Cardiovascular Exercise Physiology Lecture Review

Fick Principle & Whole-Body Oxygen Uptake

• Core Formula (Fick Equation)
  {\displaystyle \dot VO2 = Q \times (A!!!−!!V\,O2\,\text{difference})}
  • Q (cardiac output) = HR \times SV
  • (A!!!−!!V\,O_2) = arterial – venous O₂ content difference ( “oxygen extraction” )
  • Laboratories can sample arterial & venous blood to calculate this extraction per cardiac cycle.

• Acute Exercise Response
  Whole-body (\dot VO_2) rises proportionally with exercise intensity because both cardiac output and O₂ extraction increase.

Cardiac Output (Q)

• Rest vs. Exercise
  • Resting Q ≈ 5\,L\,\text{min}^{−1}
  • Heavy endurance exercise ⇒ 5-fold increase (≈ 25\,L\,\text{min}^{−1} or more in trained athletes).

• Determinants
  • Heart rate (HR) – rises linearly with work rate.
  • Stroke volume (SV) – rises until ≈ 50 % (\dot VO_2^{max}) (range 40–60 %). Beyond that point SV plateaus; further Q rise is HR-driven.

• Sympathetic Control
  β₁-receptor stimulation (epinephrine / norepinephrine) ↑ HR & ↑ contractility (↑ SV).
  Parasympathetic (vagal) withdrawal creates the initial rapid HR rise at exercise onset.

Heart Rate Dynamics

• HR vs. Intensity
  Linear increase during graded (Bruce) test until age-determined HRmax.

• Estimating HRmax
  “Tanaka” regression:
  {\rm HR_{max}\,(beats\,min^{−1}) \approx 208 − 0.7\,(\text{age\,in\,yr})}
  Age is the dominant determinant; training status has virtually no effect on HRmax.

• Mechanoreceptors & Chemoreceptors
  • Mechanoreceptors in skeletal muscle sense fiber length/tension → reflex sympathetic activation.
  • Chemoreceptors detect metabolic by-products (↑CO_2, ↑lactate, ↑H^+, ↓pH) → further sympathetic drive.

Stroke Volume (SV)

• Key Regulators
  • Preload (venous return / EDV)
  • Afterload (arterial pressure)
  • Contractility (β₁-mediated inotropy)
  • Frank–Starling Mechanism predominates at low–moderate intensity; sympathetic inotropy dominates at high intensity.

• Training Adaptation
  Endurance training ↑ maximal SV → ↑ maximal Q. (HRmax unchanged.)

Cardiovascular Drift (Prolonged Steady-State ≥ ~40 min)

• Observed Pattern
  ↑ HR (slow upward “drift”)
  ↓ SV (slow downward drift)
  Q remains constant so that metabolic demand is still met.

• Traditional (Thermoregulatory) Theory

  1. Core temperature ↑ → sweat production ↑ (fluid loss).
  2. Blood is redirected to the skin for heat dissipation.
  3. ↓ Central blood volume & venous return ⇒ ↓ preload ⇒ ↓ SV.
  4. HR drifts upward to keep Q constant.

• Alternate (Cardiac) Theory

  1. With time, HR gradually rises (sympathetic overdrive & ↓ diastolic filling time).
  2. The faster rate itself limits ventricular filling ⇒ ↓ SV.
  3. HR, not SV, is the primary driver.
     Most researchers acknowledge both mechanisms occur simultaneously.

Vascular Responses & Redistribution

• Global Pattern During Dynamic Exercise
  • ↑ Blood flow to working skeletal muscles & skin.
  • ↓ Flow to GI tract, kidneys, liver via α₁-mediated vasoconstriction.
  • Coronary circulation receives the same proportion of Q, so absolute flow ↑.

• Total Peripheral Resistance (TPR)
  Typically ↓ because widespread muscular & cutaneous vasodilation > vasoconstriction elsewhere.

• Mean Arterial Pressure (MAP)
  MAP = \dfrac{SBP − DBP}{3} + DBP
  Or conceptually MAP = Q \times TPR.
  • Systolic BP (SBP) ↑ with intensity (follows Q).
  • Diastolic BP (DBP) usually unchanged because vasodilation in active beds balances vasoconstriction in inactive beds; can fall slightly in heavy aerobic work or rise in heavy resistance work.
  • Net effect ⇒ modest ↑ in MAP.

• Systolic BP Plateau
  Near maximal effort SBP levels off because stroke work & Q reach their limit (SV plateau + HRmax).

Exercise Hyperemia (Local Muscle Blood Flow)

• Definition – The large rise in skeletal-muscle perfusion during contraction.

• Contributors

  1. Metabolic vasodilators – NO, adenosine, prostaglandins, K⁺, CO₂, H⁺, etc.
  2. Mechanical factors – rhythmic “muscle pump” & flow-mediated vasodilation ( FMD ).
  3. Endothelial shear stress → NO release → further dilation.

Heat Stress & Fluid Shifts

• Sweating & Plasma Volume
  • ↑ Core temp → large sweat losses → ↓ plasma volume (PV).
  • Intracellular & interstitial fluid shift toward plasma to partially compensate, but PV continues to fall during long or very intense bouts.
  • ↓ PV → ↓ preload ⇒ ↓ SV ⇒ higher HR than in a temperate environment at the same external workload.

• Blood Pressure in the Heat
  • Skin vasodilation ↓ TPR.
  • Lower SV offsets; SBP may stay similar or fall slightly despite higher HR.
  • DBP can drop modestly because of the vasodilatory dominance.

Pressure–Volume (P–V) Loop & Stroke Work

• Stroke Work ≈ Area within the cardiac P–V loop.
  • Exercise ↑ preload (loop widens) & ↑ ventricular pressure (higher top-left corner) → larger loop area → ↑ mechanical work.

Quick Reference: Direction of Major Acute Changes During Dynamic Aerobic Exercise

Practical / Applied Points

• Training Effect – Endurance training mainly enhances SV and (A!!!−!!V\,O2) diff, thus raising (\dot VO2^{max}). HRmax is age-limited.

• Steady-State Concept – Once workload is constant, HR, SV, Q, BP reach stable plateaus within 2–3 min. “Steady-state” applies at any absolute intensity (e.g., 40 % or 80 % (\dot VO_2^{max})).

• Cardiovascular Drift Implications – During long runs or cycle bouts, relying on HR to gauge intensity may overestimate metabolic load late in the session; hydration & cooling strategies help limit drift.

• Clinical Testing – Failure of SBP to rise (or a fall) during a graded test, or an exaggerated rise in DBP, may indicate cardiovascular pathology.

• Heat Caution – Marathons/ultras: progressive PV loss + cardiovascular drift → “hitting the wall” (~mile 20). Excessive sympathetic drive & dehydration contribute to rare post-race cardiac events.