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chap 9

CHAPTER 9: Cardiorespiratory Responses to Acute Exercise

Overview

  • Cardiovascular responses to acute exercise

  • Respiratory responses to acute exercise

  • Recovery from acute exercise

Cardiovascular Responses to Acute Exercise

  • Key Functions:

    • Increases blood flow to working muscles

    • Involves alterations in heart function and peripheral circulatory adaptations:

    • Heart rate

    • Stroke volume

    • Cardiac output

    • Blood pressure

    • Blood flow

Resting Heart Rate (RHR)

  • Normal Ranges:

    • Untrained RHR: 60 to 80 beats/min

    • Trained RHR: as low as 30 to 40 beats/min

  • Factors Affecting RHR:

    • Neural tone, temperature, altitude

  • Anticipatory Response:

    • Heart rate increases above resting level just before the start of exercise due to:

    • Decreased vagal tone

    • Increased levels of norepinephrine and epinephrine

Heart Rate During Exercise
General Responses (1 of 2)

  • Heart rate is directly proportional to exercise intensity.

  • Maximal Heart Rate (HRmax):

    • Highest heart rate achieved during all-out effort to volitional fatigue

    • Highly reproducible

    • Slight decline with age

    • Estimated HRmax formula:

    • HR_{max} = 220 - ext{age in years}

    • For older adults, better estimates:

    • HR_{max} = 208 - (0.7 imes ext{age in years})

    • HR_{max} = 211 - (0.64 imes ext{age in years})

Steady-State Heart Rate (2 of 2)

  • Definition:

    • The point of plateau; optimal heart rate for meeting circulatory demands at a specific submaximal intensity.

    • Increases with exercise intensity, adjustments take 2 to 3 minutes.

    • Serves as the basis for simple exercise tests estimating aerobic fitness and HRmax.

Heart Rate Variability

  • Definition:

    • A measure of heart rate rhythmic fluctuations due to continuous changes in sympathetic and parasympathetic balance.

  • Influenced by:

    • Body core temperature

    • Sympathetic nerve activity

    • Respiratory rate

  • Analyzed through frequency (spectral analysis) rather than time.

Stroke Volume (SV)

  • Importance:

    • Major determinant of endurance capacity.

  • Determinants of SV:

    • Volume of venous blood returned to the heart

    • Ventricular distensibility

    • Ventricular contractility

    • Aortic or pulmonary artery pressure

  • Key Concepts:

    • Preload, afterload.

Stroke Volume Changes During Exercise

  • Stroke volume increases with intensity up to 40%-60% of V̇O_2max.

    • Plateau observed beyond this point, except in elite endurance athletes.

  • At maximal exercise, stroke volume is approximately double the standing stroke volume.

  • Standing vs. supine stroke volume:

    • Supine stroke volume is much higher than standing stroke volume, indicating differences in filling capabilities.

Influences on Stroke Volume

  • Factors that Increase Stroke Volume:

    • Increased preload leads to more end-diastolic ventricular stretch, leading to increased contraction strength (Frank-Starling mechanism).

    • Increased contractility, independent of end-diastolic volume, can be caused by increased norepinephrine or epinephrine.

    • Decreased afterload due to a reduction in aortic resistance.

Cardiac Output (Q̇) Responses

  • Formula:

    • Q̇ = HR imes SV

  • Cardiac output increases with exercise intensity, plateauing near V̇O_2max.

  • Normal Values:

    • Resting Q̇: ~5 L/min

    • Untrained Q̇max: ~20 L/min

    • Trained Q̇max: ~40 L/min

    • Q̇max is a function of body size and aerobic fitness.

Fick Principle

  • Definition:

    • Calculates tissue oxygen consumption based on blood flow and oxygen extraction:

    • V̇O2 = Q̇ imes (a-v)O2 ext{ difference}

    • Also expressed as: V̇O2 = HR imes SV imes (a-v)O2 ext{ difference}.

Blood Pressure Responses
Blood Pressure Changes During Exercise (1 of 2)

  • During endurance exercise, mean arterial pressure (MAP) increases:

    • Systolic blood pressure increases proportionally with exercise intensity.

    • Diastolic blood pressure exhibits slight decreases or slight increases at maximal exercise.

  • MAP Formula:

    • MAP = Q̇ imes TPR

    • Where Q̇ increases and TPR decreases slightly due to muscle vasodilation versus sympatholysis.

Blood Pressure Changes During Exercise (2 of 2)

  • Rate-pressure product defined as:

    • HR imes SBP

    • Related to myocardial oxygen uptake and myocardial blood flow.

  • Resistance exercises lead to periodic large increases in MAP, potentially up to 480/350 mmHg.

  • More common during the Valsalva maneuver.

Blood Flow Redistribution
General Mechanisms (1 of 2)

  • Increased cardiac output enhances available blood flow, redirecting it to areas with greater metabolic needs (exercising muscles).

    • Less active regions experience blood shunting via sympathetic vasoconstriction (e.g., splanchnic circulation including liver, stomach, pancreas, GI).

    • Kidneys are also affected in similar ways.

General Mechanisms (2 of 2)

  • Local vasodilation occurs, permitting additional blood flow in exercising muscles triggered by metabolic and endothelial products.

    • Sympathetic vasoconstriction in muscle is offset by sympatholysis, and local vasodilation is greater than neural vasoconstriction.

  • As body temperature rises, skin vasodilation occurs, mediated by:

    • Decreased sympathetic vasoconstriction and increased sympathetic vasodilation, promoting heat loss.

Cardiovascular Drift

  • Associated with increased core temperature and dehydration.

  • Notable effects include:

    • Decrease in stroke volume (SV)

    • Increase in skin blood flow

    • Decrease in plasma volume due to sweating, resulting in reduced venous return and preload.

  • Heart rate (HR) will increase to maintain cardiac output (Q̇) despite the decrease in stroke volume.

Competition for Blood Supply

  • Exercise demands for blood flow can create competition with other processes:

    • Exercise (muscles) and eating (splanchnic blood flow)

    • Exercise (muscles) and heat (skin)

  • Multiple demands can lead to decreased muscle blood flow overall.

Blood Oxygen Content

  • (a-v)O2 difference (mL O2/100 mL blood):

    • Calculated as arterial O2 content minus mixed venous O2 content.

  • Resting levels are approximately ~6 mL O2/100 mL blood, increasing to ~16-17 mL O2/100 mL blood during maximal exercise.

  • Enhanced venous oxygen levels during exercise occur due to arterial blood differences becoming pronounced.

Plasma Volume Responses

  • Influenced by capillary fluid movement related to hydrostatic pressure and oncotic/osmotic pressures.

  • Exercise in an upright position typically leads to a decrease in plasma volume, which may impair exercise performance.

  • Increased MAP raises capillary hydrostatic pressure, and metabolite buildup raises tissue osmotic pressure, compounded by sweating which further reduces plasma volume.

Hemoconcentration Effects

  • Decreased plasma volume leads to hemoconcentration, with fluid percentage of blood declining and cell percentage of blood increasing.

  • As a result:

    • Hematocrit may increase up to 50%.

  • Net Effects:

    • Increased red blood cell concentration

    • Increased hemoglobin concentration

    • Enhanced oxygen-carrying capacity of the blood.

Integrated Exercise Response

  • Cardiovascular responses to exercise are complex, rapid, and finely tuned.

  • The primary priority is maintaining stable blood pressure.

  • Blood flow can only be sustained if BP is stable; maintaining blood pressure takes precedence over other physiological needs such as exercise or thermoregulation.

Central Regulation

  • Stimulation of Rapid Changes:

    • Changes in heart rate, cardiac output, and blood pressure can occur immediately with exercise initiation.

    • These changes precede the buildup of metabolites in muscles, with heart rate increasing within 1 second post-exercise onset.

  • Central Command:

    • Involves higher brain centers activating both motor and cardiovascular control centers simultaneously.

Respiratory Responses to Acute Exercise

Ventilation Changes During Exercise (1 of 2)

  • Immediate increase in ventilation before muscle contractions occurs as an anticipatory response from central command.

  • Gradual second phase of increased ventilation is driven by chemical alterations in arterial blood (e.g., increased CO2, H+), monitored by chemoreceptors.

Ventilation Changes During Exercise (2 of 2)

  • Ventilation increases in proportion to muscular metabolic needs:

    • At low intensities: Only tidal volume increases.

    • At high intensities: Both tidal volume and respiratory rate increase significantly.

  • Recovery of ventilation post-exercise is delayed, potentially taking several minutes, governed by blood pH, PCO2, and temperature.

Breathing Irregularities
Exercise-Induced Asthma (1 of 3)

  • Symptoms:

    • Lower airway obstruction

    • Coughing, wheezing, dyspnea

  • Characterized by greater water evaporating from the airway surface and injury to microvasculature.

Dyspnea and Hyperventilation (2 of 3)

  • Dyspnea:

    • Common among those with poor aerobic fitness, related to difficulty adjusting to high blood PCO2, H+.

  • Hyperventilation:

    • Can be caused by anticipation or anxiety prior to exercise leading to increased PCO2 gradient between blood and alveoli, causing decreased blood PCO2, increased blood pH, and decreased drive to breathe.

Valsalva Maneuver (3 of 3)

  • A potentially dangerous practice, often accompanying particular exercises.

  • Characterized by:

    • Glottis closure leading to increased intra-abdominal and intrathoracic pressure;

    • Results in collapse of large veins due to elevated pressure, causing decreased venous return and consequently lowered cardiac output and arterial blood pressure.

Ventilation and Energy Metabolism

  • Matching Metabolic Needs:

    • The ventilatory equivalent for O2 can be expressed as:

    • V̇E/V̇O_2 (L air breathed per L O2 consumed per minute), used to index the efficiency of breathing control to the body’s oxygen demand.

  • Ventilatory Threshold:

    • The point where the Volume of air breathed exceeds that of oxygen consumed, this is associated with both the lactate threshold and increased PCO2 levels.

Estimating Lactate Threshold

  • The ventilatory threshold is used as a surrogate measure to estimate lactate threshold.

  • Associated with excess lactic acid and sodium bicarbonate, leading to the accumulation of lactic acid and CO2.

  • Monitoring both V̇E/V̇O2 and V̇E/V̇CO2 refines the estimation of lactate threshold.

Limitations on Performance

  • Typically, ventilation does not pose limiting factors as respiratory muscles account for 10% of V̇O_2 and 15% of Q̇ during heavy exercise, and they are highly fatigue-resistant.

  • Airway resistance and gas diffusion are usually not limiting factors under sea-level conditions.

  • Exceptions may arise for:

    • Individuals with restrictive or obstructive lung disorders, especially elite endurance athletes at high intensities (known as exercise-induced arterial hypoxemia, EIAH).

Acid–Base Balance
Acid-Base Regulation (1 of 2)

  • Metabolic processes result in H+ accumulation which lowers pH.

  • The normal range pH is slightly alkaline at rest (7.1 to 7.4), high pH indicates alkalosis.

  • During exercise, the body becomes slightly acidic (6.6 to 6.9); significantly lowered pH indicates acidosis.

Acid-Base Regulation (2 of 2)

  • The body's physiological mechanisms to control pH include:

    • Chemical Buffers: Bicarbonate, phosphates, proteins, hemoglobin.

    • Increased ventilation induces H+ binding to bicarbonate.

    • Kidneys are involved in eliminating H+ from buffers and excreting excess H+.

  • Active recovery can facilitate quicker pH recovery:

    • Passive Recovery: Typically lasts 60 to 120 minutes.

    • Active Recovery: Lasts around 30 to 60 minutes.

Summary of Buffering Capacity

  • Table 9.2: Buffering Capacity of Blood Components

    • Buffers such as bicarbonate, hemoglobin, proteins, and phosphates have their respective percentages of total buffering capacity outlined.

Cardiovascular Recovery Variables

  • Post Exercise Hypotension:

    • Aerobic Exercise: Driven by peripheral vasodilation and can last for several hours; histamine plays an essential mediatory role.

    • Resistance Exercise: Driven by decreased cardiac output post-exercise.

Conclusion

  • The integration of cardiovascular and respiratory responses during acute exercise is crucial for optimizing performance and recovering efficiently from physical demands.