CV system and exercise Flashcards
3 parts of the CV system
heart
vasculature
blood
4 functions of the CV system
transport oxygen and nutrients to body
removal of co2 and waste products
circulation of hormones
regulation of body temp, pH, and fluid balance
high VO2 max and sufficient vasculature
process oxygen quicker
two circuits of the CV system
parallel - pulmonary circuit(external respiration - pulmonary artery/vein), systemic circuit (internal respiration - cellular respiration)
heart - continous linkage between the two circuits
weight of heart
310g m
260g f
function of heart
pumps - 70ml each beat (stroke volume, at rest)
1 day - 7100 L through heart, 195 mil L for a 75 y life span
blood vessels of an adult stretched in a line
100,000km
macroanatmy of heart (2)
four chambered organ that provides the drive for blood flow
both ventricles pump the same amt of blood, left ventricle is thicker to overcome increased resistance
what circuit has more resistance
systemic
valve in right side of heart
tricuspid valve
valve in left side of heart
bicuspid/mitral valve
myocardium
fibers interconnect in latticework fashion to allow the herat to function as a unit
interscalated discs
junction b//w adjacent cardiac muscle cells that forms a mechanical and electrical connections between cells (desmosomes and gap junctions - mono/bi nucleated) for communication of msgs.
syncytium
group of cells of myocardium that function collectively as a unit during depolarization for atria and ventricles
nerve innervation of the heart?
no, only cardiacmyocytes - no impulses and conducting neurons - gap junctions
SA node
pacemaker - specialized cardiac myocytes and has no equipment for crossbridging
6 pacemaker potential makers
sinoatrial - 60-100 and sets the pace of the heart bachmann's bundle atriventricular node - only way for current to travel delays signal by 100ms and takes over if SA node failes bundle of his right and left bundle branches purkinje fibres
depolarization of SA node
sodium channels open up and charges increase, ca comes in, then another kind comes in, move through the gap junctions
repolarization - opening of potassium channels
extrinsic autonomic control of the CV system
sympathetic - SA node neurotransmiter - nor epinephrine - adrenergic receptor
hormone (adrenal medulla) - epinephrine
parasympathetic - SA node or normal cells , neurotransmitter - acetylcholine - muscarinic cholinergic receptor
extrinsic control of the heart AKA
autonomic control of the heart
extrinsic control of the heart at rest (3)
increased parasympathetic
decreased sympathetic
slows down SA pacemaker potential (60) acetylcholine and less sodium and calcium
extrinsic control of the heart at exercise (3)
decrease parasympathetic
increase sympathetic - NE up to 220bpm
speeds up pacemaker potential
cardiac cycle (4)
one complete sequence of contraction and relaxation of the heart - ventricular filling - (diastole) isovolumetric contraction (Systole) ventricular ejection (systole) isovolumetric relaxation (Diastole)
systole
contraction
diastole
relaxation
characteristics of membrane potential of regular cardiomyocytes
depolarization triggered by SA node/AV node
long refractory period - L type calcium - extend depolarization period - so they dont stack
ECG
electrocardiogram
- tracing that provides a graphic illustration of the heart muscle
ECG has
leads that go around the heart that shows the diff in activity
P wave
atrial depolarization - all atrial cells depolarized and in long refractory period
QRS - ventricular depolarization - all ventricular cells depolarized
do heart cells regenerate?
no
ST segment
ventricular depolarization to repolarization - heart attack if there is a bump
STROKE volume (2)
amt of blood ejected from the ventricles with each beat of the heart
SV=EDV-ESV
ejection fraction (2)
% of EDV ejected from the heart
EF% = (SV/EDV)x100
ejection fraction influenced by 3
preload
contractility
afterload
preload
volume of blood returning to the heart
contractility
force of myocardial contraction
afterload
resistance of vasculature
more preload
more SV
preload follows what law
frank-starling
- greater the EDV, greater the stroke volume as you have stretched out the muscle
contractility stimulated by
increased SNS stimulation
- increased SV for a given EDV
cardiac output
amt of blood pumped/unit of time - in L/min
CO= SVxHR
measuring CO
difficult
Fick equation
echocardiogram
fick equation
CO = VO2/(a-vo2) with vo2 measured by metabolic cart
invasive as it requires sample of arterial and mixed venous blood
doppler - aorta and vena cava
doppler echocardiogram
calculates SV from measurements of aortic cross sectional area and time velocity integrals in the ascending aorta
myocardial oxygen consumption is influenced by
the phase of the cardiac cycle - coronary arteries are compressed in systole, so oxygen is delivered during diastole
myocardial oxygen consumption
rate pressure product
RPP=HRxSBP
during exercise bloodflow to the heart is increased through 2
vasodilation as a result of metabolic byproduct (adenosine - byproduct of atp use)
increased contractility of heart
what type of vessels have smooth muscles?
arteries
arterioles AKA
resistance vessels - ability to vasodilate and vasoconstrict
smooth muscles are under the control of 2 in order to
extrinsic factors - autonomic nervous system
intrinsic factors - metabolic, myogenic, and shear stress
change the diameter of the arterioles to permit control of blood flow
flow of the vascular system follows the
poiseuille’s law
flow = changing pressure/resistance
meta-arterioles
short vessels that connect arterioles and venules
capillaries 2
branch off metaarterioles
blood flow regulated by local metabolic factors
single layer of rolled up endothelial cells
anastomosis
shunts between arterioles and venules - present in skin and plays an important role in thermoregulation
veins AKA
2
capacitance vessels
- increased distensibility permits veins to pool large volumes of blood
venoconstriction can increase the amt of blood returning to the heart, thus increasing EDV/preload and SV
total volume of blood and its components
5-6L
plasma - fluid matrix
living cells - erythrocytes (RBC) to carry oxygen
leukocytes
hemotocrit and a normal number
% of RBC - 38-48%
what stimulates RBC production
EPO which increases the viscosity of blood, you need a hematocrit of less than 50 to compete
arterial blood pressure
force of blood against arterial walls during cardiac cycle (mmHg)
systolic blood pressure
provides estimate of work of heart and force blood exerts against arterial wall during systole
diastolic blood pressure (2)
indicates peripheral resistance or ease that blood flows from arterioles into capillaries -mean arterial pressure
average force exerted by blood against arterial wall during cardiac cycle
systole length vs diastole
systole shorter
auscultation method of measuring BP (5)
non- invasive sphygmomanometer and stethoscope first korotkoff sound =SBP fourth = DBP1 fifth = DBP 2
cardiovascular hemodynamics (2)
flow of blood through vessels is dependent on the pressure gradient along the vessel and the resistance to flow
Q= MAP/TPR
why can MAP used for changing pressure?
flow =changing pressure/resistance
pressure at vena cava is near to zero
velocity of blood is inversely related to
cross sectional area
- velocity of blood decreases in caps, allowing better exchange of gases and nutrients
3 cardiovascular control centres are in
vasomotor centre
cardio accelerator centre
cardio inhibitor center
medulla oblongata
baroreceptors
senses in increase in blood pressure and puts the brake on
vasomotor centre controls 2
skeletal muscle arterioles to vasodilate and visceral arterioles to vasoconstrict
sympathetic nerve innervates which CV control centres? what nerve is it?
vasomotor centre
cardioaccelerator centre
accelerator nerve
what CV control centre does the parasympathetic nerve innervate? what nerve is it?
cardio inhibitor center
vagus nerve
cardioaccelerator and inhibitor center have an effect on
heart
- increases HR and contractility
- decrease HR and a little contractility
3 afferents of the CV system and their receptors
glossopharyngeal - arterial baro
vagal - cardiac receptors
skeletal muscle -skeletal muscle mechnoreceptors and metaboreceptors
2 efferents of the CV system and what they control
vagal efferent - ach on the heart
sympathetic efferent - NE on the heart and systemic resistance and capacitance vessels
Heart transplant and innervation
no increase of HR through SNS, only NE from the adrenal gland so it might ake a while
lesion at C7 effect on CV
no longer hit max HR because no more SNS innervation, your parasympathetic will kick in and work when you’re at rest but will leave during exercise and your HR can go up to 100 bpm
vasoconstriction innervated by
increased sympathetic innervation of N/NE
vasodilation innervated by 2
increased sympathetic innervation of E and NE and intrinsic metabolic factors
Beta 2 receptors
activated by E/NE to relax smooth muscles and dilate vessels
Alpha 1 receptors
activated by E/NE to contract smooth muscles and constrict vessels (increase resistance to decrease flow) - redirect this blood for fight or flight
intrinsic control - localized vasodilation (3)
decreased local pO2 and pH
increased local pCO2, K, lactate and nitric oxide - (from arteriold vessels)
from depletion of ATP and fatigue related factors
exercise response to long term, moderate to heavy exercise - submax aerobic - 60-85% VO2max (3)
rapid increase in CO, SV, HR, SBP, RPP
after 30 min, development of cardiovascular shift
a lot more blood to muscles, some more to skin
Exercise response to short term, light to moderate exercise - submax aerobic exercise of 30-70 % VO2max (4)
increased Q until steady state is reached
- rapid increase in SV due to increased preload (frank-starling) and increased contractility
slight increase in MAP
- increased SBP due to increased CO with no change in DBP
- Q increased more than TPR reduced
increase in RPP - heart is taxed
blood to skeletal muscle
blood volume when exercising (3)
in the early part of aerobic exercise it rapidly drops - shift in plasma volume rather than loss of fluid
higher hemotocrit, plasma going into interstitial area
cardiovascular shift (5)
changes in observed cardiovascular variables with out a change in workload
- decreased SV (decreased preload due to thermoregulatory fluid loss and distribution of blood to skin to rid of heat - decreased EDV)
- increased HR to maintain CO
- decreased SBP with decreased TPR from vasodilation
- Increased RPP, increased in HR is greater than the drop in SBP
cerebral blood supply during any physical activity
always gets the same blood supply
incremental aerobic exercise to VO2max and effect (5)
30 -> 100%VO2max increased CO with plateau at max - SV plateaus at 50 VO2max - you dont have enough time to eject everything (increased EDV from increased preload, decreased ESV from increased contractility) increased MAP - SBP increases (22mmhg) - increased CO with simutaneous drop in TPR - constant DBP increased RPP with plateau at max HR increased gradually till VO2max
Q at rest
5.8L/min
Q at light aerobic exercise
9.4L/min
Q at heavy aerobic exercise
17.5L/min
Q at maximal exercise
25L/min
VO2max
greatest amount of oxygen that the body can take in, transport and utilize during heavy exercise
CV system determinants of VO2 max (2-3, 2-6)
central circulation - Q - arterial blood flow -hemoglobin concentration peripheral circulation - flow to non exercising regions - muscle blood flow - muscle capillary density - oxygen diffusion - oxygen extraction - hemoglobin - oxygen exchange
respiratory system determinants of VO2max (3)
oxygen diffusion
ventilation
a-vo2 difference
4 skeletal muscle/metabolic function determinants of vo2 max
myoglobin
enzymes and oxidative potential
energy stores and delivery
mitochondria size and number
3 factors that influence the SV
myocardial contractility
ventricle size
blood volume
3 factors of the metabolic oxidative potential
availability of FFA, glycogen, glucose
size and type of muslce fibre
size and number of mitochondria
3 factors for muscle bloodflow
capillary density
Nervous and hormonal control
peripheral resistance
2 factors for a-vo2 idff
metabolic oxidative potential
muslce blood flow
highest HR
Vo2 max
4 criteria for achieving VO2 max
plateau in oxygen consumption - rise less than 150ml o2/min or 2.1ml o2/kgmin
lactate greater than 8-9mmol/L
RER larger than 1.1 - anaerobic system and hydrogen buffing
+/- bpm of age predicted max HR
if any of the criteria for vo2 max is not met
its the VO2 peak - highest VO2 achieved which is slightly lower than VO2 max
order of VO2max of blind shrew, pronghorn and oskar svendsen
blind shrew
pronghorn
oskar svendsen
gender difference in VO2 max
male relative to weight can be 20-30% higher
male relative to fat free mass can be 0-15% higher
gender plays a role in which factors that determine VO2 max? (6)
blood volume ventricle size size and type of muslce fibre availability of FFA, glycogen and glucose Hb in blood nervous and hormonal control
max HR for men and women
similar
M vs F HR at relative submax
higher for F
M vs F HR and Q at absolute submax
F always higher
vo2max F vs M
F always lower
HR at rest F vs M
F higher
trend of F HR
usually higher to make up for low SV
children and VO2max 2
lower - limit Q
decrease in weight means high relative VO2max
females at puberty and vo2max
decrease
older age and vo2 max
decrease because of decreased Q and increased TPR (loss of elasticity in vessels
upper body exercise effects vs lower (3)
decreased SV due to reduced preload (decrease muscle pump from lower body)
increased HR due to sympathetic innervation
increased TPR - increased SBP and RPP
Why do people have heart attacks when they shovel snow?
large myocardial oxygen demand relative to VO2, RPP higher with snow shoveling than max treatmill test - excess strain on your heart
exercise response to static exercise (3)
muscle contraction (%MVC)
- decreased SV due to decreased preload (increased intrathoracic pressure on inf. vena cava - valsalva maneuver)
- increased afterload due to mechanical constriction of blood vessels which leads to pressor reflex
pressor reflex/response (2)
rapid/exaggerated increase in both SBP and DBP during static exercise
- results from build up of metabolic by products triggering sensory afferent nerve endings which leads to increased sympathetic innervation of increased HR and MAP
exercise response to dynamic resistance exercise
constant load /rep to failure
highly elevated MAP
- mechanical compression of the blood vessels - increased afterload
generally a decrease in TPR but may increase slighly
decreased preload so decreased SV
valsalva maneuver
decreased SV due to decreased preload
acute cardiovascular strain with heavy resistance exercise (2)
could be harmful to ind. with heart and vascular disease
- leg press strength exercise, your bp can go up to 480/350
BP recovery after exercise (2)
after submax, BP temporarily falls below pre exercise for normotensive and hypertensive ind due to peripheral vasodilation
hypotensive response can last up to 12 hrs.
occurs in response to either low or mod intensity or resistance exercise
cardiovascular fitness
ability to deliver and use oxygen under the demands of intensive, prolonged exercise of work
- evaluated by VO2max
2 adaptations to CV training
central cardiovascular adaptations - occur in the heart and contribute to an increased ability to deliver oxygen
peripheral cardiovascular adaptations - occur in the vasculature and muscles and contribute an increased ability to extract oxygen
canadian society for exercise physiology recommends
a total of 150 mins of mod to vig PA
cardiac dimensions as cardiovascular adaptations to aerobic training (3)
increased heart mass
increased left/right ventricular cavity size (increased EDV)
- volume overload - repeated exposure to increased preload
increased LV/RV mass (hypertrophy) - eccentric hypertrophy
vascular structure and function (3)
arterial remodeling - increase size/cross sectional area improved endothelial function - increased ability to dilate assist heart in meeting the demand of elevated RPP cappilarization - 20% increase - increase tortuosity - twisted
blood volume in the first 10 days of training (2)
20-25% of increase in blood volume, largely due to increases in blood plasma
absolute level of RBC does not appear to increase therefore decreased hemotocrit
blood volume after a month of training
increased RBCs = normalization of hemotocrit
How do endurance athletes achieve a large maximal Q
by increasing SV
untrained : 22000ml/min= 195beat*113ml/beat
trained: 35000ml/min=195beats/minx179ml/beat
eudurance training causes SV to (5)
increase during rest and exercise
increase contractility, blood volume, and cardiac dimension
down peripheral resistance
Plateau in SV at 40-50% VO2 max
in untrained ind, trained atletes may not have it.
endurance training causes HR to (3)
decrease at rest (increase parasympathetic)
submax HR for standard exercise decrease by 12-15 beats/min
max HR unchanged, facilitating greater Q at VO2max
aerobic endurance training adaptation to maximal oxygen consumption
increase VO2 max by 5-30%
increased Q
increased a-VO2 difference due to improved distribution of Q to active muslces and increased capacity of trained muscle to extract and process available O2
greatest influence in men post training regarding to VO2peak, Q peak and a-VO2 peak
VO2
upper body has a increased __________ innervation
sympathetic nervous system
valsalsa maneuver
metabolic byproducts induce pressor reflex
increase in SV implication to heart
eccentric stretch which increases ventricle size - hypertrophy and an increase in blood volume
overload principle
Frequency - 4-5/6 sessions/week optimal
Intensity - training mod to max for greatest improvement in VO2max
- defined relation to HR, rate of perceived exertion, or %VO2 max
Time/duration - 35-45 min sessions (mod-heavy)
greater initial fitness level associated with ______ changes in VO2max
lower
blood pressure adaptation to aerobic endurance training
in normotensive ind - little to no change
rate pressure product adaptation to aerobic endurance training
decrease at rest and submaximal exercise
resistance adaptation to aerobic endurance training
decrease at maximal exercise
endurance training adaptation due to BP, RPP and resistance are because of
improved endothelial function - how well your vessles respond to sympathetic and parasympathetic innervations
increased plasma volume and RBC means
increased total blood volume
increased total blood volume means
increased venous return
what three factors induce the increase in EDV
increased ventricular compliance, internal ventricular dimensions and VR
increased myocardial contractility means
increased ejection fraction
increased EDV and EF means 2
maximum SV - Q
max Q
increased effectiveness of Q distribution
increased effectiveness of Q distribution
increased optimization of peripheral flow
increased optimization of peripheral flow
increased blood flow to active muscles
4 adaptations to dynamic resistance training
increased left ventricular wall thickness - related to increased afterload (concentric ventricular hypertrophy)
SV may be slightly increased
resting MAP reduced (except in hypertensive pop.)
no clear evidence for increased VO2max
Upon cessation of cardiorespiratory training (4)
all adaptations reverse to baseline over period of time
- decrease VO2max, Qmax, SV, blood volume
- increased HR
84 days to fall back down to baseline
most effective strategy to maintain training adaptations of VO2
maintenance of training intensity
cardiac remodelling caused by long term deconditioning
cardiac dimensions appear to return to baseline after a long period of detraining
blood doping
misuse of certain techniques and/or substances to increases one’s RBC mass, which allows the body to transport more oxygen to muscles and therefore increase stamina and performance
3 things that blood doping can do
increase hemoglobin from 15g/dl to 19 therefore hematocrit of larger than 50%
increase blood volume to enhance cardiac output
increased vo2max by 4-13% and endurance performance by 3-34%
large vessels benefit to blood doping
inject it right into the lumen - lesser chance of getting caught
1945 blood doping
pilots started infusing RBCs to prevent blackouts
1972-76 blood doping
Lasse Viren (Finland) - 3 golds - 5k, 10k, marathon, suspicion of blood doping
1986 blood doping
banned after american cycling team admitted to blood doping
1998 blood doping
tour de france - police identified team cars full of boxes of EPO
2013 blood doping
lance armstrong confession
2 kinds of blood transfusion
autologous/homologous blood doping
autologous blood doping 4
reinfusing of your own blood
- remove 500-2000ml and reinfuse after regeneration of blood volume and RBCs (4-6wks)
- cannot be detected
- vanishing twins - new antigens
homologous blood doping
reinfusing someone else’s blood (compatible donor)
- test developed in 2004
Erythropoietin 3
hormone naturally produced by the kidneys that stimulates production of new RBCs in the spleen and bone marrow
- risk of elevated hematocrit - numerous athletes suspected to have died of heart attacks or strokes as a result of EPO
- test developed for synthetic EPO in 2000
- one study showed no effect
meldonium
created in
banned?
mechanism?
latvia 1970s - lil eng lit, no double blind, placebo control or cross-over clinical trials
jan 1st, 2016 - intention of enhancing performance
vasodilator of the heart - protective against cardiovascular ischemia - blood flow booster to treat angina
