Cardio-Respiratory and Metabolic Adjustments During Exercise

Introduction

I. CARDIOVASCULAR ADJUSTMENTS

1. Cardiac Output

• At rest: ~5.5 L/min; rises to 23 L/min in an untrained young man and up to 30-40 L/min in trained athletes during maximal exercise - a 4-6 fold increase.
• Increased cardiac output results more from increased heart rate (~3x resting) than increased stroke volume (~1.5x resting).

2. Heart Rate

• Rises from ~72 bpm at rest to 180-200 bpm during maximal exercise.
• Mediated initially by withdrawal of vagal tone and later by sympathetic activation and catecholamine release.

3. Stroke Volume

• Increases due to:
  • Frank-Starling mechanism - skeletal muscle pump enhances venous return → increased end-diastolic volume → greater stroke volume
  • Increased myocardial contractility from sympathetic stimulation and catecholamines

4. Blood Pressure

• Systolic BP rises ~30% (from ~120 to ~160-180 mmHg)
• Diastolic BP stays nearly constant or may fall slightly
• This 30% increase in pressure further augments muscle blood flow by more than doubling it.

5. Redistribution of Blood Flow

• During maximal exercise, muscle blood flow increases ~25-fold (from 3.6 to ~90 mL/100g/min).
• Blood is redistributed away from splanchnic, renal, and cutaneous circulations (via baroreceptor-mediated vasoconstriction) toward active skeletal muscles.
• Local vasodilation in active muscle is driven by metabolic byproducts: low O₂, low pH, elevated CO₂, K⁺, lactic acid, and adenosine.

6. Two Mechanisms Triggering CV Response (Early vs. Late)

II. RESPIRATORY ADJUSTMENTS

1. Minute Ventilation

• Increases from ~7.5 L/min at rest to 100-120 L/min during maximal exercise - a ~15-20 fold increase.
• Achieved by increases in both tidal volume and respiratory rate.

2. Three Phases of Ventilatory Response

1. Abrupt initial rise at the onset of exercise - due to neural signals from motor cortex (central command) and proprioceptors in muscles, tendons, and joints.
2. Gradual rise during moderate exercise - humoral factors; interestingly, arterial PO₂, PCO₂, and pH remain normal - the exact mechanism is debated.
3. Steep rise during vigorous exercise - lactic acidosis causes buffering that releases extra CO₂, further stimulating ventilation (carotid body-mediated response).

3. Ventilatory Threshold (Anaerobic Threshold)

• When exercise intensity exceeds ~50-60% VO₂max, anaerobic glycolysis produces lactic acid.
• This is buffered by bicarbonate: H⁺ + HCO₃⁻ → H₂O + CO₂
• The extra CO₂ produced causes a disproportionate rise in ventilation - this is the ventilatory threshold.
• Below the threshold: isocapnic buffering (alveolar PCO₂ stays constant).
• Above the threshold: alveolar PCO₂ falls as respiratory compensation for metabolic acidosis occurs.

4. Arterial Blood Gas Changes

• Moderate exercise: PaO₂, PaCO₂, and pH remain essentially normal (ventilation matches metabolic needs perfectly).
• Strenuous exercise: arterial pH falls (metabolic acidosis from lactic acid accumulation).

5. Ventilation/Perfusion (V/Q) Matching

• At rest, upper lung zones are under-perfused.
• During exercise, increased pulmonary blood flow leads to more uniform V/Q distribution throughout the lung, improving gas exchange efficiency.

6. Oxygen-Hemoglobin Dissociation Curve

• Shifts to the right (Bohr effect) due to:
  • Increased temperature
  • Increased CO₂
  • Decreased pH (lactic acidosis)
• This decreases Hb affinity for O₂ → facilitates O₂ unloading to muscles.

7. Oxygen Diffusing Capacity

• Increases significantly during exercise due to increased pulmonary blood flow and recruitment of previously underperfused alveolar-capillary units.
• Untrained: diffusing capacity increases ~3-fold; trained athletes: up to ~3.4-fold.

III. METABOLIC ADJUSTMENTS

1. Energy Sources Used in Sequence

• Skeletal muscle converts only ~25% of chemical energy into mechanical work; the remainder is released as heat.
• Both muscle glycogen and liver glycogen (released as blood glucose) serve as carbohydrate sources.

2. Oxygen Consumption (VO₂)

• Rises linearly with work output: from 250 mL/min at rest to 4000 mL/min in a trained athlete.
• VO₂max is the maximum oxygen consumption under maximal aerobic effort - the best single indicator of cardiorespiratory fitness.
• VO₂max in trained marathoners is ~45% greater than in untrained individuals.

3. Oxygen Debt (Excess Post-Exercise Oxygen Consumption - EPOC)

• After exercise, O₂ consumption remains elevated above basal for up to 90 minutes.
• Stimulus is elevated arterial H⁺ from lactic acidemia (not elevated CO₂ or low PO₂).
• Used to: replenish ATP and creatine phosphate, convert lactate back to glycogen in the liver (Cori cycle), restore body temperature and O₂ stores in blood.

4. Hormonal Metabolic Changes

• Catecholamines (adrenaline, noradrenaline) increase glycogenolysis, lipolysis, and gluconeogenesis.
• Glucagon increases; insulin decreases - promotes glucose release from the liver.
• Cortisol rises during prolonged exercise - promotes gluconeogenesis and fat mobilization.

Summary Table