OVERALL KINS 4630 STUDY GUIDE

atria

collect blood coming into heart

ventricles

pumping chambers that push blood out to the lungs and body

path of deoxygenated blood

right atrium → right AV valve → right ventricle → pulmonary valve → pulmonary artery → lungs

path of oxygenated blood

pulmonary vein → left atrium → left AV valve → left ventricle → aortic valve → aorta → body

arteries

high pressure highways carrying bloos away from heart

arterioles

squeeze or open up to control where blood goas (resistance vessels)

capillaries

exchange stations where oxygen and nutrients drop off into tissues, and waste gets picked up (super fragile)

venules & veins

low pressure return pipes holding lots of volume (capacitance vessels)

one way valves

located in veins

so blood doesn’t slide backward due to gravity

vasoconstriction

radius decreases

resistance shoots way up and local flow drops

vasodilation

radius increase

resistance drops and blood floods through easily

spontaneous rhythmicity

heart generates own electrical signals (~100 bpm)

pathway of heart electrical signal

SA node → across atria → AV node → interventricular septum → purkinje fibers

SA node

natural pacemaker

AV node

creates a pause in heart

P wave

atria electrical signal, squeeze last bit of blood into ventricles

QRS Complex

ventricles electrical signal, AV valves snap shut

pressure shoots up forcing pulmonary/aortic valves to open and blood pumps out

T wave

ventricles repolarize

pressure drops, valves close

blood passively flows back into ventricles from atria

cardiac output

total amount of blood pumped out of the heart PER MINUTE

Heart Rate x Stroke Volume

Stroke Volume

amount of blood pumped out in one single BEAT

SV = EDV - ESV

EDV

how much blood was in the ventricle right before it squeezed

ESV

how much blood was left over after it squeezed

ejection fraction

percentage of blood successfully pushed out compared to what started in chamber

EF = SV / EDV

cardiac muscle

short branching fibers connected by gap junctions

beats involuntarily using calcium to trigger more calcium

functional synctium

individual cells working together

skeletal muscle

long, cylindrical, multi-nucleated fibers

voluntary, strictly require a nerve signal to contract

parasympathetic nervous system

keeps resting HR lower than 100bpm via vagus nerve and acetylcholine

sympathetic nervous system

releases adrenaline/norepinephrine to speed up HR and contract harder during stress/exercise

baroreceptors

stretch sensors in aorta and carotid arteries

feel if blood pressure is getting too high or too low

integration center

brains cardiovascular control center reviews data

effectors

brain sends signals back to heart and blood vessels

heart: change HR/strength of contraction

blood vessels: changes width

metabolic control of blood flow

build up of waste acts as chemical signal telling local vessels to dilate

endothelial control of blood flow

inner lining of vessels release chemicals like nitric oxide to relax smooth muscle and increase flow

myogenic control of blood flow

vessels naturally bounce back

functional sympatholysis

active muscle tells NS to ignore constriction commands and stay wide open to get blood

extrinsic control of blood flow

SNS triggers widespread vasoconstriction in inactive tissue to channel blood toward active areas

muscle pump

muscles physically squeeze deep veins, pushing blood upward like squeezing a tube of toothpaste

respiratory pump

pressure changes in chest and belly act like vacuum, pulling venous blood up toward heart

systemic circulation

high pressure

blood must travel through body

needs thick, muscular walls to generate high pressure

pulmonary circulation

low pressure

blood only has to go right next door to lungs

low pressure to prevent fluid leaking out of lungs

how does body move O2 around?

2% dissolved in blood plasma

98% bound to hemoglobin (4 per hemoglobin)

S shaped Oxyhemoglobin saturation curve

high O2 pressure in lungs: hemoglobin grabs O2

low O2 pressure in tissues: hemoglobin unloads O2

pH & temperature effect on oxyhemoglobin curve

shift to the right

hemoglobin loosens grip, dumping extra O2 where muscles need it

haldane effect

When CO2 binds to hemoglobin, helps O2 push off

When O2 is high in lungs, helps push CO2 off

Removal of CO2

CO2 naturally flows out of muscle cells into blood because higher concentration of it in muscle rather than blood

ways CO2 travels in blood

7-10% dissolved in plasma

20-30% bound to hemoglobin

60-70% turned into bicarbonate ions

acid base balance

too much CO2 buildup, chemical buffers soak up CO2 and lungs breathe faster to remove CO2

a-vO2 diff definition

tells how much O2 your tissues actually extracted and used

(O2 in arteries going out to body) - (O2 left in veins coming back to heart)

a-vO2 diff during exercise

during exercise, muscles need more O2, so a-vO2 difference increases compared to at rest

Fick Equation

Total O2 Consumption = Cardiac Output x a-vO2 difference

to get more O2 to muscles, heart pumps more blood and body extracts more O2

hemoglobin

in red blood cells

lower affinity on oxygen

job to travel around body and release O2 easily to tissues

myoglobin

in muscle cells

super high affinity for oxygen

job is powerful magnet that pulls O2 out of blood and holds tightly as local storage tank inside muscles

factors influencing O2 delivery and uptake

1. blood content: how much hemoglobin and O2

2. blood flow: cardiac output, how well vessel direct blood to needed places

3. local conditions: temperature, pH (hot/more acidic = O2 lets go faster)

4. fick equation: delivery = cardiac output, uptake = myoglobin and a-vO2 difference

HR response to exercise

linear relationship until hit max

stroke volume response to exercise

shoots up in beginning then levels off early on

cardiac output response to exercise

skyrockets during heavy exercise to feed muscles

how to predict max HR from submaximal test

draw line straight up to their age-estimated max HR to estimate their overall fitness without exhausting them

due to HR going up in linear relationship with exercise intensity

determinants of stroke volume

1. end diastolic volume (preload)

2. aortic pressure (after load)

3. contractility

aortic pressure

resistance the heart has to push against to get blood out into the body

frank-starling mechanism

more blood that fills the heart → more heart muscle fibers stretch → more contractility

systolic blood pressure

top number

increases in straight line as intensity increases because heart is pumping a massive volume of blood into arteries per minute

diastolic blood pressure

bottom number

stays mostly flat due to local control of blood vessels

cardiovascular drift

during steady-state exercise, HR drifts upward & stroke volume drifts downward

Phase 0 of ventilation

right before movement, breathing speeds up a little bit because brain anticipates

phase 1 of ventilation

sudden surge in breathing driven by brain signals and moving joints

phase 2 of ventilation

breathing continues to rise gradually as body detects rising CO2 and acid

phase 3 of ventilation

breathing levels off and stays stable

phase 4 of ventilation

after stop, breathing stays high for a bit to pay your O2 debt then slowly returns to normal

lactate threshold

exact point during hard exercise where muscles start producing lactic acid faster than body can clear it out

ventilatory threshold

exact point where you suddenly start breathing much harder and faster

VE / VO2 and VE / VCO2

ratios tracking how hard your lungs are working compared to how much O2 youre taking in and how much CO2 you’re blowing off

bicarbonate buffer system

main one outside cells

bicarbonate grabs extra acid, turns it into weak carbonic acid, breaks it down into water and CO2

protein buffer system

inside cells and blood

amino acids on proteins can absorb or release acid as needed

phosphate buffer system

inside cells

helps mop up extra acid in cellular fluid

muscular strength

absolute maximum force a muscle can produce in one signal effort

muscular power

force x speed

how fast you can apply that maximum force

muscular endurance

muscles ability to keep contracting repeatedly over a long time without getting too tired

aerobic power

maximum capacity of your heart and lungs to deliver O2 for long steady efforts

anaerobic power

ability to generate massive energy in very short explosive burst without relying on O2

individuality

workout must be tailored to unique body, goals, and fitness level

specificity

get what you train for

progressive overload

gradually asking more of your body over time to keep making gains

reversibility (use it or lose it)

if stop training, fitness levels will drop back down

periodization & variation

changing up routine and cycling through different phases to prevent boredom, burnout, and plateaus

continuous training

low-moderate intensity at a steady, unchanging pace for longer time

best for: building strong aerobic endurance base and fat burning

interval training

alternating between bursts of hard/maximal work and periods of recovery

best for: boosting speed, pwer, and VO2max when short on time

neural phase

get stronger without muscles getting bigger

NS recruits more motor units, fires signals faster, synchronizes better, turns off opposing muscles

hypertrophic phase

actual muscle growth takes over

myofibrillar & sarcoplasmic hypertrophy

myofibrillar hypertrophy

adding more contractile proteins to make fibers bigger and stronger

sarcoplasmic hypertrophy

strengthening the fluid and connective tissue framework around the fibers to handle heavier loads

hypertrophy

existing muscle fibers get fatter and bigger

dominant mechanism for human muscle growth

hyperplasia

muscle fibers actually splitting or multiplying to create brand-new fibers

in humans, plays very minor role

satellite cells

stem cells living just outside your muscle fibers

satellite function during injury

1. activation: multiply

2. migration & fusion: donate own nuclei to muscle cell

3. repair: muscle uses those nuclei to repair fibers

muscle atrophy

shrinking of muscle fibers because protein breakdown happens faster than protein synthesis

immobilization

causes rapid and severe atrophy because of sudden mechanical unloading

requires heavy rehad to fix

training cessation

causes gradual loss of fitness

retraining is much faster due to body retaining extra nuclei and neural pathways

DOMS

ache and stiffness that hits 12-24 hours after hard workout due to microscopic tears in muscle

especially after eccentric contractions

resistance training men vs women

similarities: both build relative strength and muscle size at similar rates

differences: men have higher absolute muscle mass and breater baseline upper body strength

resistance training young vs old

similarities: older adults can still successfully building muscle and adapt neurally

differences: old adults experiences anabolic resistance, need longer recovery times, and have lower absolute ceiling for maximal strength