Review PCr

Review Glycolysis

Review TCA

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 FADH 2

Process of Beta oxidation  most fats are 16 or 18 carbons

16C Palmitate:  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  = 131 ATP  2 ATP for activation, = 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  (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