Review PCr
Review Glycolysis
Review TCA
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HSL must stimulate the
catabolism of triglyceride
(glycerol + 3 FAs)
insulin (-)
lactate (-)
epi (+)
norepi (+)
glucagon (+)
GH (+)
cortisol (+)
If in adipose: glycerol may
enter circulation, be taken up
by liver and phosphorylated to
glycerol 3-phosphate
 make new TGs
 enter the glycolytic pathway
 gluconeogenic precursor (via
dihydroxyacetone phosphate, DHAP)
FAs can enter the muscle cell
for further catabolization
Entry into cell no problem;
entry into mitochondria for
Beta oxidation is similar to
facilitated diffusion of glucose:
it takes others
FAs are converted to a CoA
derivative by fatty acyl CoA
synthase
Palmitate: 16C FA:
 Palmitate → palmitoyl CoA via long chain
acyl CoA synthase
 ATP in and AMP out; net cost?
 now ready for beta oxidation
Fatty acyl CoA must be
transported across the mito.
membrane and into the matrix
via carnitine shuttle
 notice the “drop off” of CoA to combine with
another fatty acyl CoA
 why supplement carnitine
– increased carnitine, shuttle in more fat, more fat
catabolism, even at rest
– partly b/c exercise causes an increased
excretion of carnitine in urine, maybe lowering
muscle levels
 no studies support this contention, need
mitochondria for carnitine to help
NOW, beta oxidation
 think of it as a merry-go round, dropping off
2 carbons (acetyl CoA)
Two purposes of Beta Oxidation
 cleave carbon atoms in pairs (acetyl CoA),
degrading the FA
 produce high energy reducing equivalents,
NADH +H and FADH2
Process of Beta oxidation
 most fats are 16 or 18 carbons
16C Palmitate:
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5 ATP/ spin (n/2 - 1)
12 ATP/acetyl CoA (n/2)
7 spins X 5 = 35 ATP
8 acetyl CoA X 12 = 96 ATP
35 + 96 = 131 ATP
2 ATP for activation, 131 - 2 = 129 ATP
Uneven FAs
 cleaving of pairs continues until last time, 2
C and a 3C
 3C fatty acid is propionyl CoA
 propionyl CoA is converted to succinyl CoA
Glycerol catabolism: 19 ATP
Entire TG
 129 X 3 (3 FAs) = 387
 387 + 19 (glycerol) = 406 ATP
Acetyl CoA from Beta
Oxidation must interact with
OXA to feed the TCA (CHO
flame)
Acetyl CoA may be converted
to ketones when not enough
OXA (fasting, diabetes, and
prolonged exercise)
Ketones (or ketone bodies)
 two acetyl CoA condense to acetoacetate
 acetoacetate reduced to 3-hydroxybutyrate
(if NADH:NAD ratio is high in mitochondria)
 or, acetoacetate spontaneously, slowly
undergoes a decarboxylation to acetone
 this occurs in liver
 ketones may be used for energy, especially
by heart and kidneys
Fat catabolism during low
intensity exercise
low intensity: 5 kcal/min
 most (72%) derived from fat
 3.6 kcal from fat, 0.4 gms of fat
double intensity: 10 kcal/min
 45% of energy is derived from fat
 4.5 kcal/min, 0.5 gm of fat
e.g., 5 kcal/min for 60 min = (5
X 60) = 300 kcals, 24 gm fat
10 kcal/min for 45 min = 450
kcals, 22.5 gm fat
Therefore, should you
encourage some one to
exercise at low intensity to
“burn more fat”?????
Fat facts:
 fat utilization decreases when exercise
follows a high CHO meal (increase in
circulating insulin)
 fat utilization decreases when lactate begins
to accumulate
 ability to use fat as a fuel increases with
training