Cardiovascular Responses to Exercise – Study Notes

Overview & Learning Outcomes
  • Understand acute cardiovascular responses to three exercise patterns
    • Transition from rest → constant-load submaximal work (steady-state) → recovery
    • Incremental (progressive intensity) exercise to VO2 max⁡\text{VO}_2\,\max
    • Prolonged sub-maximal exercise (≥30 min)
  • Be able to graph (with correct units & approximate values) and explain control of:
    • Heart rate (HR, beats·min−1^{-1})
    • Stroke volume (SV, mL·beat−1^{-1})
    • Cardiac output (Q, L·min−1^{-1})
    • Blood pressures – systolic (SBP), diastolic (DBP) & mean arterial pressure (MAP, mmHg)
  • Explain redistribution of blood flow from rest to exercise and the mechanisms behind it (sympathetic tone, local vasodilators, precapillary sphincters).
  • Compare responses in males vs females and arm vs leg exercise.
  • Calculate & interpret Rate Pressure Product (RPP; “double product”).
Key Definitions & Formulas
  • Q=HR×SVQ = HR \times SV (Fick principle for bulk flow)
  • HRmax⁡  (b⋅min−1)≈220−age (y)HR_{\max} \;\text{(b·min}^{-1}\text{)} \approx 220 - \text{age (y)}
  • SV=EDV−ESVSV = EDV - ESV
  • Ejection fraction =SVEDV×100= \dfrac{SV}{EDV} \times 100 (normal rest ≈ 60 – 70 %)
  • MAP=2 DBP+SBP3MAP = \dfrac{2\,DBP + SBP}{3}
  • Poiseuille’s Law for resistance to flow
    • R=L ηr4R = \dfrac{L\,\eta}{r^{4}}
    • Vessel radius (r) is the most powerful determinant of total peripheral resistance (TPR).
  • Rearranged haemodynamic relationships
    • Q=MAP×80TPRQ = \dfrac{MAP \times 80}{TPR}
    • TPR=MAP×80QTPR = \dfrac{MAP \times 80}{Q} (constant 80 converts mmHg·min·L−1^{-1})
  • Rate Pressure Product (RPP) – indirect myocardial work index
    • RPP=HR×SBPRPP = HR \times SBP (dimensionless)
Big Picture – Why Circulate Blood During Exercise?
  • Deliver O2O_2 & fuel substrates (glucose, fatty acids) from lungs & gut → working muscle mitochondria.
  • Remove metabolic by-products CO2CO_2, H+H^+, heat → lungs, skin, kidneys.
  • Fast, flexible circulation supported by:
    • Pump (heart) – HR & SV adjustments
    • Pipes (arteries, arterioles, capillaries, veins) – diameter & compliance changes
    • Fluids (blood volume/viscosity)
Capillary Architecture & Flow Control
  • Continuous, metarteriole–capillary beds with precapillary sphincters.
  • Active tissue releases local vasodilators (↓PO<em>2<em>2, ↑P</em>CO2</em>{CO_2}, ↑K+^+, adenosine, heat ➔ relax sphincters ➔ ↑regional blood flow).
  • ‘Thoroughfare channels’ sustain minimal flow when sphincters closed.
Neural–Hormonal Control of the Heart
  • Cardiovascular centre: medulla oblongata (input from higher brain, baro-, chemo-, proprio-receptors).
  • Parasympathetic (vagus) ➔ SA/AV nodes ➔ ↓HR (dominant at rest).
  • Sympathetic (cardiac accelerator nerves, adrenal catecholamines) ➔ SA/AV + myocardium ➔ ↑HR & ↑contractility.
  • Rapid HR rise at exercise onset = vagal withdrawal; further rise = ↑sympathetic drive.
Heart Rate Responses

Single-intensity (steady-state)

  • Sharp rise at onset, reaches steady state within ≈ 3 min once O2O_2 delivery meets metabolic demand.
  • Magnitude proportional to absolute workload.
  • Typical steady-state value 100–160 b·min−1^{-1} for moderate work.
  • Recovery: rapid early drop (parasympathetic re-activation) then slower to baseline.

Incremental exercise

  • HR increases ~linearly with power/VO<em>2\text{VO}<em>2 until HR</em>maxHR</em>{max}.
  • Slightly attenuated slope in highly trained due to larger SV.

Prolonged exercise (cardiovascular drift)

  • Despite constant load, HR drifts ↑ (~3–15 b·min−1^{-1} per 10–30 min) especially in heat/humidity.
  • Compensates for falling SV to maintain Q.
Stroke Volume (SV) & Its Regulation

Resting range: 60 – 100 mL (influenced by body size, sex, training status).
Determinants (Frank-Starling & inotropy)

  • Preload (EDV) – ↑venous return via skeletal muscle/respiratory pumps & venoconstriction
  • Afterload (aortic/arterial pressure) – small acute effect
  • Contractility – sympathetic β-adrenergic stimulation ↑Ca2+^{2+} availability
  • Filling time (↔ HR)
    During exercise
  • Venous return ↑ ➔ EDV ↑ ➔ SV ↑
  • Sympathetic stimulation ↑contractility ➔ ↓ESV ➔ further ↑SV
  • SV plateaus at ~40–60 % VO2 max⁡\text{VO}_2\,\max in most untrained; highly trained may keep rising (larger LV volume & compliance).
Cardiac Output (Q) Responses

Steady-state

  • Rises rapidly, plateaus within 2–3 min when Q ≈ metabolic requirement.
  • Typical moderate work: 10–15 L·min−1^{-1}.
    Incremental
  • Nearly linear ↑ driven mainly by HR after SV plateau.
  • Untrained peak: ~20–25 L·min−1^{-1}; elite endurance male ≈ 30–35 L·min−1^{-1}.
    Prolonged
  • Q maintained (or slight ↓ late) via HR ↑ offsetting SV ↓.
Blood Pressure Responses & Regulation
  • SBP ↑ linearly with intensity (≈ 8–10 mmHg per MET) due to ↑Q.
  • DBP: little change or slight ↓ (−0 to −10 mmHg) because peripheral vasodilation ↓TPR.
  • Hence MAP ↑ modestly (≈ SBP ↑ partially counteracted by DBP ↓).
    Short-term regulation
  • Baroreflex resets to higher operating point during exercise ➔ prevents excessive BP fluctuations.
    Long-term
  • Kidney-mediated volume control; not acute.
Redistribution of Blood Flow

Rest (Q ≈ 5 L·min−1^{-1})

  • Skeletal muscle 15–20 % (≈ 1 L·min−1^{-1})
  • Splanchnic 24 %, Renal 19 %, Brain 13 %, Skin 9 %, Coronary 4 %
    Maximal exercise (Q ≈ 25 L·min−1^{-1})
  • Skeletal muscle 80–85 % (≈ 22 L·min−1^{-1})
  • Skin 2 % (heat stress may raise skin flow slightly), Splanchnic 1 %, Renal 4 %, Brain ~3 %, Others negligible.
    Mechanisms
  • Global sympathetic vasoconstriction (α-adrenergic) to non-essential beds.
  • Local metabolic vasodilation in active muscle overrides sympathetic tone (functional sympatholysis).
  • Opening of more capillaries ↑surface area for gas exchange.
Rate Pressure Product (RPP)
  • Surrogate for myocardial O<em>2O<em>2 demand (closely related to coronary blood flow & MVO</em>2</em>2).
  • Resting example: HR 75 b·min−1^{-1} × SBP 110 mmHg = 8,250.
  • Progressive exercise example (21-y female):
    • 25 % VO2\text{VO}_2max ➔ 13,000
    • 50 % ➔ 22,400
    • 75 % ➔ 30,600
    • 100 % ➔ 42,000
  • RPP ↑ in proportion to both HR & SBP; useful in cardiac rehab to keep workloads below angina threshold.
Responses to Different Exercise Patterns

Rest → Steady-State Submaximal

  • HR, SV, Q & SBP all rise rapidly then plateau (~2–3 min).
  • DBP unchanged/↓; MAP slight ↑.
    Incremental (Graded Test)
  • HR & SBP: linear ↑ to maximal.
  • SV: ↑ until ~40–60 % VO2\text{VO}_2max then plateau (untrained) or continues (trained).
  • Q: near-linear ↑ (slope steeper early; becomes HR-driven after SV plateau).
    Prolonged Constant-Load (>30 min)
  • Cardiovascular drift: ↓SV (due to dehydration, ↓plasma volume, ↑body temp → skin circulation) + compensatory ↑HR, maintaining Q & SBP.
Arm vs Leg Exercise (Same Absolute Work Rate)
  • ↑HR and ↑BP during arm ergometry vs cycle/leg because:
    • Smaller active muscle mass ➔ higher sympathetic outflow to maintain power ➔ greater vasoconstriction in inactive large beds ➔ ↑TPR.
  • SV often lower (less muscle pump assistance).
Sex Differences
  • HRmaxHR_{max} predicted by age; no intrinsic sex difference.
  • Women: ↓SV (≈10–25 % lower) due to smaller heart size & lower blood volume ➔ slightly lower maximal Q.
  • Men: higher SBP/DBP responses (greater sympathetic activation; androgen effects on arterial stiffness).
    Example values (college-age, 70 kg male vs 50 kg female)
  • Rest: HR 72 vs 75 b·min−1^{-1}; SV 100 vs 70 mL; Q both ≈ 5 L·min−1^{-1}.
  • Max untrained: HR 200 b·min−1^{-1} (same); SV 110 vs 90 mL; Q 22 vs 18 L·min−1^{-1}.
  • Trained endurance:
    • Male: HR 190; SV 180 mL; Q 34.2 L·min−1^{-1}.
    • Female: HR 190; SV 125 mL; Q 23.8 L·min−1^{-1}.
Cardiovascular Drift – Mechanistic Details
  • Fluid loss (sweat) & plasma transudation → ↓central venous pressure → ↓EDV → ↓SV.
  • Skin vasodilation for thermoregulation ↑venous compliance, ↓venous return.
  • HR ↑ via baroreflex & ↑sympathetic activity to maintain MAP & Q.
  • Performance implication: perceived effort ↑, may limit endurance in heat unless fluid intake & cooling strategies employed.
Concept Integration (Cardiac Output Map)
  • Q depends simultaneously on:
    • HR (ANS modulation, intrinsic SA node rate)
    • SV determined by
    • Preload (venous return ↔ blood volume, muscle pump, respiratory pump, venoconstriction)
    • Contractility (SNS, circulating catecholamines, Frank-Starling)
    • Afterload (arterial pressure)
    • Filling time (inverse of HR)
  • Blood pressure (MAP) = Q × TPR; TPR dynamically altered via arteriolar radius.
  • Exercise sets off coordinated adjustments via central command, reflex feedback, and local metabolic control to match blood flow with metabolic demand while stabilising arterial pressure.
Worked Calculations & Quick Checks
  1. Steady-state jog, 25-y male: HR 150 b·min−1^{-1}, SV 110 mL.
    • Q=150×0.11=16.5  L⋅min−1Q = 150 \times 0.11 = 16.5\;\text{L·min}^{-1}.
  2. If SBP 180 mmHg at that workload:
    • RPP=150×180=27,000RPP = 150 \times 180 = 27{,}000 (≈3.3-fold ↑ vs rest 8,000).
  3. MAP when SBP 180 mmHg, DBP 70 mmHg:
    • MAP=2(70)+1803=3203≈107  mmHgMAP = \dfrac{2(70)+180}{3} = \dfrac{320}{3} \approx 107\;\text{mmHg}.
  4. Estimate TPR:
    • TPR=MAP×80Q=107×8016.5≈519  dyn⋅s⋅cm−5TPR = \dfrac{MAP \times 80}{Q} = \dfrac{107 \times 80}{16.5} \approx 519\;\text{dyn·s·cm}^{-5} (lower than rest ≈1,100, reflecting vasodilation).
Practical / Clinical Implications
  • RPP monitoring in cardiac patients to keep exercise below ischaemic threshold.
  • Understanding sex & modality differences informs prescription (e.g., arm ergometry elicits higher BP – caution in hypertensives).
  • Hydration & cooling strategies mitigate cardiovascular drift and maintain performance.
  • Knowledge of rapid HR recovery is used as marker of cardiovascular fitness (faster recovery = better vagal re-activation).