Chapter 9 Flashcards
circulatory system works with the
pulmonary system to bring O2 to the lungs and the lungs deliver O2 to the tissues
purposes of the cardiorespiratory system
transport O2 and nutrients to tissues
remove CO2 wastes from tissues
regulate body temp
two major adjustments of blood flow during exercise
increased cardiac output
redistribution of bloodflow from inactive organs to active muscle (thermoregulation)
pulmonary circuit
heart to lungs
on the right side of the heart
pumps DEoxygenated blood to the lungs via the pulmonary artery
returns OXYgenated blood to the left side of the heart via the pulmonary veins
systemic circuit
heart to the rest of the body
left side of the heart
pumps OXYgenated blood to the whole body via the arteries
returns DEoxygenated blood to the right side of the heart via the veins
plasma
liquid portion of the blood
contains ions, proteins, and hormones
RBCs
has Hb to carry O2
white blood cells
important in preventing infection
platelets
important in blood clotting
how to calculate hematocrit
hematocrit= height of RBCs/total height
hematocrit
what percent of blood is made of packed RBCs
average hematocrit males and females
males = 42%
females = 38%
blood flow is directly proportional to
the pressure difference between two ends of a system (change in pressure)
blood flow is inversely proportional to
resistance (increase resistance, decrease bloodflow)
blood flow equation
blood flow= change in pressure/resistance
pressure is proportional to
the difference between MAP and right atrial pressure (change in pressure)
diastole
relaxation period
pressure in the ventricles is LOW
filling with blood from the atria
AV valves open when ventricular pressure is LESS THAN atrial pressure
systole
contraction phase
pressure in ventricles rises
blood is ejected to pulmonary and systemic circulation
aortic and pulmonary semilunar valves open when ventricular pressure is GREATER than aortic pressure
at rest what is longer: diastole or systole
diastole
what happens to both systole and diastole during exercise
get shorter
appropriate order of events in left ventricle
ventricular filling - atrial contraction forces small amount of blood into ventricles
isovolumetric contraction- ventricles contract with no corresponding volume change
ventricular ejection- as pressure increases, blood is ejected into aorta
isovolumetric relaxation- ventricles relax with no corresponding volume change
cardiac output
the amount of blood pumped by the heart each minute
Q=HR x SV
what is stroke volume
the amount of blood ejected in each beat
cardiac output depends on
HR
SV
and training state and sex
typical resting HR for untrained males and females
males- 72
females- 75
typical resting SV for untrained males and females
males- 70
females- 60
typical Q for untrained males and females
males- 5.00
females- 4.5
typical max HR for untrained males and females
200 for both
typical max SV for untrained males and females
males- 110
females- 90
typical Q at max for males and females
males- 22.0
females- 18.0
parasympathetic regulation of HR
via vagus nerve- slows HR by inhibiting SA and AV node
preganglionic neuron releases ACh onto post-ganglionic neuron
post-ganglionic neuron releases ACh onto mAChr
G protein conformational change
G protein inactivates Ca2+ channel, inhibiting it from entering the cell
G protein also opens K+ channel, allowing it to exit the cell. This causes hyperpolarization as the cell becomes more negative making it harder to generate an action potential, slowing HR
sympathetic regulation of HR
via cardiac accelerator nerves- increases HR by stimulating SA, AV, and cardiac tissues
preganglionic neuron releases ACh onto post ganglionic neuron
post-ganglionic neuron releases NE onto B1-ADR
This causes a G protein conformational change which signals a 2nd messenger to open Na+ and Ca2+ channels.
Na+ and Ca2+ enter the cell, depolarizing the cell by making it more positive, making it easier to generate an action potential which increases HR
what is responsible for the increase in HR at onset of exercise
PNS withdrawl
if the function of the vagus nerve is hyperpolarizing the cell making it harder to generate an action potential, withdrawl of this function would actually increase HR and allow sympathetic pathway to take over
an increase in temperature does what to HR
increases HR to maintain perfusion pressure
if we are devoting blood to other areas of the body, the heart has to work harder to maintain perfusion pressure
Heart Rate Variability (HRV)
variation time between HRs
measured at R-R (peak to peak) interval using ECG tracing
wide range in resting HRV=
good index of a healthy balance between SNS and PNS
low variation in resting HRV =
bad
imbalance in autonomic regulation
excellent predictor of CV dysfunction
if we have low variability (same HR at rest) we lost PNS input and only have SNS input which is a sign of too much stress, no longer have vagus nerve input to AV and SA nodes)
diseases that promote a decrease in HRV:
depression
hypertension
heart disease, including myocardial infarction
physical inactivity
what activity results in increased HRV
regular bouta of aerobic exercise
EDV
end diastolic volume
aka preload
volume of blood in ventricles at the end of diastole
increased EDV does what to SV
increases SV
because volume is increasing
frank starling mechanism
EDV (preload)
greater EDV results in a more forceful contraction
- if you stretch the heart/ventricles more they get lined into a more optimal position to generate more forceful contraction
dependent on venous return and filling time
venous return is increased by
venoconstriction via SNS
skeletal muscle pump
respiratory pump
skeletal muscle pump
rhythmic skeletal muscle contractions force blood in extremities towards the heart
one way valves in veins prevent backflow of blood
exercising= constantly constricting veins= constantly moving blood back to heart = increasing preload
respiratory pump
changes in thoracic pressure pull blood towards the heart, increasing venous return, increasing preload
filling time affected by
HR
Body position
what body position increases preload
supine due to equal distribution of the blood in veins
average aortic pressure
pressure the ventricles must pump against to eject blood
aka afterload
dependent on MAP
stoke volumes relationship to afterload
stoke volume is INVERSELY proportional to afterload
increase afterload = decreases SV
a decrease in afterload results in
an increase in SV, decrease in ESV, and decrease in LVP
strength of ventricular contractility (inotropy) enhanced by
circulating Epi/NE and direct SNS stimulation of heart via cardiac accelerator nerves
less inotropy results in
less NE/Epi binding onto target cells (ventricles/cardiac tissues) resulting in a not as forceful contraction
more inotropy results in
more Epi/NE binding onto B1ADR
more G protein conformational change to 2nd messenger to open channels
makes it easier to generate action potential which depolarizes the cell increasing HR
increase inotropy results in
decreased ESV and increased SV
what is an increase in SV during exercise due to
increase EDV (preload)
increased inotropy
fick equation
VO2= Q x (a-v)O2difference
increased O2 delivery accomplished by what during exercise
increased Q
redistribution of blood flow from inactive organs to working skeletal muscle
up to 40-60% VO2 max due to
increased HR
increased SV
greater than 40-60% VO2 max due to
increased HR only
unless an elite athlete, what happens to EDV and SV
decreases and plateaus because at high HR, filling time is decreased
what body position results in an increased SV
supine position due to increase in EDV due to less pooling of blood in the legs
what happens to blood flow during exercise
increased blood flow to working skeletal muscle
at rest, what % of Q goes to muscle
15-20%
at maximal exercise, what % of Q goes to muscle
80-85%
what happens to bloodflow to less active organs during exercise
decreased bloodflow to liver, kindeys, GI tracts
redistribution of blood flow during exercise depends on
metabolic rate
regulation of muscle blood flow during exercise is primarily mediated by
local factors (autoregulation)
intrinsic control of bloodflow by increases in local metabolites (nitric oxide, prostaglandins, ATP, adenosine, and endothelium-derived hyperpolarization factors) all promote vasodilation to increase blood flow to working muscle tissues
does the a in (a-v)O2 difference ever change
no = it is the amount of O2 found in arteries
what is arteriovenous difference?
the amount of O2 that is taken up from 100mL blood
during exercise what happens to (a-v)O2difference
increases due to higher O2 uptake in tissues
used for oxidative ATP production
as you start exercising/muscles activated you are consuming more O2 which means that the partial pressure of O2 at the mitochondria/muscles decreases; this increases the gradient for O2 to move from arteries into the tissues which yields a lower value on venous or returning blood
as we consume more O2 in tissues, what happens to venous return
decreases
more O2 being pulled into tissues, lower partial pressure of O2 at mitochondria
what causes an elevated HR and BP in emotionally charged environments?
increases in SNS activity
emotional influence on HR and BP
can increase HR and BP
does not increase peak HR or BP during exercise
transition from rest to exercise: onset of exercise
rapid increase in HR, SV, Q
plateau in submaximal (below lactate threshold) exercise
HR and Q during graded exercise
increases linearly with increasing work rate
reaches plateau at 100% VO2 max
BP during graded exercise
MAP increases linearly
systolic BP increases all the way to max
Diastolic BP remains fairly constant
arm vs leg exercise: which yields a higher HR and BP
at the same absolute workload (1L/O2 in arms/legs)
the arms will yield a higher BP and HR because vascular capacity is much smaller in upper body/arms (network/# of blood vessels much smaller, but if you send same amount of blood into a smaller network, you increase pressure)
increased BP = vasoconstriction of large inactive muscle mass
increased HR= higher sympathetic stimulation
recovery of HR and BP between bouts depends on
fitness level
temp and humidity
duration and intensity of exercise
HIIT
power output constant but HR is gradually increasing between intervals (don’t have full recovery of HR before the start of the next interval= additive effect and HR slowly starts drifting to max and you potentially start to fatigue out)
this relates to EPOC as it takes a long time for HR and other things to recover at higher intensity exercises
during prolonged exercise what happens to Q
cardiac output is maintained
what happens to SV during prolonged exercise
gradual decrease in SV at a constant work rate over time due to dehydration and reduced plasma volume
as time increases, you sweat more and lose fluid, decreasing blood volume, decreasing SV and EDV
what happens to HR during prolonged exercise
gradual increase in HR (particularly in heat) aka cardiovascular drift
cardiovascular drift
not able to maintain steady state at high temps or power outputs
can also happen if you start diverting bloodflow to periphery via vasodilation, meaning the heart has to work harder to maintain perfusion pressure
how to prevent cardiovascular drift
drink water
lower intensity
cooler environment or use cooling measures during exercise
transition from exercise to recovery: during recovery
decrease in HR, SV, and Q toward resting
recovery after exercise depends on
duration and intensity of exercise
training state of subject
