Ex phys final

Cries in VO2= CO * a-vO2dif

PO2 throughout the body

in alveoli→ 105

lungs to systemic arteries→ 100

systemic veins→ about 40

PCO2 throughout body

in capillaries→ 40

Lungs to systemic arteries→ 40

Systemic veins→ 46

temperature’s affect on hemoglobin curve

warmer temps make O2 unload easier

• warm muscles are muscles in use

• cold muscles are muscles at rest

pH affect on hemoglobin curve

lower pH makes O2 unload easier

• lower pH, aka more hydrogen atoms, aka more CO2 used means muscle needs O2

respiratory control center

medulla and pons

• control rate/depth of breathing

• unconscious control

• influenced by chemoreceptors

heart rate regulation

autonomic→ parasympathetic slows heart

hormonal→ cortisol (and GH) and T4 increase HR

cardiac cycle

systole- aka contraction normally takes 1/3 of cycle

• with exercise, this is 0.2 sec

diastole, aka relaxation normally takes 2/3 of cycle

• with exercise, this is .13 sec

SV values (EDV, ESV, SV)

EDV- 120 ml/beat

ESV- 70 ml/beat

SV- at rest, 80 ml/beat

HR influences

(temp, neural, hormone)

Temp: direct relationship. Inc temp inc. HR

Neural: Sympathetic stim increases, parasympathetic decreases HR

Hormones: catecholamines, and thyroid hormones inc HR

SV influences

1. preload- End-diastolic volume

2. sympathetic stimulation

3. afterload- mean arterial blood pressure

preload influences

venous return

• venoconstriction of non-working muscle

• skeletal muscle pump

• respiratory pump

Frank-starling mechanism

sympathetic stimulation on SV

increased sympathetic stimulation will increase cardiac contractility

• including better calcium handling

• E/NE and thyroid hormones will also increase contractility

afterload affect on SV

if it is high, MABP will increase the pressure of the aorta, making the L ventricle have to work harder to push blood to the body

• hypertension:( damages the heart)

Mean arterial BP (definition and formula)

the average pressure in arteries

MABP= CO * TPR

MABP= Diastolic BP plus 1/3 pulse pressure

pulse pressure

difference between SBP and DBP

mean arterial BP, short and long term regulation

Short term:

• chemical and baroreceptors signal to SNS

• SNS will inc stimulation to vasoconstrict or decr stimulation to vasodilate

Long term:

• kidneys control blood volume and therefore BP

TPR regulation

length- you can really only change this by changing weight

viscosity of liquid- aka hematocrit. This can be changed by RAAS or aldosterone

radius of vessel- controlled be frequency of SNS stimulation

• local factors can vasodilate or vasoconstrict

• alpha 1 receptors vasoconstrict

• angiotensin II vasoconstricts

Blood pressure “formula”

BP = CO * TPR

assumptions of submax testing:

1. after 110, Hr increases linearly

2. every intensity of exercise has an O2 consumption rate

3. with incremental exercise, each level has its own steady stae

4. submax tests can be used in conjunction with HR max to predict the power output/exercise capacity

CV changes with exercise

• bloodflower redistribution (more to muscles, less to GI tract)

• inc CO

• improved a-vO2 dif

blood redistribution is controlled by:

vasoconstriction:

• myogenic stretch reflex

• sympathetic stimulation to non-working tissue

Vasodilation

• local factors from working muscles produce H+, CO2, NO which all signal for local dilation

Fick equation

VO2= CO * a-vO2 difference

basically amount of O2 used is amount of blood pumped times the amount of O2 taken up by blood

O2 demand during incremental exercise

increases much higher than at rest

will inc with every intensity

CO change with incremental exercise

CO will dramatically inc until it reaches the need, then inc slowly

SV response to incremental exercise

SV will inc rapidly, then plateau around 40% VO2 max

• in highly trained individuals, they train their heart to pump efficiently so that SV doesn’t plateau

• for 99.9% of population, all CO increase after 50% VO2max comes from HR

a-vO2 difference response to incremental exercise

changes a lot early/low intensity, increases slowly after about 50% VO2max

• inc is due to a high amount of O2 taken up for oxidative phosphoryation

BP response to incremental exercise

SBP increases. Vasoconstriction to the rest of the body requires inc in BP

DBP doesn’t really change→ this would decr filling time and EDV

criteria for meeting VO2 max

1. plateau in VO2 despite inc work rate

2. RER is over 1.15 (ratio of gases used)

3. HR in final stage is within 10 bpm of HRmax

   • (high blood lactate, RPE of 17+, HR doesn’t inc with work rate)

double product

Hr *SBP

• inc linearly with intensity

• indicates myocardial O2 consumption

stroke work

SV * mean systolic pressure

aka the amount of work the L ventricle has to do to push out blood

arm vs leg exercise (HR and BP)

• BP is higher bc there is more inactive muscle tissue (aka legs)

• HR is higher bc of more sympathetic stimulation (to stimulate for vasoconstriction)

alveolar type 1 cell

simple squamous, is the lining of the alveoli

alveolar type 2 cell

this type of cell secretes pulmonary surfactant, which prevents the alveoli from collapsing

equation for flow of gas

flow = (P_alveolar- P_atmophere)/resistance

change volume→ pressure changes→ get flow

ways O2 can exist in plasma

• hemoglobin- 98%

• dissolved in plasma- 1.5%

ways CO2 can exist in plasma

• on hemoglobin- 30%

• dissolved in plasma- 10%

• mixed in as bicarbonate- 60%

P50

partial pressure necessary to keep 50% of hemoglobin saturated with O2

things that inc HB’s affinity for oxygen

(mean it holds on to O2, muscle doesn’t need it)

• decr temp

• decr PCO2

• inc pH (more alkaline/basic)

things that decr Hb’s affinity for oxygen

(make it easier for O2 to leave, mean tissue needs O2)

• high temp

• low pH (CO2 production, more acidic, more H+)

Hering-bruer inflation reflex

prevents lungs from over-inflating

stretch receptors in (intercostals???) stop inhalation

sensors that affect pO2, pCO2, pH of blood

• peripheral chemoreceptors (in the aortic arch and carotid bodies, which supply blood to the body and brain)

• central chemoreceptor (in the medulla oblongata, directly senses ECP’s pH)

Neural controllers of breathing

• medulla oblongata is the leader/pace-setter (inspiration via phrenic n and intercostals)

• RR is modified by the pons (inhibitory, fine tuning)

P wave on EKG

atrial depolarization

QRS complex on EKG

ventricular polarization and atrial repolarization

ST segment and T wave on EKG

ventricular repolarization

IRV

inspiratory reserve volume

the amt that can be inspired after a normal inspiration

ERV

expiratory reserve volume

the amt that can be expired at end of normal expiration

VC

vital capacity

max volume inspired/expired in one breath

TV + IRV + ERV

RV

reserve volume

amount left after ERV/max exhalation

there is some amt of air needed in lungs to prevent them from collapsing

TLC

total lung volume/capacity

the amount of air in the lungs after a full inspiration

VC + RV

FVC, FEV1

forced vital capacity

VC but inhaled and exhaled forcefully

FEV1- amt air forcefully expired in1 sec

FECV1/FVC

ratio of amt of air blown out in 1 sec to amt of air you can forcefully blow out

you want to get 80% or more out to be normal

PEF (test)

peak expiratory flow- highest flow rate of air during max exhale

done after surgery to clear CO2 from lungs and inc RR

MVV

max ventilatory volume

amt of air breathed in during sustained voluntary effort

minute ventilation (V_e)

TV * RR

amt expired each minute

usually 70% of MVV

pCO2 on ventilation

CO2 drives ventilation!!!!!!

inc in this increases Ve

• inc in pO2 decreases Ve

V_e change (rest→exercise)

Ve will inc rapidly with onset, then inc steadily

pO2 and pCO2 remain unchanged relatively bc of this increase right away

ventilatory response to exercise (trained vs untrained)

trained- ventilation is less frequent at rest and at any intensity of a submax exercise

• better CV shape (SV inc, HR can relax with the same CO)

• body is better at utilizing O2

• change in aerobic capacity of locomotor muscles

untrained- ventilation is more frequent at rest and at any submax intensity of exercise

ventilatory threshold

where your RR inc disproportionately to the O2 consumption

this illustrates the shift from aerobic to anaerobic respiration (and inc CO2 production)

• untrained occurs around 50% VO2max

• trained occurs higher, maybe 75% VO2 max

myoglobin O2 affinity

much higher than hemoglobin, even at low pO2

• allows for Mb to “store” O2 as a reserve

• shuttles O2 from cell membrane to mitochondria

types of non-steroid hormones

peptide-

• hydrophilic, made in ER and golgi/stored in vescicles. enter blood as “free hormone”

Amine hormone-

• aka catecholamines and thyroid hormones

(Prostaglandins) a third type of hormone

ADH

• from posterior pituitary

• to kidneys

• prevents water loss by resorbing Na+

  • inc BP

• inc with exercise

GH

• from anterior pituitary

• to all cells

• inc use of fats/FFA as an energy source

  • decr use of carbs as a fuel

  • “supports” actions of cortisol

• Inc with exercise

Thyroid hormones

• from thyroid

• to whole body

• inc HR and contractility

  • inc FFA mobilization

  • “mimic” the affects of catecholamines in this way

• inc with exercise

  • no chronic adaptations to exercise

insulin

• from pancreas

• to whole body

• inc glucose uptake

  • decr BG

• decr with exercise

glugagon

• from pancreas

• to whole body

• decr glucose uptake

  • inc BG

  • inc protein and fat use for fuel

  • influenced by catecholamines

• inc with exercise

catecholamines

• from adrenal medulla

• to whole body

• inc HR and contractility

  • decr glucose uptake→ MAINTAIN BG

  • inc glycogenolysis in liver and lipolysis

  • vasoconstriction

• inc with exercise

  • decrease with training for same exercise-→ progressive overload!

aldosterone (mineralocorticoid)

• from adrenal cortex

• to kidneys

• resorbs Na+, inc fluid retention

  • inc BP

• inc with exercise

cortisol (glucocorticoid)

• from adrenal cortex

• to whole body

• prevent glucose uptake in body

  • inc gluconeogenesis in liver

  • inc FFA mobilization

• decr/not produced with low intensity exercise, inc with higher intensity exercies

renin

• from kidneys

• to liver

• inc water resorption

  • inc BP

  • increase vasoconstriction

how BG is maintained

1. glycogenolysis in liver

2. lipolysis in liver

3. FFA mobilization in liver

4. preventing CHO uptake in muscle tissues

beta adrenergic receptor effects

• beta 1 has no E/NE preference

• beta 2 MUCH prefers E

beta1→ inc hr, glycogenolysis, lipolysis

beta2→ inc bronchodilation, vasodilation

alpha adrenergic receptor effects

• both slightly/equally prefer E/NE

alpha1→ vasoconstriction

alpha2→ opposes actions of beta receptors

leptin

hormone that influences appetite

• from hypothalamus

• inc insulin sensitivity and FA oxidation

• too high concentration activates SNS, CV remodeling, heart failure

adiponectin

• inc insulin sensitivity and has FA oxidation

• too much inc coronary heart disease/myocardial hypertrophy risk

• too little causes visceral fat accumulation/hyperglycemia

change in appetite hormones w increased fat mas

MORE leptin

Less adiponectin

• leads to T2D and low-grade inflammation

  • fatty pancreases→ more beta cells→ more insulin-hyperinsulinemia

  • too much leptin→ decr receptors→ leptin resistance→ hyperinsulinemai

  • TSH inc→ hyperthyroidism→ inc in fat mass → HP axis inc cortisone chronically

  • ghrelin is decr→ decr growth hormone → decr lipid mobilization→ inc food uptake→ hypogonadism/hyperandrogenism

hormone signaling that would mobilize fat mass is blocked

testosterone

from testes

• anabolic (promotes tissue rebuilding/performance enhancements)

• promotes masculine characteristics

Estrogen/Progesterone

released from ovaries

• establish and maintain reproductive fn

• lack of estrogen can cause osteoporosis/athletic dysmenorrhea

• FSH/LH/estradiol change with exercise

overload

effect of training when body is exercised at lvl above what it is used to

adaptations from endurance training

• inc in VO2 (from SV and a-vO2 dif)

• inc SV (inc preload, decr afterload, inc contractility)

• inc a-vO2 dif (venous O2 changes, muscle blood flow, capillary density, mitochondrial #/size)

other adaptations/metabolic changes with endurance exercise

(aerobic enzymes, lactate Dehydrogenase form, IM fatty acid stores, FFA uptake ability, enzymes for lipolysis)

• inc aerobic enzymes

• lactate Dehydrogenase shifts to H-form (makes more lactate than pyruvate)

• inc IM fatty acid stores and glycogen

• inc FFA uptake ability

• inc enzymes for lipolysis

acute CV response to exercise

inc in: HR, SV, CO, MABP, blood flow to working muscles

• at 95% of RM1, you can see up to 320/350mmHg for BP and 170bpm

• be v careful with valsalva, this can cause reactive hyperemia

chronic CV response to exercise

decr RHR, (individual)

resting MABP is lower

inc in SV, mostly due to change in lean muscle mass

general adaptation syndrome

body gets “stressed” from resistance training and will compensate to this stress w minimal fatigue

• this is good stress and how we see adaptation

overreaching

intentionally training excessively, which leads to short term decrements

• you are out for a day or two to recover

• can be used intentionally to get out of plateaus

overtraining

when the body is way way over-stressed from workouts and this causes long-term decreases in performanve

• can last weeks-6 months

• can extend to ending athletic careers

exercise and immunity

immune system is transiently suppressed for 3-72 hrs post workout

if someone is overtrained/lacks sleep/additional stressors→ immune response is even worse

Detraining

2 days→ we see initial atrophy due to decr protein synthesis

• little later, inc protein resorption

Strength drops around 2 weeks

• we see 7-12% change/loss of strength

• you can regain muscle quicker when working out bc of neural “set point”

age-related muscle change

10% of muscle mass is lost 25-50

40% of muscle mass is lost 50-80

• loss of fast fibers and gain in slow fibers

• due to reduced PA

• regular training can improve strength/endurance but can’t eliminate this phenomena

metabolic syndrome

type 2 diabetes, dyslipidemia, obesity, hypertension