Flashcards in Unit 7 - Exercise Physiology Deck (47)
what is resting O2 ventilation as an index of EE?
-3.5 ml/min/kg = 1 MET
-to translate to calories, need to know caloric equivalent of consuming 1 L of O2, which needs you to know the type of fuel metabolized (known if RQ is known)
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?
1. ventilatory capacity and diffusion
2. cardiac output, distribution of CO, and capillarity of skeletal muscle
3. mitochondrial content
how does cardiac output change with increasing O2 consumption? max amount? distribution?
increases linearly; at max is 4-5x resting (5.5 L/min)
-arterioles controlling blood flow to active skeletal muscle will dilate to get up to 80-85% of total CO
-blood flow to inactive muscles and splanchnic area decrease due to vasoconstriction
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?
1. better capillary perfusion
2. decreased myocyte PO2
3. right shift in O2-Hb dissociation curve
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?
1. type of muscle mass being use din exercise
2. whether exercise is static or dynamic
3. body position
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
-total occlusion of blood flow at 70% of max voluntary contraction, so MAP increase as TPR increases
-extremely large increases in MAP are seen when setatic muscle contractions are performed with large muscle groups (competitive weight lifting)
--exacerbated with Valsalva maneuver
-dynamic exercise in a large muscle group will have minimal BP response
what are the components of the metabolic response to exercise?
1. anaerobic ATP production - fast to turn on in response to need, powerful in terms of max rate of ATP turnover, but limited in capacity to sustain repeated contractions
-"stored" ATP in muscle cells can support only 2-3 contractions (4-6 mM)
-levels of CrP are 3-4x greater than ATP
-glycolysis has greatest capacity of anaerobic mechanisms
2. aerobic ATP production - slower to turn on and less powerful, but greater in capacity to sustain prolonged bouts of muscle contraction
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?
1. during transition period from one level of activity to a higher level of activity
2. whenever exercise demands exceed anaerobic threshold of the individual
what is the O2 deficit?
when ATP need >> 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")
-untrained: at 50% VO2 max
-trained: 85 or 90% VO2 max
what does the RER value during exercise depend on?
1. exercise intensity
2. prior dietary history
3. exercise duration
4. fitness level
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
how much does blood glucose supply for total energy costs?
when is liver glycogenolysis and liver gluconeogenesis more important?
glycogenolysis: major source of E especially during intense exercise
gluconeogenesis: provides up to 40% of liver glucose output with mild, very prolonged exercise
why does glucose uptake by muscle increase despite decreased insulin?
enhanced insulin sensitivity
how does glycogenolysis rate change as work rate changes? what happens if muscles are depleted of glycogen?
glycogenolysis rate increases exponentially as work rate increases
-severe local muscle fatigue apparent when muscles depleted
blood free fatty acid utilization
mobilization stimulated by increased circulating levels of E, NE, GH, glucagon, and cortisol (inhibited by insulin and lactate)
-major E substrate at low exercise intensities
-contribution to total E supply decreases as exercise intensity increases