CV system and exercise Flashcards
1
Q
3 parts of the CV system
A
heart
vasculature
blood
2
Q
4 functions of the CV system
A
transport oxygen and nutrients to body
removal of co2 and waste products
circulation of hormones
regulation of body temp, pH, and fluid balance
3
Q
high VO2 max and sufficient vasculature
A
process oxygen quicker
4
Q
two circuits of the CV system
A
parallel - pulmonary circuit(external respiration - pulmonary artery/vein), systemic circuit (internal respiration - cellular respiration)
heart - continous linkage between the two circuits
5
Q
weight of heart
A
310g m
260g f
6
Q
function of heart
A
pumps - 70ml each beat (stroke volume, at rest)
1 day - 7100 L through heart, 195 mil L for a 75 y life span
7
Q
blood vessels of an adult stretched in a line
A
100,000km
8
Q
macroanatmy of heart (2)
A
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
9
Q
what circuit has more resistance
A
systemic
10
Q
valve in right side of heart
A
tricuspid valve
11
Q
valve in left side of heart
A
bicuspid/mitral valve
12
Q
myocardium
A
fibers interconnect in latticework fashion to allow the herat to function as a unit
13
Q
interscalated discs
A
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.
14
Q
syncytium
A
group of cells of myocardium that function collectively as a unit during depolarization for atria and ventricles
15
Q
nerve innervation of the heart?
A
no, only cardiacmyocytes - no impulses and conducting neurons - gap junctions
16
Q
SA node
A
pacemaker - specialized cardiac myocytes and has no equipment for crossbridging
17
Q
6 pacemaker potential makers
A
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
18
Q
depolarization of SA node
A
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
19
Q
extrinsic autonomic control of the CV system
A
sympathetic - SA node neurotransmiter - nor epinephrine - adrenergic receptor
hormone (adrenal medulla) - epinephrine
parasympathetic - SA node or normal cells , neurotransmitter - acetylcholine - muscarinic cholinergic receptor
20
Q
extrinsic control of the heart AKA
A
autonomic control of the heart
21
Q
extrinsic control of the heart at rest (3)
A
increased parasympathetic
decreased sympathetic
slows down SA pacemaker potential (60) acetylcholine and less sodium and calcium
22
Q
extrinsic control of the heart at exercise (3)
A
decrease parasympathetic
increase sympathetic - NE up to 220bpm
speeds up pacemaker potential
23
Q
cardiac cycle (4)
A
one complete sequence of contraction and relaxation of the heart - ventricular filling - (diastole) isovolumetric contraction (Systole) ventricular ejection (systole) isovolumetric relaxation (Diastole)
24
Q
systole
A
contraction
25
diastole
relaxation
26
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
27
ECG
electrocardiogram
| - tracing that provides a graphic illustration of the heart muscle
28
ECG has
leads that go around the heart that shows the diff in activity
29
P wave
atrial depolarization - all atrial cells depolarized and in long refractory period
QRS - ventricular depolarization - all ventricular cells depolarized
30
do heart cells regenerate?
no
31
ST segment
ventricular depolarization to repolarization - heart attack if there is a bump
32
STROKE volume (2)
amt of blood ejected from the ventricles with each beat of the heart
SV=EDV-ESV
33
ejection fraction (2)
% of EDV ejected from the heart
| EF% = (SV/EDV)x100
34
ejection fraction influenced by 3
preload
contractility
afterload
35
preload
volume of blood returning to the heart
36
contractility
force of myocardial contraction
37
afterload
resistance of vasculature
38
more preload
more SV
39
preload follows what law
frank-starling
| - greater the EDV, greater the stroke volume as you have stretched out the muscle
40
contractility stimulated by
increased SNS stimulation
| - increased SV for a given EDV
41
cardiac output
amt of blood pumped/unit of time - in L/min
| CO= SVxHR
42
measuring CO
difficult
Fick equation
echocardiogram
43
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
44
doppler echocardiogram
calculates SV from measurements of aortic cross sectional area and time velocity integrals in the ascending aorta
45
myocardial oxygen consumption is influenced by
the phase of the cardiac cycle - coronary arteries are compressed in systole, so oxygen is delivered during diastole
46
myocardial oxygen consumption
rate pressure product
| RPP=HRxSBP
47
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
48
what type of vessels have smooth muscles?
arteries
49
arterioles AKA
resistance vessels - ability to vasodilate and vasoconstrict
50
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
51
flow of the vascular system follows the
poiseuille's law
| flow = changing pressure/resistance
52
meta-arterioles
short vessels that connect arterioles and venules
53
capillaries 2
branch off metaarterioles
blood flow regulated by local metabolic factors
single layer of rolled up endothelial cells
54
anastomosis
shunts between arterioles and venules - present in skin and plays an important role in thermoregulation
55
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
56
total volume of blood and its components
5-6L
plasma - fluid matrix
living cells - erythrocytes (RBC) to carry oxygen
leukocytes
57
hemotocrit and a normal number
% of RBC - 38-48%
58
what stimulates RBC production
EPO which increases the viscosity of blood, you need a hematocrit of less than 50 to compete
59
arterial blood pressure
force of blood against arterial walls during cardiac cycle (mmHg)
60
systolic blood pressure
provides estimate of work of heart and force blood exerts against arterial wall during systole
61
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
62
systole length vs diastole
systole shorter
63
auscultation method of measuring BP (5)
```
non- invasive
sphygmomanometer and stethoscope
first korotkoff sound =SBP
fourth = DBP1
fifth = DBP 2
```
64
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
65
why can MAP used for changing pressure?
flow =changing pressure/resistance
| pressure at vena cava is near to zero
66
velocity of blood is inversely related to
cross sectional area
| - velocity of blood decreases in caps, allowing better exchange of gases and nutrients
67
3 cardiovascular control centres are in
vasomotor centre
cardio accelerator centre
cardio inhibitor center
medulla oblongata
68
baroreceptors
senses in increase in blood pressure and puts the brake on
69
vasomotor centre controls 2
skeletal muscle arterioles to vasodilate and visceral arterioles to vasoconstrict
70
sympathetic nerve innervates which CV control centres? what nerve is it?
vasomotor centre
cardioaccelerator centre
accelerator nerve
71
what CV control centre does the parasympathetic nerve innervate? what nerve is it?
cardio inhibitor center
| vagus nerve
72
cardioaccelerator and inhibitor center have an effect on
heart
- increases HR and contractility
- decrease HR and a little contractility
73
3 afferents of the CV system and their receptors
glossopharyngeal - arterial baro
vagal - cardiac receptors
skeletal muscle -skeletal muscle mechnoreceptors and metaboreceptors
74
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
75
Heart transplant and innervation
no increase of HR through SNS, only NE from the adrenal gland so it might ake a while
76
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
77
vasoconstriction innervated by
increased sympathetic innervation of N/NE
78
vasodilation innervated by 2
increased sympathetic innervation of E and NE and intrinsic metabolic factors
79
Beta 2 receptors
activated by E/NE to relax smooth muscles and dilate vessels
80
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
81
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
82
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
83
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
84
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
85
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
86
cerebral blood supply during any physical activity
always gets the same blood supply
87
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
```
88
Q at rest
5.8L/min
89
Q at light aerobic exercise
9.4L/min
90
Q at heavy aerobic exercise
17.5L/min
91
Q at maximal exercise
25L/min
92
VO2max
greatest amount of oxygen that the body can take in, transport and utilize during heavy exercise
93
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
```
94
respiratory system determinants of VO2max (3)
oxygen diffusion
ventilation
a-vo2 difference
95
4 skeletal muscle/metabolic function determinants of vo2 max
myoglobin
enzymes and oxidative potential
energy stores and delivery
mitochondria size and number
96
3 factors that influence the SV
myocardial contractility
ventricle size
blood volume
97
3 factors of the metabolic oxidative potential
availability of FFA, glycogen, glucose
size and type of muslce fibre
size and number of mitochondria
98
3 factors for muscle bloodflow
capillary density
Nervous and hormonal control
peripheral resistance
99
2 factors for a-vo2 idff
metabolic oxidative potential
| muslce blood flow
100
highest HR
Vo2 max
101
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
102
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
103
order of VO2max of blind shrew, pronghorn and oskar svendsen
blind shrew
pronghorn
oskar svendsen
104
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
105
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
```
106
max HR for men and women
similar
107
M vs F HR at relative submax
higher for F
108
M vs F HR and Q at absolute submax
F always higher
109
vo2max F vs M
F always lower
110
HR at rest F vs M
F higher
111
trend of F HR
usually higher to make up for low SV
112
children and VO2max 2
lower - limit Q
| decrease in weight means high relative VO2max
113
females at puberty and vo2max
decrease
114
older age and vo2 max
decrease because of decreased Q and increased TPR (loss of elasticity in vessels
115
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
116
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
117
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
118
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
119
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
120
valsalva maneuver
decreased SV due to decreased preload
121
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
122
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
123
cardiovascular fitness
ability to deliver and use oxygen under the demands of intensive, prolonged exercise of work
- evaluated by VO2max
124
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
125
canadian society for exercise physiology recommends
a total of 150 mins of mod to vig PA
126
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
127
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
```
128
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
129
blood volume after a month of training
increased RBCs = normalization of hemotocrit
130
How do endurance athletes achieve a large maximal Q
by increasing SV
untrained : 22000ml/min= 195beat*113ml/beat
trained: 35000ml/min=195beats/minx179ml/beat
131
eudurance training causes SV to (5)
increase during rest and exercise
increase contractility, blood volume, and cardiac dimension
down peripheral resistance
132
Plateau in SV at 40-50% VO2 max
in untrained ind, trained atletes may not have it.
133
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
134
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
135
greatest influence in men post training regarding to VO2peak, Q peak and a-VO2 peak
VO2
136
upper body has a increased __________ innervation
sympathetic nervous system
137
valsalsa maneuver
metabolic byproducts induce pressor reflex
138
increase in SV implication to heart
eccentric stretch which increases ventricle size - hypertrophy and an increase in blood volume
139
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)
140
greater initial fitness level associated with ______ changes in VO2max
lower
141
blood pressure adaptation to aerobic endurance training
in normotensive ind - little to no change
142
rate pressure product adaptation to aerobic endurance training
decrease at rest and submaximal exercise
143
resistance adaptation to aerobic endurance training
decrease at maximal exercise
144
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
145
increased plasma volume and RBC means
increased total blood volume
146
increased total blood volume means
increased venous return
147
what three factors induce the increase in EDV
increased ventricular compliance, internal ventricular dimensions and VR
148
increased myocardial contractility means
increased ejection fraction
149
increased EDV and EF means 2
maximum SV - Q
150
max Q
increased effectiveness of Q distribution
151
increased effectiveness of Q distribution
increased optimization of peripheral flow
152
increased optimization of peripheral flow
increased blood flow to active muscles
153
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
154
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
155
most effective strategy to maintain training adaptations of VO2
maintenance of training intensity
156
cardiac remodelling caused by long term deconditioning
cardiac dimensions appear to return to baseline after a long period of detraining
157
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
158
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%
159
large vessels benefit to blood doping
inject it right into the lumen - lesser chance of getting caught
160
1945 blood doping
pilots started infusing RBCs to prevent blackouts
161
1972-76 blood doping
Lasse Viren (Finland) - 3 golds - 5k, 10k, marathon, suspicion of blood doping
162
1986 blood doping
banned after american cycling team admitted to blood doping
163
1998 blood doping
tour de france - police identified team cars full of boxes of EPO
164
2013 blood doping
lance armstrong confession
165
2 kinds of blood transfusion
autologous/homologous blood doping
166
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
167
homologous blood doping
reinfusing someone else's blood (compatible donor)
| - test developed in 2004
168
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
169
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
