Lecture 11 & 12 - Adaptations of Aerobic Training Flashcards
two main components that make up VO2 max
Q (cardiac output) max x AVO2 difference max
basically…
resource delivery x resource utilization
how does cardiorespiratory endurance training effect the left ventricle
- endurance training will cause LV to hypertrophy which will lead to increased LV contractibility
- LV will increase in internal diameter, decreasing LV pressure, increasing BP gradient (LA to LV), causing an increased end diastolic volume and increased preload
both will lead to increases in LV contraction strength which will then cause an increased stroke volume then a greater Q
how does cardiorespiratory endurance training effect lungs/breathing rate
- endurance training will cause increases in breathing frequency rates and an increase in tidal volume
- both will increase ventilation rate which will cause an increase in respiratory pump effect (help facilitate movement)
- this will cause an increase in venous return which will lead to an increase in diastolic volume and preload…….. increasing V
how does cardiorespiratory endurance effect the blood
- endurance training will increase red blood cell volume and plasma volume, both will increase the total blood volume and lead to a greater venous return - > inc endiastolic volume….. inc Q
- increases in plasma volume will decrease blood viscosity (water vs sand) and will decrease peripheral resistance
- this will cause a decrease in afterload which will cause and increase in blood pressure gradient (LV to aorta)
- this will increase stroke volume which will increase Qmax
how does cardiorespiratory endurance training affect the autoregulation (direct blood flow) by active muscles
- when theres an increase in autoregulation by active muscles, we see an increase in vasodilation of the active muscle, allowing more blood through
- this will increase muscle arteriole radius (paired with decrease blood viscosity) which will decrease peripheral and then decreases afterload…… increase Qmax
what is the effect of exercise on the SNS influence on inactive tissue
- exercise increases SNS output to inactive tissues which will increase vasoconstriction to inactive tissues and cause an increase in the percentage of BF distribution to active muscle (this is also increased by an increase in muscle arteriole radius)
- this will cause an increase in active muscle BF volume, leading to increase O2 delivery volume to active muscle and eventually lead to an increase in AVO2diffmax
what is the effect of exercise on muscle capillaries
- it will increase muscle capillary density and recrutment and will cause an increase in capillary oxygen diffusion area
- this will cause an increase in capallary oxygen diffusion rate (vgas) and will work with the increase in O2 delivery volume to active muscle (by inc SNS output) to increase AVO2 max
how does exercise impact the capillary/muscle cells
- there will be an increase in myoglobin, mitochondria size, and oxidative activity rate which all will produce and increase in aerobic ATP production rate
- this will increase oxygen usage, leading to a decrease in muscle PO2
- this will then cause an increase in PO2 gradient (capitally to muscle) which will lead to an increase capillary O2 diffusion rate which will then increase AVO2diff max
are VT and LT the same thing?
they’re dictated by different variables; but they’re similar
- cause by buffering (bicarbonate buffering) of lactic acid leading to increase in non-metabolic CO2 production and thus increased ventilation
explain the lactate threshold
Accelerated glycolysis
- FADH produced faster than it is shuttled into mitochondria
- excess NADH in cytoplasm converts pyruvic acid to lactic acid
Recruitment of fast twitch muscle fibres
- LDH isozyme in fast fibers promotes lactic acid formation
Reduced rate of lactate removal from blood
where does the non metabolic CO2 come from
- when we have an excess of H ions we combine them to bicarbonate with carbonic anhydrase to create carbonic acid
- carbonic acid can then dissociate and become water and CO2
- CO2 is then released at the lungs leading to an increase in CO2 production without an increase in O2 uptake ventilatory threshold is where this starts to happen
how to calculate VT
V-Slope method
- find the intersection points of the slope of values below, between and after VT to determine at what point does glycolysis outpace oxidative phosphorylation
respiratory compensation point
mismatch between ventilation rates and CO2 production
- increase in expired minute ventilation (VE) with respect to CO2 output (VCO2)
- look at intersection point before, around and after VE/VCO2 slopes to see where both linear slopes intersect to find RCP
anaerobic power
NOT THE SAME
instantaneous power
- primary due to ability to apply more force at a greater velocity. Has little to do with energy availability
Anaerobic power (5 secs)
- increases are largely related to improved force production capacity
- 30 second training bouts have shown increase in (creatine kinase) CK and MK (myosin kinase). 6 secs bout have shown to strength improvements similar to 30secs, but no change in CK or MK
aerobic capacity
- 30 second training bouts have shown to lead to increases in phosphorylase, PFK, LDH or approximately 10-25%
- there does appear to be a cap on improvement. 60 second bouts show than final seconds (40-60s) are not different between pre and post training
