Cardiorespiratory Responses to Acute Exercise

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 (HR) increases above RHR just before the start of exercise.
- Decrease in vagal tone.
- Increases in norepinephrine and epinephrine.

Relationship to Exercise Intensity
- HR is directly proportional to exercise intensity.
Maximum Heart Rate (HRmax)
- HRmax is defined as the highest HR achieved during all-out effort to volitional fatigue.
- HRmax is highly reproducible and declines slightly with age.
- Estimated HRmax can be calculated using the formula:
  HR_{max} = 220 - \text{age in years}
- A more accurate estimate is:
  HR_{max} = 208 - (0.7 \times \text{age in years})

Characteristics
- As exercise intensity increases, so does steady-state HR.
- Adjustment to a new intensity typically takes 2 to 3 minutes.
Applications
- Steady-state HR is the basis for simple exercise tests estimating aerobic fitness and HRmax.

Example of Heart Rate Responses
- Graph data showing heart rate responses from rest to HRmax based on % VO2max.

Changes with Intensity
- SV increases with exercise intensity up to approximately 40 to 60% VO2max.
SV During Maximal Exercise
- SV during maximal exercise is approximately double that of standing SV.
- SV during maximal exercise is only slightly higher than supine SV, where supine end-diastolic volume (EDV) is greater than standing EDV.

Preload
- Defined as end-diastolic ventricular stretch, which increases contraction strength according to the Frank-Starling mechanism.
Contractility
- Factors affecting contractility include circulating epinephrine and norepinephrine and direct sympathetic stimulation of the heart.
Afterload
- Afterload is defined as aortic resistance (R), where decreased afterload leads to increased SV.

Mechanism of SV Increase
- Increased preload at lower intensities leads to increased SV.
- Venous return contributes to increased EDV and thus increases preload.
- Muscle and respiratory pumps along with venous reserves foster this increase.
Effect of Heart Rate
- Increased HR may lead to a slight decrease in EDV and hence a decrease in SV due to reduced filling time, but increased contractility at higher intensities leads to increased SV.
- Reduced afterload through vasodilation also contributes to increased SV.

Function and Formula
- Cardiac output (Q) is calculated using the equation:
  Q = HR \times SV
Variations with Intensity
- Cardiac output increases with exercise intensity and plateaus near VO2max.
- Normal Values
- Resting Q is approximately 5 L/min.
- Untrained Qmax is approximately 20 L/min.
- Trained Qmax is approximately 40 L/min.

Behavior During Exercise
- Mean arterial pressure (MAP) tends to increase during endurance exercise.
- Systolic blood pressure (BP) increases proportionally to exercise intensity, while diastolic BP either slightly decreases or remains steady during maximal exercise.
Pressure Calculations
- MAP is defined by the equation:
  MAP = Q \times \text{Total Peripheral Resistance (TPR)}
- Both Q increases and TPR decreases slightly due to muscle vasodilation (sympatholysis).

Definition
- Rate-pressure product is defined as:
  \text{Rate-pressure product} = HR \times SBP
- This is related to myocardial oxygen uptake and myocardial blood flow.
Responses to Resistance Exercise
- Resistance exercise may lead to periodic large increases in MAP, which can reach extreme values such as 480/350 mmHg, particularly when using the Valsalva maneuver.

Mechanism
- Increased cardiac output results in more available blood flow.
- Blood flow must be redirected to areas with the greatest metabolic need (exercising muscles).
- Sympathetic vasoconstriction shifts blood away from less active regions (e.g., splanchnic circulation, kidneys).
Local Responses
- Local vasodilation allows increased blood flow in exercising muscles, triggered by metabolic and endothelial products.
- Sympathetic vasoconstriction in muscles is offset by sympatholysis, where local vasodilation overrides neural vascular constriction.
- As temperature rises during exercise, skin vasodilation occurs due to decreased sympathetic vascular constriction and increased sympathetic vasodilation, thus promoting heat loss through the skin.

Competing Demands
- Exercise combined with other demands (e.g., eating, heat) leads to competition for limited cardiac output (Q). This can result in decreased blood flow to muscles.

(a-v)O2 Difference
- This difference is calculated as:
  (a-v)O2 \text{ difference} = \text{Arterial O2 content} - \text{Mixed venous O2 content}
- Normal resting difference is approximately ~6 mL O2/100 mL blood and can increase to ~16 to 17 mL O2/100 mL blood during maximal exercise.

Central Command
- The initial signal driving cardiovascular responses emerges from higher brain centers and is fine-tuned by feedback from:
- Chemoreceptors
- Mechanoreceptors
- Baroreceptors

Ventilation Trends
- Linear increases in ventilation occur up to approximately 50-75% VO2max.
- An exponential increase in ventilation occurs beyond this point, characterized by the ventilatory threshold (Tvent), which is the inflection point where ventilation increases exponentially.

Regulatory Mechanisms
- The respiratory control center, located in the medulla oblongata, receives neural and humoral input from feedback mechanisms, including:
- CO2 levels in the blood
- Information from muscles
- This center regulates ventilatory rate accordingly.

Conditions
- Alterations from typical breathing patterns can include:
- Hyperventilation
- Dyspnea
- Valsalva Maneuver

Submaximal Exercise
- The pulmonary system is generally not seen as a limiting factor in submaximal exercise.
Maximal Exercise
- The pulmonary system is typically not considered limiting in healthy individuals at sea level but may become a limiting factor in elite endurance athletes due to exercise-induced hypoxemia.