4.3 Cardiac output, stroke volume, and heart rate during exercise

Cardiac output, stroke volume, and heart rate are crucial factors in understanding how our hearts respond to exercise. These parameters work together to meet the increased oxygen demands of our muscles during physical activity.

As we exercise, our bodies undergo remarkable changes. Our hearts pump more blood, our stroke volume increases, and our heart rates climb. These adaptations allow us to perform physical tasks more efficiently and improve our overall cardiovascular fitness.

Cardiac Output Components and Exercise

Defining Key Cardiovascular Parameters

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• Cardiac output measures blood volume pumped by heart per minute (L/min)
• Stroke volume represents blood ejected from left ventricle during one contraction (mL)
• Heart rate counts heart beats per minute (bpm)
• Cardiac output calculation uses formula $CO = SV × HR$
• Exercise increases cardiac output to meet elevated oxygen demands of working muscles
• Relationship between cardiac output, stroke volume, and heart rate changes dynamically based on exercise intensity and duration

Exercise-Induced Cardiovascular Changes

• Sympathetic nervous system activation boosts heart rate and myocardial contractility
• Enhanced venous return from muscle pump action and respiratory pump increases preload
• Increased preload leads to higher stroke volume through Frank-Starling mechanism
• Reduced parasympathetic activity decreases heart inhibition, allowing increased heart rate
• Elevated blood volume and improved ventricular filling during diastole enhance stroke volume
• Catecholamine release (epinephrine, norepinephrine) further augments cardiac contractility and heart rate
• Peripheral vasodilation in working muscles reduces afterload, facilitating greater stroke volume

Cardiac Output Regulation During Exercise

Nervous System and Hormonal Influence

• Sympathetic nervous system activation increases heart rate and myocardial contractility
  • Sympathetic nerves release norepinephrine at sinoatrial node
  • Norepinephrine binds to beta-1 adrenergic receptors, increasing heart rate
• Decreased parasympathetic activity reduces inhibitory effects on heart
  • Vagus nerve activity decreases, reducing acetylcholine release
  • Reduced acetylcholine leads to faster depolarization of sinoatrial node
• Catecholamine release augments cardiac function
  • Epinephrine and norepinephrine secreted by adrenal medulla
  • Catecholamines increase heart rate and myocardial contractility
  • Also cause peripheral vasoconstriction in non-exercising tissues

Mechanical Factors Affecting Cardiac Output

• Enhanced venous return increases preload
  • Muscle pump action squeezes veins, propelling blood back to heart
  • Respiratory pump creates negative intrathoracic pressure, facilitating venous return
• Increased preload leads to greater stroke volume via Frank-Starling mechanism
  • Greater ventricular filling stretches cardiac muscle fibers
  • Stretched fibers generate more force during contraction
• Peripheral vasodilation in working muscles reduces afterload
  • Local metabolites cause vasodilation in active muscles
  • Reduced resistance allows for easier ejection of blood from ventricles
• Improved ventricular filling during diastole enhances stroke volume
  • Longer diastolic filling time at lower intensities allows for greater ventricular filling
  • Enhanced ventricular compliance in trained individuals improves filling capacity

Stroke Volume and Heart Rate Changes

Stroke Volume Response to Exercise

• Stroke volume increases rapidly at exercise onset
  • Initial increase due to enhanced venous return and sympathetic activation
  • Plateaus at moderate intensities (40-60% of maximal oxygen uptake)
• Trained individuals exhibit higher stroke volumes
  • Enlarged heart chambers and improved myocardial contractility
  • Greater blood volume and enhanced venous return
• Stroke volume may slightly decrease at very high intensities
  • Reduced ventricular filling time due to extremely high heart rates
  • Potential limitation in highly trained athletes during maximal exercise

Heart Rate Dynamics During Exercise

• Heart rate increases linearly with exercise intensity
  • Rises from resting levels to maximal exertion
  • Rapid initial increase followed by steady climb
• Trained individuals typically have lower resting heart rates
  • Enhanced parasympathetic tone at rest
  • Greater stroke volume allows for lower heart rate at given cardiac output
• Heart rate reserve (HRR) concept used in exercise prescription
  • HRR = Maximum heart rate - Resting heart rate
  • Allows for individualized exercise intensity recommendations
• Cardiovascular drift observed during prolonged exercise
  • Gradual increase in heart rate over time at constant workload
  • Compensates for slight decrease in stroke volume due to dehydration and increased core temperature

Limits on Cardiac Output at Maximal Exercise

Physiological Constraints on Heart Function

• Maximal heart rate primarily limited by genetics and age
  • General formula: Maximum heart rate = 220 - age (individual variation exists)
  • Sympathetic stimulation reaches maximum effect
• Diastolic filling time becomes limiting factor at very high heart rates
  • Shortened diastole reduces ventricular filling
  • May lead to decreased stroke volume at maximal intensities
• Ventricular compliance and contractility limitations
  • Untrained individuals may reach limits of myocardial adaptability
  • Cardiovascular disease can impair ventricular function

External Factors Affecting Cardiac Output

• Dehydration and hyperthermia reduce plasma volume
  • Decreased blood volume leads to reduced venous return
  • Negatively impacts stroke volume and overall cardiac output
• Pulmonary diffusion capacity indirectly limits cardiac output
  • Oxygen uptake in lungs may not keep pace with increased blood flow
  • Can lead to arterial desaturation in some highly trained athletes
• Blood oxygen-carrying capacity affects tissue oxygen delivery
  • Hemoglobin concentration and oxygen saturation influence oxygen transport
  • Anemia or other blood disorders can limit oxygen delivery despite high cardiac output
• Skeletal muscle oxygen extraction capacity
  • In some elite athletes, cardiac output may exceed muscle's ability to utilize oxygen
  • Peripheral limitations become primary constraint on performance