2. Review PCr

3. Review Glycolysis

4. Review TCA

5. HSL must stimulate the catabolism of triglyceride (glycerol + 3 FAs)  insulin (-)  lactate (-)  epi (+)  norepi (+)  glucagon (+)  GH (+)  cortisol (+)

6. 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)

7. FAs can enter the muscle cell for further catabolization

8. Entry into cell no problem; entry into mitochondria for Beta oxidation is similar to facilitated diffusion of glucose: it takes others

9. FAs are converted to a CoA derivative by fatty acyl CoA synthase

10. Palmitate: 16C FA:  Palmitate → palmitoyl CoA via long chain acyl CoA synthase  ATP in and AMP out; net cost?  now ready for beta oxidation

11. 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

12.  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

13. NOW, beta oxidation  think of it as a merry-go round, dropping off 2 carbons (acetyl CoA)

14. 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

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

16. 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  35 + 96 = 131 ATP  2 ATP for activation, 131 - 2 = 129 ATP

17. 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

18. Glycerol catabolism: 19 ATP

19. Entire TG  129 X 3 (3 FAs) = 387  387 + 19 (glycerol) = 406 ATP

20. Acetyl CoA from Beta Oxidation must interact with OXA to feed the TCA (CHO flame)

21. Acetyl CoA may be converted to ketones when not enough OXA (fasting, diabetes, and prolonged exercise)

22. 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

23.  this occurs in liver  ketones may be used for energy, especially by heart and kidneys

24. Fat catabolism during low intensity exercise

25. low intensity: 5 kcal/min  most (72%) derived from fat  3.6 kcal from fat, 0.4 gms of fat

26. double intensity: 10 kcal/min  45% of energy is derived from fat  4.5 kcal/min, 0.5 gm of fat

27. e.g., 5 kcal/min for 60 min = (5 X 60) = 300 kcals, 24 gm fat

28. 10 kcal/min for 45 min = 450 kcals, 22.5 gm fat

29. Therefore, should you encourage some one to exercise at low intensity to “burn more fat”?????

30. 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