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Carbohydrate Metabolism During
Exercise
Importance of Carbohydrate
Metabolism
• Involved in resynthesis of ATP during highintensity exercsise
• Also provide substrate for Krebs/TCA cycle
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
Carbohydrate Supplementation
Attenuates Fatigue
• Ingestion of carbohydrates during
prolonged exercise maintains intracellular
concentration of Krebs intermediates
• Also attenuates increased levels of IMP
accumulation
Exercise Intensity Limited in the
Absence of CHO
• If lipid is the sole energy source, exercise
above 50-60 % VO2max cannot be
sustained
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
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 % - 120 %VO2max
results in squaring the rate [100 fold increase in
this case])
• 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
Insert fig 2.1
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
Is Glycogenolysis Confined to
Exercising Muscle
• In animals, prolonged exercise results in
glycogen loss in non-exercising muscles
• In humans the data is equivocal
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 cycling @ 20 % VO2max
• 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
exercise @ 55% VO2max
• 65% decline in VL glycogen content
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
PHOS
• Oh no, not again!!!
How does CHO intake affect PHOS
activity?
• In animals, elevated blood glucose decreases
glycogen breakdown
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
High Intensity Exercise
• At high intensity 70-75%, elevated blood
glucose has no effect on glycogen levels
• Still ergogenic, maintains blood glucose
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
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
Some other proposed modulators
• Inhibitors
– Citrate
– Phosphoglycerate
– Phophoenolpyruvate
– Mg2+
• Promoters
– AMP and ADP
– Pi
– NH4+
– Fructose –2,6 diphosphate
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
30-60 s time frame
• May be a factor as Krebs and fat metabolism
become more predominant
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
Hormonal Regulation of Glucose
Metabolism
• Under non-exercising conditions, insulin
needed to stimulate glucose entry into cell
• Is insulin needed during exercise?
– Permissive amount?
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?
GLUT 4
• Both exercise and insulin translocate GLUT
4 to the cell membrane
• Different pools of GLUT 4?
– Effects are synergistic
GLUT proteins
• 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?
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
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??
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
Glucose-Fatty Acid Cycle
• Randall proposed that increased FFA oxidation resul
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.
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
Lactate Production
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
The Cori cycle: lactate as a fuel
source
Muscle fuel sources in highly trained
endurance athletes
Contributions of four energy sources over
prolonged time in endurance athletes