Glycolysis / LA system Flashcards
glyconeolysis
The energy pathway responsible for the initial catabolism of glucose that begins with glucose or glycogen
- end w pyruvate (aerobic/slow)
- end w lactate (anaerobic/fast)
glycogenesis
production of glycogen in the muscle and liver
Glyconeogenesis
The creation of glucose (in the liver) from noncarbohydrate sources, primarily glycerol, lactate, pyruvate and alanine
Embden-Meyerhof pathway
glycolytic/lactic acid system
- glucose or glycogen substrate
- catabolic pathway
- peak 15-30sec, last 45-120sec
GLUT-1
transporter in sarcolemma to bring glucose diffuse into cell
- cannot bring in glucose fast enough so need help of GLUT 4
GLUT-4
internal vesicle to help GLUT1 bring glucose into cell with high-blood glucose levels
- beta cells make insulin and tell GLUT 4 to move from internal to cell membrane
insulin independent method
Ca high from muscle contraction tell glut4 to go to cell membrane (get more glucose into cell since exercising)
Phosphorylase
enzyme to turn glycogen into glucose 1-Phosphate
- increase w more Ca, P and epinephrine
hexokinase
enzyme turns glucose into glucose 6-phosphate
- ATP + glucose = ADP + G6P
phosphofructokinase
enzymes turn to fructose-6-P to fructose-1,6-P
- F6P + ATP = F1,6P + ADP
- glycolysis rate limiting factor
- affected by low ATP, high H+ and P and ADP/AMP
glycolysis facts
- in sarcoplasm
- breakdown glucose/glycogen for ATP
- aerobic/slow = pyruvate
- anaerobic/fast = lactate and H
- energy to activate pathway (HK and PFK)
- 2 net ATP (glucose) or 3 (glycogen)
Lactate Dehyrogenase
enzyme turn pyruvate = lactate by oxidizing NAD
- LDH1 = cardiac muscle, MI marker
- LDH5 = skeletal muscles
G3P dehydrogenase
G3P to 1,3-bisphosphoglycerate
resting lactate levels
Remain relatively unchanged with long-term cardiovascular training. As a result of proper cardiovascular training, less lactic acid will be produced at submaximal workloads during exercise.
1-2mmol/L
glycolysis influenced by
- NAD/NADH ratio: high NAD = faster glycolysis
- ADP/ATP ratio: high ATP = faster glycolysis
- substrate avaliability: low glucose = slow glycolysis (fasting, disease, malnutrition, prior exercise)
LA system summary
- substrates are glucose (blood) and glycogen (muscle)
- sarcoplasm
- fast glycolysis (more H = discomfort)
- peak at 15-30 sec
mod-high power; mod-low capacity (45-120 sec)
pH of blood and muscles
- resting blood: 7.4-7.45pH
- resting muscle: 6.9-7pH
- after exercise in muscle: 6.4pH
where is H from in heavy exercise
modern view is H is made from steps 1, 3, 6 of glycolysis and fast rates of ATP hydrolysis
consequences of H in fast glycolysis
- more H accumulation = pain
- inhibit PFK and phosphroylase activity and Ca bind to troponin and O2 to Hb
- decrease ATPase (less Na/K transport, less mATPase, contractions)
consequences of La in fast glycolysis
more La:
- accumulate in muscle
- more oxidation of La- in muscle
- more efflux to blood and muscles (lead to excretion, gluconeogenesis, oxidation of La)
Lactate in Recovery
- 50-75% used as fuel (oxidized into pyruvate to be used for kreb and ECT)
- 10-25% for gluconeogenesis (liver)
- 5-10% as provide C for Amino acids in transamination
Lactate Clearance
- oxidation (turn to pyruvate, oxidize ATP, CO2, H2O for Krebs – using intracellular and extracellular shuttles)
- reconverted to glucose (liver prefers to make glycogen) via gluconeogenesis
- oxidative and glycolytic fibers turn La into alanine via transamination
- some La leaves via circulate in blood (heart loves it in exercise!) or via sweat
lactate production
- muscle contractions
- enzyme activity
- muscle fiber type
- sympathetic neurohormonal activity
- insufficient oxygen
intracellular lactate shuttle
transport lactate from cytoplasm to mitochondria where it is turned back into pyruvate by LDH1 and use for Krebs Cycle stages 2, 3, 4
These lactate cant be measured in blood lactate levels
extracellular lactate shuttle
transport lactate between tissues. lactate is cleared into slow-oxidative fibers by oxidation and transamination ; into circulation/skin/liver by gluconeogenesis and transamination
Transports out due to MCT4
Transports in due to MCT1
Gluconeogenesis importance
- glucose is essential for brain and CNS
- GNG important for starvation, prolong exercise (low blood sugar)
- precursors are pyruvate, lactate, glycerol, alanine, FFA,
- occur in liver
Improving Buffering Capacity
-Better buffering capacity = more glycolytic capacity = higher post exercise blood lactate
-Not good at buffering = use H back into glycolysis = slow it down
buffering capacity
HCO3, Pi, histidine, and Hb in RBC
- maintain muscle pH
- extend anaerobic power production
- reduces power drop off
- trainable in sprint trained athletes and breath holding mammals
bicarbonate (baking soda) loading
↑ in blood pH (not muscle pH) ingest 5-6mmol/L 1 - 3 hours prior to exercise
↑ buffering potential, therefore improving anaerobic performance
↑ rate of H efflux due to ↑ gradient
- has fewer bad side effects
B-alanine supplementation
B-alanine + L-histidine = Carnosine
- Carnosine = important intramuscular buffer
- Decrease 800m running times
lactic system and training
- ↑ activity of PFK, HK, phosphorylase and LDH5, which ↑ power of system
- ↑ skeletal muscle buffering capacity (resist pH change), which ↑ capacity of system
- ↑ glycogen stores in muscle, important for ↑ capacity and power of system
