Final Exam - Review

Cardiovascular System: Components

• A pump that provides continuous linkage w/ the other three components; heart

• A high-pressure distribution circuit; arterial circulation

• Exchange vessels; capillaries

• A low-pressure collection & return circuit; venous circulation

The Heart: Rate, Stroke & Output

• Four-chambered organ that provides the drive for blood flow

• Cardiac output stays the same

• Stroke volume changes during exercise

Circulatory System: Arterial

• High-pressure tubing that propels oxygenated blood to tissues

• Blood pumped from left ventricle enters aorta & is distributed throughout the body through a network of arteries & arterioles

• Smooth muscle in arteriole walls either constrict or relax to regulate blood flow to periphery

Circulatory System: Capillaries

• The precapillary sphincter consists of a ring of smooth muscle that encircles the capillary at its origin & controls its diameter

• Two factors trigger precapillary sphincter relaxation to open more capillaries:

  1. Driving force of increased local BP plus intrinsic neural control

  2. Local metabolites produced in exercise

Circulatory System: Venous

• Valves within veins allow blood to flow in only one direction toward the heart

• Prevent backflow of blood

• Blood moves through veins by action of nearby active muscle

• Contraction of smooth muscle

Blood Pressure

• Force of blood against arterial walls during cardiac cycle

• Darcy’s Law

  • Arterial blood pressure reflects the combined effects of arterial blood flow per minute & resistance to flow in peripheral vasculature

Blood Pressure (con’t)

• Systolic Blood Pressure (SBP)

  • Provides estimate of work of heart & force blood exerts against arterial walls during systole

• Diastolic Blood Pressure (DBP)

  • Relaxation phase of cardiac cycle

  • Indicates peripheral resistance or ease that blood flows from arterioles into capillaries

• Mean Arterial Pressure (MAP)

  • Avg. force exerted by blood against arterial wall during cardiac cycle

Blood Pressure (con’t)

• After an initial rapid rise from resting level, SBP increases linearly w/ exercise intensity

• DBP remains stable or decreases slightly at higher exercise levels

• SBP may increase to 200 mmHg or higher in healthy, fit individuals during maximum exercise

Blood Pressure (con’t)

• Increased blood flow during steady-rate exercise rapidly increases SBP during the first few minutes

• SBP often declines as steady-rate exercise continues b/c arterioles in active muscles continue to dilate, further reducing peripheral resistance to blood flow; DBP generally remains unchanged throughout exercise

Post-Exercise Hypotension

• The hypotensive response to exercise can last up to 12 hrs

• Occurs in response to either low- and moderate-intensity aerobic exercise or resistance exercise

Myocardial Work

• Rate-Pressure Product

  • Estimate of myocardial workload and VO2

    • 𝑅𝑃𝑃 = 𝑆𝐵𝑃 ∙ 𝐻𝑅

  • Index of relative cardiac work

  • Ranges from 6000 at rest to ≥40,000 during exercise, depending on intensity & mode

Electrocardiogram (ECG)

• The ECG represents a composite record of the heart’s electrical events during a cardiac cycle

• These electrical events can monitor HR during physical activities & exercise stress testing

  • P wave = Atrial depolarization

  • QRS = Ventricular depolarization

  • T wave = Ventricular repolarization

Extrinsic Regulation of Heart Rate

• Heart Rate is increased by:

  • Nerves directly supply myocardium; sympathetic nerves

  • Chemical “messengers” that circulate in the blood; epinephrine

• Stimulation of sympathetic cardioaccelerator nerves releases epinephrine & norepinephrine

  • Cause chronotropic (affecting heart rate) and inotropic (affecting heart contractility) effects on heart

Extrinsic Regulation of Heart Rate (con’t)

• Parasympathetic neurons release acetylcholine, which delays rate of sinus discharge to slow HR

• At start & during low/moderate intensity exercise, HR increases largely by inhibition of parasympathetic stimulation

• HR in strenuous exercise increases by additional parasympathetic inhibition & direct activation of sympathetic cardioaccelerator nerves

Extrinsic Regulation of Heart Rate: Central command

• Anticipatory effect

• Impulses originating in brain’s higher somatomotor central command centre continually modulate medullary activity

• Central command provides greatest control over HR during exercise

Extrinsic Regulation of Heart Rate: Peripheral Feedback - Ergoreceptors

Modifies either parasympathetic or sympathetic outflow to bring about the appropriate cardiovascular & respiratory responses to various intensities of physical activity

Extrinsic Regulation of Heart Rate: Peripheral Feedback - Baroreceptors

• Specific mechanoreceptor feedback governs central nervous system’s regulation of blood flow & BP during dynamic exercise

• Baroreceptors located on aortic arch & carotid sinus

  • Sensitive to pressure & stretch

Distribution of Blood Flow - Muscle Pump

Rhythmic propulsion of blood facilitates venous return & thus cardiac output

Distribution of Blood Flow - Vasodilator Mechanisms

• Increased blood flow leads to shear stress on the vascular endothelium

• Nitric oxide facilitates blood vessel dilation & decreases vascular resistance

Distribution of Blood Flow - Blunted sympathetic vasoconstriction

Contracting skeletal muscle can overcome sympathetically-mediated vasoconstriction, which allows for a blood flow that meets demand

Cardiac Output

• Cardiac output expresses the amount of blood pumped by the heart in 1 min

• Methods to assess cardiac output:

  1. Direct Fick

  2. Indicator dilution

  3. CO2 rebreathing

Fick Equation

Expresses relationships b/w VO2 (ml⋅min -1 ) & a-vDO2 (ml ⋅dl -1 blood) to determine cardiac output (ml⋅min -1 )

Cardiac Output: Rest

• Can vary considerably during rest

  • Influencing factors incl. emotional states that alter cortical outflow to cardio-accelerator nerves & nerves that modulate arterial resistance vessels

• Effect of chronic exercise training:

  • Same cardiac output, different means

    • Trained have lower HR & higher SV

Cardiac Output: Exercise

• Increases linearly w/ intensity of exercise (VO2 ) – Fick’s equation

• Trained individuals have a much greater cardiac output due entirely to an increase in SV

• Maximal HR does not change – it is related to age, not training status

Mechanisms that could increase SV during exercise:

1. Enhanced cardiac filling in diastole followed by a more forceful systolic contraction

2. Normal ventricular filling w/ subsequent more forceful ejection & emptying during systole

3. Training adaptations that expand blood volume & reduce resistance to blood flow in peripheral tissues

Frank-Starling Law

• Describes the relationship b/w cardiac filling & cardiac output

• Force of contraction of cardiac muscle remains proportional to its initial resting length

  • Increased preload = increase cardiac contractility = increase SV

Cardiovascular Drift

• Generally associated w/ increased core temperature & dehydration, but also occurs during steady-state exercise in a thermoneutral environment

• Submaximal exercise for >15 minutes decreases plasma volume, thus decreasing SV

• Reduced SV initiates a compensatory HR increase to maintain a nearly constant cardiac output

Cardiac Output: Distribution

• At rest,

  • One fifth (20%) flows to muscle tissue

  • Major portion of remaining blood flows to digestive tract, liver, spleen, brain, & kidneys receive major portions of the remaining blood

  • Heart (4%), Brain (14%)

• During exercise,

  • Diverts to active muscle (85%)

  • Heart (4%), Brain (4%)

Cardiac Output & Oxygen Transport: Exercise

• Untrained individual

  • An increase in maximal cardiac output produces proportional increase in capacity to circulate O2 & increases VO2max

Cardiac Output: Age & Sex-Differences

• Cardiac output & VO2 are linearly related during graded exercise across the lifespan. The Q:VO2 relationship is unaffected by sex

• Higher submaximal exercise HR in children don’t compensate for a smaller SV

Factors that affect the a-vDO2:

• Central & peripheral factors interact to increase O2 extraction in active tissue during exercise

• Large portion of the cardiac output diverts to active tissue

• Exercise training redirects a greater portion of central circulation to active muscle

Gross Structure of Skeletal Muscle

• There are 600+ muscles in the human skeleton

• Skeletal muscles contain wrappings of fibrous connective tissue

• Primary roles of muscle:

  1. Posture

  2. Movement

  3. Organ Function

  4. Heat Production

Skeletal Muscle: Levels of Organization

• Epimysium

  • Surrounds entire muscle

• Perimysium

  • Surrounds a bundle of fibres called a fasciculus

• Endomysium

  • Wraps each muscle fibre & separates it from neighboring fibres

• Sarcolemma

  • Surrounds each muscle fibre & encloses fiber’s cellular contents

• Sarcoplasm

  • Contains nuclei that house genes, mitochondria, & other specialized organelles

• Sarcoplasmic reticulum (SR)

  • Provides structural integrity; calcium release & reuptake

Skeletal Muscle: Chemical Composition

• Skeletal muscle is composed of:

  • Water = 75%

  • Protein = 20%

    • Myosin, actin, and tropomyosin are most abundant muscle proteins

  • Salts and other substances = 5%

Vascularization

• Arteries & veins lie parallel to muscle fibres

• During intense exercise, vascular bed delivers large quantities of blood through active tissues to accommodate increased O2 need

Capillarisation

• Enhanced capillary microcirculation expedites removal of heat & metabolic byproducts from active tissues & facilitates delivery of O2, nutrients, & hormones

• Vascular stretch/shear stress on vessel walls from increased blood flow during exercise stimulates capillary development

Skeletal Muscle: Ultrastructure

• Muscle fibres contain myofibrils that lie parallel to the long axis

• Myofibrils contain a series of sarcomeres & smaller subunits called myofilaments that lie parallel to long axis of myofibril

• Myofilaments consist of actin & myosin that account for ~85% of myofibrillar complex

Sarcomere

• Lie in series & their filaments have a parallel configuration within a given fibre

• Each sarcomere contains actin (thin) & myosin (thick)

Crossbridges

• ATP hydrolysis activates myosin’s two heads to bind actin’s active sites

• Tropomyosin & troponin regulate make-&-break contacts b/w the myofilaments during muscle action

Muscle Fibre Alignment

• Differences in sarcomere alignment & length affect muscle’s force- & power-generating capacity

  • Fusiform = run parallel; facilitate rapid muscle shortening

  • Pennate = lie at oblique pennation angle up to 30°; generate considerable power

• Pennate muscles differ from fusiform muscles:

  • Contain shorter fibres

  • Possess more individual fibres

  • Exhibit less ROM

Sliding-Filament Theory

• Proposes that muscle shortens or lengthens b/c thick & thin filaments slide past each other w/o changing length

• Produces change in relative size within sarcomere’s zones & bands; & produces a force at Z bands

Excitation-Contraction Coupling

Represents physiologic mechanism whereby an electrical discharge at muscle initiates chemical events at cell surface to release intracellular Ca2+ & produce muscle action

Slow-Twitch Muscle Fibres (Type I)

• Generate ATP through aerobic energy systems

• Characteristics include:

  • Large amounts of myoglobin (red)

  • Many mitochondria

  • Many blood capillaries

  • Reside in deep tissue (close to bone)

  • Slow contraction velocity

Fast-Twitch Muscle Fibres (Type II)

• High myosin-ATPase activity

• Few mitochondria

• Rapid Ca 2+ release & uptake by efficient sarcoplasmic reticulum

• High rate of crossbridge turnover

• Fatigue quickly

Fast-Twitch Muscle Fibres (Type II) (con’t)

• Activation predominates in anaerobic-type sprint activities & other forceful muscle actions that rely entirely on anaerobic energy transfer

• Activation plays an important role in stop-and-go or change-of-pace sports such as basketball, soccer, lacrosse, or field hockey

Length-Tension Relationship

• Describes relationship b/w length of sarcomere & amount of tension developed

  • Optimal sarcomere length = optimal overlap

  • Too short or too stretched = little or no force develops

Force-velocity relationship

• Concentric:

  • Maximal force development decreases at higher speeds

• Eccentric:

  • Maximal force development increases at higher speeds

Human nervous system consists of two parts:

1. Central nervous system (CNS): brain & spinal cord

2. Peripheral nervous system (PNS): nerves that transmit

   info to & from the CNS

CNS: The Brain - Regions of Interest for Exercise

• Primary motor cortex (frontal lobe)

  • Conscious control of skeletal muscle movement

  • Premotor cortex: Learned repetitive or patterned movements

• Basal ganglia

  • Help initiate sustained or repetitive movements

  • Walking, running, posture, muscle tone

• Thalamus

  • Major sensory relay center

CNS: The Brain - Regions of Interest for Exercise (con’t)

• Hypothalamus

  • Maintains homeostasis, regulates internal environment

  • BP, HR, breathing, body temp

• Cerebellum

  • Controls rapid, complex movements

  • Coordinates timing, sequence of movements

  • Accounts for body position, muscle status

• Reticular formation

  • Coordinates skeletal muscle function & tone

  • Controls cardiovascular & respiratory function

PNS: Subdivisions

• 2 divisions

  • Sensory: carries sensory information from the body via afferent fibres to the CNS

  • Motor: transmits information from CNS via efferent fibers to target organs

PNS: Sensory division

Relay sensory information from receptors in periphery (blood & lymph, internal organs, sense organs, skin, muscle) to the CNS

PNS: Motor division

1. Autonomic

   • Autonomic nerves (i.e., involuntary): produce either excitatory or inhibitory effect on smooth or involuntary muscles

2. Somatic

   • Somatic nerves (i.e., motor neurons): innervate skeletal muscle & produce excitatory response to activate muscle

Reflex arc

Provides the basic mechanism to process “automatic” muscle actions

Motor Unit

• Represents an α-motor neuron & the fibres it innervates

• Motor neuron pool represents all the α-motor neurons that

  innervates one muscle

Neuromuscular Communication - How does the brain communicate with peripheral tissues?

• Electrical signal for communication b/w the brain & the periphery via neurons

Motor Unit: Functional Characteristics

• A motor unit contains only one specific muscle fibre type (type I or type II)

• 3 physiologic & mechanical properties of the muscle fibres they innervate:

  1. Twitch characteristics

  2. Tension characteristics

  3. Fatigability

Twitch Characteristics

• Characteristics include:

  • Force/tension development

  • Contraction speed

  • Rate of fatigue

Tension Characteristics

• A stimulus strong enough to trigger a motor neuron action potential; activates all muscle fibres in the motor unit to contract synchronously

• A motor unit does not exert a force gradation

Tension Characteristics (con’t)

• Force of muscle action varies from slight to maximal via two mechanisms:

  • Increased number of motor units

  • Increased frequency of motor unit discharge

Fatigue

Decrements in muscular performance w/ continued effort, accompanied by sensations of “tiredness”

Central & Peripheral Fatigue

• Central Fatigue = progressive reduction in voluntary activation of muscle during exercise

• Peripheral Fatigue = fatigue produced by changes at or distal to the neuromuscular junction

What causes fatigue?

• Central fatigue is difficult to assess

  • the causes are unclear

• Peripheral fatigue has been associated w/

  • Inadequate energy delivery/metabolism

  • Accumulation of metabolic by-products

  • Failure of muscle contractile mechanism

Proprioceptors

• Sensory receptors in muscles & tendons sensitive to stretch, tension & pressure

• There are two main types of proprioceptors:

  1. Muscle spindles (type Ia & II)

  2. Golgi-tendon organs (type Ib)

Muscle Spindles

• Provide information about changes in muscle fibre length

• Respond to stretch of a muscle & initiate counter muscle action

• Lie parallel to extrafusal muscle fibres

Golgi Tendon Organ

• Connect to extrafusal fibres near tendon’s junction to muscle

• Detect differences in tension generated by muscle

• Provides feedback to monitor discharge impulses from:

  • Tension created in muscle when it shortens

  • Tension when muscle stretches passively

Overload Principle

• Regular application of a specific exercise overload enhances physiologic function to induce a training response

• Can be achieved by manipulating:

  • Training frequency

  • Intensity

  • Duration

Specificity Principle

Training-derived adaptations are specific to the type, intensity, duration, frequency of exercise

Anaerobic Training

• Activities that demand a high level of anaerobic metabolism induce specific changes in the immediate & short-term energy systems

  1. Increased levels of anaerobic substrates

  2. Increased quantity & activity of key enzymes

  3. Increased capacity to generate & tolerate high levels of blood lactate

Aerobic Training: Metabolic Adaptations

• Increased oxidative enzyme activity

• Increased fat metabolism

  • Evident within 2 weeks of training

• Increased carbohydrate metabolism

  • Enhanced capacity to oxidize carbohydrate during maximal exercise

• Muscle fibre-type modifications

  • The fibres become “more oxidative”

  • Type I fibre hypertrophy

Aerobic Training: Metabolic Adaptations (con’t)

• The muscle

  • a-vO2 diff resting oxygen extraction is not affected by training

  • During exercise, maximal a-vO2 diff increases

Aerobic Training: Cardiovascular Adaptations

• The Heart

  • Long-term aerobic training generally increases heart mass & volume

  • Resting heart rate declines

  • Increases resting stroke volume

  • Cardiac output = increases w/ training

Aerobic Training: Cardiovascular Adaptations (con’t)

• The Blood

  • +10-20% within 3-6 training sessions

• Blood Flow

  • Submaximal Exercise

    • Trained individuals have a lower cardiac output than untrained individuals

  • Maximal Exercise

    • Greater total muscle blood flow in trained relative to untrained individuals

Aerobic Training: Pulmonary Adaptations

• No changes in pulmonary function parameters

• Greater encroachment on maximal ventilatory capacity

• Some degree of increase in respiratory muscle strength/endurance

Aerobic Training: Lactate Threshold

• Lactate Threshold increases w/ aerobic training, due to:

  • Decreased rate of lactate formation during physical activity

• Increased rate of lactate clearance (removal) during physical activity

• Combined effects of decreased lactate formation & increased lactate removal

Aerobic Training: Determining Factors

1. Initial level of aerobic fitness

   • Greater benefit for those who have the most room to improve

2. Training intensity

   • The higher the intensity, the better

   • Aerobic capacity improves if effort intensity regularly maintains HR b/w 55-70% of max

3. Training frequency and duration

   • Difficult to define a threshold

Overtraining

Prolonged & intense endurance training can precipitate the syndrome of overtraining or staleness, w/ associated alterations in neuroendocrine & immune functions

Physiological Adaptations to RT - Neural Adaptations

1. Greater efficiency in neural recruitment patterns

2. Increased motor neuron excitability

3. Increased CNS activation

4. Improved motor unit synchronization & increased firing rates

5. Lowering of neural inhibitory reflexes

6. Inhibition of Golgi tendon organs

Physiological Adaptations to RT - Structural Adaptations

1. Muscle fibre hypertrophy

   • Increase protein synthesis, more myofibrils, actin, connective tissue

2. Muscle fibre hyperplasia

   • Occurs through fibre splitting

3. Muscle fibre-type shifts

   • Type II fibres more oxidative w/ aerobic training

   • Type I fibres more anaerobic w/ anaerobic training

4. Metabolic Adaptations

Detraining

• Leads to decrease in 1RM

  • Strength losses can be regained (approx. 6 weeks)

Immobilization

• Major changes after 6 h

  • Lack of muscle use → reduced rate of protein synthesis

• First week: strength loss of 3 to 4% per day

  • Decreased size/atrophy

• Effects on Types 1 & II fibres

  • Cross-sectional area decreased, cell contents degenerate

Muscle Soreness - Acute

• During, immediately after exercise bout

  • Accumulation of metabolic by-products

  • Tissue edema

  • Edema → acute muscle swelling

Delayed-Onset Muscle Soreness (DOMS)

• Temporary soreness that occurs after exercise

  • 1 to 2 days after exercise bout

• Major cause: eccentric contractions

  • Ex: level run pain < downhill run pain

Factors that produce DOMS

• Minute tears in muscle tissue

• Muscle spasms

• Overstretching & tearing

• Acute inflammations

Hypothermia

• Core temp <35°C

• Effects:

  • Shivering, dizziness, weak pulse, shallow breathing, death (if severe)

Hyperthermia

• Core temp >38.3°C

• Effects:

  • Muscle spasms, dehydration, skin irritation, nausea, seizures, dizziness, death (if severe)

Thermoregulation

• Metabolic Heat Production (M)

  • >75% energy from ATP breakdown

• External Work (W)

  • <25% energy from ATP breakdown

• Conduction (K) -+

  • Heat transfer from one solid material to another through direct molecular contact (negligible)

• Convection (C) -+

  • Heat transfer by movement of gas or liquid

    across a surface

  • Major daily thermoregulatory factor

• Radiation (R) -+

  • Heat exchange in the form of infrared rays

  • Major daily thermoregulatory factor

• Evaporation (E) -

  • Can only cause heat loss, not gain

  • “Sweating”

  • Sweat dripping doesn’t equal heat loss

Heat Balance during Exercise

During exercise, the body responds to different thermal “stressor” by altering the aforementioned heat exchange mechanisms

Thermoregulatory Control

• T_core is regulated by the brain

  • Preoptic-anterior hypothalamus (POAH)

    • Body’s “thermostat” located in the brain

    • When body temp deviates, POAH activates thermoregulatory mechanisms

  • Sensory receptors

    • Peripheral thermoreceptors in skin

    • Central thermoreceptors in brain, spinal cord

  • Respond to heat or cold

Thermoregulatory Responses:

• Sweating

  • Increases heat loss via evaporation

• Piloerection

  • Hairs “stand on end” in order to trap still air layer against skin

• Skin Blood Flow

  • Vasodilation & vasoconstriction

• Shivering

  • Elicited by reductions in skin temp

  • Increases metabolic heat production by up to 5 times

Thermoregulatory “Effectors":

• Skin arteriole effectors

  • SNS vasoconstriction (VC) minimizes heat loss

  • SNS vasodilation (VD) enhances heat loss

• Eccrine sweat gland effectors

• Skeletal muscle effectors

• Endocrine gland effectors

Environmental Conditions

• Dry Bulb Temperature

  • Temp measured by a conventional thermometer

• Globe Temperature

  • Index of the amount of “radiant energy” in the air. Reflects the degree of radiant heat gain experience the body in a given environment

• “Wet-bulb” Temperature

  • The lowest temp that can be reached under current ambient conditions by the evaporation of water only

• Humidity

  • Impacts Evaporation

Why does core temp increase during exercise?

• Biophysical factors are important to consider

• An individual’s morphological characteristics

  • Body mass

  • Surface area

  • Tissue insulation

  • Sweat Gland density

Exercising in the heat

• Effects on cardiovascular function

  • Skin arterioles VD to increased dry heat loss, requires increased blood flow compared to exercise in the cold

• Limitation: cardiovascular system overload

  • Heat cannot provide sufficient blood flow to both exercising muscle & skin

  • Impaired performance, increased risk of overheating

Physiological Responses to Altitude- Respiratory

• Pulmonary ventilation increases immediately

• Increased ventilation at altitude = hyperventilation

• Kidneys excrete more bicarbonate

• Gas exchange at muscles decrease

Physiological Responses to Altitude- Cardiovascular

• Short term: plasma volume decreased within few hours

• RBC count increases after weeks/months

• Cardiac output increases for a given VO₂

• Muscles extract more O₂

Physiological Responses to Altitude- Metabolic

• Basal metabolic rate increases

• More reliance on glucose vs. fat

• Increases anaerobic conditions, expected increased lactic acid

Impact of Altitude on Performance

• VO2max decreases as altitude increases

  • Anaerobic performance largely unaffected

  • As little as 500m incurs a decrease in VO2max

Acute Mountain Sickness

• Illness that can affect mountain climbers, hikers, skiers, or travellers at high altitudes, usually >2400m

• Key factors:

  • Headache

  • GI issues

  • Fatigue

High-altitude pulmonary edema (HAPE)

• Etiology (Cause)

  • Related to hypoxic pulmonary vasoconstriction

  • Clot formation in pulmonary circulation

• Symptoms

  • Decreased blood O2

  • Shortness of breath, cough, tightness

• Treatment

  • Supplemental oxygen

  • Immediate descent to lower altitude