Lecture 7 ExPhys

Definition and Scope of Acute Exercise

• Definition of Acute Exercise: Acute exercise refers to exercise of a relatively short duration or a single bout of exercise.

• Acute vs. Chronic: Unlike exercise training (chronic), which involves repeated bouts over time to induce long-term adaptations, acute exercise describes the immediate physiological responses to a specific session.

• Practical Example: A typical example of acute exercise provided is asking an entire group to get up and run a single mile immediately.

Overview of Cardiovascular Responses to Acute Exercise

• Primary Goal: The central objective of the cardiovascular system during exercise is to increase blood flow to the working muscles.

• Components of Adjustment: The cardiovascular system achieves this goal through specific adjustments in the following components:     * Heart rate (HR)     * Stroke volume (SV)     * Cardiac output (CO)     * Blood pressure (BP)     * Blood flow redistribution     * Blood composition and characteristics

Heart Rate Responses

• Resting Heart Rate (RHR):     * Averages: Typically ranges between $60\text{-}80\,bpm$.     * External Influences: RHR can be impacted by factors such as training status, medications, stimulants, and environmental conditions.     * Anticipatory Response: Just before exercise begins, the heart rate typically increases above normal resting values. This is driven by:         * An increase in Sympathetic Nervous System (SNS) activity.         * The release of norepinephrine (NE) and epinephrine (E).         * Vagal tone withdrawal (a decrease in Parasympathetic Nervous System or PNS activity).

• Heart Rate During Exercise:     * Linear Increase: When exercise starts, HR increases in direct proportion to exercise intensity.     * Plateau: As maximal exercise intensity is reached, HR begins to plateau, even if the workload continues to rise. This plateau indicates the maximal heart rate ($HR_{max}$).     * Maximal Heart Rate ($HR_{max}$):         * The highest HR value achieved during an all-out effort to the point of exhaustion.         * It is used in clinical testing to prescribe exercise intensity for training and rehabilitation.         * While it remains constant day-to-day, it decreases annually as an individual ages.         * Estimation Formula: If maximal testing is unavailable, the common equation used is:
          $HR_{max} = 220 - \text{age (years)}$

• Steady-State Heart Rate:     * When exercise intensity is held constant at a submaximal level, HR increases rapidly before reaching a plateau known as the steady-state heart rate.     * It generally takes $1\text{-}3\,\text{minutes}$ to reach a new steady-state value for every increase in intensity; higher intensities require more time to achieve this state.     * Fitness Correlation: A lower steady-state heart rate at a fixed intensity is a valid predictor of superior cardiorespiratory fitness.

• Heart Rate Variability (HRV):     * Definition: A measure of the rhythmic fluctuation in HR resulting from continuous changes in the sympathetic-parasympathetic balance controlling the sinus rhythm.     * Influencing Factors during Acute Exercise: Factors include increases in core body temperature, sympathetic nerve activity, and respiratory rate.     * Mathematical Utility: Researchers use HRV to mathematically examine the impact of training or disease on individual contributors to autonomic regulation.

Stroke Volume (SV) Dynamics

• Determinants of Cardiorespiratory Endurance: At near-maximal and maximal intensities, SV is a critical determinant of endurance capacity as HR nears its peak.

• Four Determining Factors of SV:     1. Venous Return: The volume of blood returned to the heart; the heart can only pump what it receives.     2. Preload: The capacity of the ventricle to stretch to allow for maximal filling.     3. Afterload: The pressure the ventricles must contract against (specifically pressure in the pulmonary and aortic arteries).     4. Contractility: The muscle's capacity to contract forcefully.

• Categorization of Factors:     * Venous return and preload influence the filling capacity and determine the End-Diastolic Volume (EDV).     * Afterload and contractility influence the ventricle's ability to empty during systole.

• Stroke Volume during Exercise Progression:     * SV increases above resting values as intensity increases up to approximately $40\text{-}60\%\,VO_2max$, after which it typically plateaus.     * Untrained Individuals: SV may increase from resting levels of $60\text{-}70\,ml/beat$ to maximal levels of $110\text{-}130\,ml/beat$.

• Impact of Body Position:     * SV does not increase as significantly in the supine (laying down) position compared to an upright position.     * This is due to differences in gravity affecting blood distribution and return.

• Overcoming Reduced Filling Time:     * At rest ($HR = 70\,bpm$), the filling time between beats is $0.55\,s$.     * During intense exercise ($HR = 195\,bpm$), the filling time drops to $0.12\,s$.     * Despite this reduction in time, SV increases through specific physiological mechanisms.

• Mechanisms of SV Increase:     * Preload and the Frank-Starling Mechanism: As blood fills the ventricle (increasing EDV), the ventricular walls stretch. This stretch increases the number of actin-myosin cross-bridges in the myocardial cells, leading to a more forceful contraction. This is supported by the muscle pump and respiratory pump.     * Enhanced Contractility: Driven by the SNS and circulating catecholamines (E & NE), contractility can increase SV even without increased EDV by raising the ejection fraction.     * Reduced Afterload: Vasodilation in the blood vessels of active skeletal muscles (decreasing Total Peripheral Resistance or TPR) makes it easier for the ventricle to eject blood.

• Plateau Reasoning: SV eventually plateaus because, as HR continues to rise, the reduced ventricular filling time eventually reaches a limit where venous return and EDV cannot keep up.

• Measurement Techniques:     * Echocardiography: Utilizing sound waves for imaging.     * Radionuclide Techniques: Tagging red blood cells with radioactive tracers.

Cardiac Output (CO)

• Equation:
      $CO = HR \times SV$

• Baselines and Ranges:     * Resting CO: Approximately $5.0\,L/min$.     * Exercise CO: Can increase to $20\text{-}40\,L/min$ depending on training and body size.

• Relationship with Intensity: CO increases linearly with exercise intensity to meet increased oxygen demands.

• The Fick Equation: States that oxygen consumption ($VO_2$) depends on blood flow and oxygen extraction from the tissue.
      $VO_2 = CO \times (a\text{-}v)O_2 \, \text{difference}$

• Compensatory Changes: When transitioning from laying down to standing, blood pools in the legs, decreasing SV. To maintain CO, HR must increase proportionally.

• Phase Distribution: CO increases via both HR and SV until $40\text{-}60\%\,VO_2max$. Beyond this point, further increases in CO are primarily driven by HR.

Blood Pressure (BP) Regulation

• Systolic Blood Pressure (SBP):     * Increases in direct proportion to intensity (e.g., from $120\,mmHg$ at rest to $200\,mmHg$ or more during exercise).     * The increase facilitates blood flow through the vasculature.

• Diastolic Blood Pressure (DBP):     * Generally remains unchanged or may slightly decrease due to functional sympatholysis (local vasodilation).

• Mean Arterial Pressure (MAP): Increases initially at a steady state primarily because of the increase in SBP.

• Upper Body vs. Lower Body Exercise:     * Upper body exercise produces a higher BP response at the same absolute energy expenditure due to smaller muscle mass and the need for stabilization.

• Rate-Pressure Product (RPP):     * $RPP = HR \times SBP$     * This value tracks myocardial oxygen demand and uptake.

• Resistance Exercise Extremes:     * BP can reach extreme levels, such as $480/350\,mmHg$, especially during heavy lifts involving the Valsalva maneuver (exhaling against a closed glottis), which spikes intrathoracic pressure.

Blood Flow and Blood Composition Changes

• Redistribution: SNS activation causes vasoconstriction in metabolically inactive areas (liver, kidneys, intestines) and the skin (unless heat dissipation is required).

• Functional Sympatholysis: Local vasodilators like Nitric Oxide (NO) and metabolites override SNS vasoconstriction in working muscles to increase blood flow.

• Oxygen Content:
      * The $(a ext{-}v)O_2$ difference (the gradient between arterial and venous oxygen) increases because more oxygen is extracted by the muscles. Arterial oxygen remains stable, while venous oxygen decreases.

• Plasma Volume (PV):     * PV can reduce by $10\text{-}15\%$ during prolonged exercise as fluid leaves the vessels for the interstitial space due to increased BP and sweat loss.

• Hemoconcentration: As PV decreases, the cellular portion of the blood (RBCs) represents a higher percentage of total volume. This increases blood viscosity but does not involve an increase in the absolute volume of RBCs.

Integrated Control of Cardiovascular Function

• The Medulla: Acts as the primary regulator for cardiovascular function in the brain.

• Autonomic Control: The medulla regulates HR via the pacemaker in the right atrium using sympathetic and parasympathetic nerves.

• Motor Cortex and Sensory Nerves: The motor cortex stimulates the medulla based on muscle recruitment. Sensory nerves provide feedback on the metabolic status of the muscle.

• Baroreceptors:     * High-Pressure Baroreceptors: Located in large arteries; they monitor arterial blood pressure.     * Low-Pressure Baroreceptors: Located in the right side of the heart and large veins; they monitor heart filling. Increased filling causes these receptors to signal the brain to lower resistance to exercising muscles to maintain arterial pressure.