Chapter 3- Fuel for Muscle and Exercise Metabolism Flashcards
what provides energy for muscle contraction?
the breakdown of ATP into inorganic phosphate and ADP
what are type I fibers ?
slow-acting, more myoglobin therefore more capacity for oxidative metabolism
what are type II fibers
fast-acting, fewer mitochondria and capillary supply, fatigue rapidly
what are the three things contained in skeletal muscle
75% water
20% protein (myosin, actin, tropomyosin)
5% salts and substances
the hydrolysis of ATP yields how many kJ? kcal ?
31 kJ or 7 kcal
what is the formula of ATP hydrolysis ?
ATP + H2O=> ADP+ Pi + H+
what are the three mechanisms involved in resynthesis of ATP
PCr hydrolysis
glycolysis
TCA cycle
what is the resting concentration of ATP in muscle? what does this imply
4-5 mmol/kg ww muscle (only enough energy for a few seconds)
when does PCr hydrolysis begin ? what is its purpose
at immediate onset of contraction to buffer ADP accumulation after you use up the initial quantity of ATP in muscle. this prevents rapid acidification of the muscle and therefore premature fatigue
how much is [PCr] in sarcoplasm compared to ATP
3-4x
why can’t we rely only on PCr hydrolysis ?
rate of PCr hydrolysis declines after only a few seconds of maximal force contraction
where does PCr hydrolysis occur
the sarcoplasm
how does glucose uptake from blood happen? with help from what ?
GLUT4 transporter
what occurs to prevent the loss of glucose from the cell after it passes through the transporter in the muscle ?
an irreversible phosphorylation catalyzed by hexokinase.
glucose + ATP => ADP+ glucose-6-phosphate
why is the transformation of glucose into glucose-6-phosphate irreversible in the muscle and not the liver?
because skeletal muscles lack the enzyme glucose-6-phosphatase, but the liver does not
how does one control the production of glucose-6-phosphate in the skeletal muscle ?
by negative feedback on hexokinase
how does one break down muscle glycogen in order to utilize it ? (formula)
glycogen phosphorylase breaks off glucose molecule from glycogen
glycogen + Pi => glucose-1-phosphate + glycogen shorter by one glucose
then, glucose-1-phosphate has the Pi placed on a different carbon to become glucose-6-phosphate with phosphoglucomutase
what is the amount of ATP used in glycogen breakdown ?
none
you use an inorganic phosphate to bind to glucose so no ATP needed
what does phosphoglucomutase do
in glycogen breakdown, glucose-1-phosphate has the Pi placed on a different carbon to become glucose-6-phosphate
what are the two sources for glycolysis
glucose and glycogen
what is the main step between glucose/glycogen and pyruvate in glycolysis ?
fructose-1,6-bisphosphate is cleaved by aldolase into 2 glyceraldehyde-3-phosphate
when pyruvate is produced, what are the two pathways for it ?
either it becomes lactate or acetyl CoA
how does pyruvate become lactate
with lactate dehydrogenase
pyruvate+ NADH => lactate+ NAD+
how does pyruvate become acetyl coA
with pyruvate dehydrogenase
pyruvate+ CoA + NAD+ => Acetyl CoA + NADH
in glycolysis from glucose, what is the total ATP produced ? the net ATP produced ?
total ATP = 4 (2 from each glyceraldehyde-3-phosphate)
net = 4-2 = 2
in glycolysis from glycogen, what is the total ATP produced ? the net ATP produced ?
total ATP = 4
net= 4-1 = 3
what happens if glycolysis is too fast?
availability of NAD+ (necessary cofactor) becomes the limiting factor, and the reaction is limited at the 2 3C chain split (stays at glyceraldehyde 3-phosphate)
how can one regenerate the NAD+ in muscle ?
reduction of pyruvate to lactate
when does lactate formation occur ?
always, it’s just that it accumulates in heavy exercise
how does the body deal with lactic acid accumulation ?
lactate brought to liver and converted back to glucose in the Cori Cycle
what does the Cori Cycle do
lactate brought to liver and converted back to glucose
what is the main goal of the Cori Cycle
gluconeogenesis
in resting state, how many ATP and lactate are needed in the Cori Cycle to produce 1 glucose ?
2 lactate and 6 ATP
where is the Cori Cycle taking place ? why
the liver because lactate can only go to pyruvate and therefore glucose in the liver
what does TCA cycle stand for
tricarboxylic acid cycle (Krebs)
what are the two main sources of energy for the TCA cycle
fats and carbs
where does the TCA cycle occur ?
in the mitochondrion
where does glycolysis occur ?
cytoplasm/sarcoplasm
how does a pyruvate get into the TCA cycle ?
it has to first go to the mitochondrion from the cytoplasm
what are the two nutrients needed in enzymatic reactions ?
NADH and FADH2
what and where is the electron transport chain
creates a proton gradient across inner membrane and mitochondrial matrix
what does oxygen do in the ETC
removes electrons from the chain
how much ATP is made from ETC ?
38 ATP
after how long is glycogen depleted in exercise ?
1-2 h
what determines the sustainability of an exercise ?
glycogen stores
what is the enzyme responsible for lipolysis
?
hormone-sensitive lipase
what are the 5 hormones that stimulate HSL ?
epinephrine norepinephrine glucagon cortisol growth hormone
what inhibits HSL ?
insulin
what does HSL do ?
breaks down triacylglycerol into glycerol and 3 FA which go into the blood
break down the source of the 38 ATP from the complete oxidation of one glucose molecule
from glycolysis:
2 + 6 (from NADH)
from TCA:
24 (from NADH) + 4 (from FADH2) + 2 (from GTP)
therefore 38 in total
how do fatty acids enter the mitochondria ?
< or = to 12 carbons without membrane transporter
> or = to 14 carbons with membrane transporter
why does insulin inhibit HSL ?
bc it promotes TG synthesis
during prolonged moderate exercise, what is the rate of lipolysis and the rate of entry of FA into circulation like ?
adipose tissue blood flow increases
during intense exercise, what is the rate of lipolysis and the rate of entry of FA into circulation like ?
SNS vasoconstriction causes fall in adipose tissue blood flow, meaning accumulation of FA in adipose tissue
the concentration of what limits fat mobilization during intense exercise
lactate because a high amount promotes re-esterification (more TG) and therefore limits entry of FA into bloodstream
what happens to glycerol once it’s in the circulation ?
taken up by liver or converted into glucose
what happens to FA once they are in circulation ?
loosely bounded with albumin for the most part
what is uptake of FA by muscle related to directly ?
the plasma FA concentration
how do long chain (= or > 14 carbon) FFA get into the mitochondria for oxidation ?
via the carnitine shuttle
what is the carnitine shuttle ?
two forms of carnitine-acyl-transferase in the mitochondrial membrane of the muscle. CAT-I outside membrane, CAT-II on inner surface.
FFA becomes FA-CoA or acyl-CoA with acyl-CoA synthetase
then, at the outer membrane, acyl-CoA releases its CoA and binds to carnitine (fatty acyl-carnitine + free CoA) which transports it across membrane in carnitine transporter.. then in the mitochondrion, carnitine is removed and fatty acyl-CoA is reformed
what is the main rate-limiting step in utilization of FFA for energy ?
carnitine shuttle