Biochem Exam 2: Energy Metabolism Of Muscle

Front 1

cardiac muscle is rich in _____ but have very little ______

Back 1

mitochondria; glycogen

Front 2

how does cardiac muscle mainly obtain energy?

Back 2

oxidative phosphorylation

Front 3

what are two main molecular components of muscle contraction?

Back 3

Myosin and actin

Front 4

what three molecular components of muscle contraction regulate muscle contraction?

Back 4

troponins, tropomyosin and calcium ion

Front 5

what are the three major causes of muscle diseases?

Back 5

insufficient energy supply, impaired neurological control, and loss of function mutations in structural proteins

Front 6

What provides energy for muscle contraction?
what are two possible causes of insufficient energy supply?

Back 6

ATP

ischemia and genetic diseases of fuel metabolism

Front 7

what is a possible cause of impaired neurological control?

Back 7

myasthenia gravis

(not enough intracellular Ca2+)

Front 8

what are two possible loss of function mutations in muscle structural proteins?

Back 8

muscular dystrophies and cardiomyopathies

Front 9

what are both duchenne and becker muscular dystrophies caused by?

Back 9

mutations in dystrophin genes

(result in patients wheel chair bound by age 13 or 16, Duschenne more severe)

Front 10

what is dystrophin?

Back 10

molecule that participates in linking muscle cytoskeleton to membrane proteins in the sarcolemma

Front 11

what are the two major sources of ATP in muscle?

Back 11

glycolysis and oxidative phosphorylation

Front 12

what are the two sources of glucose for glycolysis?

Back 12

glycogen and blood glucose

Front 13

what are the four sources of NADH and FADH2 of oxidative phosphorylation?

Back 13

TCA cycle, beta oxidation of fatty acids, oxidation of branched-chain amino acids, and conversion of lactate to pyruvate

Front 14

what is the preferred source used for energy production depent on?

Back 14

muscle type and physiological conditions

Front 15

why is it not feasible to store ATP?

Back 15

ATP is an allosteric regulator of many enzymes

Front 16

in what form are high energy phosphate groups stored?

Back 16

creatine phosphate

Front 17

CPK/CK is a diagnostic tool for __________

Back 17

myocardial infarction
(muscle damage)

Front 18

the synthesis of creatine involves two different tissues, what are they?

Back 18

liver and kidney

Front 19

the liver is the main metabolic site of what amino acid necessary for the synthesis of creatine?

Back 19

methionine (from S-A-M)

Front 20

in the synthesis of creatine, when glycine is converted to guanidinoacetate, what is arginine converted to?

Back 20

ornithine

Front 21

creatine phosphate decomposes through _________ _______ that produces creatinine

Back 21

spontaneous cyclization

Front 22

what does the daily urine creatinine excretion depend on?

Back 22

muscle mass

Front 23

what is the excretion of creatinine: fluctuating or constant?

Back 23

constant

Front 24

what is increase creatinine levels indicative of?

Back 24

impaired kidney function

Front 25

what does an increase in AMP upregulate?

Back 25

glycolysis, glycogenolysis and b-oxidation of fatty acids

Front 26

what enzyme converts ADP to ATP?

What is produced as a bi-product in this reaction?

Back 26

adenylate kinase

AMP

Front 27

What would be the expected ADP/AMP ratio in the contracting muscle of an individual who has skeletal muscle adenylate kinase deficiency?

Back 27

The ratio would be higher than normal, because ADP is not being converted to ATP and AMP

Front 28

what induces phosphofructokinase 2 (PFK2) in the liver?

Back 28

glucagon and epinephrine
(opp of muscles)

Front 29

in which of the three (liver, skeletal muscle and cardiac muscle) is glycolysis upregulated by PFK2?

in which is it downregulated?

Back 29

cardiac muscle

liver

Front 30

what induced PFK2 in the heart?

Back 30

insulin, epinephrine, AMP levels

Front 31

which of the three (liver, cardiac muscle, skeletal muscle) has a non-phosphorylated PFK2? why?

Back 31

skeletal; because the enzyme that is phosphorylated in liver is absent in skeletal. In skeletal PFK2 is always on.

Front 32

Does PFK2 regulate glycolysis in skeletal muscle?

Back 32

no

Front 33

what inhibits carnitine palmitoyl transferase-1?

Back 33

malonyl CoA

Front 34

the level of malonyl CoA is dependent on the activities of what in reference to b-oxidation in muscle?

Back 34

(+) acetyl CoA carboxylase-2 (ACC-2)
(makes Malonyl Coa from acetyl CoA)
and
(-) malonyl CoA decarboxylase (MCoADC)
(makes acetyl Coa from malonyl CoA)

Front 35

what regulates ACC-2 and MCoADC?

Back 35

AMP, which activated AMP-PK
AMP-PK affects:
(+) MCoADC
(-) ACC-2

Front 36

High AMP level (AMP/ATP ratio) facilitates _____________, and leads to (activation/inhibition) of PFK1 and PFK2

Back 36

glucose uptake

activation of PFK1 and PFK2

Front 37

where does most of the energy come from in cardiac muscle under fasting blood glucose levels?

Back 37

long chain fatty acids

(FA degradation produces Acetyl-CoA, high Acetyl-CoA halts TCA and releases citrate substrate into cytosol)

Front 38

high levels of acetyl CoA and citrate will limit energy production from glucose through glycolysis via what two enzymes?

Back 38

PFK-1 and PDH which are inhibited

Front 39

At high blood glucose levels (well-fed) insulin fascilitates ________ through Glut 4 and activates _____ which in turn will cause the activation of ______, increasing glycolysis.

Back 39

glucose uptake; PFK2; PFK1

Front 40

what does a lack of oxygen inhibit in cardiac muscle?

Back 40

mitochondrial ATP synthesis (TCA) and B oxidation of FAs

Front 41

why is pyruvate converted to lactate during ischemia in cardiac muscle?

Back 41

because oxidative phosphorylation cannot work without oxygen therefore inhibiting the TCA cycle
(acetyl-CoA is backed up from TCA and beta-ox. preventing pyruvate from becoming acetyl-coA)

Front 42

the inhibition of oxidative phosphorylation leads to _______ in the cytosol

Back 42

acidosis

Front 43

where does all the energy for resting skeletal muscle come from?

Back 43

aerobic metabolism (oxidative phosphorylation)

Front 44

most of the energy in resting muscle is provided by what specific type of oxidative phosphorylation?

what can also be oxidized for energy?

Back 44

B-oxidation of fatty acids

branched chain AAs
(if AA levels high)

Front 45

If skeletal muscle has high energy during rest, high levels of citrate will reduce what two processes?

Back 45

glycolysis (inhibitiing PFK-1) and beta oxidation of fatty acids (activating ACC-2-->malonyl CoA)

Front 46

what is the preferred fuel in skeletal muscle during fasting?

Back 46

fatty acids

(less GLUT-4. less glucose can enter cell)

Front 47

Fatty acids are the preferred fuel during fasting because:
low ATP levels leads to ___1___ AMP levels that activate ___2____.
___3_____ will deactivate ___4___ leading to low malonyl CoA. This then will activate CPTI and facilitate _____5___ of fatty acids producing large amounts of ____6___. This then inhibits __7____ and limits the use of glucose as energy source.

Back 47

1) high
2) AMP-PK
3) AMP-PK
4) ACC
5) b-oxidation
6) acetyl CoA
7) PDH

Front 48

how long does it take for resting ATP levels to be used up?

Back 48

1.2 seconds at the start of exercise

Front 49

how long does it take for phosphocreatine to be used up if not regenerated?

Back 49

about 9 seconds

Front 50

Due to limited delivery of oxygen, how long after the onset of exercise is increased oxidative phosphorylation possible?

Back 50

1 min

Front 51

during the onset of exercise, what type of glycolysis can provide a quick ATP supply?

Back 51

anaerobic

Front 52

what two processes does anaerobic glycolysis activate?

Back 52

glycolysis and glycogenolysis

Front 53

why does increased intracellular Calcium during exercise also stimulate glycogen degradation?

Back 53

it binds to the allosteric activation of the calmodulin subunit of phosphorylase kinase

Front 54

which is a more sensitive indicator of energy need in exercising muscle AMP or ATP?

Back 54

AMP

Front 55

during high intensity exercise why is lactate produced?

Back 55

b oxidation and TCA cycle cannot produce enough ATP fast enough causing an accumulation of AMP which activates PFK-1 and glycolysis(anaerobic) creating pyruvate which is then converted to lactate.

Front 56

Why can't high intensity exercise be maintained for very long?

Back 56

1. depletion of muscle glycogen stores
2. lactic acidosis causes muscle pain and damage

Front 57

lactate produced in exercising skeletal muscle can be used by what three parts of the body?

Back 57

resting skeletal muscle, cardiac muscle and liver

Front 58

what do resting skeletal muscle and cardiac muscle use lactate as?

Back 58

energy because they will convert lactate to pyruvate using lactate dehydrogenase. (if NADH is low)

Front 59

what does the liver use lactate for?

Back 59

converts lactate to pyruvate then glucose through gluconeogenesis. Then glucose can be release into circulation to be used for energy. (Cori cycle)

Front 60

what is the source of energy in long term exercise?

Back 60

aerobic oxidation of fatty acids and glucose

Front 61

up to 40 minutes of exercise, what is the main source of blood glucose?

Back 61

liver glycogen

Front 62

by 4 hours of exercise _______ increases and _______ decreases.

Back 62

gluconeogenesis; glucogenolysis

Front 63

why does overall glucose production decrease by 4 hrs of exercise?

Back 63

by that time muscle will increase its use of fatty acids as energy source

Front 64

what percentage of ATP can branched chain amino acids provide in resting skeletal muscle?

Back 64

20%

Front 65

(slow/fast) twitch muscle fibers have low glycogen content, high myoglobin content, high oxidative capacity, and high resistence to fatigue, in contrast to (slow/fast) twitch fibers.

Back 65

slow

fast

Front 66

What changes in metabolite (ATP, creatine-phosphate, lactate) levels would be observed in biceps femoris after a 100 meter sprint?

Back 66

ATP-reduced
Creatine-phosphate- reduced
Lactate- increased

Front 67

When AMP levels rise during high intensity exercise, what cycle is accelerated?

Back 67

purine nucleotide cycle

(makes fumarate for TCA and ammonia for urine excretion of H+, decreasing acidosis)

Front 68

What enzymatic modification is the most characteristic in the liver of someone who has been running 35 minutes?
Why?

Back 68

phosphorylation of glycogen phosphorylase

activated glycogen degradation in liver, main energy source up to 40 mins

Front 69

How does acetate provide energy for skeletal muscle?

Back 69

It can be converted to acetyl CoA and used in TCA

Front 70

What is the main activator of glycolysis and glycogen degradation in exercising skeletal muscle?
What enzymes does it activate?

Back 70

AMP

glycolysis- activates PFK1
glycogen degradation- activates glycogen phosphorylase