1
Q
which 2 of the 3 can you measure from BP = Qc * TPR
A
cardiac output and bp.
2
Q
how does the regulation of bp and co change during exercise
A
when we exercise we deliver more blood to our muscles, backing off the resistance and keeping enough pressure to ensure flow into the muscles
3
Q
at rest how would the Qc equation change for a trained person
A
they would have similar Qc values at rest as they do not need to increase this but are achieving it more efficiently, as they have a greater SV and do not need as much of a high HR.
4
Q
at exercise how would the Qc equation change for a trained person
A
trained people have a greater SV, greater ventricular strength and can pump more in any given beat and they have improved cappilarisation which allows more less total peripheral resistance.
5
Q
what does increase pressure do to force of flow
A
increased pressure increase the driving forve for flow.
6
Q
what does increased resistance cause
A
increased pressure or redistribution of flow.
7
Q
what is the flow = equation
A
flow = change in pressure / resistance. and change in pressure * radius ^4 / length * viscosity.
8
Q
what happens to MAP in exercise
A
it is upregulated immediatly, and is proportional to exercise intensity
9
Q
what mediates the MAP upregulation
A
central command and ergoreceptors input.
10
Q
different BP responses to dynamic and static exercise
A
you know this, think back to what kane said
11
Q
what is the VO2max equation
A
= (BP/TPR) * (a-vo2 diff)
12
Q
how does cardiac output change in exercise and where does the blood go in dynamic exercise
A
5-8 fold increase in CO. decrease to the GI organs, increased blood flow to strated muscle flow, increased to brain but largely decrease relatively.
skin decrease slightly but then starts to increase with longer durations
13
Q
what is striated muscle flow
A
the flow of nutrienst and blood in and out of the skeletal and caridac muscle tissue
14
Q
what does distribution of blood flow to diff tissues depend on?
A
SNS nerves and receptors, myogenic autoregulation and metabolic autoregulation.
15
Q
where is myogenic auto regulation of the blood flow redistribution most prominent.
A
brain and kidney
16
Q
where is metabolic autoregulation most prominent for blood flow and what mediates it
A
in striated muscle and is mediated by temperature, pH, co2, ATP, adenosine, potassium and magnesium
17
Q
how is NO released for blood flow
A
by the capil endothelium and also circulating Hb. It’s produced in response to mechanical stress (like increased blood flow or shear stress on vessel walls) and hypoxia (low oxygen levels).
18
Q
how does NO act autocrine
A
if effects the same cells that release it, so the smooth muscle and vessles will dilate.
19
Q
NO is particulary important for exercise …
A
because it directs blood flow to the areas being used. as it is localised.
20
Q
how is NO changed for CVD patients
A
NO production is often reduced, which can impair blood flow regulation and vascular health. However, exercise training can increase NO production in the early stages of adaptation — improving blood flow and vessel function until the vessels enlarge and structural changes occur.
21
Q
where is adenosine released from
A
muscle and endothelial cells
22
Q
where is ATP and NO released from
A
all 3 cells (endothelial, RBCs and muscle)
23
Q
are ATP, NO and adenosine vasodilate localised?
A
yes
24
Q
what happens when ATP is needed somewhere and what does this cause for blood flow.
A
Increased SNS activity whichconstricts vessels systemically, but local metabolic and ATP-related vasodilators override this in active tissue, ensuring oxygen delivery matches metabolic demand.
25
with training how does the SNS actiavtion with atp change
decrease afferent fdbk to SNS, more ATP release and they will so stringly overrides SNS constrcition.
26
what is blood made up of
plasma volume and cells
27
what is the cells part
red cells, white cells and platelets
28
what is in the plasma
90% water, electrolytes, proteins, gases, hormones, metabolites, and substartes.
29
how do water and electrolyrtes exchange
freely from PV to ISF.
30
can albumin escape
yes it is the largest particle that can, although some white cells can. depenging on how leaky tissue caps are.
31
where are leaky caps tissues seen
liver
32
where are tight tissue caps
BBB and gut tight junctions.
33
what can cause some of the tight tissue caps to degrade
excess stress (heat + ischaemia).
34
commonly how does BV usually chnage during exercise
decrease 10-15% at onset (regardless of fitness or hydration), then will recover over minutes, then decrease over hours (dehydration). and then will rise over days.
35
why does BV rise over days after exercise
and by a lot PV by 20-25%, due to sterss hormones. AVP, aldosterone and albumin synthesis. which cause the body to have a greater uptake of fluid.
36
why does BV decrease at onset of exercise
due to the shift of fluid into the working muscles
37
how does BV change after exercise (recovery)
usually risen by next day.
38
what would posture do to the BV in recovery
if supine in first three hours no increase.
39
mechanisms of BV change after exercuse
lympathtic return, albumin synthesis, albumin retention and sodium retention.
40
why do we need to measure Hb as well at HCt for dehydration
because RBC will decrease when dehydrated whihc increase the concentration of HB, so should ise the RBC and HB formula instead.
41
Hct formula
easy, cheap and fast
42
what do both HCt and HCT/Hb formulas assume
no production or loss of RBC
43
Hct and Hb formula
increase in money and may be less reliable
44
BV chronic effects
massive differences accross different sports and training status.
45
what is haemodilution mean in reagrds to BV response to short term training
increase in PV before RCV
46
does haemodilution affect vo2max
doesnt seem to
47
what can SIT do to RBC
decrease by 6% in three sessions
48
what is an importnat determinnat of Vo2max
RBC. More RCV = more haemoglobin = greater oxygen-carrying capacity
49
effects of PV on ex physiol
increase SV and therefore decrease HR. decrease SNS response, decrease RPE, provides a fluid reserve for thermoregulation (sweating, perfusion).
50
can everyone get to the elite level in regards to heart related
not really, training will help but a large and strong heart is needed to get to an elite level, need both training and genetics
51
what are the differences for PNS on the SA node for trained and untrained
for a trained person, hard breaks inhibiting as they have much more to come off from.
52
what are the differences for SNS on the SA node for trained and untrained
the same for both, if anything untrained cannot activate it as much as it makes their HR lower.
53
what can heat stress do the SA node?
heat stress itself can act on the SA node, increasing 7 bpm / degree in rise of temp.
54
what things increase stroke volume
EDV "preload" and ventricular contractility.
55
what is the Frank Starling mechanism?
increase in meters and therefore increase in force, so from greater preload or stretch of the heart it will increase the ventricular contractility.
56
what can help EDV?
SNS can create venous constriction which will increase venous return. ventilatory and muscle pumps will also increase venous return.
57
what inhibits SV
MAP (=afterload).
58
where does afterload come from
arteiole constriction from the SNS.
59
different ways to measure CO
direct fick or indirect fick
60
what are the two things that can affect heart rate max
genes and age.
61
what is the direct fick equation
CO= Vo2/ a-vo2diff. invasive and specialist.
62
what is indirect fick
thermal or dye dilution, has same issues as above.
63
physiological growth of the heart from aerobic exercise
eccentric LV hypertrophy, LV dilation and protional LVWT, mild RV dilation, biatrial enlargement, cardio proliferation, activation of progenitor cells and reversible.
64
physiological growth of the heart from resistance exercise
concentric LV hypertrophy, LVWT and minimal change in LV volume, mild LA hypertrophy, activation of progenitor cells and reversible.
65
training adaptations for heart that aid cardiac output
lower HR at rest which increase the HR range and decreases the amount of cardiac work at any given time. increae in EDV and contracility (SV). increase rate of filling.
66
what are the three levels of injury for the heart
reperfusion induced arrhythmias - ischaemia of 1-5min. myocardial stunning, ischaemia 5-20min, reversable damage. 3. infraction (cell death)
67
why does does myocardial vascularisation happen
from increase in capillary density and collateral circulation
68
when does increasing in capillary density happen in the heart
weeks
69
when does collateral circulation increase in the heart
months - years
70
what can protect the heart from ischaemia?
oxidants, calcium, calpain, hydrogen and atp
71
what can protect the heart from reperfusion?
oxidants, calcium, calpian, caspase-3 and leukocytes.
72
what are other cardiac adaptations that help with resiliance
within heart muscle cells, heat shock proteins, antioxidants can be key mediators and atp-sensitive potassium channels.
73
what do heat shock proteins do?
help, make, maintain and repair proteins
74
how are antioxidants key mediators.
Exercise increases ROS, which signal mitochondrial adaptation.
MnSOD (mitochondrial antioxidant) neutralises ROS to prevent damage while allowing signalling.
Exercise upregulates MnSOD, strengthening antioxidant defences.
If MnSOD is blocked, mitochondrial adaptations and protection from exercise do not occur.
75
where are and what do atp sensitive potassium channels do?
in the mitochondiral and sacrolemmal memb. shorten action potential, so decrease calcium accumulation.
76
lifelong exercise and age related factors of cardiac adaptations
prevents stiffening and degeneration of heart valves. less benefit of increase compliance if start when old, but some age-related decrease in cardiomyocyte # and ventricular volumes.
77
HI or LI for cardiac adaptations
85-95% HRmax seemed to increase all levels of intrinsic cardiac adaptation more.
78
what may intervals do - exercise prescription
may increase aerobic power by way of potent myocardial remodelling rather than BV effects.
79
decay or adaptation faster for cardiac adaptation
decay faster but reinduction maybe quicker.
80
cardiac function (functional capacity) development timeframe and regression
development 1-2wk 12 wk.
regression 2wk 4wk
81
morphology (hypertrophy) development timeframe and regression
D 8-10wk 3-6mon
R 1-2 wk 4wk
82
electrical alterations development timeframe and regression
D 8 wk 3-6mon
R 2wk 12wk
83
current exercise prescriptions for aerobic
150-300 min of moderate-intensity PA, 75-150 of vigorous intensity PA, or a combination of both
84
current prescription for muscle strengthing
muscle-strengthing activities at moderate or greater intensity that involve all major muscle groups on 2 or more days.
85
sedentarism - current prescription
limiting the amount of time spent being sedentary.
86
What does the equation Flow = Pressure / Resistance tell us about vascular function?
Increasing resistance decreases flow; vascular function determines how easily blood moves through vessels to deliver oxygen and nutrients.
87
Why is vascular function important in the lungs?
It prevents excessive pressure that would impair gas exchange; too much pressure causes constriction, uneven flow, and hypoxia.
88
Why is vascular control important in the brain and kidneys?
These organs are pressure-sensitive; high pressure damages small vessels, while adequate control maintains perfusion and prevents stroke.
89
Why does skeletal muscle vascular function matter for performance?
Muscles need enough flow to deliver oxygen, remove waste, and use glucose and fat efficiently — key for endurance and metabolic health.
90
acute myogenic vascular response
vessels will resist ti the higher pressure, which causes the muscle to restrict against HBP. esp. in the brain and kidney
91
metabolic acute vascular response
we want them to respond to these things, NO, oxygen, heat, hydrogen and ions, esp. in muscles
92
neural acute vascular responses
almost all not the heart react to SNS, the heart will vasodilate under the same signal. with training we can learn to ignor this signal.
93
shear stress acute vascular responses.
as flow comes through the blood vessles, it bends the endothelial cells, these cells get bent forward (affecting the antegrade stress). if you have forward facing flow, it bends them more that way producing more dilating properties, the process that removes shear stress it will not flow as much abd they will not bend.
94
antegrade shear in the blood vessels is
forward vasodilatory + angiogenic - more capillarisaion
95
retrograde shear in the blood vessels is
backward. vasoconstrictive and atherogenic.
96
how to test conduit arteries
measure the flow and diameter, put a cuff on the forearm so no blood gets into the arm, then release the cuff, roaring of the blood, as the blood gets through it bends the cells more, producing NO to dilate. measure the blood vessel. FMD = how much the vessel grows in response to a higher flow.
97
how does FMD affect change with training
not used as much as you have grown the vessels, therefore it does not have such a high response as it already has a greater vascular repsonse.
98
functional change of the blood vessel is due to..
local factors (esp. NO) then heat and pH.
99
structural changes and main reasoning of vessel changes
due to systemic factors, changes the wall thickness, stufness and the lumen diameter.
100
flow change of blood vessels when can you see this and what chanegs it
small structural changes will cause big effect in flow. do not see anything at rest have to put someone under stress.
101
what will cause structural and fucntional changes in vascular
anything.
102
deacy rate of vascualr adaptations
lose in days - week. fucntional effect less robust.
103
what exercise prescription for effective anti-hypertension therapy
a wide variety
104
what can high GI intake do the pressor response to isometric ex
acutelu will increase it
105
how can exercise acutely protect against fat mediated dysfunction.
not due to reducing fat or glucose in blood but it protects bioavail of NO. ex around 18 hr before the meal.
106
how can exercise acutely protect against stress mediated dysfunction
once again protects bioavail of NO, rapid benefit even from small amount of stress.
107
why may exercise protection be more important in menopause
oestrogen can protect vascular responsiveness, and so exercise proteins may exert similar effects. but important to insure that you vascular health is higher before aswell then when you lose some you will not lose as much, as the baseline is higher.
108
how can excessive exercise impair CVS fucntion acutely - cardiac
exercise volume rather than intensity damages myocytes causing increase myocardial contractile proteins in plasma. does not neccassarily mean its any problem in long term.
109
how can excessive exercise impair CVS fucntion acutely - vascular
resistance ex and HI dynamic ex can both impair vascular function from increase oxidative stress and decrease NO bioavailability.
110
whats the but with "resistance ex and HI dynamic ex can both impair vascular function from increase oxidative stress and decrease NO bioavailability."
some studies show HIIT then increases antioxidants more than in endurance.
111
how can excessive exercise impair CVS function acutely - blood
many, maximal efforts sprints can lyse red cells, and decrease RCV.
112
why is PNS - SNS balance important
PNS gives more cardiac rest, and SNS increase BP.
113
what is a progonstic of longevity
low HR and high HRV.
114
why may HIT not aid CV health
may decrease HRV (ANS fucntion and inflammation), may increase collafen formation in heart and vessels. along w larger chamber, underlies cardiac arrhythmias in elite athletes. be non-protective in ultra distance runners.
115
how much does the brain weigh
1300-1400 g
116
how much blood does brain need
around 750ml/min or 50% own weight in blood/min
117
where does the blood for the brain come from?
70% via internal carotid arteries and 30% via vertebral arteries.
118
how much of the energy from the brain goes in neural signalling?
75%
119
what are astrocytes?
critical for controlling the blood to the brain and availability of nutrients. regulates the flow to meet all ongoing demands
120
what are the 5 major CBF mechanisms
metabolism, blood pressure, neurogenic, chemical arterial PO2 and CO.
121
what mechanism for CBF has the most sensitive effect
co2 then blood pressure.
122
CO, mechanics for CBF
not a massive problem, would have to undergo a big adaptation before this becomes a problem. the brain does well to resist against increase, to a point.
123
what is the most important mechanisms for CBF?
chemical arterial PO2
124
how does CBF change with exercise?
increase upto 20%, once above VT2 it will decrease, even though the met requirement is higher, but because of increase breathing it can lower.
125
why does rowing not have the same effect on CBF
it will continue to increase even after hyperventilation, because you are not working against gravity (thoraic pressure)
126
how to check vascular health in the brain
cannot measure FND effect, so you want to look at the steepness of the co2 and flow.
127
what happens in the heat to CBF
decrease, as carotid bodies in your throat get more active to make you hyperventilate.
128
how does voluntary under-breath effect CBF
will increase CBF, does not mean we should do this as it comes down for a reason
129
how can lack of oxygen affect CBF
can destabilise CBF, in high altitude or heavily polluted areas.
130
how does swimming increase you CBF
just by lying down increase CBF (die to increase blood flow in general), hydrostatic increases blood flow to chest and head, co2 build up, more homunculus activity,
131
how sub-concussive activities effect CBF and cognition
evidence of impaired CBF regulation and possibly poorer cognition
132
how does CBF change over a lifetime?
drops by 50% across life, but fitter people will have an increased blood flow at any given time.
133
what is an increase cognitive aspects closely linked to in young adults?
having better chemical control (co2 sensitivity) of their CBF.
134
do fit people have an increase in CBF.
yes fit people have a greater increase in exercise
135
why is increase in CBF not always good?
may slightly impair tolerance to orthostatic stress, it can increase intracranial pressure and it may impair autoregulation (the brain’s ability to maintain stable flow).
303
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