exam 4
CHAPTER 9: Cardiorespiratory Responses to Acute Exercise
Overview
Key Areas Discussed:
Cardiovascular responses to acute exercise
Respiratory responses to acute exercise
Recovery from acute exercise
Cardiovascular Responses to Acute Exercise
Overall Adjustments:
Increases blood flow to working muscles
Involves altered heart function and peripheral circulatory adaptations
Key Factors in Cardiovascular Responses
Heart Rate
Stroke Volume
Cardiac Output
Blood Pressure
Blood Flow
Cardiovascular Responses: Resting Heart Rate (RHR)
Normal Ranges:
Untrained individuals: 60 to 80 beats/min
Trained individuals: as low as 30 to 40 beats/min
Influencing Factors:
Neural tone
Temperature
Altitude
Anticipatory Response:
Heart Rate (HR) increases above RHR just before the start of exercise
Vagal tone decreases
Norepinephrine and epinephrine levels increase
Cardiovascular Responses: Heart Rate During Exercise
Heart Rate Variability
Definition: Measure of HR rhythmic fluctuation due to continuous changes in sympathetic and parasympathetic balance
Influences on HRV:
Body core temperature
Sympathetic nerve activity
Respiratory rate
Heart Rate Characteristics
Maximal HR:
Highest HR in an all-out effort to volitional fatigue
Highly reproducible with slight decline with age
Estimation Formula:
$HR_{max} = 220 - ext{age in years}$
For older adults, alternative estimates include:
$HR_{max} = 208 - (0.7 imes ext{age in years})$
$HR_{max} = 211 - (0.64 imes ext{age in years})$
Steady-state Heart Rate:
Point where HR plateaus to meet circulatory demands at a given submaximal intensity
Takes 2 to 3 minutes to adjust to a new intensity
Cardiovascular Responses: Stroke Volume (SV)
Importance: Major determinant of endurance capacity
Determinants of SV:
Volume of venous return to the heart
Ventricular distensibility (ability of the ventricles to stretch)
Ventricular contractility
Aortic or pulmonary artery pressure
Key Concepts:
Preload: End-diastolic ventricular stretch
Afterload: Resistance the ventricle must overcome to eject blood
SV Response to Intensity:
Increases from rest to 40%-60% V_{O2max}, plateau beyond this intensity
Maximally, exercise SV is approximately double that at rest
Stroke Volume Changes During Exercise
Influencing Factors:
Increase in venous return leads to increased preload
Muscle and respiratory pumps enhance venous return
HR increase can reduce filling time, potentially causing a slight decrease in EDV and SV
Increased contractility at higher intensities leads to increased SV
Decreased afterload due to vasodilation supports increased SV
Cardiovascular Responses: Cardiac Output (Q)
Formula:
Q = HR imes SV
Changes with Intensity:
Increases with intensity until it reaches a plateau near V_{O2max}
Normal Values:
Resting Q ~ 5 L/min
Untrained Qmax ~ 20 L/min
Trained Qmax ~ 40 L/min
Fick Principle
Definition:
Calculation of tissue O2 consumption depending on blood flow and O2 extraction
Formula:
V{O2} = Q imes (a-v)O{2} ext{ difference}
V{O2} = HR imes SV imes (a-v)O{2} ext{ difference}
Cardiovascular Responses: Blood Pressure
Overview:
Increase in mean arterial pressure (MAP) during endurance exercise
Characteristics:
Systolic BP increases proportionally with exercise intensity
Diastolic BP may decrease or slightly increase at maximum exercise
Key Relationships:
MAP = Q imes ext{TPR}
Cardiac output increases while total peripheral resistance decreases slightly due to muscle vasodilation
Blood Flow Redistribution
Mechanisms:
Cardiac output increases blood flow distributed toward exercising muscles
Blood is redirected away from less active regions
Sympathetic Vasoconstriction:
Occurs in splanchnic (liver, stomach, pancreas, GI) and renal circulation
Local Vasodilation:
Triggered to allow more blood flow to exercising muscle
Heat Response:
As body temperature rises, additional vasodilation occurs in skin to facilitate heat loss
Cardiovascular Responses: Hemoconcentration
Definition:
Reduction in plasma volume leading to an increase in the concentration of red blood cells (hematocrit)
Net Effects:
Increased red blood cell concentration
Increased hemoglobin concentration
Enhanced O2-carrying capacity
Cardiovascular Responses: Central Regulation
Key Stimulus for Rapid Changes:
Increases in HR, Q, and blood pressure during exercise precede metabolite buildup
HR begins to increase within 1 second of exercise onset
Mechanism:
Driven by "central command," involving higher brain centers and coactivation of motor and cardiovascular centers
Respiratory Responses: Ventilation During Exercise
Initial Changes
Anticipatory Response:
Immediate increase in ventilation before muscle contractions initiate
Second Phase Increase:
Gradual increase driven by chemical changes in arterial blood (increased CO2 and H+ detected by chemoreceptors)
Tidal Volume and Breathing Rate
Ventilation Proportional to Metabolic Demand:
At low intensity: only tidal volume increases
At high intensity: both rate and tidal volume increase
Recovery Phase
Delayed Recovery:
Recovery of ventilation takes several minutes and is affected by blood pH, PCO2, and temperature
Respiratory Responses: Breathing Irregularities
Common Irregularities
Exercise-induced Asthma:
Characterized by lower airway obstruction, coughing, wheezing, and dyspnea
Dyspnea:
Common with poor aerobic fitness, often associated with inability to cope with high blood PCO2 and H+
Hyperventilation:
May occur due to anticipation or anxiety, affecting blood PCO2 and subsequent drive to breathe
Valsalva Maneuver
Mechanism:
Involves closing the glottis, resulting in increased intra-abdominal and intrathoracic pressures, causing potential collapse of great veins leading to decreased venous return
Recovery From Acute Exercise: Cardiovascular Variables
Postexercise Hypotension (Aerobic and Resistance):
Driven by peripheral vasodilation and decreased cardiac output respectively, with lasting effects for several hours
Conclusions
Integration of Responses:
Cardiovascular and respiratory responses are complex, fast, and finely tuned to maintain blood pressure and blood flow with respect to metabolic demands during exercise.