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 Epinephrine via blood exerts only control over HR Exercise response severely impaired - -limited CO -impaired VO2

Functional Capacity of CV System

Functional Capacity Cardiac Output (CO): Amount of blood pumped by the heart in 1 minute (L/min) CO = HR x Stroke Volume (SV) Maximal CO reflects functional capacity of CV system to meet physical demand of exercise

Functional Capacity Calculating Q via Direct Fick Method: To calculate Q, must know: Average difference between O2 content of arterial blood and venous blood (a-v O2 difference) 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: Training increases vagal tone (parasympathetic) and decreased sympathetic drive – (Lowers HR) Training increases blood volume, myocardial contractility, compliance of LV (Increases SV)

Functional Capacity II. Cardiac output during exercise: Blood flow increases directly with exercise intensity Untrained - Q increases 4-fold during exercise (Q) 22,000 mL/min = 195 (HR) x 113 mL (SV) 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 Increased SV accounts for large increase in Q during exercise Fig 21.11 Fig 21.10

Functional Capacity Stroke Volume during exercise: 3 mechanisms increase SV during exercise: Enhanced diastolic filling Greater systolic emptying 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 filling Frank-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) At rest, 40% of EDV remains in left ventricle after systole Greater systolic ejection occurs when there is reduced “Afterload” (resistance to BF from increased SBP)

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 Balloon idea

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