what is resting O2 ventilation as an index of EE?
O2 consumption
respiratory quotient and kcal/L O2 for CHO, fat, and PRO
CHO: 1.0 RQ, 5.05 kcal/L O2
fat: 0.7 RQ, 4.7 kcal/L O2
PRO: 0.8 RQ, 4.5 kcal/L O2
what is respiratory exchange ratio?
RER = RQ whenever body’s total o2 content stays constant (usual) AND when total CO2 content stays constant (variable depending on breathing strategies)
what is a rough approximation of caloric expenditure?
O2 consumption x 5.0 kcal/L (noting that 1 MET = 1 kcal/kg/hr)
how is O2 consumption determined?
via measuring inspired and expired air passing through flow meter and O2 and CO2 gas analyzers
-O2 inspired - O2 expired = volume inspired * flow of inspiration - volume expired * flow of expiration
how does O2 consumption change with increasing work rate?
initially increases, but doesn’t continue indefinitely, and at some point increases in work rate won’t elicit further increase
what pulmonary, cardiovascular, and muscle factors that limit max VO2?
how does cardiac output change with increasing O2 consumption? max amount? distribution?
increases linearly; at max is 4-5x resting (5.5 L/min)
how does heart rate change with increasing O2 consumption? how do nervous systems play into this?
HR increases fairly linearly with O2 consumption
-sympathetic input to SA node increases, and parasympathetic input decreases
how does stroke volume change with exercise? with venous return? contractility?
exercise: increases initially at mild to moderate exercise, but may level off or decline at higher work rates (due to shorter filling time and lower EDV)
venous return or contractility: SV increases
why does the arterial-venous O2 difference widen with increasing exercise?
what is max O2 ventilation limited by?
left ventricular output, but if heart could deliver more O2 to exercising muscle, the muscle would use it
what is the exception where the ability of skeletal muscle to consume O2 limits VO2 max?
highly deconditioned individuals (bed rested, COPD, dialysis patients)
-not usually in normal, healthy individuals
what are 4 things that affect the blood pressure response?
why does CO increase more than TPR decreases, causing MAP to increase?
due to an increase in SBP rather than DBP, which is expected to remain near resting levels during exercise in a healthy person
what happens to SBP and DBP during large muscle work (leg) VS small muscle work (arm)?
leg: vasodilation to large active group, and vasoconstriction to small inactive group
- SBP increases much more than DBP increases, so MAP only increases a bit
arm: MAP is higher due to increasing TPR
dynamic VS static contractions
static/isometric contractions occlude flow when contraction exceeds more than 30% of max tension
what are the components of the metabolic response to exercise?
what is the myokinase reaction? what is it important for?
creatinine phosphate + ADP –> ATP + creatine
-important to maintain ATP/ADP ratio to determine muscle contractile ability in anaerobic ATP production
when is anaerobically provided ATP important?
what is the O2 deficit?
when ATP need»_space; ATP being made aerobically
-anaerobic ATP sources are mobilized to create “deficit” that is repaid post-exercise
what is the anaerobic threshold? what is it if trained VS untrained?
when anaerobic processes supplement ATP production (also “lactate threshold”)
what does the RER value during exercise depend on?
how does RER change as VO2 changes? what if if exercise intensity is prolonged?
RER increases as VO2 increases, reflecting increased CHO use (and less fat use) at steady state conditions, or hyperventilation at non-steady state
if exercise is prolonged, RER decreases if normal of high CHO diet, but if higher fat diet, the RER is already low and while they can’t work as long, RER doesn’t change