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Intensity effects on substrate utilization
Low: lipids-mainly plasma fatty acids, some intramuscular triglycerides and blood
glucose
Moderate: 50/50-plasma fatty acids, intramuscular triglycerides, muscle glycogen, some
blood glucose
High: Carbohydrates-muscle glycogen, blood glucose, intramuscular triglycerides, fatty
acids
CHO and lipids are used concurrently, intensity effects which one is dominating
Muscle substrates are used at higher intensities
Energy producing system: Immediate (1-10 sec)
Anaerobic
ATP stored in muscles
Adenylate kinase rxn
ATP-PCr system
quick energy, 2 min to recover PCr levels, very limited storage, creatine is everywhere-
acts as a shuttle system
Still occurs at the same time as the others
Energy producing system: Short term (10sec-2min)
Glycolysis, forms ATP fast but not as fast as ATP-PCr, the pay-off is only 2ATP/glucose
Anaerobic ends in lactate accumulation at high intensities/lactate threshold (60-
70%VO2max)
Aerobic ends in pyruvate to acetyl-coA to TCA/krebs to ETC
Still occurs at the same time as the others
Energy producing system: Long term (>2min)
Aerobic metabolism
Provides large amounts of ATP
Assessed by measuring VO2/O2 consumption
PDH is important for this-forms Acetyl-CoA which is a key intermediate linking metabolic
pathways
Oxidative Phosphorylation (ETC)
Still occurs at the same time as the others
muscle gylcogen
The main energy source for muscle contraction during high intensity exercise
The more you have the more time it takes for you to fatigue
Replenished fastest in the first 2 hours after exercise
, INTENSITY is the most important variable in determining rate of muscle glycogen
breakdown-determines how long your glycogen stores last
Carbohydrates
Most CHO are stored as muscle glycogen -400g
Body doesn't store much CHO so diet is important
rate of energy transfer is twice that of lipids and proteins
Liver
Produces glucose via liver glycogenolysis (increases 0-60min and during high
intensities) and gluconeogenesis (steady increase, slight increase across intensities)
Liver glucose production increases across intensities
Stores glucose that maintains our blood sugar during fasting
Fed state
insulin promotes glycogen synthesis, inhibits glycogenolysis and gluconeogenesis
Fasted state/exercise
Epinephrine inhibits insulin, promotes gluconeogenesis and glycogenolysis
Glucagon inhibits glycogen synthesis and promotes gluconeogenesis and
glycogenolysis.
Glycogenolysis
Hormone attaches to beta adrenergic receptor
adenylate cyclase turns ATP to cAMP
cAMP activate protein kinase
Protein kinase activates phosphorylase kinase-P with the help of ATP
Phosphorylase kinase-P turns phosphorylase b to phosphorylase a-P with the help of
ATP, Ca2+
Phosphorylase a-P turns glycogen into G1P
Glycolysis
Glycogen phosphorylase-activated by ADP, Pi, AMO, Ca2+ and epi
inhibited by ATP/ADP, citrate
PFK- activated by ADP, Pi, AMP
inhibited by ATP/ADP, citrate
PDH- activated by ADP, Pi, AMP
inhibited by ATP/ADP, acetyl-CoA
Lower number of steps/faster rate is why glucose is the preferred substrate for ATP
during exercise over lipid
Liver glycogenolysis
Same as glycogenolysis but initiated by glucagon instead of catecholamines
Gluconeogenesis
Done mainly in liver
precursors must first convert to oxaloacetate
special enzymes bypass exergonic steps- glucose 6 phosphate and fructose 1,6
bisphosphate
Reciprocally regulated with glycolysis
GLUT 4
On the muscle membrane
Activity increases with exercise duration