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MSK exam 1 > metabolic profile of muscles > Flashcards

metabolic profile of muscles Flashcards

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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
formation of creatine
glycine to guanidino-acetate via arginine to ornithine in the kidney guanidino-acetate to creatine via SAM to s-adenosyl homocysteine in liver
26
formation of creatinine
creatine phsphate to creatinine via spontaneous cyclization in muscle and brain
27
three sources of energy stored in typical skeletal muscle
ATP CP Glycogen
28
AMP activates
glycogen phosphorylase B (glycogenolysis)
29
AMP, Pi & NH3 activates
phosphofructokinase-1 (glycolysis)
30
ADP activates
isocitrate dehydrogenase (TCA cycle)
31
Ca2+ ion activates
``` glycogen phosphorylase (b->a) (glycogenolysis) pyruvate dehydrogenase (glycolysis -> TCA) isocitrate dehydrogenase (TCA) oxoglutarate dehydrogenase (TCA) ```
32
how is ATP replenished when muscles contract
AMP concentration is increased as ATP is used and then phosphorylase b and PFK-1 are activated and more ATP is made
33
3 mechanisms for activation of glycogen phosphorylase
muscle contraction nerve impulse epinephrine
34
muscle contraction to activate glycogen phosphorylase
AMP increase activates change from glycogen phosphorylase b -> a
35
nerve impulse to activate glycogen phosphorylase
Ca2+ is released, calmodulin causes phosphorylase kinase which then causes change from glycogen phosphorylase b->a
36
epinephrine to activate glycogen phosphorylase
cAMP activates protein kinase A activates phosphorylase kinase which causes change from glycogen phosphorylase b->a
37
activation of glycogen breakdown (glycogenolysis)
AMP and Ca2+ ions activate glycogen phosphorylase b (inactive form) change to glycogen phosphorylase a (active)
38
when is epinephrine used to change glycogen phosphorylase b -->a?
at times of stress
39
mcardle's disease
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
activation of glycolysis
AMP,Pi, NH3 activate PFK-1 | AMP is primarily responsible for initial activation
41
activation of TCA cycle
Ca2+ activates: pyruvate, isocitrate and a-oxoglutarate dehydrogenase ADP activates isocitrate dyhydrogenase
42
skeletal muscle (well fed state)
carbohydrate metabolism insulin up due to blood glucose up glucose transport up via GLUT-4 by insulin
43
carbohydrate metabolism
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
Fat in skeletal muscle (well fed state)
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
amino acids in skeletal muscle (well fed state)
protein synthesis increased as required | metabolism of branched chain AA
46
energy metabolism in muscle (fibers)
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
type IIb fibers (white)
energy production by anaerobic glycolysis (largely from glycogen to lactate) oxygen debt, cori cycle, muscle fatigue, replenishment of glycogen levels
48
advantages of carbohydrates over fat
catabolism can be switched on faster maximum rate of ATP formation is greater yield of ATP peroxygen molecule is greater
49
major disadvantage of carbohydrate
produces about 7 times less energy per gram (stored hydrated)
50
oxygen debt
the continued consumption of oxygen after vigorous sustained exercise is over (see slide 35 diagram)
51
cori cycle
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
muscle fatigue
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
replenishment of glycogen levels
insulin activates glycogen synthase (b to a form) G=6-P also activates the inactive b form see slide 39
54
type I and IIa (red)
catabolize glucose and fats as available (mostly fats) sources of fats: triacylglycerols (VLDL and chylomicra) and free FA from adipocytes (bound to albumin)
55
glucose-fatty acid cycle
fat spares glucose vice-versa according to availability (slide 42 and 43)
56
muscle metabolism in the fasted state: starvation
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
skeletal muscle starvation
carbohydrate-glucose uptake decrease (low insulin) heance little carbohydrate metabolism glucagon does not activate glycogen phosphorylase in muscle
58
skeletal muscle (starvation) fat
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
skeletal muscle (starvation) protein
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
synthesis of ketone bodies
liver mitochondria excess acetyl CoA is converted to acetoacetate, B-hydroxybutyrate and acetone (slide 49)
61
utilization of ketone bodies as fuel
muscles and other extra hepatic tissue | KB are converted back to 2 molecules of acetyl CoA
62
muscle metabolism in starvation
slide 51
63
muscle: metabolic role during starvation
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
cardiac muscle
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
cardiac muscle metabolism in the fasted state
it is also in poorly controlled diabetes oxidizes FA and ketone bodies KB can become a major substrate
66
cardiac muscle metabolism in ischemic conditions
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
cardiac muscle activation of anaerobic glycolysis in ischemic condtions
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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