regulation and integration
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Regulation and Integration. Integrated Exercise Response:. Before Exercise: Central command increases HR and myocardial contractility (suppression of parasympathetic). As Exercise Continues: Mechanoreceptors/Chemoreceptors feedback on CV center (Medulla) - PowerPoint PPT PresentationTRANSCRIPT
Regulation and Integration
Integrated Exercise Response:
Before Exercise:
Central command increases HR and myocardial contractility (suppression of parasympathetic)As Exercise Continues:
Mechanoreceptors/Chemoreceptors feedback on CV center (Medulla)
Local metabolic factors (CO2, NO, etc.) dilate blood vessels, reduce peripheral resistance, increase BF
Centrally mediated vasoconstriction occurs in vasculature of non-exercising tissue (kidney, splanchnic region, inactive muscles)
Muscle pump and ventilation ensure venous return and adequate cardiac output
Regulation and Integration
Orthotopic (Heart) Transplantation:
Sympathetic nerves stimulate medulla to release epinephrine
Epinephrine via blood accelerates SA node and dilates coronary vessels
Regulation and Integration
Orthotopic (Heart) Transplantation:
Higher resting HR, lower HR max prior to transplantation
Exercise response severely impaired -
-limited CO
-impaired VO2
Epinephrine via blood exerts only control over HR
Functional Capacity of CV System
Functional Capacity
Cardiac Output (CO):
Amount of blood pumped by the heart in 1 minute (L/min)
Maximal CO reflects functional capacity of CV system to meet physical demand of exercise
CO = HR x Stroke Volume (SV)
Functional Capacity
Calculating Q via Direct Fick Method:To calculate Q, must know:
1. Average difference between O2 content of arterial blood and venous blood (a-v O2 difference)
2. O2 consumed in 1 min
Q = VO2 (mL/min)
a-v O2 difference (mL/100 mL)X 100
Functional Capacity
Direct Fick Method:
Question:
How much blood circulates during each minute to account for observed O2 consumption, given the amount extracted?
Functional Capacity
I. Cardiac output at rest:
Average values:
5 L/min for 70 kg male (154 lb)
4 L/min for 56 kg female (123 lb)
Untrained:
(Q) 5000 mL/min = (HR) 70 bpm x (SV) 71 mL
Trained:
(Q) 5000 mL/min = (HR) 50 bpm x (SV) 100 mL
Functional Capacity
I. Cardiac output at rest:
Two factors contribute to differences in trained and untrained:
1. Training increases vagal tone (parasympathetic) and decreased sympathetic drive – (Lowers HR)
2. Training increases blood volume, myocardial contractility, compliance of LV (Increases SV)
Functional Capacity
II. Cardiac output during exercise:
Untrained - Q increases 4-fold during exercise
(Q) 22,000 mL/min = 195 (HR) x 113 mL (SV)
Blood flow increases directly with exercise intensity
Trained - Q increases 7-fold during exercise
(Q) 35,000 mL/min = 195 (HR) x 179 mL (SV)*Trained increase Q solely through increase SV
Functional Capacity
Fig 21.11 Fig 21.10
Increased SV accounts for large increase in Q during exercise
Functional Capacity
Stroke Volume during exercise:
3 mechanisms increase SV during exercise:
1. Enhanced diastolic filling
2. Greater systolic emptying
3. Training adaptation – expanded blood volume and reduced peripheral resistance
Functional Capacity
1. Enhanced Diastolic Filling:
Increased end diastolic volume (EDV) occurs when there is increased venous return or slowing of heart (Preload)
Frank-Starling mechanism – contractile force increases as resting length of cardiac fibers increases
Preload (increased EDV) stretches cardiac fibers and initiates powerful ejection (increases SV)
Functional Capacity
1. Enhanced Diastolic Filling:
Increased end diastolic volume (EDV) occurs when there is increased venous return or slowing of heart
Preload – enhanced ventricular fillingFrank-Starling mechanism – contractile force increases as resting length of cardiac fibers increases
Preload stretches cardiac fibers and initiates powerful ejection (increases SV)
Functional Capacity
2. Systolic Emptying:
Catecholamine release (sympathetic
NS) during exercise increases ventricular contractile force (facilitates systolic emptying)
Greater systolic ejection occurs when there is reduced “Afterload” (resistance to BF from increased SBP)
At rest, 40% of EDV remains in left ventricle after systole
Functional Capacity
3. Training Adaptations:
Increased plasma volume
Increased EDV
Higher SBP increases “afterload”
Reduced peripheral resistance (reduced afterload)
Functional Capacity
3. Training Adaptations:
Increased plasma volume (chronic exercise response)
Increases EDV
Reduced peripheral resistance (MAP/CO) occurs during exercise
Reduced afterload
Functional Capacity
Heart Rate During Exercise:
HR increases during submaximal “steady rate” exercise (after ~15 minutes)Cardiovascular Drift – Increase in HR and decrease in SV during exercise
Due to:
Plasma volume shift (sweating/cooling)
Decreased Preload
Reduced SV (HR compensation)
Functional Capacity
Heart Rate During Exercise:
Cardiovascular Drift – 2nd explanation
Fig 17.2
*HR increase (not cutaneous BF) reduces SV during exercise
Functional Capacity
Distribution of Cardiac Output:
Rest –
1/5 of Q to muscle (4-7 mL/100 g)
Functional Capacity
Distribution of Cardiac Output:
Exercise –
~85% of Q to muscle (50-75 mL/100 g)
300-400 mL/100 g to specific portions of muscle
Functional Capacity
Cardiac Hypertrophy (Hypertension):
Heart mass also increase with hypertension - NOT a positive adaptation
Heart chronically works against excessive resistance to blood flow
No "recuperation" periods to induce training effect (like RT or endurance training)
Constant tension weakens left ventricle
"Hypertrophied" heart becomes enlarged, distended, and functionally inadequate to deliver blood to tissues
Cardiovascular Response to Exercise
Aerobic Exercise Training and Hypertension:
Systolic and diastolic blood pressure decrease by ~6 - 10 mm Hg with aerobic exercise
Exercise training exerts its greatest effect on patients with mild hypertension
Regular aerobic exercise may control the tendency for blood pressure to increase over time (aging)
Cardiovascular Response to Exercise
9 months of aerobic training significantly reduced systolic BP (11 mm Hg) and diastolic BP (9 mm Hg)
Improved anti-hypertensive drug effect
BP began to rise again after only 1 month of detraining
Fig. 32.9