lab exam Flashcards
5 factors that influence VO2 max:
genetics = health conditions, stroke volume
body size = different lung capacities may impact aerobic capacitiy - no necessarily VO2 max
sex = males often have greater SV and HB content, less HR variation
mode of exercise = long distance runner would have higher aerobic capacity than others
environmental factors = temperature (cold temp irritates lungs), altitude (less O2 @higher) , motivations (music, fans)
do the lungs and ventilation limit VO2 max?
not if healthy
ventilation perfusion mismatch:
causes?
inadequate airflow/bloodflow to lungs for match O2 needs
- high HR
- asthma/ inflamed bronchioles
- allergies
- smoking
- humidity
- temp
pulmonary diffusing capacity
as CO rises, not enough time for gas exchnage in alveoli in lungs
main limiting factor in O2 delivery?
poor delivery due to poor ingestion causes limited VO2
central cardiac factors:
cardiac output = HR x stroke volume
how does training alter HR and SV?
- SV increases
- max HR shows less variance
peripheral factors of CO:
what do they affect?
fiber type distribution = higher slow twitch allows for more O2 utilization, higher mitochondrial density
capillary density
muscles ability to take up and use oxygen
how does training alter fiber type and capillary density?
- aerobic training = shift type IIa to act like type I
- increase density around muscle, increase transit time (more O2 gets taken up)
oxygen deficit:
Difference between O2 uptake in the first minutes of exercise and uptake during an equal period of time after steady state has been obtained
caused by time between activation of ATP-PC and aerobic activation
EPOC aka excess post exercise oxygen consumption:
occurs during recovery post exercise - body requires additional O2 to recover and fuel bodys increased metabolic rate
increased body temp, HR, BR, Circulating epi and norepi
does EPOC change depending on exercise intensity? why?
yes = as intensity increases, magnitude and duration of EPOc increases bc
- higher body temp
- greater depleted PC - require more O2 for resynthesis
- higher blood lactate levels = require O2 for conversion to glucose
- epi and norepi levels rising
rapid epoc
- resynthesis of stored PC
- muscle and blood O2 stores replensished
slow epoc
due to
Elevated body temperature and elevated blood levels of epinephrine and
norepinephrine
ii. heart rate and breathing, remain elevated to meet energy needs (ATP
production)
iii. O2 required to convert lactate to glucose
why is RER high post exercise and doesnt drop like VO2?
VCO2 takes longer to go down bc buffering system is working to remove H+ and buffer lactatee
how many kcal is a pound of body fat?
3500kcal
what happens to HR and VO2 as power output is inceased?
HR = increases (increased blood flow, ATP production, CO, sympathetic activity)
VO2 = increases (O2 demand increases, RER)
how would increase in body temperature and blood acidity alter oxygen delivery ?
weakens bonds between O2 and Hb, increased unloading to active tissues
- dissociation curve would shift right
ventilatory threshold (Tvent)
Tvent is the inflection point when there is no longer a linear relationship between Ve and
VO2. When it becomes exponential, the Tvent has been surpassed
- high ventilation rate cannot match O2 demand
tvent for trained
- minimal slope prior (dominant aerobic metabolism longer), but more substantial inflection
- better at buffering acidosis
lactate threshold (Tlactate)
when blood lactate levels begin rising exponentially during incremental exercise:
caused by:
i. Increased rate of glycolysis (from increased levels of epinephrine)
ii. Decreased removal of blood lactate
iii. Decreased muscle oxygen content
iv. Switch over from predominant usage of Type I fibers to predominant usage of Type II fibers.
how does mood and illness impact HRV?
mood = depressed people have lower HRV
illness = decreased
chronic exercise on HRV:
increases
lower resting HR
when does VO2 drift occur?
when body can’t dissapate heat during exercise = ventilation and catecholamine circulation are enhanced - further enhancing the sympathetic response and inhibiting the acquisition of steady state. With this, VO2, heart rate, and ventilation continue to increase.
cardiovascular drift:
i. drift due to increase in body temperature with dehydration and reduction in plasma volume
ii. This reduction in plasma volume causes decreased SV as there is reduced venous return
iii. HR increases to compensate for decreased SV
iv. While this occurs during prolonged exercise, increased HR and decreased
stroke volume will be exaggerated during hot/humid environments
heat acclimation
Physiological adjustments produced by exposure to artificial conditions in experimental chambers or natural environments (acclimatization) -
typically 10-14 day exposure.
- increased plasma volume
cardiopulmonary factors related to fatigue
cardiopulmonary Factors:
i. Increase with exercise
- Heart Rate - not at max, genetics factor
- Stroke volume - reached max (b/c Vo2 went above 40-50%)
- Cardiac Output - not at max b/c HR not maxed, therefore cardiac
output reserve
- Blood pressure - not a noticeable difference - Vo2 - not at max
hyperaemic response post occlusion
Fundamental stimulus with occlusion is tissue hypoxia
Buildup of vasodilatory metabolites (NO, CO2, prostaglandins etc.)
Flow becomes elevated after occlusion d/t action of metabolites resulting in
decreased vascular resistance
what happens during and after occlusion?
During occlusion there was a build up of metabolites that then quickly
reperfused the active tissue (reactive hyperemia) this excess of vasodilation may allows for blood flow that allow for enhanced performance in the vertical jump after occlusion
- Tissues that were occluded have high o2 demand which is replenished by reactive hyperemia - however, as there is no cardiac demand since occlusion is passive, this would explain why post-exercise reactive hyperemia is more pronounced than occlusion-hyperemia as after exercise there is cardiac demand that helps re-perfuse the area
If the participant were to repeat the intervals with active recovery, how might results differ
- increased removal of lactate and wastes during recovery
- decreased VO2 changes between exercise and rest
- spike ctive recovery increases total workload and utilization of aerobic pathways so this may slowly increase aerobic pathways usage throughout exercise, instead of the spike in VO2 and HR we observed
