Cardiovascular Exercise Physiology – Acute & Prolonged Responses

Overview & Fundamental Equation (Fick)

• Whole-body O$_2$ consumption rises proportionally to exercise intensity.

  • Captured by the Fick Equation: \dot V O2 = Q \times (a\,! -!v)O2\, \text{difference}

  • Q = Cardiac Output (HR × SV)

  • (a! -!v)O2 = Arterial–venous O$2$ difference (i.e., oxygen extraction).

• VO$_2$max therefore limited by:

  1. Maximal cardiac output (central factor).

  2. Maximal O$_2$ extraction at the capillaries (peripheral factor).

Cardiac Output Components

• Resting Q ≈ 5\;\mathrm{L\,min^{-1}}; can increase ≈ 5× (to \sim25\;\mathrm{L\,min^{-1}}, even higher in elite endurance athletes).

• Determinants:

  • Heart Rate (HR)

  • Stroke Volume (SV)

• Sympathetic stimulation (\uparrow epinephrine & norepinephrine → β$_1$ receptors):

  • ↑ HR (chronotropy)

  • ↑ Contractility → ↑ SV (inotropy)

• Parasympathetic withdrawal permits rapid initial HR rise.

Neural & Reflex Feedback

• Mechanoreceptors (in skeletal muscle)

  • Detect muscle length & tension changes.

  • Signal CV centers → ↑ sympathetic outflow.

• Chemoreceptors (in skeletal muscle)

  • Sense metabolic by-products (CO$_2$, H$^+$, lactate, ↓pH).

  • Further ↑ sympathetic drive as exercise continues.

Heart-Rate Dynamics

• HR increases almost linearly with workload (e.g., Bruce treadmill protocol).

• Age is the primary predictor of HR$_{max}$ (Tanaka equation).

  • Training status has little effect; two 40-year-olds (marathoner vs. sedentary) have similar HR$_{max}$.

• Estimation formula (commonly cited): HR_{max}=208-0.7\times\text{age} (Tanaka).

Stroke-Volume Dynamics

• SV rises with intensity until ≈ 50 % VO$_2$max (±10 %); plateaus thereafter.

• Acute determinants:

  1. Preload (venous return → end-diastolic volume)

  2. Afterload (aortic pressure / TPR)

  3. Contractility (β$_1$ stimulation)

• Mechanistic weighting:

  • Low-moderate intensity → Frank–Starling (stretch) predominates.

  • Higher intensity → Sympathetic inotropy predominates due to shortened filling time.

• Chronic adaptation: Endurance training ↑ max SV → ↑ max Q (HR$_{max}$ unchanged).

Steady-State Exercise

• Definition: Constant workload (regardless of absolute intensity or fitness level).

• During sub-max steady state:

  • Q, HR, and SV rise rapidly then plateau at values that match metabolic demand.

  • More aerobically trained individuals can sustain higher absolute workloads at steady state (e.g., 8 min/mile vs. 2 mph walk).

Cardiovascular Drift

• Observed during prolonged (≈ ≥45 min) steady-state aerobic work; smaller drifts reported as early as 15–20 min.

• Classic pattern:

  • ↑ HR (gradual)

  • ↓ SV (gradual)

  • Q remains ≈ constant (compensation).

• Traditional ("Stroke-Volume driven") theory:

  1. ↑ Core temp → ↑ sweating → fluid loss (↓ plasma volume).

  2. Blood redistributed to skin for cooling.

  3. ↓ Venous return → ↓ preload → ↓ SV → HR drifts ↑ to maintain Q.

• Alternative ("Heart-Rate driven") theory:

  1. Prolonged sympathetic activation + shorter diastole → HR rises first.

  2. Reduced filling time → ↓ SV.

• Likely both mechanisms act simultaneously.

• Practical outcome: Even at a fixed speed, HR "floats" upward; important for prescribing long-duration training/rehab.

Vascular Redistribution & VO$_2$

• During exercise, a greater % of Q directed to skin & working skeletal muscles; reduced to GI tract, kidneys, liver.

• %Q to myocardium remains constant, but absolute flow ↑ because total Q ↑.

• Purposes:

  1. Deliver O$_2$ & substrates.

  2. Remove CO$_2$, H$^+$, heat, and metabolites.

• Resultant rise in whole-body VO$2$ is primarily due to ↑ Q with a modest ↑ (a-v)O$2$ difference.

Blood-Pressure Responses

• Formula reminder: MAP = Q \times TPR and MAP = DBP + \frac{1}{3}(SBP-DBP)

• Exercise effects:

  • Systolic BP (SBP) ↑ with intensity (driven by ↑ Q).

  • Plateaus before absolute max due to SV limitation.

  • Diastolic BP (DBP) typically ≈ unchanged (± small ↓) during dynamic aerobic work because systemic vasodilation ≈ vasoconstriction in inactive beds → net TPR change modest.

  • Mode-specific: Heavy resistance exercise can ↑ DBP markedly.

• Net: MAP rises modestly with intensity.

Total Peripheral Resistance (TPR) & Vasodilators

• Dynamic aerobic exercise → ↓ TPR due to widespread vasodilation in active muscle & skin.

• Local metabolic/chemical vasodilators:

  • Nitric oxide (NO)

  • Adenosine

  • Prostaglandins

  • ↑ CO$_2$, ↑ H$^+$, ↑ K$^+$, ↑ temperature

• Magnitude of TPR drop depends on:

  1. Number of muscles recruited

  2. Exercise intensity → ↑ metabolite production

Exercise Hyperemia

• Defined: Exercise-induced ↑ muscle blood flow.

• Contributors:

  1. Metabolic vasodilation (chemicals above).

  2. Mechanical action of contractions (muscle pump).

  3. Flow-mediated dilation (FMD): Transient occlusion → reactive hyperemia (basis for clinical FMD tests).

• Example: Inflating a BP cuff to >200\;\mathrm{mmHg} for 10 min → release → surge in forearm blood flow (research method described by lecturer).

Exercise in the Heat

• ↑ Environmental temp → ↑ core temp sooner & higher → ↑ sweating.

• Consequences:

  • ↓ Plasma volume (fluid loss via sweat & respiratory evaporation).

  • Fluid shift from intracellular → extracellular → plasma to support sweat.

  • ↓ SV → Compensatory ↑ HR at given workload (higher HR vs. cool conditions).

  • ↑ Skin blood flow (vasodilation) → ↓ TPR; SBP may be slightly lower or similar; DBP often ↓.

• Practical/ethical point: Extended marathon/ultra-events + heat can push CV system to limits → potential collapse; monitor hydration & pacing.

Formulas & Numerical References

• Fick: \dot V O2 = Q \times (a\,! -!v)O2

• HR${max}$ (Tanaka): HR{max}=208-0.7\times\text{age}

• Stroke-Volume plateau: ≈ 50 % VO$_2$max (range 40–60 %).

• Resting Q ≈ 5\;\mathrm{L\,min^{-1}}; trained max Q can exceed 30\;\mathrm{L\,min^{-1}}.

• Cardiovascular drift onset: classically ≈ 45 min continuous moderate exercise.

Study / Self-Test Checklist

• Can you write & explain the Fick equation?

• Trace blood flow & describe where vasoconstriction vs. vasodilation occurs during running.

• List acute changes (↑, ↓, ↔) for: HR, SV, Q, SBP, DBP, MAP, TPR during (a) light jog, (b) maximal graded test, (c) prolonged steady run.

• Explain two theories of cardiovascular drift.

• Differentiate mechanoreceptor vs. chemoreceptor feedback.

• Predict BP response differences between aerobic cycling vs. heavy squatting.

• Discuss why HR$_{max}$ is age- but not training-dependent.

• Outline how heat stress alters SV, HR, and BP.

Tip: Create your own blank table with variables down the left and exercise conditions across the top; fill in ↑ / ↓ / ↔ to solidify recall.

Overview & Fundamental Equation (Fick)

• Whole-body O$_2$ consumption rises proportionally to exercise intensity.

• Captured by the Fick Equation:
  Mixed\;venous\;O_2\;content\; (ml\;O_2/dL)\newline\dot V O_2 = Q \times (a-v)O_2\;\text{difference}
  

• 
  Q = \text{Cardiac Output (L/min)} = \text{Heart Rate (beats/min)} \times \text{Stroke Volume (L/beat)}
  

• (a-v)O_2 = Arterial–venous O$_2$ difference (i.e., oxygen extraction). This represents the amount of oxygen removed from the blood by the tissues as it passes through the capillaries.

• VO$_2$max therefore limited by:

  1. Maximal cardiac output (central factor): The ability of the heart to pump blood.

  2. Maximal O$_2$ extraction at the capillaries (peripheral factor): The capacity of working muscles to extract and utilize oxygen from the blood.

Cardiac Output Components

• Resting Q \approx 5\;\mathrm{L\,min^{-1}}; can increase
  \approx 5\times\; (\text{to }\sim25\;\mathrm{L\,min^{-1})
  }, even higher in elite endurance athletes (e.g.,

30\;\mathrm{L\,min^{-1}}

).

• Determinants:

  • Heart Rate (HR)

  • Stroke Volume (SV)

  • Sympathetic stimulation (increased epinephrine & norepinephrine binding to β$_1$ adrenergic receptors in the heart):

  • ↑ HR (chronotropy): Increases the rate of pacemaker firing in the SA node.

  • ↑ Contractility → ↑ SV (inotropy): Increases the force of myocardial contraction and the amount of blood ejected with each beat.

  • Parasympathetic withdrawal permits a rapid initial HR rise by reducing vagal tone on the SA node.

Neural & Reflex Feedback

• Mechanoreceptors (in skeletal muscle): Specialized sensory receptors (e.g., muscle spindles, Golgi tendon organs) in active muscles and joints.

  • Detect changes in muscle length, tension, and joint position; provide feedback on the mechanical state of the muscle.

  • Signal cardiovascular control centers (medulla oblongata) → ↑ sympathetic outflow to the heart and blood vessels.

• Chemoreceptors (in skeletal muscle and arterial system, e.g., carotid bodies): Sensitive to chemical changes in the muscle interstitial fluid and blood.

  • Sense metabolic by-products (CO$_2$, H$^+$, inorganic phosphate, lactate, ↓pH, ↓O$_2$).

  • Further ↑ sympathetic drive as exercise continues, promoting increased blood flow and oxygen delivery to match metabolic demand.

Heart-Rate Dynamics

• HR increases almost linearly with workload (e.g., Bruce treadmill protocol).

• Age is the primary predictor of HR$_{max}$ (Tanaka equation).

• Training status has little effect; two 40-year-olds (marathoner vs. sedentary) have similar HR$_{max}$.

• Estimation formula (commonly cited): HR_{max}=208-0.7\times\text{age} (Tanaka).

Stroke-Volume Dynamics

• SV rises with intensity until
  \approx 50\%\;VO_2\;max\; (\pm10\%)
  
  ; plateaus thereafter.

• Acute determinants:

  1. Preload (venous return → end-diastolic volume): The degree of myocardial stretch at the end of diastole.

  2. Afterload (aortic pressure / TPR): The resistance the heart must overcome to eject blood.

  3. Contractility (β$_1$ stimulation): The intrinsic ability of the heart muscle to contract.

• Mechanistic weighting:

  • Low-moderate intensity → Frank–Starling mechanism (stretch-induced increase in contractility due to greater venous return) predominates. Greater venous return stretches the cardiac muscle fibers, leading to a more forceful contraction.

  • Higher intensity → Sympathetic inotropy predominates due to shortened filling time. Increased sympathetic activity enhances calcium release within myocardial cells, leading to stronger contractions despite reduced filling time.

• Chronic adaptation: Endurance training ↑ max SV by increasing ventricular volume and contractility → ↑ max Q (HR$_{max}$ unchanged).

Steady-State Exercise

• Definition: Constant workload (regardless of absolute intensity or fitness level), where physiological responses (HR, Q, SV, VO$_2$) reach a plateau.

• During sub-maximal steady state:

  • Q, HR, and SV rise rapidly then plateau at values that match metabolic demand.

  • More aerobically trained individuals can sustain higher absolute workloads at steady state (e.g., 8 min/mile run vs. 2 mph walk) due to a higher aerobic capacity achieved at a lower relative intensity.

Cardiovascular Drift

• Observed during prolonged \approx \ge45\;\text{min} steady-state aerobic work; smaller drifts reported as early as 15–20 min.

• Classic pattern:

  • ↑ HR (gradual)

  • ↓ SV (gradual)

  • Q remains
    \approx\;\text{constant}\; (\text{compensation})
    
    .

• Traditional ("Stroke-Volume driven") theory:

  1. ↑ Core temp → ↑ sweating → fluid loss (↓ plasma volume).

  2. Blood redistributed to skin for cooling, and some pooling in peripheral vasculature.

  3. ↓ Venous return → ↓ preload → ↓ SV → HR drifts ↑ to maintain cardiac output.

• Alternative ("Heart-Rate driven") theory:

  1. Prolonged sympathetic activation + shorter diastole (due to initial HR rise) → HR rises first.

  2. Reduced filling time (due to higher HR) → ↓ SV.

• Likely both mechanisms act simultaneously and contribute.

• Practical outcome: Even at a fixed speed, HR "floats" upward over time; important for prescribing long-duration training/rehab where %HRmax zones might be influenced.

Vascular Redistribution & VO$_2$

• During exercise, a greater % of Q is directed to working skeletal muscles and skin (for thermoregulation); blood flow is significantly reduced to less active organs such as the GI tract, kidneys, and liver via sympathetic vasoconstriction.

• %Q to myocardium remains constant, but absolute flow ↑ because total Q ↑.

• Purposes:

  1. Deliver O$_2$ & substrates (glucose, fatty acids) to active tissues.

  2. Remove CO$_2$, H$^+$, heat, and metabolites from active tissues.

• Resultant rise in whole-body VO$_2$ is primarily due to ↑ Q with a modest ↑ (a-v)O$_2$ difference (indicating increased oxygen extraction by muscles).

Blood-Pressure Responses

• Formula reminder: MAP = Q \times TPR and MAP = DBP + \frac{1}{3}(SBP-DBP)

• Exercise effects:

  • Systolic BP (SBP) ↑ with intensity (driven by ↑ Q and ↑ SV).

  • Plateaus before absolute max due to SV limitation.

  • Diastolic BP (DBP) typically
    \approx\;\text{unchanged}\; (\pm\;\text{small}\;\downarrow)
    
    during dynamic aerobic work because systemic vasodilation in active muscles roughly counteracts vasoconstriction in inactive beds → net TPR change is modest relative to Q increase.

  • Mode-specific: Heavy resistance exercise can ↑ DBP markedly due to sustained muscle contractions compressing blood vessels and high intrathoracic pressure (Valsalva maneuvers).

• Net: MAP rises modestly with intensity during aerobic exercise.

Total Peripheral Resistance (TPR) & Vasodilators

• Dynamic aerobic exercise → ↓ TPR due to widespread vasodilation in active muscle & skin vascular beds.

• Local metabolic/chemical vasodilators (acting directly on vascular smooth muscle or endothelium):

  • Nitric oxide (NO): Released by endothelial cells in response to shear stress; potent vasodilator.

  • Adenosine: Released from metabolically active cells; causes smooth muscle relaxation.

  • Prostaglandins: Local hormones involved in inflammation and vasodilation.

  • ↑ CO$_2$, ↑ H$^+$ (from lactic acid), ↑ K$^+$, ↑ temperature: Locally produced during metabolism; directly relax arteriolar smooth muscle.

• Magnitude of TPR drop depends on:

  1. Number of muscles recruited: More active muscle mass leads to greater cumulative vasodilation.

  2. Exercise intensity → ↑ metabolite production: Higher intensity produces more vasodilatory by-products.

Exercise Hyperemia

• Defined: Exercise-induced ↑ muscle blood flow, typically far exceeding resting levels.

• Contributors:

  1. Metabolic vasodilation (chemicals above): Primary driver, matching blood flow to metabolic demand.

  2. Mechanical action of contractions (muscle pump): Rhythmic contractions compress veins, forcing blood toward the heart and promoting venous return, which in turn facilitates arterial inflow.

  3. Flow-mediated dilation (FMD): Endothelium-dependent vasodilation in response to increased shear stress (friction of blood flow against vessel walls); basis for clinical FMD tests.

• Example: Inflating a BP cuff to

200\;\mathrm{mmHg}

for 10 min → release → surge in forearm blood flow (reactive hyperemia, a research method described by lecturer).

Exercise in the Heat

• ↑ Environmental temp → ↑ core temp sooner & higher → ↑ sweating.

• Consequences:

  • ↓ Plasma volume (fluid loss via sweat & respiratory evaporation) impacting venous return.

  • Fluid shift from intracellular → extracellular → plasma to support sweat production.

  • ↓ SV due to reduced preload from fluid loss and increased skin blood flow → Compensatory ↑ HR at given workload (higher HR vs. cool conditions) to maintain Q.

  • ↑ Skin blood flow (vasodilation) for heat dissipation → ↓ TPR; SBP may be slightly lower or similar; DBP often ↓.

• Practical/ethical point: Extended marathon/ultra-events + heat can push CV system to limits → potential collapse; rigorous monitoring of hydration & pacing is crucial.

Formulas & Numerical References

• Fick:
  \dot V O_2 = Q \times (a-v)O_2
  

• HR$_{max}$ (Tanaka): HR_{max}=208-0.7\times\text{age}

• Stroke-Volume plateau:
  \approx 50\%\;VO_2\;max\; (\text{range } 40\text{–}60\%)
  
  .

• Resting Q
  \approx 5\;\mathrm{L\,min^{-1}}
  
  ; trained max Q can exceed
  30\;\mathrm{L\,min^{-1}}
  
  .

• Cardiovascular drift onset: classically
  \approx 45\;\text{min}
  
  continuous moderate exercise, though earlier smaller drifts may occur.

Study / Self-Test Checklist

• Can you write & explain the Fick equation?

• Trace blood flow & describe where vasoconstriction vs. vasodilation occurs during running.

• List acute changes (↑, ↓, ↔) for: HR, SV, Q, SBP, DBP, MAP, TPR during (a) light jog, (b) maximal graded test, (c) prolonged steady run.

• Explain two theories of cardiovascular drift.

• Differentiate mechanoreceptor vs. chemoreceptor feedback.

• Predict BP response differences between aerobic cycling vs. heavy squatting.

• Discuss why HR$_{max}$ is age- but not training-dependent.

• Outline how heat stress alters SV, HR, and BP.

Tip: Create your own blank table with variables down the left and exercise conditions across the top; fill in ↑ / ↓ / ↔

to solidify recall.

Here are the answers to your study questions, based on the provided notes:

1. Fick Equation Explanation:
   The Fick Equation is:

   \dot V O_2 = Q \times (a-v)O_2

   • \dot V O_2 (Whole-body O$_2$ consumption) is the rate at which the body uses oxygen.

   • Q (Cardiac Output) is the volume of blood pumped by the heart per minute (HR \times SV).

   • (a-v)O_2 (Arterial–venous O$_2$ difference) is the amount of oxygen extracted from the blood by the tissues as it passes through the capillaries.

   In essence, it states that oxygen consumption is equal to the amount of blood pumped by the heart multiplied by the amount of oxygen the tissues extract from that blood.

2. Blood Flow and Vaso- (Running):
   During running, blood flow is redistributed to prioritize active muscles and skin, with reduced flow to less active organs:

   • Vasodilation: Occurs in working skeletal muscles and skin (for thermoregulation) due to local metabolic/chemical vasodilators (e.g., nitric oxide, adenosine, prostaglandins, ↑CO$_2$, ↑H$^+$, ↑K$^+$, ↑temperature) and mechanical action of contractions (muscle pump). Flow-mediated dilation (FMD) also contributes.

   • Vasoconstriction: Occurs in inactive vascular beds, primarily in the gastrointestinal tract, kidneys, and liver, via sympathetic nervous system activation, to divert blood to active areas.

   • Blood flow to the myocardium (heart muscle) increases in absolute terms, but its percentage of total cardiac output (Q) remains constant.

3. Acute Cardiovascular Changes During Exercise:

   Variable	Light Jog (Sub-Max Steady State)	Maximal Graded Test (Increasing Intensity)	Prolonged Steady Run (\ge45 min, Cardiovascular Drift)
   HR	↑ (rapidly then plateaus)	↑ (linearly to max)	↑ (gradual drift upward)
   SV	↑ (rapidly then plateaus)	↑ (until

   \approx 50\%\;VO_2\;max

   then plateaus) | ↓ (gradual drift downward) |
   | Q | ↑ (rapidly then plateaus) | ↑ (to max) | ↔ (remains approximately constant) |
   | SBP | ↑ | ↑ (with intensity, then plateaus) | ↑ (may be slightly lower or similar due to heat) |
   | DBP | ↔ ($\pm$ small ↓) | ↔ ($\pm$ small ↓) | ↓ (often, due to increased skin blood flow) |
   | MAP | ↑ (modestly) | ↑ (modestly) | ↑ (modestly, but affected by DBP changes in heat) |
   | TPR | ↓ | ↓ (due to widespread vasodilation) | ↓ (due to widespread vasodilation, especially in skin) |

4. Two Theories of Cardiovascular Drift:
   Cardiovascular drift is the phenomenon observed during prolonged steady-state aerobic work where HR gradually increases and SV gradually decreases, while cardiac output (Q) remains relatively constant.

   • Traditional ("Stroke-Volume Driven") Theory: Proposes that increased core temperature leads to greater sweating and fluid loss (↓ plasma volume). Blood is redistributed to the skin for cooling, and some pooling may occur in peripheral vasculature. This results in ↓ venous return and ↓ preload, causing ↓ SV, which is then compensated by an ↑ HR to maintain Q.

   • Alternative ("Heart-Rate Driven") Theory: Suggests that prolonged sympathetic activation and a shorter diastolic filling time (due to the initial rise in HR) lead to an earlier increase in HR. This higher HR then reduces filling time, subsequently causing a ↓ SV.
     Both mechanisms likely act simultaneously and contribute.

5. Mechanoreceptor vs. Chemoreceptor Feedback:
   Both are neural feedbacks from skeletal muscle to cardiovascular control centers:

   • Mechanoreceptors: Located in active muscles and joints (e.g., muscle spindles, Golgi tendon organs). They detect physical changes like muscle length, tension, and joint position. Their signals provide feedback on the mechanical state of the muscle, leading to an ↑ in sympathetic outflow.

   • Chemoreceptors: Located in skeletal muscle interstitial fluid and arterial system (e.g., carotid bodies). They sense chemical changes and metabolic by-products of exercise, such as CO$_2$, H$^+$, inorganic phosphate, lactate, ↓pH, and ↓O$_2$. Their signals further ↑ sympathetic drive as exercise continues to enhance blood flow and oxygen delivery.

6. BP Response Differences (Aerobic Cycling vs. Heavy Squatting):

   • Aerobic Cycling (Dynamic Aerobic Work): Systolic BP (SBP) increases with intensity due to increased cardiac output. Diastolic BP (DBP) typically remains largely unchanged or slightly decreases because widespread vasodilation in active muscles roughly counteracts vasoconstriction in inactive areas, leading to a modest net change in TPR. Mean Arterial Pressure (MAP) rises modestly.

   • Heavy Squatting (Heavy Resistance Exercise): SBP also increases significantly. However, DBP can increase markedly due to sustained muscle contractions compressing blood vessels and high intrathoracic pressure from Valsalva maneuvers (holding breath). The sustained muscle tension can restrict blood flow and elevate peripheral resistance more substantially.

7. HR$_{max}$ Age- vs. Training-Dependent:

   • HR$_{max}$ is primarily age-dependent and decreases predictably with age, as described by formulas like the Tanaka equation (HR_{max}=208-0.7\times ext{age}).

   • HR$_{max}$ is not significantly training-dependent. Two individuals of the same age, regardless of their training status (e.g., a marathoner vs. a sedentary person), will have similar maximal heart rates. Endurance training primarily affects submaximal HR (lowering it for a given workload) and maximal stroke volume, but not the inherent maximal beating capacity of the heart itself.

8. How Heat Stress Alters SV, HR, and BP:

   • SV (Stroke Volume): ↓ Decreases due to reduced plasma volume from increased sweating and respiratory evaporation, and increased blood flow diversion to the skin for cooling, which reduces venous return and preload.

   • HR (Heart Rate): ↑ Increases compensatorily at a given workload to maintain cardiac output, as stroke volume decreases.

   • BP (Blood Pressure): SBP may be slightly lower or similar. DBP often ↓ decreases due to widespread vasodilation in the skin for thermoregulation, leading to a greater drop in Total Peripheral Resistance (TPR). The net effect is typically a slightly