1. Cardiovascular response to exercise

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26 Terms

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Acute Adaptations

Increase blood flow to muscles, reduce blood flow to low activity tissues

  1. Increase o2 delivery to working muscles

  2. Reduce delivery to e.g. intestines

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Chronically Adaptations

More effective o2 delivery during sub-maximal exercise + increased maximum o2 consumption (VO2 Max)

  1. Delivers more o2 to active muscles mass

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Cardiovascular factors that influence O2 Uptake + VO2 Max

  1. Cardiac strucutre and function

  2. Blood (plasma) vol - widen heart

  3. Blood flow/distribution - in active muscles

  4. o2 Extraction - arterio venous difference

  • Peripheral - what’s been taken up by the muscle

<ol><li><p><span style="color: yellow;"><strong>Cardiac strucutre and function</strong></span></p></li><li><p><span style="color: yellow;"><strong>Blood (plasma) vol </strong></span>- widen heart</p></li><li><p><span style="color: yellow;"><strong>Blood flow/distribution</strong></span> - in active muscles</p></li><li><p><span style="color: yellow;"><strong>o2 Extraction</strong></span> - arterio venous difference</p></li></ol><p></p><ul><li><p>Peripheral - what’s been taken up by the muscle</p></li></ul><p></p><p></p>
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Cardiac Output 

The volume of blood pumped out the heart per minute 

Heart Rate x Stroke Volume

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Stroke Volume

The volume of blood ejected out the left ventricle per beat

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o2 Extraction: (a-v) o2 Difference

  1. Training increases submaximal + maximal values in muscles

  2. Active muscle - utilise o2 more efficiently

  3. Increase oxidative capacity (higher oxidative enzyme content)

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Physiological Cardiac Hypertrophy

enlarged heart (mass and size)

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Heart Structure

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Venous return

The volume of blood returning to the heart via the veins

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Vascular resistance

the force that must overcome to push blood through the circulatory system

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Preload

The amount of blood in the ventricle before contraction (end diastolic volume)

  1. Determines cardiac muscle length before contraction

  2. Determined by venous return

  3. Increase CO + HR = Preload increase

  4. Increase in moderate intensity

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Afterload

The pressure against which the ventricle must contract (vascular resistance)

  1. Higher the afterload, less blood ejected per heartbeat

  2. Heart has limited force

  3. Moderate intensity - can decrease, vessels open for o2

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Ventricle valves during Systole and Diastole

Systole = contraction of heart (emptying)

Diastole = relaxation phase of heart (filling)

<p><span style="color: rgb(180, 51, 204);"><strong>Systole</strong></span> = contraction of heart (emptying)</p><p><span style="color: rgb(182, 45, 224);"><strong>Diastole </strong></span>= relaxation phase of heart (filling)</p>
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Contractility: The Frank-Starling Mechanism

Contractility = intrinsic ability of the heart muscle (myocardium) to generate force and to shorten during contraction, independent of how much it’s stretched (preload) or how much resistance it’s pumping against (afterload)

  1. Principle based on length-tension relationship of ventricle

  2. Greater stretch, greater contraction

  3. Preload (end diastolic vol) increases, ventricular fiber length increases, increasing muscle tension

<p><span style="color: rgb(203, 48, 226);"><strong>Contractility</strong></span> = intrinsic ability of the heart muscle (myocardium) to generate force and to shorten during contraction, <em>independent</em> of how much it’s stretched (preload) or how much resistance it’s pumping against (afterload)</p><ol><li><p>Principle based on length-tension relationship of ventricle</p></li><li><p>Greater stretch, greater contraction</p></li><li><p>Preload (end diastolic vol) increases, ventricular fiber length increases, increasing muscle tension</p></li></ol><p></p>
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Athlete’s Heart: Potential Mechanisms

  1. Left ventricular Mass - heavier in all athletes

  2. Left ventricular Vol - larger in ENDURANCE athletes

  • Increased CO stretches out heart

  • Increased preload, Increases SV, Eccentric hypertrophy

  1. Posterior wall/Septal thickness - larger in RESISTANCE

  • Beefier

  • Increased Afterload, Decreases SV, Concentric hypertrophy

  • Work against high resistance, decreases SV

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Endurance training adaptations: Stroke Volume

  1. Increased preload (ventricular filling) = Increase ventricular dimensions

  2. Increased diastolic filling time due to bradycardia

  3. Bradycardia = slow HR

  4. Increased contractility

  5. Increased maximal SV

<ol><li><p>Increased preload (ventricular filling) = Increase ventricular dimensions</p></li><li><p>Increased diastolic filling time due to bradycardia</p></li><li><p><span style="color: rgb(214, 40, 223);"><strong>Bradycardia</strong></span> = slow HR</p></li><li><p>Increased contractility</p></li><li><p>Increased maximal SV</p></li></ol><p></p>
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Endurance Training Adaptations: Heart Rate

  1. Increased SV = Decreased HR for the same CO (sub-maximal exercise)

  2. Max HR unchanged

<ol><li><p>Increased SV = Decreased HR for the same CO (sub-maximal exercise)</p></li><li><p>Max HR unchanged</p></li></ol><p></p>
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Endurance Training Adaptations: Cardiac Output (Q)

Product of SV x HR

  1. Most significant adaptation - major determinant of VO2 Max

  2. Sub-Max Exercise = lower CO (increased o2 extraction)

  3. Better muscle oxidative capacity - higher a-vO2 diff (more enzymes)

<p><strong>Product of SV x HR</strong></p><ol><li><p>Most significant adaptation - major determinant of VO2 Max</p></li><li><p>Sub-Max Exercise = lower CO (increased o2 extraction)</p></li><li><p>Better muscle oxidative capacity - higher a-vO2 diff (more enzymes)</p></li></ol><p></p>
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Acute Blood Redistribution

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Acute Blood Flow Regulation

Muscle activity, pH go up

  1. Muscle metabolites + Temp

  2. Dilator substances produced by endothelium e.g. NO (open BV’s)

  3. Pressure changes within vessels - myogenic

  4. Symp Acticvity - reduce blood flow to low activity tissues (adrenalin receptors) 

<p>Muscle activity, pH go up</p><ol><li><p>Muscle metabolites + Temp</p></li><li><p>Dilator substances produced by endothelium e.g. NO (open BV’s)</p></li><li><p>Pressure changes within vessels - myogenic</p></li><li><p>Symp Acticvity - reduce blood flow to low activity tissues (adrenalin receptors)&nbsp;</p></li></ol><p></p>
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Training the heart through increases in blood vol?

Primary Mechanisms for Blood Vol Increase:

  1. Increase in plasma proteins - Albumin (Osmotic effect)

  2. Increase in total body water - alterations in kidney function (Reduced urine output, Increased water retention)

<p>Primary Mechanisms for Blood Vol Increase:</p><ol><li><p><span style="color: yellow;"><strong>Increase in plasma proteins</strong> </span>- Albumin (Osmotic effect)</p></li><li><p><span style="color: yellow;"><strong>Increase in total body water</strong> </span>- alterations in kidney function (Reduced urine output, Increased water retention)</p></li></ol><p></p>
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Effects of Various Training Modalities on Blood Volume

  1. Increased Haemoglobin = Increased VO2 Max

  2. Strong relationship

<ol><li><p>Increased Haemoglobin = Increased VO2 Max</p></li><li><p>Strong relationship</p></li></ol><p></p>
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Blood Volume Changes

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March 2019, Nordic skiing: Blood doping scandal rocks sport as five athletes arrested

  1. EPO = induces production of RBC

  2. Blood Transfusions - blood doping

  • Autologous - own blood

  • Homologous - another person’s blood

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Aerobic training adaptations overview: increasing oxygen delivery to muscle

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Summary

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