Acute & Chronic Responses to Exercise

Cardiac Terminology

• Cardiac Output (CO): Amount of blood pumped by the heart per minute.

  • Formula: CO(Q) = HR x SV

• Stroke Volume (SV): Amount of blood ejected by the heart per beat.

  • Approx. 70 mL in a healthy human at rest.

• Heart Rate (HR): Beats per minute (bpm).

  • Resting average: 70 bpm.

• End-Diastolic Volume (EDV): Peak volume of blood that fills the ventricles during relaxation.

• End-Systolic Volume (ESV): Volume of blood remaining in the ventricles after ejection.

  • Formula: SV = EDV - ESV.

• Systolic Blood Pressure (SBP): Pressure exerted on systemic arterial walls during ventricular contraction (systole).

• Diastolic Blood Pressure (DBP): Pressure exerted during ventricular relaxation (diastole).

Central Nervous System

• Autonomic Nervous System (ANS)

  • Sympathetic Branch: Acts as an "accelerator."

    • Releases norepinephrine, stimulating the SA and AV nodes, increasing HR to > 100 bpm.

  • Parasympathetic Branch: Acts as "brakes."

    • Releases acetylcholine, keeping HR < 100 bpm.

• Somatic Nervous System: Responsible for voluntary actions.

CV Responses to Exercise

• Metabolic Demand: Oxygen requirement can rise 15 to 20 times during exercise.

• Limitation: The CV system has a finite amount of blood (5–6 L) to be circulated.

• Strategies to Overcome Limitation:

  1. Increase Cardiac Output (CO = HR x SV).

  2. Redirect blood from non-active to active tissues via vasoconstriction/vasodilation.

  3. Extract more oxygen from the blood.

Acute Response - Heart Rate

• HR Response: Increases rapidly within the first few minutes of activity.

  • Controlled by the SA node.

  • Decrease in parasympathetic activity allows HR to rise.

  • Gradual increase in sympathetic activity further increases HR.

• Steady-State HR: If exercise intensity is constant, HR reaches a plateau and remains stable during sub-maximal exercise.

• Progressive Increase: HR continues to rise with increasing intensity to meet oxygen demands.

Acute Response - Stroke Volume

• SV Response: Increases abruptly at the start of exercise.

  • Release of norepinephrine enhances ventricular contraction force.

  • Increased venous return leads to higher EDV and SV.

• Sympathetic Activity: Vasoconstriction raises venous pressure, driving blood back to the heart.

• Skeletal Muscle Contraction: Aids blood return via the muscle pump.

• Preload Effect: Increased preload stretches the myocardium, enhancing ventricular contraction force.

Acute Response - Cardiac Output

• Increase in CO: 2-3 fold increase driven by HR and SV rises.

• Prolonged Exercise: HR gradually increases, SV slowly declines, while CO stabilizes; this is known as "CV drift."

Acute Response - Blood Pressure and Total Peripheral Resistance (TPR)

• Blood Pressure Changes: Elevated SBP, stable DBP (~70–80 mm Hg), and decreased TPR at the onset of exercise.

• Increased BP During Exercise:

  • Abrupt rise in Q (Cardiac Output).

  • Decrease in parasympathetic activity releasing "brakes."

  • Increased sympathetic activity leads to vasoconstriction of veins and arterioles.

• Decreased TPR: Results in peripheral vessel vasodilation, enhancing blood flow and oxygen delivery to muscles.

Acute Response - Pulmonary Ventilation (V̇E)

• Ventilation Increase: V̇E rises at exercise onset.

  • Driven by increased tidal volume (VT) and respiratory rate (RR).

• Continued Rise: V̇E continues to increase during prolonged submaximal exercise.

Acute Response - Airway Resistance

• Bronchodilation: Airways dilate, reducing airway resistance.

  • Withdrawal of parasympathetic activity and norepinephrine release cause dilation in bronchial smooth muscle.

• Stable Resistance: Bronchodilation and reduced resistance remain stable with extended exercise duration at a constant workload.

Chronic Aerobic Training - HR, SV, CO

• Heart Rate (HR):

  • Rest: Decreased HR (often below 60 bpm) due to increased vagal tone and decreased sympathetic activity.

  • Submaximal: Reduced HR with similar mechanisms.

  • Maximal: No change or slight decrease in max HR.

• Stroke Volume (SV):

  • Rest: Increased SV from larger chamber size and longer filling time.

  • Submaximal: Continued increase in SV due to same mechanisms.

  • Maximal: Increased SV with added plasma volume.

• Cardiac Output (CO):

  • Rest: No change in CO at rest.

  • Submaximal: Greater increase in CO as intensity rises.

  • Maximal: Increased CO from rising SV for a given HR.

Chronic Aerobic Training - Blood Plasma

• Plasma Volume Increase: Can increase by 500 mL or more with training.

  • Leads to increased contractile force and SV.

  • Allows for a decreased HR, making the heart more efficient in maintaining Q at rest.

Chronic Aerobic Training - Oxygen Extraction

• Improved Oxygen Extraction: Enhanced capacity to extract oxygen from blood during exercise.

  • Increased capillary density in muscle.

  • Improved local blood flow and greater surface area for gas exchange.

  • Enhanced ability to redistribute blood flow to working muscles.

  • Vasodilation lowers vascular resistance, improving oxygen and nutrient delivery.

Chronic Aerobic Training - Pulmonary Ventilation

• Resting Changes: No significant changes in pulmonary system at rest; resting ventilation volume remains unchanged.

  • Resting ventilation rate may decrease due to heightened parasympathetic control.

• Submaximal Changes: Decreased V̇E compared to untrained individuals.

  • Result of later ventilatory threshold and enhanced endurance of ventilatory muscles, along with better blood pH regulation.

Ventilatory Threshold

• Ventilation Definition: V̇E represents minute ventilation or gas volume exhaled per minute.

• Exercise Response: At low-to-moderate intensities, V̇E rises and stabilizes at steady-state exercise.

  • With higher intensities, the bicarbonate buffering system becomes insufficient against metabolic acidosis.

  • The respiratory system compensates by increasing V̇E.

• Ventilatory Threshold: The moment V̇E deviates from linearity concerning oxygen uptake is termed ventilatory threshold (VT1).

Athlete’s Heart vs. Hypertrophic Cardiomyopathy (HCM)

• Athlete’s Heart:

  • Symmetrical increase in heart size due to endurance training.

  • Uniform cardiac wall thickness, enhancing SV and CO.

• Hypertrophic Cardiomyopathy (HCM):

  • Asymmetrical heart enlargement with abnormal thickness in specific regions (interventricular septum and left ventricle).

  • Normal thickness elsewhere.

  • Significant risk, as it can lead to sudden cardiac death.