Cardiovascular Responses to Exercise – Comprehensive Notes

Organization of the Circulatory System

• Cardiopulmonary / cardiorespiratory system = cardiovascular + pulmonary systems
• Principal goals of system
  • Transport: O$_2$, nutrients to tissues
  • Removal: CO$_2$, metabolic wastes
  • Regulation: body temperature via blood distribution and sweating
• 4 major vessel categories
  • Arteries & arterioles: high-pressure conduits → tissues
  • Capillaries: site of gas & nutrient exchange
  • Venules & veins: low-pressure return → heart; contain majority of blood volume (≈64 %)

Cardiac Anatomy & Blood Flow

• Heart positioned within pericardial sac
  • Layers: epicardium, myocardium, endocardium
  • Pericardial fluid reduces friction
• Chambers & valves
  • Right atrium (RA) → tricuspid → right ventricle (RV) → pulmonary semilunar → pulmonary artery
  • Left atrium (LA) → mitral/bicuspid → left ventricle (LV) → aortic semilunar → aorta
• Coronary circulation
  • RCA supplies RA, RV, SA node, most AV node; branches → PDA (posterior ⅓ septum), acute marginal
  • LMCA branches → LAD (anterior ⅔ septum, anterior LV) & LCx (LA + post-lat LV); minor: obtuse marginal, diagonals, septal perforators

Pulmonary vs. Systemic Circuits

• Pulmonary circuit (right heart): de-oxygenated blood → lungs via pulmonary arteries, returns O$_2$-rich via pulmonary veins
• Systemic circuit (left heart): O$2$-rich blood → body; returns O$2$-poor via vena cavae

Myocardium Characteristics & Training Effects

• High oxidative demand; supplied by coronary arteries
• Structural comparison to skeletal muscle
  • Short, branching fibers, single nucleus, intercalated discs, endomysium only, primarily aerobic metabolism
  • No satellite cells → negligible regeneration
• Exercise training is cardioprotective
  • ↓ incidence & severity of myocardial infarction (MI)
  • Mechanisms: ↑ antioxidant capacity, improved ATP-sensitive K$^+$ channel function
  • Trained vs. untrained: ~40 % less tissue damage during MI

The Cardiac Cycle

• Systole = contraction / ejection (≈⅓ volume expelled/beat)
• Diastole = relaxation / filling
  • At rest: diastole longer (0.5 s) vs. systole (0.3 s)
  • Heavy exercise: both shorten; total cycle ~0.33 s at 180 b·min$^{-1}$
• Pressure events
  • AV valves open when P{ventricle}
  • Semilunar open when P{ventricle}>P{aorta/pulmonary}
• Heart sounds: S$1$ = AV closure; S$2$ = semilunar closure

Arterial Blood Pressure & Hypertension

• Expressed as SBP/DBP (normal 120/80\,\text{mmHg})
• Pulse pressure = SBP − DBP; Mean arterial pressure (MAP):
  \text{MAP}=\text{DBP}+0.33(\text{SBP}-\text{DBP})
• Hypertension: BP > 140/90\,\text{mmHg}
  • Primary (essential) ≈ 90 %; multifactorial
  • Secondary: renal, endocrine, etc.
  • Risks: LV hypertrophy, atherosclerosis, stroke, renal damage
• Determinants of MAP \text{MAP}=Q \times TPR (cardiac output × total peripheral resistance)
  • Short-term control: baroreceptors, SNS
  • Long-term: kidneys (blood volume)

Electrophysiology & Electrocardiography

• Conduction pathway: SA node → atrial myocardium → AV node (delay) → AV bundle → R/L bundle branches → Purkinje fibers
• ECG components
  • P wave: atrial depolarization
  • PR segment/interval: AV nodal delay & bundle conduction
  • QRS: ventricular depolarization (+ atrial repolarization)
  • ST segment: early ventricular repolarization (isoelectric)
  • T wave: ventricular repolarization
• Normal sinus rhythm 60–100 b·min$^{-1}$; bradycardia
• Diagnostic exercise testing: ST-segment depression ≥1 mm suggests myocardial ischemia

Coronary & Myocardial Pathologies

• MI = total/near-total coronary occlusion → ischemic necrosis
  • ECG: ST-T changes, peaked T, arrhythmias (PVCs, VT, VF)
  • Acute pericarditis → diffuse ST elevation
• Ventricular hypertrophy
  • LVH common in chronic HTN; may cause baseline ST changes, false-positive stress tests
• Sudden cardiac death (~1/200,000 youth athletes)
  • Children: congenital coronaries, cardiomyopathy, myocarditis
  • Adults: CAD, cardiomyopathy

Cardiac Output (Q̇)

• Definition: blood pumped per minute
  Q=HR \times SV
• Typical values (college-age)
  • Rest: ~5 L·min$^{-1}$ (trained & untrained)
  • Max untrained: 18–22 L·min$^{-1}$
  • Max trained male: ≈34 L·min$^{-1}$, female ≈24 L·min$^{-1}$
• Stroke volume determinants
  • End-diastolic volume (preload)
  • Afterload (MAP)
  • Contractility (SNS, EPI/NE)
• Frank–Starling: ↑ EDV → ↑ fiber length → ↑ SV
  • Venous return enhanced by venoconstriction (SNS), skeletal muscle pump, respiratory pump
• Sympathetic stimulation shifts SV-EDV curve upward (↑ contractility)

Regulation of Heart Rate

• Parasympathetic (vagus): ↓ HR via SA/AV inhibition (acetylcholine)
• Sympathetic (cardiac accelerator): ↑ HR & contractility via β$_1$ receptors
• Resting bradycardia in endurance athletes due to ↑ vagal tone
• HR increase at exercise onset
  • First phase: parasympathetic withdrawal to ~100 b·min$^{-1}$
  • Further rise: SNS activation
• Max HR estimation
  HR{max}=220-\text{age} or HR{max}=208-0.7\times\text{age}
• β-blockers: compete for β receptors → ↓ HR, contractility; used in CAD/HTN, alter exercise prescription
• Heart Rate Variability (HRV)
  • SD of R–R intervals; reflects sympathovagal balance
  • Low HRV predicts morbidity/mortality in CVD

Blood Composition & Hemodynamics

• Blood = plasma (ions, proteins, hormones) + cells (RBCs, WBCs, platelets)
• Hematocrit = % cells (≈42 %)
• Flow relationships
  • Flow \propto \dfrac{\Delta P}{R}
  • Resistance: R=\dfrac{\text{length}\times\text{viscosity}}{\text{radius}^4} (radius has greatest influence)
• MAP falls across systemic tree; largest drop across arterioles ("resistance vessels")
• Venous pressures influenced by gravity; skeletal muscle pump & valves prevent pooling

Oxygen Delivery & Fick Equation

• Muscular O$_2$ demand during exercise = 15–25× rest
• Achieved via ↑ Q̇ and blood redistribution
• a-vO$_2$ difference widens with intensity (↑ extraction)
• Fick:
  \dot V{O2}=Q \times (a!−!v\,O_2\,\text{difference})

Cardiovascular Responses to Dynamic Exercise

1. Cardiac Output
   • HR & Q̇ rise linearly to VO$_2$ max
   • SV: untrained plateau at 40–60 % VO$_2$ max; trained athletes continue to rise (no plateau)
2. Blood Pressure
   • SBP & MAP ↑ linearly; DBP ~constant
   • Rate-pressure product (double product): HR\times SBP reflects myocardial O$_2$ demand
3. Redistribution of Flow
   • Rest: 15–20 % Q̇ → muscle; max exercise: 80–85 %
   • Visceral organs constrict to 20–30 % of resting flow (SNS α-adrenergic)
   • Local vasodilation (autoregulation) via ↓O$2$, ↑CO$2$, H$^+$, K$^+$, adenosine, nitric oxide
4. Special cases
   • Arm exercise at same VO$_2$ → ↑ HR & BP vs. leg (less muscle mass, more SNS activation)
   • Resistance exercise: transient peaks up to 320/250 mmHg with Valsalva; SV ↓ concentric / ↑ eccentric; Q̇ may rise
   • Prolonged steady exercise: Q̇ maintained; SV ↓ (dehydration); HR drifts upward (cardiovascular drift)
   • Intermittent exercise recovery depends on fitness, environment, bout intensity/duration
5. Environmental & Emotional factors
   • Heat/humidity amplify HR, BP responses
   • Pre-exercise anxiety elevates resting but not peak HR/BP

Neural & Reflex Control

• Central Command: feed-forward drive from motor cortex → CV control center
• Peripheral feedback fine-tunes via:
  • Muscle mechanoreceptors (group III)
  • Metaboreceptors (group IV; K$^+$, lactate, H$^+$, ATP)
  • Baroreceptors (pressure)
  • Heart mechanoreceptors
• Exercise Pressor Reflex: afferents → medulla → ↑ SNS → ↑ HR, BP, vasoconstriction non-active tissues
  • Exaggerated in HF, HTN, PAD
• Functional Sympatholysis: local metabolites (NO, prostaglandins, adenosine, H$^+$, K$^+$) blunt SNS-mediated vasoconstriction in active muscles
  • Impaired in hypertension; restored by ARBs, nebivolol, training

Chronic Adaptations to Training

• Endurance (aerobic)
  • Eccentric LV hypertrophy (volume overload): chamber dilation, proportional wall thickening, ↑ myocyte length; no fibrosis/dysfunction; reversible
  • Mild RV dilation & bi-atrial enlargement; ↑ cardiomyocyte proliferation
• Resistance training
  • Concentric LV hypertrophy (pressure overload): ↑ wall thickness, little chamber dilation; ↑ myocyte width; reversible
• Hypertension pathologic remodeling
  • Concentric → eccentric hypertrophy → HFpEF / HFrEF depending on MI etc.

Substrate Use by Heart During Exercise

• At rest: 40–70 % ATP from fatty acids, 20–30 % glucose, 5–15 % lactate
• During intense exercise: ↑ circulating fatty acids (lipolysis), ↑ lactate uptake, ↓ blood glucose reliance

Beta-Blockers Beyond Cardiology

• Often misused by musicians/performing artists for anxiety control
• Risks if unsupervised: hypotension, bradycardia, reduced exercise capacity, fine-motor impairment

Sudden Cardiac Death & Screening

• Rare but catastrophic; pre-participation screening (history, physical, ECG) identifies high-risk individuals (coronary anomalies, HCM, arrhythmogenic syndromes)

Summary Diagram of Acute Exercise Responses

• ↑ Q̇ via ↑ HR & SV (Frank–Starling + SNS)
• Metabolic vasodilation in muscle ↔ SNS vasoconstriction in viscera (functional sympatholysis)
• Muscle pump & deeper breathing → ↑ venous return
• Central & reflex controls coordinate to maintain MAP and O$_2$ delivery