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