Unit 4: Circulatory Response to Exercise and Thermoregulation

Circulatory system’s purpose

¤Transport O₂ and nutrients to tissues

¤Removal of CO₂ wastes from tissues

¤Regulation of body temperature

How does the cardiorespiratory system regulate body temp

Vasoconstriction - ex: when cold, shunts blood away from periphery

Vasodilation- ex: when hot, there’s gradient from skin to atmosphere, heat is radiated to the environment

Two major adjustments of blood flow during exercise

¤Increased cardiac output

¤Redistribution of blood flow

The 3 regulation of MAP during exercise

¤Determinants

¤Exercise pressor reflex

¤Central command

Chordae tendinae

• keeps the valves closed so NO regurgitation (backflow)

What happens if NO chordae tendinae or NO papillary muscles

blood will go to opposite direction of where it’s supposed to go, based on the press gradient

Heart does what

creates pressure and press gradient to drive blood flow

Arteries and arterioles

Carry blood away from the heart

Capillaries

Exchange of O₂, CO₂, and nutrients with tissues

Veins and venules

Carry blood toward the heart

Describe this image

• Aorta —> very compliant (meaning very stretchy)

• Arteriole —> tiny but has mix of smooth muscles

• small arteries —> have smooth muscle

• Vein: temporay storage unit, and very compliant and could hold a lot of blood vol w/o significant change in blood press

Pulmonary circuit vs Systemic circuit

Pulmonary:

¤Right side of the heart

¤Pumps deoxygenated blood to the lungs via pulmonary arteries

¤Returns oxygenated blood to the left side of the heart via pulmonary veins

lower pressure + compliant due to not having to send blood to rest of the body

Systemic circuit:

¤Left side of the heart

¤Pumps oxygenated blood to the whole body via arteries

¤Returns deoxygenated blood to the right side of the heart via veins

MAP of pulmonary circuit and why?

25 mmHg

b/c they are very compliant and have low resistance

MAP of systemic circuit and why?

90 mmHg

b/c it has to pump blood much farther and against more SVR

Normal resting cardio output and is it for sympathetic or pulmonary

5 L/min and it is both

• both CO on each sides are the same

endocardium

innermost and closer to blood vessels

myocardium

smooth muscle

epicardium

upper layer of heart

Heart attack aka _________ is caused by what?

• aka myocardial infarction

• caused by blood clotting (myocardial ischemia) which if prolonged causes the death of myocardial cells (myocardial infarction)

Exercise training protects heart b/c

¤Reduce incidence of heart attacks

¤Improves survival from heart attack

¤Exercise reduces the amount of myocardial damage from heart attack b/c

• Improvements in heart’s antioxidant capacity

Endurance Exercise Protects Against Cardiac Injury During Heart Attack

• lowered risk of myocardial infarction for trained/endurance athletes

• also if trained athletes does have myocardial infarction, they experience less symptoms

Resistance training can ______ cardiovascular health

enhanced

Myocardium structure

¤Only one fiber type (similar to type I)

• High capillary density

• High number of mitochondria

• Striated

¤Cardiac muscle fibers connected by intercalated discs

• Desmosomes: hold cells together

• Gap junctions:  rapidly conduct action potentials

Myocardium vs Skeletal Muscle

¤Skeletal muscle cells

• Large, long, unbranched, multinucleated

• Intermittent, voluntary contractions

• Na+ induced Ca⁺⁺ release from SR

¤Myocardial cells

• Small, short, branched, one nucleus

• Continuous, involuntary rhythmic contractions

• Ca++ induced Ca++ release

Ca2+ induced release

• Ca2+ from SR floods the heart and is key signal of depolarization in the heart

• improved Ca2+ handling results in more forceful contraction

What signals depolarization for Skeletal muscles

Na+

damage to myocyte

No help or repair

Events of Cardiac cycle in order

1) Ventricular filling (mid-to-late diastole)

• ventricular filling + atrial contraction

2) Ventricular systole (atria in diastole)

• Isovolumetric contraction + Ventricular contraction

3) Early diastole

• Isovolumetric relaxation

4) back to Ventricular filling

then the process repeats itself

systole

¤Contraction phase

¤Ejection of blood

• ~2/3 or 60% blood is ejected from ventricles per beat

Diastole

¤Relaxation phase

¤Filling with blood

At rest diastole is _____ than systole

During exercise both systole and diastole are ______

¤At rest, diastole longer than systole

• @ rest you’re in diastole for 2/3 of overall cardiac cycle

¤During exercise, both systole and diastole are shorter

• b/c HR increases —> makes the cardiac cycle go faster

Ventricular filling (mid-to-late diastole)

1) Ventricular filling

• AV valves are open b/c Patrial >> Pvent

• passive Blood flow goes atria —> ventricles

• Ventricles are at diastole, Aortic + Pulmonary valves closed

2) Atrial contraction

• pace maker stimulates + depolarization of atria

• causes atrial contract

• this atrial contraction gives more boost/ more blood to ventricle (atrial kick)

  • this boost is good for exercise

Ventricular systole (atria in diastole)

3) Isovolumetric contraction

• ventricles depolarize then causes contraction

• all valves are closed.

4) Ventricular ejection

• since Ventricular press >> aortic press + pulmonary press

  • it causes Aortic/semilunar valve (left) and Pulmonary/semilunar valve (right) to bust open

• This causes ejection of blood

• we then lose blood volume. —→ SV = EDV - ESV

Isovolumetric relaxation (early diastole)

• Not enough pressure and gradually relaxes myocytes

• all valves are closed

Ventricular filling

return to it and higher BV

what type of pressure is close to BP?

aortic pressure when it is 120/80

x-descent

downward wave, reflecting right atrial relaxation and the AV valve moving down during ventricular contraction

C-wave

Since ventricular contraction squeezes against all closed gates

• there’s pressure build up that causes the bump in atrial pressure

• (this is due to bulging of AV values back into atrial chamber)

V-wave

final pulling/increasing atrial press before AV valves open and pushing blood to ventricles

• occurs btw late ventricular systole and early diastole

which wave has highest atrial volume

v-wave

Dicrotic notch

Reverberation, incisura/dicrotic notch

Reverberation:

• makes dicrotic point

Dicrotic notch/ incisura

• a small dip or notch on the arterial blood pressure

• marks the closure of the aortic valve as systole ends, causing a brief backward flow of blood

Explain EMPV

ECG

• SA node fires (electrical activity) to stimulate heart to contract or relax

Mechanical event

• shortening or enlarging of chamber

• systole or diastole (contraction)

Pressure event

• pressure created + squeeze on chamber

Volume

• after pressure gradient, it is the blood flow

P-wave

atrial depolarization (contraction)

T-wave

ventricular repolarization (diastole/relaxation)

QRS wave complex

ventricular depolarization (contraction)

Heart sounds

First: closing of AV valves —> lub

Second: closing of A + P valves —> dub

Pulse pressure

difference btw systolic + diastolic

Clinical MAP

MAP = DBP + 0.33 (SBP - DBP)

• it is 1/3 of pulse pressure b/c @ rest, you are in diastole for 2/3 of overall cardiac cycle

  • meaning 1/3 of the time you are generating high pressure

Systolic BP

• pressure generated during Ventricular contraction

• turbulent flow

Diastolic BP

• pressure in arteries during cardiac relaxation

• disappearing sound —> which then reestablishes lamellar flow

this a graph of what?

graph of Aortic

Stroke volume equation

SV = EDV - ESV

EDV is measured after isovolumetric relaxation

ESV is measured after isovolumetric contraction

What sounds are we hearing when measuring BP w/ occlusion

korotkoff sounds (turbent flow)

No sound is produced meaning the flow is

lamellar

Physiological MAP

MAP = CO x SVR

SVR = TPR = TVR

Cardiac Output

• delivery

• HR x SV

Short term regulation of MAP

• Sympathetic NS (

• Baroreceptors in aorta and carotid arteries

  • sensed Increase in BP → decreased SNS act

    • which then decreases CO and poss Resistance → higher BP

  • sensed Decrease in BP → Increased SNS act

    • which then increases CO and poss Resistance → lower BP

Long-term regulation of MAP

• In days, weeks, years

• Kidneys

  • control BV

    • Ex: low BV → low SV x low CO → low BP

More trained person has ____ HR and ___ SV

lower HR and higher SV due to using less energy

Regulation of HR

Parasympathetic NS

• thru Vagus nerve / parasympathetic tone (like a break on a car)

• inhibits SA and AV node —> slows HR

Sympathetic NS

• thru cardiac accelerator nerves

• stimulates SA + AV node → increases HR (chronotropy)

LOW resting HR is due to ______ tone

parasympathetic tone

_____ in HR at start of exercise and why?

• increase in HR @ start b/c of parasympathetic withdrawal

  • up to 100 bpm

• later increase is due to increase activation of SNS

Regulation of SV

1.End-diastolic volume (EDV)

¤Volume of blood in the ventricles at the end of diastole (“preload”) 

• getting more blood —> higher SV

2. Average aortic blood pressure

   ¤Pressure of the heart that be overcome for ventricles to eject blood (“afterload”)

   • Mean arterial pressure

   • higher afterload —> lower SV

3. Strength of the ventricular contraction (contractility)

   ¤Enhanced by circulating Epi/Noepi and direct sympathetic stimulation of heart

• more contractility —> more blood ejected —> Higher SV

4. HR

Hypertension ____ afterload, which results in _______ ESV, and _____ SV

Frank- Starling Law of Heart

¤Preload: degree of stretch of cardiac muscle cells before they contract (Frank-Starling law of the heart)

¤Cardiac muscle exhibits a length-tension relationship

¤At rest, cardiac muscle cells are shorter than optimal length

¤Slow heartbeat and exercise increase venous return

VR increased by

1.Venoconstriction

¤Via SNS —> reduces compliance and capacitance (storage) of veins → increases blood flow to the heart

2.Skeletal muscle pump (helpful during exercise)

¤Rhythmic skeletal muscle contractions, squeeze on veins to let blood flow in the extremities toward the heart

¤One-way valves in veins prevent backflow of blood

• increases SV too

• generates more force via gaining more contractile proteins —> further increasing VR

3.Respiratory pump (NOT helpful @ rest due to not intensely breathing)

¤Changes in thoracic pressure pull blood toward heart

• inhalation →

  • increased vol and decreased press of thoracic cage compared to abdominal cavity —> blood flows to thoracic cage to the heart

    • (due to blood flow HP → LP)

Heart Rate

purple: steady state exercise

blue: high intensity exercise

Effects of Sympathetic Stimulation on Stroke Volume

Strength of Contraction

¤Contractility (Inotropy): contractile strength at a given muscle length, independent of muscle stretch and EDV

• Positive inotropic agents increase contractility

  • Increased Ca⁺⁺ influx due to sympathetic stimulation

  • Hormones (thyroxine, glucagon, and epinephrine)

¤Negative inotropic agents decrease contractility

• Acidosis (too much acid / decrease in pH)

  • this is dangerous b/c it will cause the aerobic heart to rely on anaerobic processes

• Increased extracellular K⁺

• Calcium channel blockers

Intrinsic Control of Blood Flow

Ability of local tissues to constrict or dilate arterioles that serve them

• alters regional flow based on needs

¤Metabolic mechanisms (VD) —→ (IMPORTANT FOR EXERCISE)

• Buildup of local metabolic by-products

• decrease in O₂

• Increase in CO₂, K⁺, H+, lactate

• causes Functional sympatholysis

¤Endothelial mechanisms (mostly VD)

• Substances secreted by vascular endothelium

• Nitric oxide (NO), prostaglandins, EDHF

¤Myogenic mechanisms (VC, VD)

• Local pressure changes can cause Vasoconstriction (VC), Vasodilation (VD)

• Increase in P → Increase VC

• Decrease in P → increase VD

Central Command

• initial signal to drive cardiovasc sys and reset the set point coming from higher brain centers b/c of centrally generated motor signals

• Anticipation that you’ll exercise —> your set point is reset to higher set point

Central command is fine-tuned by feedback from

¤Heart mechanoreceptors

¤Muscle chemoreceptors

• Sensitive to muscle metabolites (K⁺, lactic acid)

¤Muscle mechanoreceptors

• Sensitive to force and speed of muscular movement

¤Baroreceptors

• Sensitive to changes in arterial blood pressure

Exercise Pressor Reflex (EPR)

¤Metaboreflex

• Chemicals (metabolites) released from contraction stimulate chemoreceptors

• Stimulation of chemoreceptors send afferent information to the medullary CV centers via group IV afferent nerves.

• This causes a “shift” in MAP control: baroreflex resetting

¤Mechanoreflex

• Mechanical deformation (movement) from contracting/moving limbs stimulate mechanoreceptors (propioceptors)

• Stimulation of mechanoreceptors send afferent information to the medullary CV centers via group III afferent nerves

• This causes a “shift” in MAP control: baroreflex resetting

Our set point if everyone’s around 120/80 BP, is

MAP (90 mmHg)

Isolation of mechanoreceptors

• lay down on ground, you are inactive

• but, if diff person puts your feet in a bicycle-like pedal and that person is connected to you, but in a diff bicycle

• every time that person moves the pedals, it moves your pedal

• b/c of this mechanoreceptors would fire b/c they detect that your legs are moving

  • then BP increases

isolation of chemoreceptors

• occluding blood flow in arm and make person do forearm grip exercise

• you will accumulate metabolites

• since you occluded blood flow → metabolites do NOT deposit anywhere

• but as soon as you release them —> BP increases

  • even if NO body movement

• This is due to chemoreceptors firing

Functional sympatholysis

SNS's vasoconstrictive response is lowered in exercising skeletal muscles, allowing for optimized blood flow to meet metabolic demands

During exercise MAP = CO x SVR

increase MAP = increase CO x SVR

• skin

  • do intense in hot environment

    • vasodilates skin (lowers SVR)

  • can be up to 8 L/min for CO in hot environment

• muscles

  • engaging more muscle + doing harder exercise

  • metabolites accumulate in the active muscles

    • causes functional sympatholysis → vasodilating muscle → increase blood flow to muscles

  • lower SVR

Cardiovascular Adjustments to Exercise ( in order)

1. Central command

• anticipation of exercise withdraws parasympathetic tone

2. Mechanical

• mechanoreceptors detect movement, activating part of the exercise pressor reflex to reset MAP to a higher set point

• skeletal muscle pump increases venous return, which increases SV.

• respiratory pump increase venous return and SV, but the increased breathing rate is caused by metabolite buildup

3. Metabolic

• metabolite buildup triggers metaboreceptors to activate part of the exercise pressor reflex to raise MAP to a higher set point, increases breathing rate (increasing respiratory pump), and triggers functional sympatholysis (vasodilation to working muscles)

4. Autonomic

• parasympathetic withdrawal and sympathetic nerve activity increases from increased firing of metaboreceptors: increased HR, increased contractility of heart, increased SVR (except skin and muscles), increased afterload, increased venoconstriction (increases venous return and SV)

5. Humoral

• increased norepinephrine and epinephrine, which also increase HR, contractility, venoconstriction

During exercise

• your muscles work harder, meaning more O2 than @ rest

• in order to deliver O2, heart beats faster → faster pulse

Why is it good to exercise regularly

• your heart gets used to moving more blood thru body

• left ventricle hypertropies and stronger contraction

• w/ each heart beat pumping more blood-

  • the heart beats less often → lower HR during exercise and lower HR during rest

Calculation of VO2 max

VO2 max = CO X a-VO2 difference max

• CO = delivery

  • HR x SV

• a-VO2 difference max = extraction

Short-term vs Long-term exercise CV adaptation

Short term exercise ( w/in 1-4 months)

• initial VO2 max increases by 26%

  • this is due to retaining more plasma volume → increases SV → increases CO

  • increasing SV > increasing a-vO2 → not good @ extraction

Long term exercise ( w/in 28-32 months)

• VO2 max increases by 42%

  • increasing a-vO2 > increasing SV → Get better @ extraction

Training-induced increased maximal SV

Increased Preload (EDV)

• increased plasma volume @ start

• increased VR

  • b/c increased plasma

• increased Ventricular volume

  • b/c increased plasma

Decreased Afterload (TPR)

• decreased arterial constriction

• increased max muscle blood flow w/ NO change in MAP

  • This is all b/c you get better @ blood flow distribution, where you’re more conditioned to vasodilate and do functional sympatholysis in appropiate places

  • this then lowers resistance → causing low afterload

Increased Contractility

• eccentric hypertrophy (expansion of chamber) good in exercise b/c it is accompanied by concentric hypertrophy (thicker, stronger muscle around chamber)

Left ventricular hypertrophy w/o exercise is good or bad?

bad b/c it is a response to hypertension

What is concentric hypertrophy a response to?

to higher pressure (from resistance training or chronic hypertension, which increases afterload and puts more stress on left ventricle), it wants to overcome the pressure

• it does this by the walls thickening —> sarcomeres added in parallel

• ex: constantly picking up heavier weight

What is eccentric hypertrophy a response to?

due to volume overload that occurs w/ aerobic training → increased Vr → increases filling of LV → sarcomeres add in series

based on increased VR (filling a lot)

• needing more vol

Thickened muscle w/o expansion of chamber volume, what happens

• you get smaller size of chamber vol → smaller size of chamber

• since the chamber size is small → you get smaller preload

Resistance exercise

gray area

• b/c it has some eccentric hypertrophy, but def has concentric hypertrophy

Arteriovenous O2 difference

Increased Muscle blood flow

• decreases SNS vasoconstriction

Improved ability of the muscle to extract oxygen from the blood

• increased capillary density (more SA)

  • better extraction

  • fast blood flow via muscle

• increased mitochondrial # @ SK muscle

  • increased metabolism

  • better extraction

For exercise training and diffusion distance

exercise training

• increases more blood vessel to drop off stuff → reducing pressure on diffusion

Diffusion distance

• Increased diffusion distance causes innermost layer of the heart to be more @ risk of ischemia

• smaller diffusion distance causes innermost layer of the heart to be less @ risk of ischemia