primary blood supply to heart provided by coronary arteries from aorta
cardiac veins return deoxygenated blood to inferior and superior vena cava
Heart and exercise:
heart generates pressure to drive oxygenated blood through vessels to skeletal muscles
driven by demands of muscle for O2
what does it do:
removes CO2 and wastes
transports hormones and molecules
supports temperature balance and fluid regulation
maintains acid-base balance
Matching systemic O2 supply with O2 demand:
VO2 = Q x a-vO2difference
Q = HR x SV
a-vO2difference = CaO2 - CvO2
important to increase Q with increase intensity because we would not be able to generate big enough VO2max
Q allows us to manage higher intensity
CvO2 decreases with increased intensity because more O2 is dropped off at tissue
Q and O2 utilization:
as VO2 increases, Q increases in proportion
increase demand = increase CO2
~ 6:1 ratio
for every 1 L increase in VO2, we get a 6 L output of CO2
Cardiac output (Q):
total volume of blood pumped by ventricle each minute
influenced by HR and SV
HR control:
2 mechanisms to control HR:
intrinsic control:
cardiac muscle generates own signal
pacemaker (SA node) establishes sinus rhythm
without external control (~100 bpm)
extrinsic control:
systems modulate intrinsic
causes HR to speed up or slow down
adjusts HR to ~35-40 bpm at rest
maximal effort, HR = ~220 bpm
Intrinsic regulation of HR:
SA node —> atria —> AV node —> purkinje fibres —> ventricles
SA node = spontaneous depolarization and repolarization to provide innate heart stimulus
AV node = delays impulse to provide time for atria to finish contracting and finish giving blood to ventricles
bundle of His
purkinje fibres = carry impulse rapidly through ventricles
Extrinsic regulation of HR:
3 systems:
parasympathetic:
releases ACh to slow down HR
sympathetic:
releases NE to speed up HR and increase contractility
innervates heart at SA node
endocrine:
release of Epi to affect SA node and increase HR
HR during exercise:
at low intensities, increase in HR due to decrease in PSNS activity
as intensity increases, increase in HR due to SNS activation
HR vs O2 uptake:
tight connection between HR, Q, and exercise intensity up to VO2max
SV:
amount of blood left in heart after contraction
EDV - ESV = SV
ejection fraction (EF):
percent of EDV pumped
SV/EDV = EF
Components of SV:
preload:
volume of blood in heart during diastole (before contraction)
end-diastolic filling
Frank Starling Law of Heart:
relationship between contractile and resting length of heart muscles
force of contraction equals initial muscle length
preload stretched ventricles in diastole to produce more forceful ejection
Components of SV:
contractility/inotropy:
enhanced contractile force to increase SV and facilitate emptying
myocardial contractility:
inotropy = increasing muscle tension for given preload and rate of muscle tension development
increase inotropy = increase SV
During exercise, increase inotropy:
increases SNS
decreases PSNS
increases endocrine (catecholamines)
Components of SV:
afterload:
Pressure heart must generate to open aortic valve
increase afterload = more pressure
decrease afterload = less pressure
exercise = reduction in afterload which causes increase in SV, Q, and O2
SV vs O2 uptake:
rapid rise in SV due to decreased afterload, increased inotropy, and increased preload
SV plateaus as exercise continues
increase exercise = increase HR, which decreases the amount of time we have to fill the heart, therefore decreasing slope at which SV rises as intensity increases = plateau
Qmax and VO2max:
increase Q = increase VO2max
endurance athletes that have high VO2max also have high Q
HR = limiting factor for ability to sustain higher intensities
Fick principle:
increase in VO2 is determined by Q
VO2max related to maximum ability of heart to pump blood
Central delivery of O2 blood:
SV fills chambers during diastole —> increases with increased intensity
CV system:
arteries = carry blood away from heart
arterioles = control blood flow
capillaries = area of exchange
venules = collect blood from capillaries
veins = carry blood to heart
Arteries and arterioles:
high-pressure tubing
pressure = high on arterial side, low on venous side
connect left ventricle to tissue
walls contain circular layers of smooth muscle that constrict and relax to control blood flow
innervated by SNS (NE released = constriction)
no gas exchange
Capillaries:
exchange
gas, nutrients, and waste products
velocity decreases as blood moves to and through capillaries because blood is moving away from area of high pressure (heart) to low pressure (veins)
Blood flow and VO2:
they follow each other
as one rises/lowers, the other rises/lowers
blood flow and VO2 rise to match O2 demands
relationship with metabolic rate of muscles
Hemodynamics:
pressure:
force that drives flow
provided by heart contraction
from region of high pressure to low pressure (no gradient = no flow)
resistance:
force that opposes flow
provided by physiological properties of vessels —> pressure differential
modification of vessel radius
Blood flow (Q):
total volume of blood pumped through vessel per minute
Q = MAP / TPR
increase pressure and decrease resistance = increase Q
decrease pressure and increase resistance = decrease Q
MAP:
P = arterial pressure - venous pressure
arterial pressure = 2/3 DBP + 1/3 SBP
Arterial blood pressure:
systolic = highest pressure in artery during contraction
diastolic = lowest pressure in artery during relaxation
mean arterial pressure (MAP) = average pressure on arterial vessel walls over entire cardiac cycle
Facts about pressure:
diastolic pressure stays the same with varying intensities
but systolic pressure changes (ex. increases with greater intensity)
MAP:
venous pressure = CVP (central venous pressure)
represents blood coming back to heart
Venous blood pressure:
CVP:
blood pressure taken in vena cava or right atrium pressure
reflects amount of blood returning to heart and ability of right heart to pump blood into pulmonary circulatory
range = 0-8 mmHg.
right atrial pressure doesn't change much during exercise
TPR:
resistance = n x L x r^4
we only really manipulate radius (r^4) because viscosity (n) and length of vessel (L) don’t change as often
r^4 has a powerful impact on resistance
increase r^4 = decrease resistance
decrease r^4 = increase resistance
TPR:
resistance to Q offered by all systemic vasculature, excluding pulmonary vasculature
3 factors affect resistance of Q:
Poiseuille’s Law —> n, L, r^4
we can only acutely change r^4 (vasoconstriction and vasodilation)
arterioles = resistance vessels (they control TPR; responsible for 70-80% of pressure drop from left ventricle to right atrium)
TPR = MAP / Q
Blood flow and exercise:
at rest, muscles receive ~ 1L/min of Q
with increased intensity, blood to muscle rises (80-85% of total Q)
brain always receives steady flow of blood
vessels constrict to redirect blood from areas that do not need it to areas that do (kidneys and splanchic)
Distribution of blood flow:
blood to sites that most need it
at rest:
liver and kidneys receive 50% of Q
muscles receive 20% of Q
exercise:
muscles receive 80% of Q
Q and muscle blood flow:
active muscle = decrease resistance
non-active muscle = increase resistance
Muscle blood flow:
resistance = most powerful tool to modify blood flow
Arterioles and smooth muscle:
arterioles have strong muscular walls of smooth muscle
smooth muscle uses cross-bridge cycling, actin and myosin, and Ca2+