Exercise cardiovascular physiology

Acute Response - The Engine Roars

• Central command (motor cortex) & muscle mechanoreceptors/chemoreceptors initiate the response.
• Cardiac Output (CO) ↑ up to 4-7x via ↑ Heart Rate (HR) & ↑ Stroke Volume (SV). $CO = HR \times SV$.
  • HR increases linearly with intensity (max ≈ 220 - age).
  • SV increases, then plateaus at 40-60% of VO₂ max.
• Blood Pressure Changes:
  • Systolic BP ↑ due to ↑ CO.
  • Diastolic BP shows minimal change or ↓ due to ↓ total systemic vascular resistance (SVR).

⭐ In dynamic exercise, total peripheral resistance drops significantly. A rise in diastolic BP may suggest underlying pathology.

Chronic Adaptations - Built to Last

• Physiological Hypertrophy ("Athlete's Heart"): Balanced growth, non-pathological.
  • Endurance Training (Aerobic): Volume load → Eccentric hypertrophy (↑ LV cavity size > ↑ wall thickness).
  • Strength Training (Isometric): Pressure load → Concentric hypertrophy (↑ wall thickness > ↑ LV cavity size).
• Hemodynamic Changes:
  • Rest: ↑ Vagal tone → ↓ Resting HR. ↑ SV. Resting CO is unchanged.
  • Max Exercise: ↑↑ SV & cardiac contractility → ↑ Max CO.
• Peripheral Adaptations:
  • ↑ Skeletal muscle capillary density.
  • ↑ Mitochondrial number and density.
  • ↑ Arteriovenous O₂ difference ($A-vO_2$ diff).

⭐ Athlete's heart shows enhanced diastolic filling and normal systolic function, unlike pathological hypertrophy which often has diastolic dysfunction.

Oxygen Dynamics - The Fick Principle

• The Fick principle states that cardiac output (CO) can be calculated as the rate of oxygen consumption ($VO_2$) divided by the arteriovenous oxygen difference ($C_aO_2 - C_vO_2$).
• Formula: $CO = \frac{VO_2}{C_aO_2 - C_vO_2}$
  • $VO_2$: Total body O₂ consumption (mL/min).
  • $C_aO_2$: Arterial O₂ content (mL O₂/L blood).
  • $C_vO_2$: Mixed venous O₂ content (mL O₂/L blood).
• This principle is a cornerstone for measuring cardiac output, especially in exercise physiology and critical care settings.

⭐ During exercise, the relationship between cardiac output and oxygen consumption ($VO_2$) is linear. For every 1 L/min increase in $VO_2$, CO increases by approximately 5-6 L/min.

Blood Flow Control - The Traffic Cop

• Local Metabolic Autoregulation: Dominant mechanism in exercising muscle and coronary circulation. Matches blood flow to metabolic demand.
  • Key vasodilators: Adenosine, K⁺, H⁺, CO₂, lactate.
• Systemic Sympathetic Response: ↑ norepinephrine causes vasoconstriction in non-essential tissues (e.g., splanchnic, renal), shunting blood to active muscles.
• Functional Sympatholysis: Local metabolic factors in exercising muscle functionally override systemic sympathetic vasoconstriction, causing net vasodilation.

⭐ During intense exercise, coronary blood flow increases 4-5x. This is driven almost entirely by local metabolic vasodilation (adenosine is key), which overcomes the reduced diastolic filling time.

High‑Yield Points - ⚡ Biggest Takeaways

• Cardiac output increases dramatically, driven first by stroke volume and heart rate, then mainly by heart rate.
• Systolic blood pressure ↑ due to ↑ cardiac output, while diastolic blood pressure remains stable or ↓ due to vasodilation in muscles.
• This leads to an increased pulse pressure.
• Total peripheral resistance ↓ significantly as metabolic demands in skeletal muscle cause marked vasodilation.
• The arteriovenous O₂ difference widens, reflecting increased oxygen extraction by tissues.