Cardiorespiratory Changes During Isotonic Exercise

CARDIOVASCULAR CHANGES

1. Heart Rate (HR)

• Increases promptly at onset of exercise - even before metabolic changes occur
• Initial rise is largely due to decreased vagal (parasympathetic) tone; later, increased sympathetic discharge contributes
• Maximal HR: up to 200+ beats/min in children, rarely exceeds 195 beats/min in adults, and is lower in the elderly
• Trained athletes have a lower resting and exercise HR for any given workload due to larger stroke volume

2. Stroke Volume (SV)

• Markedly increased - this is the key feature distinguishing isotonic from isometric exercise
• Increased by:
  • Enhanced myocardial contractility via sympathetic (β₁) stimulation
  • Greater venous return (Frank-Starling mechanism)
  • Venoconstriction (noradrenergic) reducing venous pooling
• Represented by an increased pulse pressure (Costanzo)

3. Cardiac Output (CO)

• CO = HR × SV; both components increase, driving CO to very high levels
• Can exceed 35 L/min during strenuous isotonic exercise (resting ~5 L/min)
• Increase is directly proportional to the rise in O₂ consumption
• In trained athletes, maximal CO is higher; VO₂max averages ~38 mL/kg/min in active men, ~29 mL/kg/min in active women
• Ganong's Review of Medical Physiology, 26th Ed.

4. Blood Pressure

• Systolic BP rises moderately (increased CO)
• Diastolic BP remains unchanged or falls - due to net fall in total peripheral resistance from vasodilation in exercising muscle
• This contrasts with isometric exercise where both systolic AND diastolic BP rise sharply
• After exercise, BP may transiently drop below baseline as residual metabolites keep muscle vessels dilated

5. Total Peripheral Resistance (TPR)

• Net fall in TPR - this is the hallmark of isotonic exercise
• Results from massive vasodilation in actively contracting skeletal muscle
• Locally mediated by: ↓tissue PO₂, ↑tissue PCO₂, accumulation of K⁺ and other vasodilator metabolites, local temperature rise
• 10- to 100-fold increase in the number of open capillaries in exercising muscle

6. Blood Flow Redistribution

• Skin, splanchnic regions, kidneys, and inactive muscles (α₁ receptors → ↑resistance, ↓flow)

• Exercising skeletal muscle (local metabolic override of sympathetic tone)
• Coronary circulation (↑O₂ demand)
• Cerebral circulation (maintained throughout)
• Skin (late - biphasic response: initial vasoconstriction, then vasodilation for heat dissipation as body temperature rises)

7. Venous Return

• Greatly increased, enabling the rise in cardiac output
• Mechanisms:
  • Muscle pump - rhythmic skeletal muscle contractions squeeze veins
  • Thoracic (respiratory) pump - increased breathing depth creates greater negative intrathoracic pressure
  • Mobilization of blood from splanchnic reservoirs (increases arterial blood volume by ~30%)
  • Noradrenergic venoconstriction reduces venous capacitance
• Ganong's Review of Medical Physiology, 26th Ed.

RESPIRATORY CHANGES

1. Ventilation (Minute Ventilation, V̇E)

• Increases dramatically and nearly linearly with O₂ consumption (and CO₂ production) during moderate exercise
• Can rise from a resting ~6 L/min to >100 L/min during heavy exercise
• Two phases:
  • Immediate (neurogenic) phase: rapid increase at the very onset of exercise - before any blood gas changes - driven by central command from the cerebral motor cortex and signals from muscle mechanoreceptors
  • Chemical phase (30-40 seconds in): CO₂ released from active muscles matches the increased ventilation, and arterial PCO₂ returns to normal

2. Arterial Blood Gases

• PaO₂: remains essentially normal during moderate isotonic exercise
• PaCO₂: initially falls slightly (over-ventilation from central command), then returns to ~40 mmHg as CO₂ output from muscles rises to match ventilation
• pH: maintained near normal during moderate exercise; falls (lactic acidosis) during severe exercise beyond the anaerobic threshold
• Key point: arterial blood gases do NOT change significantly during moderate exercise, confirming that the primary driver is neurogenic, not chemical

3. Mechanism of Ventilatory Control During Exercise

• Central command: cerebral motor cortex sends parallel signals to muscles AND to the brain stem respiratory center - explains the "anticipatory" increase in ventilation
• Proprioceptive input: muscle and joint mechanoreceptors send afferent signals to the respiratory center
• Chemical fine-tuning: peripheral chemoreceptors (for PO₂, PCO₂, H⁺) make final adjustments
• The neurogenic shift of the PCO₂-ventilation response curve is ~20-fold upward during heavy exercise, keeping arterial PCO₂ near 40 mmHg throughout
• This neurogenic response is partly learned - cerebral cortex involvement allows progressive adaptation with training

4. Oxygen Consumption (VO₂)

• Rises in proportion to exercise intensity
• Skeletal muscle O₂ extraction increases (widened arteriovenous O₂ difference)
• VO₂max represents the ceiling and is the product of maximal CO × maximal tissue O₂ extraction - both increase with training

KEY COMPARISON: Isotonic vs. Isometric Exercise

• Ganong's Review of Medical Physiology, 26th Ed. - "Circulatory Changes during Exercise"
• Guyton and Hall Textbook of Medical Physiology - "Regulation of Respiration During Exercise"
• Costanzo Physiology, 7th Ed. - "Central Command" and "Overall Responses to Exercise"