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Exercise Physiology > CV system and exercise > Flashcards

CV system and exercise Flashcards

1
Q

3 parts of the CV system

A

heart
vasculature
blood

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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

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3
Q

high VO2 max and sufficient vasculature

A

process oxygen quicker

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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

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5
Q

weight of heart

A

310g m

260g f

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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

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7
Q

blood vessels of an adult stretched in a line

A

100,000km

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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

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9
Q

what circuit has more resistance

A

systemic

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10
Q

valve in right side of heart

A

tricuspid valve

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11
Q

valve in left side of heart

A

bicuspid/mitral valve

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12
Q

myocardium

A

fibers interconnect in latticework fashion to allow the herat to function as a unit

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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.

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14
Q

syncytium

A

group of cells of myocardium that function collectively as a unit during depolarization for atria and ventricles

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15
Q

nerve innervation of the heart?

A

no, only cardiacmyocytes - no impulses and conducting neurons - gap junctions

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16
Q

SA node

A

pacemaker - specialized cardiac myocytes and has no equipment for crossbridging

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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
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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

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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

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20
Q

extrinsic control of the heart AKA

A

autonomic control of the heart

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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

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22
Q

extrinsic control of the heart at exercise (3)

A

decrease parasympathetic
increase sympathetic - NE up to 220bpm
speeds up pacemaker potential

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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)
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24
Q

systole

A

contraction

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25
Q

diastole

A

relaxation

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26
Q

characteristics of membrane potential of regular cardiomyocytes

A

depolarization triggered by SA node/AV node

long refractory period - L type calcium - extend depolarization period - so they dont stack

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27
Q

ECG

A

electrocardiogram

- tracing that provides a graphic illustration of the heart muscle

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28
Q

ECG has

A

leads that go around the heart that shows the diff in activity

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29
Q

P wave

A

atrial depolarization - all atrial cells depolarized and in long refractory period
QRS - ventricular depolarization - all ventricular cells depolarized

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30
Q

do heart cells regenerate?

A

no

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31
Q

ST segment

A

ventricular depolarization to repolarization - heart attack if there is a bump

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32
Q

STROKE volume (2)

A

amt of blood ejected from the ventricles with each beat of the heart
SV=EDV-ESV

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33
Q

ejection fraction (2)

A

% of EDV ejected from the heart

EF% = (SV/EDV)x100

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34
Q

ejection fraction influenced by 3

A

preload
contractility
afterload

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35
Q

preload

A

volume of blood returning to the heart

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36
Q

contractility

A

force of myocardial contraction

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37
Q

afterload

A

resistance of vasculature

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38
Q

more preload

A

more SV

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39
Q

preload follows what law

A

frank-starling

- greater the EDV, greater the stroke volume as you have stretched out the muscle

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40
Q

contractility stimulated by

A

increased SNS stimulation

- increased SV for a given EDV

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41
Q

cardiac output

A

amt of blood pumped/unit of time - in L/min

CO= SVxHR

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42
Q

measuring CO

A

difficult
Fick equation
echocardiogram

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43
Q

fick equation

A

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

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44
Q

doppler echocardiogram

A

calculates SV from measurements of aortic cross sectional area and time velocity integrals in the ascending aorta

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45
Q

myocardial oxygen consumption is influenced by

A

the phase of the cardiac cycle - coronary arteries are compressed in systole, so oxygen is delivered during diastole

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46
Q

myocardial oxygen consumption

A

rate pressure product

RPP=HRxSBP

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47
Q

during exercise bloodflow to the heart is increased through 2

A

vasodilation as a result of metabolic byproduct (adenosine - byproduct of atp use)
increased contractility of heart

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48
Q

what type of vessels have smooth muscles?

A

arteries

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49
Q

arterioles AKA

A

resistance vessels - ability to vasodilate and vasoconstrict

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50
Q

smooth muscles are under the control of 2 in order to

A

extrinsic factors - autonomic nervous system
intrinsic factors - metabolic, myogenic, and shear stress
change the diameter of the arterioles to permit control of blood flow

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51
Q

flow of the vascular system follows the

A

poiseuille’s law

flow = changing pressure/resistance

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52
Q

meta-arterioles

A

short vessels that connect arterioles and venules

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53
Q

capillaries 2

A

branch off metaarterioles
blood flow regulated by local metabolic factors
single layer of rolled up endothelial cells

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54
Q

anastomosis

A

shunts between arterioles and venules - present in skin and plays an important role in thermoregulation

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55
Q

veins AKA

2

A

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

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56
Q

total volume of blood and its components

A

5-6L
plasma - fluid matrix
living cells - erythrocytes (RBC) to carry oxygen
leukocytes

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57
Q

hemotocrit and a normal number

A

% of RBC - 38-48%

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58
Q

what stimulates RBC production

A

EPO which increases the viscosity of blood, you need a hematocrit of less than 50 to compete

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59
Q

arterial blood pressure

A

force of blood against arterial walls during cardiac cycle (mmHg)

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60
Q

systolic blood pressure

A

provides estimate of work of heart and force blood exerts against arterial wall during systole

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61
Q

diastolic blood pressure (2)

A

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

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62
Q

systole length vs diastole

A

systole shorter

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63
Q

auscultation method of measuring BP (5)

A 
non- invasive 
sphygmomanometer and stethoscope 
first korotkoff sound =SBP 
fourth = DBP1 
fifth = DBP 2
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64
Q

cardiovascular hemodynamics (2)

A

flow of blood through vessels is dependent on the pressure gradient along the vessel and the resistance to flow
Q= MAP/TPR

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65
Q

why can MAP used for changing pressure?

A

flow =changing pressure/resistance

pressure at vena cava is near to zero

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66
Q

velocity of blood is inversely related to

A

cross sectional area

- velocity of blood decreases in caps, allowing better exchange of gases and nutrients

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67
Q

3 cardiovascular control centres are in

A

vasomotor centre
cardio accelerator centre
cardio inhibitor center
medulla oblongata

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68
Q

baroreceptors

A

senses in increase in blood pressure and puts the brake on

69
Q

vasomotor centre controls 2

A

skeletal muscle arterioles to vasodilate and visceral arterioles to vasoconstrict

70
Q

sympathetic nerve innervates which CV control centres? what nerve is it?

A

vasomotor centre
cardioaccelerator centre
accelerator nerve

71
Q

what CV control centre does the parasympathetic nerve innervate? what nerve is it?

A

cardio inhibitor center

vagus nerve

72
Q

cardioaccelerator and inhibitor center have an effect on

A

heart

  • increases HR and contractility
  • decrease HR and a little contractility
73
Q

3 afferents of the CV system and their receptors

A

glossopharyngeal - arterial baro
vagal - cardiac receptors
skeletal muscle -skeletal muscle mechnoreceptors and metaboreceptors

74
Q

2 efferents of the CV system and what they control

A

vagal efferent - ach on the heart

sympathetic efferent - NE on the heart and systemic resistance and capacitance vessels

75
Q

Heart transplant and innervation

A

no increase of HR through SNS, only NE from the adrenal gland so it might ake a while

76
Q

lesion at C7 effect on CV

A

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
Q

vasoconstriction innervated by

A

increased sympathetic innervation of N/NE

78
Q

vasodilation innervated by 2

A

increased sympathetic innervation of E and NE and intrinsic metabolic factors

79
Q

Beta 2 receptors

A

activated by E/NE to relax smooth muscles and dilate vessels

80
Q

Alpha 1 receptors

A

activated by E/NE to contract smooth muscles and constrict vessels (increase resistance to decrease flow) - redirect this blood for fight or flight

81
Q

intrinsic control - localized vasodilation (3)

A

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
Q

exercise response to long term, moderate to heavy exercise - submax aerobic - 60-85% VO2max (3)

A

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
Q

Exercise response to short term, light to moderate exercise - submax aerobic exercise of 30-70 % VO2max (4)

A

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
Q

blood volume when exercising (3)

A

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
Q

cardiovascular shift (5)

A

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
Q

cerebral blood supply during any physical activity

A

always gets the same blood supply

87
Q

incremental aerobic exercise to VO2max and effect (5)

A 
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

Q at rest

A

5.8L/min

89
Q

Q at light aerobic exercise

A

9.4L/min

90
Q

Q at heavy aerobic exercise

A

17.5L/min

91
Q

Q at maximal exercise

A

25L/min

92
Q

VO2max

A

greatest amount of oxygen that the body can take in, transport and utilize during heavy exercise

93
Q

CV system determinants of VO2 max (2-3, 2-6)

A 
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
Q

respiratory system determinants of VO2max (3)

A

oxygen diffusion
ventilation
a-vo2 difference

95
Q

4 skeletal muscle/metabolic function determinants of vo2 max

A

myoglobin
enzymes and oxidative potential
energy stores and delivery
mitochondria size and number

96
Q

3 factors that influence the SV

A

myocardial contractility
ventricle size
blood volume

97
Q

3 factors of the metabolic oxidative potential

A

availability of FFA, glycogen, glucose
size and type of muslce fibre
size and number of mitochondria

98
Q

3 factors for muscle bloodflow

A

capillary density
Nervous and hormonal control
peripheral resistance

99
Q

2 factors for a-vo2 idff

A

metabolic oxidative potential

muslce blood flow

100
Q

highest HR

A

Vo2 max

101
Q

4 criteria for achieving VO2 max

A

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
Q

if any of the criteria for vo2 max is not met

A

its the VO2 peak - highest VO2 achieved which is slightly lower than VO2 max

103
Q

order of VO2max of blind shrew, pronghorn and oskar svendsen

A

blind shrew
pronghorn
oskar svendsen

104
Q

gender difference in VO2 max

A

male relative to weight can be 20-30% higher

male relative to fat free mass can be 0-15% higher

105
Q

gender plays a role in which factors that determine VO2 max? (6)

A 
blood volume 
ventricle size 
size and type of muslce fibre 
availability of FFA, glycogen and glucose 
Hb in blood 
nervous and hormonal control
106
Q

max HR for men and women

A

similar

107
Q

M vs F HR at relative submax

A

higher for F

108
Q

M vs F HR and Q at absolute submax

A

F always higher

109
Q

vo2max F vs M

A

F always lower

110
Q

HR at rest F vs M

A

F higher

111
Q

trend of F HR

A

usually higher to make up for low SV

112
Q

children and VO2max 2

A

lower - limit Q

decrease in weight means high relative VO2max

113
Q

females at puberty and vo2max

A

decrease

114
Q

older age and vo2 max

A

decrease because of decreased Q and increased TPR (loss of elasticity in vessels

115
Q

upper body exercise effects vs lower (3)

A

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
Q

Why do people have heart attacks when they shovel snow?

A

large myocardial oxygen demand relative to VO2, RPP higher with snow shoveling than max treatmill test - excess strain on your heart

117
Q

exercise response to static exercise (3)

A

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
Q

pressor reflex/response (2)

A

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
Q

exercise response to dynamic resistance exercise

A

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
Q

valsalva maneuver

A

decreased SV due to decreased preload

121
Q

acute cardiovascular strain with heavy resistance exercise (2)

A

could be harmful to ind. with heart and vascular disease

- leg press strength exercise, your bp can go up to 480/350

122
Q

BP recovery after exercise (2)

A

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
Q

cardiovascular fitness

A

ability to deliver and use oxygen under the demands of intensive, prolonged exercise of work
- evaluated by VO2max

124
Q

2 adaptations to CV training

A

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
Q

canadian society for exercise physiology recommends

A

a total of 150 mins of mod to vig PA

126
Q

cardiac dimensions as cardiovascular adaptations to aerobic training (3)

A

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
Q

vascular structure and function (3)

A 
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
Q

blood volume in the first 10 days of training (2)

A

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
Q

blood volume after a month of training

A

increased RBCs = normalization of hemotocrit

130
Q

How do endurance athletes achieve a large maximal Q

A

by increasing SV
untrained : 22000ml/min= 195beat*113ml/beat
trained: 35000ml/min=195beats/minx179ml/beat

131
Q

eudurance training causes SV to (5)

A

increase during rest and exercise
increase contractility, blood volume, and cardiac dimension
down peripheral resistance

132
Q

Plateau in SV at 40-50% VO2 max

A

in untrained ind, trained atletes may not have it.

133
Q

endurance training causes HR to (3)

A

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
Q

aerobic endurance training adaptation to maximal oxygen consumption

A

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
Q

greatest influence in men post training regarding to VO2peak, Q peak and a-VO2 peak

A

VO2

136
Q

upper body has a increased __________ innervation

A

sympathetic nervous system

137
Q

valsalsa maneuver

A

metabolic byproducts induce pressor reflex

138
Q

increase in SV implication to heart

A

eccentric stretch which increases ventricle size - hypertrophy and an increase in blood volume

139
Q

overload principle

A

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
Q

greater initial fitness level associated with ______ changes in VO2max

A

lower

141
Q

blood pressure adaptation to aerobic endurance training

A

in normotensive ind - little to no change

142
Q

rate pressure product adaptation to aerobic endurance training

A

decrease at rest and submaximal exercise

143
Q

resistance adaptation to aerobic endurance training

A

decrease at maximal exercise

144
Q

endurance training adaptation due to BP, RPP and resistance are because of

A

improved endothelial function - how well your vessles respond to sympathetic and parasympathetic innervations

145
Q

increased plasma volume and RBC means

A

increased total blood volume

146
Q

increased total blood volume means

A

increased venous return

147
Q

what three factors induce the increase in EDV

A

increased ventricular compliance, internal ventricular dimensions and VR

148
Q

increased myocardial contractility means

A

increased ejection fraction

149
Q

increased EDV and EF means 2

A

maximum SV - Q

150
Q

max Q

A

increased effectiveness of Q distribution

151
Q

increased effectiveness of Q distribution

A

increased optimization of peripheral flow

152
Q

increased optimization of peripheral flow

A

increased blood flow to active muscles

153
Q

4 adaptations to dynamic resistance training

A

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
Q

Upon cessation of cardiorespiratory training (4)

A

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
Q

most effective strategy to maintain training adaptations of VO2

A

maintenance of training intensity

156
Q

cardiac remodelling caused by long term deconditioning

A

cardiac dimensions appear to return to baseline after a long period of detraining

157
Q

blood doping

A

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
Q

3 things that blood doping can do

A

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
Q

large vessels benefit to blood doping

A

inject it right into the lumen - lesser chance of getting caught

160
Q

1945 blood doping

A

pilots started infusing RBCs to prevent blackouts

161
Q

1972-76 blood doping

A

Lasse Viren (Finland) - 3 golds - 5k, 10k, marathon, suspicion of blood doping

162
Q

1986 blood doping

A

banned after american cycling team admitted to blood doping

163
Q

1998 blood doping

A

tour de france - police identified team cars full of boxes of EPO

164
Q

2013 blood doping

A

lance armstrong confession

165
Q

2 kinds of blood transfusion

A

autologous/homologous blood doping

166
Q

autologous blood doping 4

A

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
Q

homologous blood doping

A

reinfusing someone else’s blood (compatible donor)

- test developed in 2004

168
Q

Erythropoietin 3

A

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
Q

meldonium
created in
banned?
mechanism?

A

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

Exercise Physiology (17 decks)

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