Lecture 4 - Training Prescription for Anaerobic Adaptation Flashcards
What reactions do these enzymes catalyse? ATPase Creatine Kinase Adenylate Kinase Glycogen Phosphorylase Phosphofructokinase
ATP break down to ADP and Pi Resynthesis PCr - in mitochondria Inter-conversion of adenine molecules Breaks down muscle/liver glycogen (increased AMP) Regulates glycolysis (increased AMP)
What is heavier… dry weight or wet weight?
Wet weight muscle mass is generally measured as less than dry muscle weight
What did Gaitanos (1993) find in relation to muscle metabolism during intermittent maximal exercise?
What happened after the first 6 second sprint?
What happened after 10 second sprints?
Increased AMP = Increased ATP
Reduction in ATP and PCr concentrations - ADP same
Peak and Mean Power output both reduced due to PCr depletion and enzyme impairment
Drops in glycogenolytic, glycolytic and glycogen degradation rates
Why does the contribution of glycolysis to ATP production reduce during intermittent sprints?
Reduced Glycogen Phosphorylase activity
Reduced PFK activity = Reduced glycolysis
Reduced starting glycogen stores
What are some of the metabolite changes during a 30s sprint?
ATP conserved until 30 secs
Free AMP = more in the muscle = glycogen breakdown should raise
PCr stores at the 3rd bout are depleted
What does an individual with increased mitochondria therefore have?
Increased ATP storage and increase in amount of PCr synthesised for exercise
What went on in the last 30 second sprint in terms of GP and glucose release?
What is the inhibitor of GP activation
Increase in GP activation - inhibited by G-6-P
If G-6-P accumulates then more glucose is outside than inside the fibre
During sprints large amounts of glucose is release but G-6-P allows only small amounts to come into the cell
What were the total contributions at the 2nd 30s sprint?
1st 6 seconds = aerobic - PCr and Glycolysis similar
As GP drops, anaerobic turnover drops so more dependent on oxidative system
Oxidative cannot meet ATP demand so muscle contraction and PPO reduce
What were the total contributions at the 3rd 30s sprint?
What is a key adaptation required to work and adapt the anaerobic system?
60% from oxidative
Why sprint interval training may not be beneficial to make any anaerobic adaptations
Increase in amount of mitochondria
What did MacDougall find on chronic adaptations using a Wingate protocol?
Training increases PPO and ability to sustain repeated sprints
However this is not due to GP/LDH activity
PFK and hexokinase both increase by 49% and 56%
Does sprint interval training affect VO2 max and oxidative metabolism?
NO! Cardiac Output is main inhibitor of VO2 max
Sprint interval = increases SV and Q
Increased mitochondria increases VO2 max
What are some of the mitochondrial markers we look for?
MDH (malate dehydrogenase), SDH (succinate dehydrogenase) and CS (citrate synthase) all increase post training
Increase in oxidative enzymes
By what % did VO2 max increase by after 7 week Wingate training?
7% - helped by short recovery periods
