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What brain centers regulate cardiovascular function?
Medulla oblongata: cardioacceleratory, cardioinhibitory, and vasomotor centers.
How does the sympathetic nervous system affect the heart?
Increases heart rate (chronotropic), contractility (inotropic), and causes vasoconstriction.
How does the parasympathetic nervous system affect the heart?
Decreases heart rate (via vagus nerve), minimal effect on contractility.
Define chronotropic effect.
An effect that changes heart rate.
Define inotropic effect.
An effect that changes force of myocardial contractility.
What catecholamines are involved in CV regulation?
Epinephrine and norepinephrine.
What receptors do catecholamines act on?
β1 (↑HR & contractility), β2 (vasodilation in muscle), α1 (vasoconstriction in vessels).
What is central command in cardiovascular control?
Anticipatory activation of the CV system by the brain before and at onset of exercise.
What are the main receptors involved in neural regulation of circulation?
Baroreceptors, chemoreceptors, mechanoreceptors (group III/IV afferents).
What is the Frank-Starling mechanism?
Greater EDV stretches ventricles more, leading to stronger contraction and increased stroke volume.
What increases blood flow to the heart during exercise?
Muscle pump, respiratory pump, venoconstriction, one-way valves, and coronary vasodilation.
What influences end-diastolic volume (EDV)?
Preload, blood volume, body position, intrathoracic pressure, and heart rate.
How does endurance training affect stroke volume?
Increases due to improved EDV and stronger myocardium.
How does training affect resting and submax HR?
Decreases due to increased parasympathetic tone (resists fight or flight).
How does training affect HR recovery?
Faster recovery post-exercise.
What vascular changes occur with training?
Better blood flow distribution and increased capillarization.
How does blood distribution change during exercise?
More blood to working muscles (up to 85%); less to organs like GI tract.
How does exercise influence vessel diameter?
Vasodilation in active muscles; vasoconstriction elsewhere.
What is the role of nitric oxide in blood flow?
Released by endothelium; causes local vasodilation in response to shear stress.
What is cardiovascular drift?
Gradual ↑ HR and ↓ stroke volume during prolonged exercise, especially in heat.
What causes cardiovascular drift?
Dehydration, blood volume loss, and increased skin blood flow.
What is the Fick equation for
CO = VO₂ / (a-v O₂ difference)
What methods measure cardiac output?
Fick method, dye dilution, thermodilution, echocardiography, impedance cardiography, CO₂ rebreathing.
How does lower body exercise affect cardiovascular responses?
Greater muscle mass → higher venous return and stroke volume, lower HR at same workload.
How does upper body exercise affect cardiovascular responses?
Smaller muscle mass → higher HR and BP at same workload due to greater SNS activation and vasoconstriction.
How does training affect cardiac output during submaximal exercise?
Remains similar, but achieved with lower HR and higher stroke volume.
How does training affect blood volume?
Increases plasma volume, supporting better venous return and thermoregulation.
What is the role of baroreceptors in CV regulation?
Detect pressure changes and adjust HR and vessel tone to maintain BP homeostasis.
Gas Exchange Dependency
Gas exchange is influenced by partial pressure gradients, gas solubility, and the surface area and thickness of the alveolar-capillary membrane.
Henry's Law
Henry's Law states that the amount of gas that dissolves in a liquid is proportional to its partial pressure and solubility.
Gas Movement Direction
Gases move from areas of high partial pressure to areas of low partial pressure.
Alveolar Gas Gradients at Rest
At rest, the partial pressure of oxygen decreases from 100 to 40 mmHg in the alveoli, while carbon dioxide increases from 40 to 46 mmHg.
Tissue Gas Exchange at Rest
At rest, oxygen diffuses from blood (100 mmHg) to tissue (40 mmHg), and carbon dioxide diffuses from tissue (46 mmHg) to blood (40 mmHg).
Tissue Gas Exchange During Exercise
During exercise, increased oxygen demand and carbon dioxide production enhance gas diffusion rates.
Oxygen Transport
Approximately 98% of oxygen is bound to hemoglobin, while 2% is dissolved in plasma, driving diffusion.
Carbon Dioxide Transport
Carbon dioxide is transported as 60% bicarbonate, 20% bound to hemoglobin, and 10% dissolved in plasma.
Oxygen-Hemoglobin Dissociation Curve
The oxygen-hemoglobin dissociation curve illustrates the relationship between PO₂ and hemoglobin saturation and is influenced by several physiological factors.
Bohr Effect
Increased CO₂ or decreased pH lowers hemoglobin's affinity for O₂, promoting O₂ unloading at tissues.
Haldane Effect
Deoxygenated hemoglobin binds CO₂ more easily, aiding CO₂ transport from tissues to lungs.
Factors Shifting Oxyhemoglobin Curve Right
Increased CO₂, H⁺ (↓pH), temperature, and 2,3-BPG; enhances O₂ offloading.
AVO₂ Difference
Difference in O₂ content between arterial and venous blood; increases with exercise due to higher O₂ extraction by muscles.
Myoglobin
Muscle protein that stores and releases O₂; has higher O₂ affinity than hemoglobin, effective during intense exercise.
Bicarbonate
Primary form of CO₂ transport; buffers pH via reaction: CO₂ + H₂O \rightleftharpoons H₂CO₃ \rightleftharpoons H⁺ + HCO₃⁻.
Neural Control of Ventilation
Involves respiratory centers (medulla, pons) and mechanoreceptors that respond to stretch and movement.
Humoral Control of Ventilation
Regulation based on blood chemistry (pH, PO₂, PCO₂) detected by chemoreceptors.
Chemoreceptors
Central receptors detect CO₂ via H⁺ in CSF; peripheral receptors respond to ↓PO₂, ↑PCO₂, ↓pH.
Ventilation at Rest
Controlled primarily by CO₂ levels through chemoreceptor feedback.
Ventilation in Abnormal Conditions
Hypoxia or acidosis increases peripheral chemoreceptor activity to stimulate ventilation.
Steady-Rate Physical Activity
Ventilation increases proportionally to O₂ demand, allowing aerobic metabolism to meet energy needs.
Minute Ventilation (VE)
Total air volume moved per minute = tidal volume × breathing rate; increases with exercise intensity.
Ventilatory Threshold
Point during exercise when ventilation increases disproportionately to VO₂ due to rising CO₂ from buffering lactic acid.
Lactate Threshold
Exercise intensity where lactate starts accumulating faster than it can be cleared, typically 50–80% VO₂max.
Onset of Blood Lactate Accumulation (OBLA)
Point when blood lactate reaches ≥4.0 mmol/L; indicates significant anaerobic metabolism.
Energy Cost of Breathing
approx. 2% of VO₂ at rest; up to 11% during maximal exercise and 40
Acute Neuromuscular Changes
immediate changes in the nervous and muscular systems during exercise, including increased motor unit recruitment and firing frequency.
Acute Neuromuscular Changes (Muscle)
Temporary changes in muscle behavior, such as increased muscle fiber recruitment and activation, leading to greater force production during exercise.
Acute Neuromuscular Changes (Neural)
Increased motor unit recruitment, firing rates, and enhanced synaptic transmission improve strength and muscle activation during exercise.
Chronic Neuromuscular Changes
increased motor unit recruitment, muscle hypertrophy, improved neuromuscular efficiency, and changes in synaptic transmission.
Chronic Neuromuscular Changes (Muscle)
Muscle hypertrophy, increased muscle fiber size, and improved muscle endurance result from prolonged resistance or endurance training.
Chronic Neuromuscular Changes (Neural)
Enhanced motor unit recruitment, improved synchronization, and more efficient neuromuscular communication lead to better muscle coordination and strength.
Difference Between Acute and Chronic Neuromuscular Changes
Acute (Immediate):
Occur during or right after exercise
Increased motor unit recruitment and rate coding
Greater EMG activity due to heightened neural drive
Temporary fatigue or post-activation potentiation
No structural muscle change
Chronic (Adaptations):
weeks to months of training
Improved motor unit synchronization and recruitment of high-threshold motor units
Reduced antagonist co-activation
Muscle hypertrophy and sometimes hyperplasia
Fiber type transition (e.g., Type IIx → Type IIa)
Neuromuscular efficiency improves performance and strength
Influence of Training Type on Neuromuscular Changes
Resistance training increases muscle strength and size through hypertrophy and motor unit recruitment, while endurance training improves neuromuscular efficiency and muscle endurance without significant hypertrophy.
Neural vs Muscular Adaptations Time Course
Neural adaptations (motor unit recruitment, firing rate) occur early in training,
muscular adaptations (hypertrophy, endurance) take longer.
Neural Adaptations Time Course
occur within the first few weeks, as the nervous system becomes more efficient at recruiting motor units and increasing firing rates.
Muscular Adaptations Time Course
occur after several weeks or months of training, as muscle fibers increase in size and endurance improves.
ex: hypertrophy
Concurrent Training
Training that combines resistance and endurance exercises to improve both muscular strength and cardiovascular endurance.
Benefits of Concurrent Training
Beneficial for individuals aiming to improve both muscle strength and aerobic endurance simultaneously, such as athletes needing both capabilities for performance.
Impact of Concurrent Training on Strength
Endurance training may inhibit some muscle hypertrophy due to interference with muscle growth pathways, especially if not well-balanced.
Key Characteristics of Concurrent Training
Requires careful balancing of endurance and resistance components, with adequate recovery to minimize negative impacts on strength development.
Acute cardiovascular changes with exercise (with training)
HR, SV increases, CO increases. Systolic blood pressure increases. Oxygen uptake increases. Minute ventilation (tidal volume and breathing rate) increases.
Blood flow redistributes to working muscles.
Chronic cardiovascular changes at rest (with training)
Heart rate decreases. Stroke volume increases. Cardiac output remains the same. Blood pressure decreases (both systolic and diastolic)
Chronic cardiovascular changes with submaximal exercise (with training)
Heart rate decreases at the same intensity. Stroke volume increases. Cardiac output remains the same. Blood pressure decreases at the same intensity. Muscle glycogen use decreases. Oxygen consumption (VO_2) remains unchanged or slightly improves.
Chronic cardiovascular changes with maximal exercise (with training)
Heart rate: No change in maximal heart rate. Stroke volume increases significantly. Cardiac output increases. Systolic blood pressure increases significantly. Diastolic blood pressure remains the same or decreases slightly. VO_2 max increases significantly.
Athlete’s heart (with training)
Chronic aerobic training results in increased left-ventricular end-diastolic volume (EDV), greater preload and left-ventricular cavity size, wall thickening, and heart volume 25% larger than sedentary individuals.
Pulmonary ventilation adaptations (with training)
Maximal exercise: Minute ventilation (VE) increases due to increased tidal volume and breathing rate.
Submaximal exercise: Lower O_2 cost of breathing, reduced fatigue of ventilatory muscles, and more oxygen available for active muscles.
Plasma volume adaptations (with training)
12-20% increase in plasma volume with aerobic training, increasing stroke volume, end-diastolic volume, and oxygen transport, and improves temperature regulation during activity.
Heart rate adaptations (with training)
Training decreases intrinsic firing rate of the sinoatrial node, contributing to resting and submaximal exercise bradycardia.
Stroke volume adaptations (with training)
Stroke volume increases during rest and exercise due to increased left-ventricular volume and mass, reduced cardiac and arterial stiffness, increased diastolic filling time, and reduced heart rate.
Cardiac maximal output adaptations (with training)
increases due to improved stroke volume.
Aerobic metabolic adaptations (with training)
Increased
slow-twitch fibers and capillary density,
myoglobin concentration,
mitochondrial size and number,
increased enzymes for aerobic respiration (e.g., citrate synthase), and
increased glycogen storage and fat oxidation.
Anaerobic training adaptations (with training)
Increased size of fast-twitch fibers. Enhanced enzymes for anaerobic metabolism (creatine phosphokinase, phosphofructokinase). Improved buffering capacity (bicarbonate).
Blood lactate concentration adaptations (with training)
Endurance training lowers blood lactate levels, extending time before lactate accumulation (OBLA) due to decreased rate of lactate formation and increased rate of lactate clearance.
Oxygen extraction adaptations (with training)
Aerobic training increases O2 extraction from circulating blood and enhances muscle capacity to extract and process O2.
Factors that influence aerobic training
Initial fitness level, training intensity, duration, and frequency, and training type and progression.
Training intensity measurement
measured by % HRmax, energy expenditure, power output, % VO2 max speed at or above lactate threshold, and Rating of Perceived Exertion (RPE).
VO2 max improvement timeline (with training)
improvements in aerobic fitness occur within several weeks, with cardiovascular adaptations occurring rapidly, within 10 days of training.
Tapering (with training)
Tapering involves reducing training intensity and/or volume to reduce stress and optimize performance. A 1-3 week taper reduces training volume by 40-60% while maintaining intensity.
Overtraining (with training)
Overtraining is a chronic overload with failure to adapt, leading to performance deterioration, increased injury, and psychological stress. Symptoms include fatigue, disturbed mood, elevated resting pulse, insomnia, and increased infection susceptibility.
Additional benefits of endurance training (with training)
Endurance training provides additional benefits such as improved body composition (increased lean mass, decreased fat), improved bone density, ligament/tendon strength, improved lipid profile (increased HDL, decreased LDL), enhanced insulin sensitivity, and improved blood flow redistribution.
Insulin
Function: Regulates blood glucose levels by promoting glucose uptake into cells, especially muscle and fat tissue, for energy storage. Glands Involved: Pancreas.
Glucagon
Function: Raises blood glucose levels by promoting glycogen breakdown in the liver (glycogenolysis) and glucose production. Glands Involved: Pancreas.
Cortisol
Function: A stress hormone that increases glucose availability by promoting gluconeogenesis and lipolysis. It also aids in protein breakdown during prolonged stress (exercise). Glands Involved: Adrenal glands.
Catecholamines (Epinephrine and Norepinephrine)
Function: Increase heart rate, blood pressure, and metabolism during exercise. Stimulate glycogen breakdown and fatty acid oxidation to provide energy. Glands Involved: Adrenal glands.
Growth Hormone (GH)
Function: Promotes muscle, bone, and connective tissue growth. Supports fat metabolism by stimulating lipolysis and maintaining plasma glucose levels during exercise. Glands Involved: Anterior pituitary gland.
Antidiuretic Hormone (ADH)
Function: Helps conserve body fluids by promoting water retention in the kidneys. Glands Involved: Posterior pituitary gland.
Testosterone
Function: Plays a key role in muscle growth, strength, and anabolic processes. Supports fat metabolism and recovery. Glands Involved: Gonads (testes in males, ovaries in females).
Prolactin
Function: Involved in milk production and has roles in metabolic processes and stress responses. Glands Involved: Anterior pituitary gland.
Aldosterone
Function: Regulates sodium and potassium balance and water retention via kidney influence. Glands Involved: Adrenal glands.
Thyroid Hormones (T3 and T4)
Function: Regulate metabolism and energy production, increasing metabolic rate and supporting energy demands during exercise. Glands Involved: Thyroid gland.