Cardiovascular Responses to Exercise and Training Adaptations

Neural Stimulation and Metabolic Demand

• Sympathetic Nervous System (SNS) and Motor Unit Recruitment

  • Exercise requires significant SNS stimulation and motor stimulation to contract high-threshold motor units.

  • High-Threshold Motor Units: Specifically, the Type IIx (fast-twitch glycolytic) fibers.

  • Metabolic Correlation: The recruitment of these fibers corresponds heavily with catecholamine production (epinephrine and norepinephrine) and, consequently, lactate production.

Acute Exercise Responses and the Fick Equation

• Heart Rate and Steady State Exercise

  • When starting exercise, heart rate increases rapidly until it reaches a steady state.

  • Steady State Definition: A point where the heart rate flatlines and remains stable because the metabolic demand has been met.

  • Homeostatic Significance: Reaching a steady state indicates a homeostatic norm for oxygen delivery, adequate tissue oxygenation, and effective blood $CO_2$ removal.

  • Cardiac Efficiency: A lower steady-state heart rate at a specific given workload indicates a more efficient heart.

• The Fick Equation

  • A fundamental formula for understanding oxygen uptake ($VO_2$):

  • $VO_2 = Q \times (a-vO_2\,\text{difference})$

  • Where:

    • $VO_2$ = Oxygen consumption/uptake.

    • $Q$ = Cardiac output.

    • $(a-vO_2\,\text{difference})$ = Arterial-venous oxygen difference (the amount of oxygen extracted by tissues).

  • Control Mechanisms: Humans do not have moment-to-moment independent control over oxygen extraction ($a-vO_2$ difference); however, we can control cardiac output.

  • Direct Relationship: Because $VO_2$ and cardiac output ($Q$) are in a direct relationship, any adaptation in $VO_2$ is mirrored by cardiac output.

• Cardiac Output ($Q$)

  • Formula: $Q = \text{HR} \times \text{SV}$

  • Where:

    • $\text{HR}$ = Heart Rate.

    • $\text{SV}$ = Stroke Volume.

  • During submaximal exercise after chronic training, $VO_2$ remains unchanged. Therefore, Cardiac Output ($Q$) also remains unchanged.

  • If heart rate ($\text{HR}$) is lower after training, Stroke Volume ($\text{SV}$) must increase to maintain the same Cardiac Output.

Stroke Volume Dynamics and Filling Mechanics

• Stroke Volume Adaptation

  • Stroke volume increases with increasing work rate but generally plateaus at approximately $40\,\%\,\text{to}\,60\,\%\,\text{of}\,VO_2\,\text{max}$.

  • Limiting Factors: At very high contraction rates, the time available for the heart to fill with blood is limited, which leads to the plateau.

  • Averages (Textbook Values for Adults):

    • Resting SV: Average of approximately $70\,ml/\text{beat}$.

    • Exercise SV: Average of approximately $120\,ml/\text{beat}$.

    • Variability: Larger individuals may reach peaks of $130\,ml/\text{beat}\,\text{or}\,140\,ml/\text{beat}$, while smaller individuals may max out at $90\,ml/\text{beat}\,\text{or}\,100\,ml/\text{beat}$.

• Stroke Volume Components

  • Stroke volume is the difference between End-Diastolic Volume ($\text{EDV}$) and End-Systolic Volume ($\text{ESV}$):

  • $\text{SV} = \text{EDV} - \text{ESV}$

  • At Maximal Intensities:

    • $\text{EDV}$: Tends to become stagnant or drop mildly because of reduced filling time.

    • $\text{ESV}$: Continues to decrease significantly due to increased myocardial contractility driven by the SNS.

    • Result: Stroke volume stays relatively the same at peak intensities because the decrease in $\text{ESV}$ compensates for the flatlined $\text{EDV}$.

Factors Influencing Venous Return

• The Frank-Starling Mechanism

  • An increase in blood returning to the heart (venous return) result in greater stretching of the ventricles, which facilitates a more forceful contraction.

• Venoconstriction

  • SNS causes mild venoconstriction during exercise.

  • Paradoxical Effect: While constriction in arteries increases resistance, in veins it reduces "distensibility" (floppiness). This prevents veins from ballooning out and helps streamline the blood volume back toward the heart.

• The Skeletal Muscle Pump

  • Rhythmic contractions of skeletal muscles compress veins, forcing blood toward the heart.

  • One-Way Valves: Veins contain valvulets (leaflets) that allow universal flow toward the heart but close to prevent backflow.

  • Toothpaste Analogy: If you squeeze a tube of toothpaste in the middle (like a muscle contracting against a vein) and the end is crimped (like a valve), the paste must go out the nozzle.

• The Respiratory Pump

  • Changes in thoracic pressure during breathing (expanding the thoracic cage) create negative pressure.

  • This negative pressurization acts like a suction, pulling blood volume into the thoracic cavity and back into the heart.

Acute Blood Pressure Responses and Static Exercise

• Standard Exercise Response

  • Systolic Blood Pressure (SBP): Increases linearly with exercise intensity.

  • Diastolic Blood Pressure (DBP): Largely does not change or remains stagnant for most normative exercise intensities.

  • Mean Arterial Pressure (MAP): Increases linearly due to the drastic increase in SBP.

• Static Exercise and Heavy Lifting

  • Static/isometric exercise can cause extreme spikes in blood pressure due to muscle contraction compressing blood vessels indefinitely.

  • Extreme Values: Studies using intra-arterial catheters during a near-maximal leg press have recorded pressures as high as $480/350\,mmHg$.

• The Valsalva Maneuver

  • Definition: Exerting pressure against a closed glottis (often used when lifting heavy weights or when constipated).

  • Physiological Effect: Increases intrathoracic and systemic pressure, which can increase tissue perfusion but also presents a risk of passing out during a lift.

Cardiovascular Drift and Blood Flow Redistribution

• Cardiovascular Drift

  • Occurrence during prolonged, constant-intensity endurance exercise.

  • Observation: Heart rate gradually "drifts" upward (e.g., from $120\,bpm\,\text{to}\,135\,bpm$) for the same workload, while stroke volume decreases.

  • Cause: Primarily due to a loss of blood volume (plasma) through sweat and heat loss (dehydration).

• Redistribution of Blood Flow

  • During rest, internal organs (kidneys, liver, GI tract) receive high perfusion.

  • In maximal exercise, up to $80\,\%$ of blood flow is redirected toward active skeletal muscle tissue.

  • GI Tract: Perfusion to the stomach and intestines is reduced dramatically because digestion is parasympathetically driven, whereas exercise is sympathetically driven.

VO2 Max: Measurement and Calculations

• Aerobic Capacity

  • Known as the upper limit of a person's ability to consume oxygen.

  • It is an indicator of cardiorespiratory endurance and is inversely correlated with cardiovascular disease risk.

• Absolute vs. Relative $VO_2\,\text{max}$

  • Absolute: Measured in liters of oxygen per minute ($L/min$).

    • Resting: approximately $0.25\,L/min$.

    • High: approximately $3.5\,\text{to}\,4.0\,L/min$.

  • Relative: Measured in milliliters of oxygen per kilogram of body weight per minute ($ml/kg/min$). This allows for direct comparison between people of different sizes.

  • Highest Recorded Value: Statistically, cross-country skiers often have the highest values (up to $92\,ml/kg/min$) due to extreme core and upper body engagement.

• Sample Calculation

  • Given: Absolute $VO_2 = 4.9\,L/min$, Body weight = $70\,kg$.

  • 1. Convert Liters to Milliliters: $4.9 \times 1000 = 4900\,ml$.

  • 2. Divide by Mass: $\frac{4900}{70} = 70\,ml/kg/min$.

Training Adaptations and Blood Volume

• Blood Volume (BV) Increases

  • Regular endurance training increases overall blood volume by approximately $10\,\%\,\text{to}\,15\,\%$.

  • Plasma Volume ($75\,\%$ of the increase): Occurs rapidly (within 24–48 hours) due to increased osmolality and water retention.

  • Red Blood Cell/Erythrocyte Volume ($25\,\%$ of the increase): Takes roughly three weeks of continuous regular training to see a measurable increase due to the time required for cellular synthesis.

  • Viscosity: This specific ratio (more plasma than cells) is vital to keep the blood from becoming too thick or viscous, which prevents extreme cardiac strain.

• Cardiac Hypertrophy

  • Chronic Adaptation: The heart is a muscle and undergoes hypertrophy with training.

  • Healthy vs. Maladaptive: Exercise-induced hypertrophy involves increased myofibrillar density and density of cardiomyocytes (good). Pathological hypertrophy (e.g., from hypertension) involves collagen deposition and fibrosis, making the heart rigid (bad).

Chronic Cardiovascular Training Effects

• Resting State Adaptations

  • Heart Rate: Decreases (average of $5\,bpm$) due to increased parasympathetic/vagal tone.

  • Stroke Volume: Increases due to higher blood volume and increased filling time.

  • Blood Pressure: Resting values can decrease by $6\,\text{to}\,7\,mmHg$ in borderline hypertensive individuals.

• Submaximal Training Adaptations

  • Heart Rate: Lower at a given workload (the workload is perceived as easier).

  • Cardiac Output ($Q$) and $VO_2$: Remain statistically unchanged because metabolic demand for a specific submaximal speed is constant.

  • Stroke Volume: Higher at the same submaximal workload.

  • Recovery: Heart rate returns to resting levels much faster post-exercise because of lower circulating epinephrine/norepinephrine levels.

• Maximal Training Adaptations

  • $VO_2\,\text{max}$: Increases by approximately $15\,\%$ on average. Highly sedentary individuals can see gains of $50\,\%$\text{+}.

  • Non-Responders: Approximately $10\,\%\,\text{to}\,15\,\%$ of the population does not show major $VO_2\,\text{max}$ adaptations despite training.

  • Cardiac Output ($Q$): Increases by roughly $15\,\%$\text{ at maximum}.

  • Maximal Heart Rate: Largely unchanged statisticaly (remains roughly $220 - \text{age}$).

  • Stroke Volume: Significantly higher at maximum.

  • Systolic BP: Increased at max because the heart is stronger.

  • Diastolic BP: Decreased at max due to increased vascular compliance.

Questions & Discussion

• Interaction on Blood Flows: The instructor noted that blood flow to kidneys and the liver is significantly reduced during exercise because they are not active organs in that context.

• Anecdote on Toothpaste Usage: The instructor shared a story about his wife squeezing a tube of toothpaste from the middle (like a "Neanderthal") to illustrate how valves (crimps) allow flow to go in one direction toward the nozzle (the heart).

• Genetics and Athleticism: Discussion of "athletic families," mentioning Arch Manning, The Manning Brothers (Peyton/Eli), and Deion Sanders and his son (Shedeur Sanders), to illustrate that $50\,\%\,\text{to}\,60\,\%$ (up to $80\,\%$) of $VO_2\,\text{max}$ and response to training is genetically predisposed.

• The Y2K and 2012 Scares: The instructor discussed the fear of computer calendars switching to "00" causing nuclear warheads to launch during the Y2K transition and the Maya calendar predicting the end of the world in 2012 to define the term "millennium" and "milli-."

• Clinical Disconnect: The instructor shared an anecdote about a PhD meeting where medical professionals were hesitant to exercise-train mice because they didn't want them to be "muscular," highlighting a lack of understanding regarding the systemic inflammatory and cardiovascular benefits of exercise.

• The "Polypill": Mentioned a 2004 paper titled "Exercise is a Real Polypill" which supports exercise as an effective medical intervention for reducing blood pressure and inflammation.

• Hypertension Anecdote: Mentioned an old neighbor who put salt on watermelon, illustrating how high sodium intake and fluid retention drive chronic hypertension.