type IIa-intermediate
type IIb-low

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18
Q

fiber diameter of skeletal muscle fibers

A

type I-small
type IIa-intermediate
type IIb-large

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19
Q

cardiac muscle

A

metabolism almost totally aerobic
lots of mitochondria (40% of cytoplasmic space)
much myoglobin
can use-FA, glucose, KB, lactate
glycogen and lipid stored for emergencies
prefers FA

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20
Q

smooth muscle

A

most energy from glycolysis
less oxidative capacity than cardiac muscle (less mitochondria)
can also use lactate

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21
Q

energy for muscle contraction

A

immediate source is ATP

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22
Q

myosis ATPase is used in

A

ATP——->ADP +Pi

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23
Q

creatine kinase (CK) reaction

A

ATP+Creatine phosphocreatine+ADP

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24
Q

adenylate kinase (AK) reaction

A

2ADP ATP+AMP

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25
Q

formation of creatine

A

glycine to guanidino-acetate via arginine to ornithine in the kidney

guanidino-acetate to creatine via SAM to s-adenosyl homocysteine in liver

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26
Q

formation of creatinine

A

creatine phsphate to creatinine via spontaneous cyclization in muscle and brain

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27
Q

three sources of energy stored in typical skeletal muscle

A

ATP
CP
Glycogen

28
Q

AMP activates

A

glycogen phosphorylase B (glycogenolysis)

29
Q

AMP, Pi & NH3 activates

A

phosphofructokinase-1 (glycolysis)

30
Q

ADP activates

A

isocitrate dehydrogenase (TCA cycle)

31
Q

Ca2+ ion activates

A 
glycogen phosphorylase (b->a) (glycogenolysis)
pyruvate dehydrogenase (glycolysis -> TCA)
isocitrate dehydrogenase (TCA)
oxoglutarate dehydrogenase (TCA)
32
Q

how is ATP replenished when muscles contract

A

AMP concentration is increased as ATP is used and then phosphorylase b and PFK-1 are activated and more ATP is made

33
Q

3 mechanisms for activation of glycogen phosphorylase

A

muscle contraction
nerve impulse
epinephrine

34
Q

muscle contraction to activate glycogen phosphorylase

A

AMP increase activates change from glycogen phosphorylase b -> a

35
Q

nerve impulse to activate glycogen phosphorylase

A

Ca2+ is released, calmodulin causes phosphorylase kinase which then causes change from glycogen phosphorylase b->a

36
Q

epinephrine to activate glycogen phosphorylase

A

cAMP activates protein kinase A activates phosphorylase kinase which causes change from glycogen phosphorylase b->a

37
Q

activation of glycogen breakdown (glycogenolysis)

A

AMP and Ca2+ ions activate glycogen phosphorylase b (inactive form)

change to glycogen phosphorylase a (active)

38
Q

when is epinephrine used to change glycogen phosphorylase b –>a?

A

at times of stress

39
Q

mcardle’s disease

A

type V glycogen storage disease
myopathy due to defect in glycogen breakdown
deficiency of muscle glycogen phosphorylase
painful muscle cramps and unusual fatigue
usual incs [lactate] on exercise is absent
vigorous anaerobic exrc leads to rhabdomyolysis
patients should exercise gently
prior ingestion of sucrose beneficial

40
Q

activation of glycolysis

A

AMP,Pi, NH3 activate PFK-1

AMP is primarily responsible for initial activation

41
Q

activation of TCA cycle

A

Ca2+ activates: pyruvate, isocitrate and a-oxoglutarate dehydrogenase

ADP activates isocitrate dyhydrogenase

42
Q

skeletal muscle (well fed state)

A

carbohydrate metabolism
insulin up due to blood glucose up
glucose transport up via GLUT-4 by insulin

43
Q

carbohydrate metabolism

A

glucose transport up (insulin incrs GLUT-4)
glycogen synthesis up (type IIb-if glycogen stores depleted)

insulin activates glycogen synthase
insulin inactivates glycogen phosphorylase

glucose available-no recruitment for glycogen as energy source

glycolysis for ATP production

44
Q

Fat in skeletal muscle (well fed state)

A

FA released from chylomicra and VLDL

fat oxidation will be less important until glucose level falls (insulin decreases circulating level of fatty acids through inhibition of hormone-sensitive lipase in adipose tissue)

45
Q

amino acids in skeletal muscle (well fed state)

A

protein synthesis increased as required

metabolism of branched chain AA

46
Q

energy metabolism in muscle (fibers)

A

type IIb-glycogen can be mobilized for rapid release of metabolic substrate

type IIb fibers-lacrate produce by anaerobic glycolysis

type I and IIa-most energy produced by oxidative metabolism

47
Q

type IIb fibers (white)

A

energy production by anaerobic glycolysis (largely from glycogen to lactate)

oxygen debt, cori cycle, muscle fatigue, replenishment of glycogen levels

48
Q

advantages of carbohydrates over fat

A

catabolism can be switched on faster
maximum rate of ATP formation is greater
yield of ATP peroxygen molecule is greater

49
Q

major disadvantage of carbohydrate

A

produces about 7 times less energy per gram (stored hydrated)

50
Q

oxygen debt

A

the continued consumption of oxygen after vigorous sustained exercise is over (see slide 35 diagram)

51
Q

cori cycle

A

particularly relevant to exercising skeletal muscle
RBC turns glucose to lactate and ATP
lactate taken up to liver and turned to glucose
glucose is taken back to RBC

52
Q

muscle fatigue

A

increase in Pi (major contributor)
fall in pH (inhibits PFK-1 and release of Ca2+ from SR)

failure to maintain synthesis of Ach in an adequate rate

Try increase in brain leads to serotonin increase (relaxation)

53
Q

replenishment of glycogen levels

A

insulin activates glycogen synthase (b to a form)

G=6-P also activates the inactive b form

see slide 39

54
Q

type I and IIa (red)

A

catabolize glucose and fats as available (mostly fats)

sources of fats: triacylglycerols (VLDL and chylomicra) and free FA from adipocytes (bound to albumin)

55
Q

glucose-fatty acid cycle

A

fat spares glucose vice-versa according to availability (slide 42 and 43)

56
Q

muscle metabolism in the fasted state: starvation

A

glucose reserved for brain and RBC
muscle uses FA and KB
muscles provides AA c-skeletons for liver to make glucose
AA largely released as alanine and glutamine

57
Q

skeletal muscle starvation

A

carbohydrate-glucose uptake decrease (low insulin) heance little carbohydrate metabolism

glucagon does not activate glycogen phosphorylase in muscle

58
Q

skeletal muscle (starvation) fat

A

FA-major source of fuel after 4h
FA and KB major source of fuel after 1-2 days
FA major source of fuel after 3 weeks

59
Q

skeletal muscle (starvation) protein

A

breakdown of muscle protein to provide C atoms for gluconeogenesis (rapid during days 1-2 stimulated by cortisol)

breakdown decreases after 2 days as KB take over from glucose as major fuel (especially in the brain)

60
Q

synthesis of ketone bodies

A

liver mitochondria
excess acetyl CoA is converted to acetoacetate, B-hydroxybutyrate and acetone

(slide 49)

61
Q

utilization of ketone bodies as fuel

A

muscles and other extra hepatic tissue

KB are converted back to 2 molecules of acetyl CoA

62
Q

muscle metabolism in starvation

A

slide 51

63
Q

muscle: metabolic role during starvation

A

degradation of muscle proteins provides C-atom for gluconeogenesis

released from muscle as AA-mostly alanine glutamine

major site of metabolism of branch chain aa

64
Q

cardiac muscle

A

metabolism in the fed state
oxidative catbolism supplies >95% energy requirement (fatty acids 60-90%, glucose 10-40%)
can oxidize lactate under extreme cicumstances

at high blood glucose, insulin enhances uptake and metabolism of extra glucose

(stimilates uptake of GLUT-4 into cardiac cell membrane nad stimulate PFK-2 to produce more F-2,6 bisphosphate)

small stores of glycogen for extreme circumstances

65
Q

cardiac muscle metabolism in the fasted state

A

it is also in poorly controlled diabetes
oxidizes FA and ketone bodies
KB can become a major substrate

66
Q

cardiac muscle metabolism in ischemic conditions

A

myocardial infarction

ATP levels fall
AMP levels rise

anaerobic glycolysis is stimulated to compensate for the loss of aerobic ATP production by 2 AMP-mediated mechanisms

67
Q

cardiac muscle activation of anaerobic glycolysis in ischemic condtions

A

myocardial infarction

AMP activates AMP-activated protein kinase which phosphorylates PFK-2 (activation)
this leads to prodcution of F-2,6-BP which activates PFK-1

AMP activates PFK-1 directly, allosteric binding

slide 57

MSK exam 1 (3 decks)

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