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MSK exam 3 AP lower limb > energy metabolism in muscle > Flashcards

energy metabolism in muscle Flashcards

1
Q

the main types of fuel used by muscle for energy metabolism are what?

A

glycogen
glucose
free fatty acids

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2
Q

what does muscle use predominantly at rest?

A

fatty acids

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3
Q

what does muscle use during high intensity isometric exercise?

A

anaerobic glycolysis

creatine kinase reaction

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4
Q

during low intensity submaximal exercise, the main sources of energy are ….

A

blood glucose and free fatty acids

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5
Q

with high intensity submaximal exercise what happens to the proportion of energy derived from glycogen and glucose?

A

it is increased, glycogen becomes the main sources

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6
Q

when does fatigue happen?

A

when glucose and glycogen stores are depleted

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7
Q

during the first hour of mild, low intensity exercise (jogging) what is the major source of energy ?

A

glucose
glucagon
free fatty acids

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8
Q

the uptake of free fatty acids by muscle increases when?

A

during one to four hours of mild to moderate prolonged exercise

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9
Q

what happens after four hours of exercise?

A

lipid oxidation becomes the major source of energy

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10
Q

muscle contraction and relaxation depend primarily on what

A

hydrolysis of ATP

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11
Q

when does anaerobic glycolysis occur usually

A

during conditions of high intensity, sustained isometric muscular activity (lifting heavy objects)

particularly in the setting of limited blood flow and oxygen supply to exercising muscle fibers

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12
Q

increased concentrations of lactate within muscles, and the accumulation of Pi, ADP and movovalent form of organic phosphate are related to what?

A

fatigue

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13
Q

aerobic glycolysis is important when?

A

during dynamic forms of exercise, such as walking, running.

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14
Q

what is the main source of energy is muscle and other cells?

A

oxidative phosphorylation

this system produces 17-18 times as much adenosine triphosphate from the same amount of glucose

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15
Q

when is the phosphocreatine pathway utilized?

A

during very high intensity exercise

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16
Q

what is the process of the phosphocreatine pathway?

A

rapid formation of ATP can be accomplished through the reaction of phosphocreatine with ADP, catalyzed by creatine kinase

this is very BRIEF b/c of small amount of phosphocreatine in the muscle

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17
Q

where is creatinephosphate synthesize and subsequently transported?

A

synthesized in the liver and transported to the muscle cells via the bloodstream

for storage in skeletal muscle and the brain

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18
Q

when can creatine phosphate donate a phosphate group to ADP to form ATP?

A

during the first 2-7 seconds following an intense muscular or neuronal effort

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19
Q

what does ATP derived from creatininephosphate supply?

A

immediate short bursts of contractile energy

high jumps, sprints, etc

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20
Q

what can you do with excess ATP during a period of low effort ?

A

convert to creatininephosphate making an energy reservoir for rapid buffering and regeneration of ATP

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21
Q

what organs can you find creatine kinase in?

A

heart
brain
lung
skeletal muscle

22
Q

where do you find CK1 (aka CK-BB)

A

brain
smooth muscles
lungs

23
Q

CK-2 is found where? aka CK-MB

A

mostly in the heart

24
Q

CK3- aka CK-MM is found where?

A

mostly in skeletal muscle

25
Q

CK is assayed in blood tests and an elevation of CK is an indication of what?

A

myocardial infarction

rhabdomyolysis (severe muscle breakdown)

muscular dystrophy, myasthenia gravis, myositis

acute renal failure

drugs (statins, anticoagulants, aspirin, cocaine, etc.)

26
Q

what is the purine nucleotide cycle ?

A

intensely exercising muscle can generate ATP over a short period of time using adenylate kinase reaction

this reaction catalyzes the conversion of two ADP molecules into one molecule of ATP and AMP

this cycle tries to catch up with insufficient ATP supply by converting ADP to ATP

2ADP–> ATP–> AMP—> IMP–> NH3

27
Q

what is a cause of metabolic myopathy?

A

AMP deaminase converts AMP to IMP and releases an NH3 molecule in the process

deficiency of AMP deaminase is apparently a cause that is common of exercise-induced myopathy and metabolic myopathy

28
Q

lipid metabolism in muscle occurs via what?

A

beta and omega oxidation of fatty acids

29
Q

long chain fatty acids constitute a major source of energy for what?

A

prolonged low intensity exercise, lasting for more than 40-50 minutes

30
Q

the mitochondrial membrane is not permeable to long-chain fatty acids so what must happen?

A

a multistep process

in cytoplasm–> long chain fatty acids are first activated by long-chain acyl-CoA synthetase to their CoA thioesters

CoA thioesters then linked with carnitine by the enzyme Carnitin palmitoyltransferase (CPT I)

this is now acylcarnitine and is transferred across the inner mitochondrial membrane by carnitine;acylcarnitine transferase

once in the mitochondrial matrix it is converted back to free acyl-CoA derivative and carnitine by CPT II

the long chain acyl-CoA enters the beta-oxidation pathway

31
Q

what happens to 95 percent of Acetyl-Coa that is hepatic ?

A

it is converted to ketones which are important sources of energy for all tissues, particularly the brain

during prolonged fasting ketones provide an important source of energy in brain tissue because the BBB is impermeable to long chain fatty acids

32
Q

what is omega-oxidation of fatty acids ?

A

during prolonged fasting 20 percent of total cellular oxidation of fatty acids is accomplished in liver peroxisomes through omega-oxidation
producing DCA’s (dicarboxylic acids)

33
Q

what is different about peroxisomes?

A

beta oxidation occurs via a flavin-containing oxidase that generates H2O2, and then through peroxisomal catalase H20 and O2, therefore some energy is wasted

34
Q

in metabolic defects of intramitochondrial fatty acid oxidation what is going on?

A

mitochondrial beta-oxidationof DCA’s is impaired at a time when the production of DCA’s is increased due to the recruitment of peroxisomal omega-oxidation, hence FINDING OF DCA”S IN THE URINE

35
Q

what is a useful marker of diagnosing inborn errors of fatty acid oxidation?

A

detection of acylcarnitine derivatives in serum and the detection of dicarboxylic acids and acylglycines in urine

36
Q

what is the cori cycle?

A

recycling of lactic acid

cori cycle operates more efficiently when the muscular activity has stopped

in muscle glucose–> pyruvate–> lactate

lactate then goes to the liver

lacate–> pyruvate – > glucose

glucose goes back to muscle via blood

37
Q

what is the significance of the cori cycle?

A

the prevention of lactic acidosis in the muscle under anaerobic conditions

the conversion of lactate to pyruvate provides about 30 percent of the glucose for gluconeogenesis in liver

38
Q

what makes lactate

A

lactate dehydrogenase

39
Q

in exercising skeletal muscle what happens when NADH production exceeds the oxidative capacity of the respiratory chain?

A

this results in elevated NADH/NAD+ ratio, favoring reduction of pyruvate to lactate

THEREFORE during intense exercise, lactate accumulates in muscle causing a drop in intracellular pH, resulting in CRAMPS

40
Q

how does the ratio of NADH/NAD+ in the liver and heart compare to exercising muscle?

A

the ratio is lower in heart and liver

41
Q

what does the liver convert pyruvate into ?

A

glucose by gluconeogenesis or oxidized in the TCA cycle

42
Q

what does the heart excluseivley oxidize lactate to?

A

CO2 and H20 via the TCA cycle

43
Q

what is lactic acidosis ?

A

elevated concentrations of lactate in the plasma

occurs whemn there is a myocardial infarction, PE, uncontrolled hemorrhage, or when an individual is in shock

the failure to bring adequate amounts of oxgyen to the tissues results in impaired oxidative phophorylation and decreased ATP synthesis

to survive the cell relies on anaerobic glycolysis which prodcuces lactic acid as end product

44
Q

elevated muscle lacate accounts for what?

A

fatigue and pain induced by strenuous exercise

45
Q

how is NAD+ regenerated in anaerobic conditions?

A

NAD+ is regenerated by further metabolism of pyruvate

electrons are transferred from NADH to pyruvate by lactate dehydrogenase forming NAD+ and lactate

46
Q

what are the symptoms of metabolic myopathy

A

exercise intolerance

muscle pain and cramps

47
Q

what are some causes of metabolic myopathies?

A

carnitine deficiency syndrome

fatty acid transport defects

defects of beta-oxidation enzymes

48
Q

what is a primary carntitine deficiency

A

lack of carnitine in the cell (such as a mutation in the carnitine transporter) and is associated with lipid myopathy

fatty acid oxidation is significantly reduced
DON”T SEE elevated levels of acyl carnitine

49
Q

what is a secondary carnitine deficiency

A

occurs when the carnitine is sequestered in the form of acyl-carnitine (carnitine cannot be removed from acyl group, such as defects in carnitine acyl transferase 2)

WOULD SEE ELEVATED levels of ACYL CARNITINE fatty acid oxidation is significantly reduced

50
Q

fatty acids can only be used in

A

aerobic metabolism

MSK exam 3 AP lower limb (15 decks)

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