1. Carbohydrate Metabolism During Exercise

2. Importance of Carbohydrate Metabolism
Involved in resynthesis of ATP during high-intensity exercsise
Also provide substrate for Krebs/TCA cycle

3. Carbohydrate Depletion and Fatigue
Glycogen depletion or hypglycemia often associated with exercise fatigue
Glycolysis provides pyruvate which feeds into Krebs/TCA
If glucose is insufficient to fuel glycolysis, Krebs may be slowed as a result

4. Carbohydrate Supplementation Attenuates Fatigue
Ingestion of carbohydrates during prolonged exercise maintains intracellular concentration of Krebs intermediates
Also attenuates increased levels of IMP accumulation

5. Exercise Intensity Limited in the Absence of CHO
If lipid is the sole energy source, exercise above % VO2max cannot be sustained

6. McCardles Disease as a Model
McCardles patients do not have PHOS
Cannot utilize glycogen as a fuel source
Exercise capacity only 50 % of predicted
Also greater ATP degradation
Elevated IMP levels compared to normals

7. Glycogenolysis
Glycogen breakdown is both exercise intensity and duration dependent
Glycogenolysis is most rapid during short duration exercise
Rate is exponentially related to intensity
(ie. Doubling intensity 60 % %VO2max results in squaring the rate [100 fold increase in this case])

8. As exercise proceeds, glycogneolytic rate decreases
Could be reduction in glycogen stores
remember previous exercise
Could be change in the levels of allosteric regulators of PHOS as a result of lower intensity
If duration is longer, intensity must be lower

9. Insert fig 2.1

10. Why is Glycogenolysis Higher with High Intensity Exercise?
For low intensity exercise, primarily type I fibers involved
As intensity increases, type II s are recruited
At maximal intensity all fibers are recruited
Type II fibres have greater glycogenolytic capacity

11. Is Glycogenolysis Confined to Exercising Muscle
In animals, prolonged exercise results in glycogen loss in non-exercising muscles
In humans the data is equivocal

12. Glycogenolysis in Non-exercising Muscle
For
Forearm lactate release in prolonged leg exercise
Lactate could not be accounted for by glucose uptake
Lactate release from legs during recovery from arm exercise
Muscle glycogen declined 20 % in non-exercising leg during 4 hours one-legged 20 % VO2max

13. Against
No change in non-exercising muscle glycogen content after glycogen depleting exercise
No change in 2 hours of one-legged cycling
No change in deltoid content with 2 hours leg 55% VO2max
65% decline in VL glycogen content

14. Why would you want glycogenolysis in non-exercising muscles?
If glycogenolysis occurs, glucose can be broken down via glycolysis
Pyruvate may be converted to lactate which can then be released from non-exercising muscle
Lactate can be converted to glucose via gluconeogenesis
Maintains blood glucose

15. PHOS
Oh no, not again!!!

16. How does CHO intake affect PHOS activity?
In animals, elevated blood glucose decreases glycogen breakdown

17. Low Intensity Exercise
During low intensity exercise (50% VO2max) w/ 30 s sprints, elevated blood glucose attenuates glycogen breakdown
Hypoth-between sprints, high glucose promoted glycogen resynthesis
This led to reduced NET breakdown

18. High Intensity Exercise
At high intensity 70-75%, elevated blood glucose has no effect on glycogen levels
Still ergogenic, maintains blood glucose

21. Phosphofructokinase (PFK) regulation
Most important regulator of PFK activity is ATP
ATP can bind to PFK at two sites and alter its activity
Binds to catalytic site with high affinity
Can also bind to allosteric site

22. PFK cont’d Binding to the allosteric site inhibits activity
So,… when [ATP] in the cell is high, PFK will be inhibited
no need for glycolysis, plenty of ATP
H+ can enhance ATP affinity for allosteric site
Provides feedback inhibition

23. Some other proposed modulators
Inhibitors
Citrate
Phosphoglycerate
Phophoenolpyruvate
Mg2+

24. Promoters
AMP and ADP Pi
NH4+
Fructose –2,6 diphosphate

25. Citrate Probably not a major factor during short, intense exercise
Aerobic metabolism does not contribute greatly until later (>30 s)
Citrate probably does not accumulate within the s time frame
May be a factor as Krebs and fat metabolism become more predominant

26. Promoters
ADP and AMP will accumulate rapidly at the onset of anaerobic exercise
Breakdown of PCr
H+ may be reduced at the onset of exercise
Removing the ATP induced inhibition

27. Hormonal Regulation of Glucose Metabolism
Under non-exercising conditions, insulin needed to stimulate glucose entry into cell
Is insulin needed during exercise?
Permissive amount?

28. Insulin Not Necessary During Exercise
During exercise insulin levels decline
Glucose transport is stimulated by exercise in the absence of insulin
Effects of exercise and insulin are additive
Different mechanisms?

29. GLUT 4
Both exercise and insulin translocate GLUT 4 to the cell membrane
Different pools of GLUT 4?
Effects are synergistic

30. GLUT proteins

31. So, insulin is not necessary for glucose transport during exercise
But, exercise increases cellular sensitivity to insulin
Hyperinsulinemia at the onset of exercise results in rapid drop in blood glucose
Implications for competition meals?

32. Epinephrine
Effects on glucose uptake are equivocal at best, confusing at worst
Can’t say one way or the other
Epi will activate PHOS though
This will stimulate glycogenolysis and possibly elevate G-6-P, in effect reducing glucose uptake

33. Glycogen Availability
Inverse relationship between glycogen levels and glucose uptake
Leg glucose uptake directly related to percentage glycogen-empty muscle fibers
Also, inversely related to muscle G-6-P levels
Inhibition through G-6-P levels??

34. Blood Glucose Availability
Glucose uptake is elevated during exercise when blood glucose levels are high
During the latter stages of exercise, as blood glucose drops, glucose uptake also decreases
High rates of glucose uptake can be achieved late in exercise if blood glucose levels are maintained
Carbs not ergogenic if glycogen stores elevated

35. Glucose-Fatty Acid Cycle
Randall proposed that increased FFA oxidation resulted in citrate ,mediated inhibition of PFK
Resulting elevations in G-6-P inhibited hexokinase, glucose phosphorylation and uptake
Experimental results equivocal to this point
This may work in a test tube, but it’s hard to show physio.

36. Lactate Metabolism
Lactate originally believed to be a “waste” product of anaerobic glycolytic metabolism
More recently believed to participate in carbohydrate metabolism, serve as an energy source as well as metabolic regulator

37. Lactate Production

38. Factors Affecting Lactate Production
O2 availability
Classic pathological factor affecting lactate production (ischemia)
Rate of glycogenolysis and glycolysis
Diet
High CHO diet results in more lactate formation
Catecholamines

39. The Cori cycle: lactate as a fuel source

42. Muscle fuel sources in highly trained endurance athletes

43. Contributions of four energy sources over prolonged time in endurance athletes