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Kinesiology 2230A/B Midterm: CV

Course Code
Kinesiology 2230A/B
Glen Belfry
Study Guide

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Blood volume at rest - 5L
VO2 of brain can double during cerebral activity
Arteries are resistance vessels
o Change diameter quickly
Veins are capacitance vessels
o Side where most blood is stored at rest (64%)
Cardiac Structure and Function - Fick Equation
VO2 = HR x SV x (a-VO2diff)
o Heart - HR x SV
o Tissue - a-VO2diff
A-VO2 difference and how much O2 is being delivered determines O2 consumption
o If a-VO2 difference is greater, O2 consumption will increase
The Heart - Internal vs. External
Venous circulation - blood returns to the heart via inferior and superior vena cava - right atrium -
right ventricle - right and left pulmonary arteries - aorta - systemic circulation
Right side - to lungs
Left side - rest of body
Arteries - blood away from the heart
Veins - towards the heart
Major Arteries
Right and left coronary arteries
Circumflex artery
Anterior and posterior interventricular arteries
Initiation of Heart Contraction and Relaxation
SA node:
o Cluster of cells that depolarize spontaneously and generate electric current
o No external stimulus
o Wave of depolarization from SA node to atria to muscle contraction
o Goes to AV node next
AV node:
o Cluster of cells at the barrier of the atrium and ventricle
o Functions to slow the movement of the depolarization wave from the atrium into the
o Mostly lipid and doesn’t conduct
o Enables to completely depolarize atria before ventricles
o Small delay
Bundle of His and Purkinje Fibres:
o Bundle branches allow the whole heart to receive the depolarization wave quickly
o Synchronous contraction of ventricles
o Depolarization wave moves through these and myocardium
Phases of a Resting ECG
P - atrial depolarization
AV node - delay
QRS - initial depolarization moving through the septum
o Ventricle depolarization
T - ventricular repolarization after ventricular contraction
Bradycardia - slow heart rate (less than 60)

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Tachycardia - fast HR (over 100)
Stroke Volume
Volume of blood pumped per heart beat
Diastole - filling and relaxed heart
Systole - contraction of the heart
Stroke volume - EDV - ESV
o Ejection fraction
Q (cardiac output) - HR x SV
Blood Pressure and Exercise
Driving force which keeps blood flowing
At rest:
o 80-120 mmHg systemic
o 10-25 mmHg pulmonary
Pressure is in the arteries
Originating from the left ventricle (systemic) or right ventricle (pulmonary)
o Left wall is thicker
Mean Arterial Pressure (MAP)
Measure of the driving force
Average pressure that is being maintained
Diastolic is the lowest it will get\multiply by 1/3
MAP = diastolic BP + (0.33[systolic BP - diastolic BP])
o = 80 + (0.33[120-80])
o = 93.3 mmHg
Hypertrophic Cardiomyopathy
Most common cause of sudden death in youth
Left ventricular wall is thicker
Myofibril disarray that becomes more prevalent with age
Chambers can’t eject blood
Contractile protein signalling occurs - not getting enough CO or SV, hypertrophy increases
Blood Pressure and Exercise
Continuous blood flow through the arterial system
Pressure in arteries is maintained during filling
o Arteries expand when blood is ejected
o Once ejection stops, the elasticity of the arteries pushes the blood forwards, creating a
pressure wave
Rate pressure product (RPP) - estimate of cardiac work
o Systolic BP x HR
Valsalva - forced expiration with a closed glottis - whole body isometrically contracts
o Thoracic region becomes rigid
o This occludes blood flow in the body
o Stops blood from leaving and returning to the heart
o Brief increase in BP, then a dramatic drop
Blood Pressure and Rhythmic Exercise
Diastolic pressure doesn't change
o Directly associated with the elasticity of the arterial system
Systolic BP increases linearly with work rate
MAP does not change much

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o Slight MAP change is associated with resistance to flow
The more the area works, the more the capillaries open
o As the radius increases, resistance to flow decreases
Cardiac Structure and Function
CO affects O2 use
Without any changes in CO, O2 use increases
As HR goes down, ability to deliver O2 decreases
Factors Affecting SV
Contractibility - the force with which the heart contracts
Increased SNS stimulation and circulating catecholamines (EPI/NE)
Increased contractibility - more EDV is pumped out
o Changes amount of blood that leaves the heart
There is a sympathetic stimulus from the hardwiring and hormonal response
o Direct sympathetic stimulus innervates the heart and increases contractibility
o Delayed response from adrenal glands receives innervation from spine during the onset of
exercise - catecholamines
o When a stimulus is given, force and speed of contraction increases
SV and EDV:
o An increase of exercise intensity = increase in EDV
o As EDV increases, SV increases
o If we superimpose the effects of sympathetic stimulation on the initial EDV response, we see
that SV is greater at any EDV
Factors Affecting EDV
1. Venous tone (sympathetic)
Increase in venomotor tone (vasoconstriction) increases venous return, which increases preload,
and the smooth muscles of the veins will contract
As it contracts, it will reduce the radius of the veins and push blood to the heart
2. Ventricular size and distensibility
The larger the chamber, the larger the SV
Distensibility - stretch under pressure, elasticity of the heart itself
If the tissue is less elastic, there will be a decrease in SV
A decrease in distensibility, the heart can't increase its volume as quickly
3. Respiratory pump
Heart is enclosed in pleural space
Ribs go out during breathing and increase volume in chest
This reduces pleural pressure
This drop draws blood towards the heart
4. Muscle pump
When a muscle contracts, veins are compressed, pushing the blood back to the heart
Muscle pump uses a one-way valve
This increases EDV
5. Supine or prone exercise
Decreased hydrostatic load
Lower HR, larger SV
When laying down, there is no vertical displacement
Standing requires more work
When first standing up, there is a period where SV is lower - blood accumulates in the lower
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