Cardiovascular System: Functions, Physiology, and Exercise Adaptations

Functions of the cardiovascular system

Delivers oxygen and nutrients to tissues; removes CO₂ and metabolic waste; transports hormones; regulates temperature and pH; supports immune function; and must increase oxygen delivery up to 25× during exercise.

Heart's unique physiology

Cardiac muscle is highly aerobic with dense mitochondria, branched fibers, and intercalated discs (desmosomes + gap junctions) that allow coordinated contractions without fatigue.

Reason cardiac muscle has many mitochondria

The heart must beat continuously without rest, so it relies entirely on aerobic metabolism and needs abundant ATP.

Intercalated discs

Specialized junctions containing desmosomes (structural anchoring) and gap junctions (electrical continuity) enabling the heart to contract as a syncytium.

Functional syncytium

The property of cardiac muscle that allows all fibers to contract together due to gap junctions transmitting electrical impulses rapidly from cell to cell.

Intrinsic cardiac conduction system

SA node → AV node → Bundle of His → Bundle branches → Purkinje fibers, allowing coordinated electrical and mechanical activity.

Intrinsic firing rates

SA node 60-100 bpm, AV node 40-60 bpm, Purkinje fibers 20-40 bpm ensuring the heart can beat independently even without nervous input.

Why the SA node controls HR

It has the fastest spontaneous depolarization rate, making it the natural pacemaker.

Parasympathetic control of HR

Vagus nerve (CN X) releases ACh to hyperpolarize the SA and AV nodes, reducing HR; dominant at rest.

Vagal tone

The parasympathetic influence that keeps resting HR lower than the SA node's intrinsic rate.

Sympathetic control of HR

Norepinephrine increases SA node firing, increases contractility, and speeds conduction, raising HR during exercise.

Why HR rises instantly at exercise onset

Central Command immediately withdraws vagal tone before movement begins, allowing HR to jump within 1 second.

Cardiac cycle

Systole (contraction/ejection) and diastole (relaxation/filling); at rest, diastole is about ⅔ of the cycle for optimal filling.

Why diastole is longer at rest

Ventricles need more time for adequate filling to maintain stroke volume.

Effect of increased HR on diastole

As HR rises, diastole shortens significantly, limiting filling and contributing to SV plateau during exercise.

Arteries vs arterioles vs capillaries

Arteries carry blood away; arterioles regulate resistance and distribution; capillaries allow gas/nutrient exchange due to thin walls.

Importance of arterioles in exercise

They control blood distribution by vasodilation of active muscles and vasoconstriction of inactive areas under metabolic + sympathetic control.

Veins and venous valves

Veins store ~64% of blood volume; valves prevent backflow and allow the muscle pump to assist venous return.

Plasma volume changes with exercise

Plasma decreases acutely due to sweating but increases chronically with training, improving stroke volume and thermoregulation.

Hematocrit definition

Percentage of blood volume composed of RBCs, WBCs, and platelets.

Function of RBCs

Carry hemoglobin which binds oxygen (4 O₂ per hemoglobin); each RBC carries about 1 billion O₂ molecules.

Polycythemia

Excess RBCs increasing viscosity and clot risk.

Anemia

Low RBC count reducing oxygen-carrying capacity and causing fatigue.

Blood distribution at rest

Liver 27%, kidneys 22%, muscle 15%, and veins store 64% of total blood volume.

Blood distribution during exercise

Up to 80% of cardiac output directed to muscle; GI and kidney blood flow decrease; skin blood flow increases for cooling.

Local metabolic vasodilation

Active muscle releases H+, CO₂, K+, adenosine, and nitric oxide to cause vasodilation and overcome sympathetic vasoconstriction.

Stroke volume (SV)

SV = EDV - ESV; determined by preload (filling), afterload (resistance), and contractility.

Preload (EDV)

The volume of blood in the ventricle before contraction; increased by venous return and Frank-Starling mechanism.

Afterload

The resistance the left ventricle must overcome to eject blood; mainly influenced by arterial pressure.

Contractility

Strength of ventricular contraction; increases with sympathetic stimulation (via Ca²⁺).

Frank-Starling mechanism

Increased EDV stretches myocardial fibers, increasing cross-bridge formation and enhancing contractile force, increasing SV.

Venous return mechanisms

Muscle pump, respiratory pump, and venous valves move blood back to the heart.

Cardiac output (Q)

Q = HR × SV; increases with exercise and is the major determinant of VO₂max.

Why stroke volume plateaus at 40-60% VO₂max

Diastolic filling time decreases due to high HR, limiting further increases in EDV.

Endurance athletes and SV plateau

Highly trained athletes often don't plateau due to larger, more compliant ventricles and greater blood volume.

Blood pressure during dynamic exercise

SBP increases due to increased contractility and Q; DBP stays the same or decreases due to vasodilation.

Blood pressure during resistance exercise

BP can spike extremely high due to the Valsalva maneuver and increased intrathoracic pressure.

MAP formula and limitation

MAP = DBP + ⅓(SBP - DBP); accurate only at rest because exercise shortens diastole.

Cardiovascular drift

During prolonged exercise, plasma volume decreases → SV drops → HR rises to maintain Q.

a-vO₂ difference

Amount of oxygen extracted by tissues; increases from 4-5 mL at rest to 15-18 mL at maximal exercise.

Central Command Theory

The brain anticipates exercise by withdrawing vagal tone and increasing sympathetic activity, adjusting HR, BP, and blood distribution.

Vascular remodeling with training

Chronic training increases arterial diameter, collateral circulation, nitric oxide availability, and vascular compliance, reducing resistance.

Resting HR with training

Decreases due to increased vagal tone and increased stroke volume.

Submax HR with training

Decreases because the heart becomes more efficient and muscles extract more oxygen.

Max HR with training

Unchanged because it is age-determined.

Stroke volume changes with training

Increases at rest, submax, and maximal exercise due to larger LV, increased plasma volume, and improved contractility.

Cardiac output changes with training

Rest and submax unchanged; maximal Q increases due to higher maximal SV.

Capillary density adaptation

Increases with training to enhance gas exchange, reduce diffusion distance, and improve endurance.

Blood pressure changes with training

Resting and submax BP decrease due to improved vascular function and lower peripheral resistance.

Purpose of warm-up

Increases tissue temperature, HR, and blood flow; enhances nerve conduction; prepares muscles for exercise.

Purpose of warm-down

Maintains muscle pump to prevent blood pooling, assists venous return, and helps remove metabolic waste.

Varicose veins

Occur when venous valves fail, causing blood pooling and vessel distention; worsened by static exercise.

Function of the respiratory system

Bring in oxygen, remove carbon dioxide, and regulate pH.

Conducting zone

Airway passages that warm, filter, and humidify air but do not engage in gas exchange.

Respiratory zone

Alveoli and capillaries where gas exchange occurs; has a huge surface area and extremely thin membrane.

Inspiration mechanics

Active process using the diaphragm and external intercostals to expand the thoracic cavity and decrease pressure.

Expiration mechanics

Passive at rest but active during exercise using abdominal and internal intercostal muscles.

Diffusion requirements

Adequate air supply, blood supply, and pressure gradient across the respiratory membrane.

Fick's Law of Diffusion

Gas diffusion depends on surface area, membrane thickness, diffusion constant, and pressure gradient.

Partial pressure of oxygen at sea level

PO₂ = 159 mmHg (drives oxygen diffusion into blood).

Oxygen transport

98% bound to hemoglobin and 2% dissolved in plasma.

Carbon dioxide transport

70% bicarbonate, 20% bound to hemoglobin, 10% dissolved.

Oxyhemoglobin dissociation curve

Graph showing hemoglobin's affinity for oxygen under different conditions.

Bohr Effect

A rightward shift caused by increased temperature, CO₂, and H+ that reduces hemoglobin's affinity for O₂, enhancing unloading to muscles.

Ventilation during exercise

Increases in rate and depth to supply oxygen, remove CO₂, and maintain pH.

Ventilatory threshold

Point where ventilation increases disproportionately to VO₂ due to lactate buffering (H⁺ + HCO₃⁻ → CO₂).

Dyspnea

Shortness of breath caused by inability to regulate CO₂ and H+ or weak/overworked respiratory muscles.

Hyperventilation

Excessive ventilation that reduces CO₂, causing dizziness and increasing breath-hold time.

Breath holding physiology

Rising CO₂—not lack of O₂—stimulates the urge to breathe; hyperventilation lowers CO₂ and can cause blackout.

Stitch in the side

Likely caused by diaphragm ischemia, ligament stretching, or shallow breathing during exercise.

Tidal volume

Normal breathing volume (~400-600 mL); increases with exercise.

Vital capacity

Maximal air exhaled after maximal inhalation (higher in men).

Residual volume

Air remaining in lungs after maximal exhalation, preventing collapse.

Minute ventilation (VE)

Breathing rate × tidal volume; increases dramatically with exercise.

MET definition

1 MET = 3.5 mL O₂/kg/min, representing resting oxygen consumption.

Altitude primary issue

Reduced barometric pressure lowers PO₂, reducing oxygen diffusion into blood.

Acute altitude responses

Increased ventilation, increased HR, decreased stroke volume, increased catecholamines, reduced VO₂max.

Chronic altitude adaptations

Increased EPO, RBCs, hemoglobin, capillaries, mitochondria, and 2,3-DPG production; improved buffering.

Lactate paradox

Despite lower VO₂max at altitude, lactate levels decrease after acclimatization due to reduced sympathetic drive and glycolysis.

Training at altitude

HR zones become inaccurate because rest HR ↑ 10% and max HR ↓ 10%, requiring reduced intensity and longer recovery.

Best altitude strategy

Live high, train low (2000-2500 m for 4+ weeks) to increase RBC mass while maintaining training intensity.

Competition timing after altitude

Best performance occurs within 3 weeks after returning to sea level.