Blood Flow
how does blood get redistributed to active regions during exercise
SNS increases epi and norepi being released which tells smooth muscle around arterioles to vasoconstrict or vasodilate
changes in PP, metabolites released in response to hypoxia, and acidity signals SNS to cause vasodilation
vo2 max range for athletes vs normal healthy people vs cardiac patients
70/80 vs 30/40 vs 10/20
not born with high vo2max, have to train, but some people still born with better vo2max and can train easier
training increases shift from fast to slow fibers
increase in capillarization
what factors increase vo2max
increase in preload = higher plasma volume and increased SV
decrease in afterload = decrease in BP and increased SV
sending more blood to muscle and having more mitochondrial/capillary density to use up o2 increases avo2diff
what is autoregulation and what effect does this have on skeletal muscle blood flow
autoregulation is when blood flow is automatically increased to meet metabolic demands of the tissue, this is due to changes in o2 and co2 tensions (PP), nitric oxide, potassium, adenosine, and pH (these all signal the SNS)
causes vasodilatory effect (bc SNS)
HRmax, SVmax, avo2diffmax for normal person
HR: 195
SV: 0.1
avo2diff: 160
overall, how does endurance training influence exercise performance
enhances exercise performance
results in numerous adaptations in muscle fibers that assist in maintaining homeostasis
increased mitochondrial volume
increases in number of ATP transporters in the mitochondrial membrane allows for faster ADP uptake into the mitochondria and lower cytosolic ADP
more machinery to take up AcoA and break down fats to use FFA
more mitochondria = more ability to respond to signals to ramp up to start producing more energy = smaller o2 deficit
what direction does contraction follow, what receives the depolarization
follows depolarization, direction goes toward center of heart from RA, AV node receives depolarization because it's in the center and it pauses the momentum momentarily for the ventricles to fully fill, contracts from top to bottom
what is avo2diff and how does it change during exercise
avo2diff is the amount of o2 taken up from 100ml blood (o2 extraction, ateriovenous difference)
increases with exercise due to higher amount of o2 being extracted from blood because the muscles are in need
HRmax, SVmax, avo2diffmax for athlete
HR: 190
SV: 0.2
avo2diff: 160
what are the intracellular signaling responses that lead to endurance training adaptations
endurance training leads to increase in Ca, ATP and free radicals -> these activate PGC1A -> this activates the fast-to-slow fiber shift, mitochondrial biogenesis, and synthesis of antioxidant enzymes
changes in fuel utilization
plasma glucose is spared due to the increased FFA transporters due to increased capillary and mitochondrial density which increases uptake of FFA, which increases utilization of FFA
what happens to diastolic pressure during aerobic exercise
nothing :P
how does an increase in avo2diff during exercise occur
as intensity increases, we move more o2 from the blood (85% total o2 from blood during maximal exercise)
what are the differences between HRmax, SVmax, VO2max, and avo2diffmax for normal vs athlete
HRmax in athlete is slightly blunted/smaller
SV in athlete is doubled
VO2max is doubled
avo2diff doesnt change
what is the master switch for endurance training adaptations and what signals from exercise turn the switch on
PGC1A is the switch, increase in Ca, ATP, and free radicals all activate/turn on switch
increases in antioxidant capacity
the more we exercise, the more enzymes we will make which increases capacity for antioxidants
stroke volume equation
sv = edv - esv
how does max avo2diff change with endurance training
less SNS vasoconstriction which increases muscle blood flow
better ability to extract o2 from blood with training due to increased mitchondrial and capillary density
what is the average change in vo2max after a few months of endurance training
15-20% in 4 months
SV decreases rapidly in response to rapid loss of plasma volume
decrease in max avo2diff occurs but slower than SV decline
due to big drops in mitochondria, oxidative capacity, and 2a fibers
it takes less time to retrain after detraining because you're just relearning instead of from scratch
vo2max decreases because of decrease in its variables (SV, Q, avo2)
improvements in acid-base regulation
what does the stress of exercise cause
protein synthesis to be activated which makes more mitochondria
mRNA activity goes up in response to stress of exercise