ES380-Chapter 9: Cardiorespiratory responses to acute exercise

what is the main goal of the CV with exercise?

increase bloodflow to working muscle to meet O2 demand

Heart rate increase will affect what 5 other functions?

Stroke volume

cardiac output=Q

blood pressure

blood flow

blood

what is the equation for the fick principle that quantifies VO2 uptake?

VO2=Q x (a-v)O2difference

O2 use depends on what 2 factors?

Tissue bloodflow

O2 extraction

what is the mean BPM

75

what 3 things affects the BPM

Vagal tone(PNS)

Temperature

Altitude

Big point: what is the anticipatory response?

Increase HR above RHR just before exercise

Big point: what are the 2 steps that affect the anticipatory response?

1. withdrawal of vagal tone(PNS)

2. increased SNS causing increased NE and Epi

how does HR increase with exercise intensity?

linearly

what are the 4 steps of increasing HR in response to exercise intensity?

1. decreased PNS(until HR of 100)

2. increased SNS(over HR of 100)

3. group III/IV muscle afferents

4. SNS stimuli Epi/NE secretion

True/false: maximum HR is not reproducible and not good for exercise prescription

FALSE

HRmax is highly reproducible and thus very good for exercise prescription

what is the timeframe for the physiologic adjustment period?

2-3 mins

what is the main activity that maintains HR after the adjustment period and what functions control that?

Sympathetic activity

-command center + muscle metaboreceptors

how much does HR have to increase above VO2max to increase CO(in a percent)?

above 50% of the VO2 max

why does SV increase during low to moderate intensity?

what 3 mechanisms cause this?

compensation of mobilization of venous blood

-oneway valves, muscle pump, respiratory pump

training status and exercise mode dependent

what are the 5 mechanisms that increase SV during exercise?

-Frank-starling mechanism

-Increased SNS/ circulating NE or Epi

-Anrep and bowditch effects

-decreased afterload

-torsional contraction of the ventricles

4 effects of frank-starling mechanism during exercise?

increased EDV causes Increased ventricular stretch causes increased Ca2+ which causes increased contractility

effects of SNS activity on SV?

increased SNS-> increased NE/Epi-> increased Ca2+-> contractility

BIG POINT: what is the biggest cause for increased SV during low to intermediate work and what mechanisms cause that(think about cause and effect and work backwards)?

VO2 max increased SV b/c EDV increases caused by increased preload from frank starling mechanism

BIG POINT: what is the biggest cause for increased SV during intermediate to peak work and what mechanisms cause that(think about cause and effect and work backwards)?

VO2 max, increased SV b/c decreased ESV from SNS/NE, ANREP and bowditch effects, as well as torsional contraction

BIG POINT: what is the biggest determining effect of VO2 max?(think about what could we increase to have the most prevalent effect)

increases in SVmax

what are 7 other factors that can affect VO2 max?

blood volume, cardiac size/mass/compliance, muscle BF, capillary density, mitochondrial content

why does cardiac output have the greatest rate of change(rise the fastest) during the beginning of exercise?(think about Q=HR x SV)

fast increase in SV to accommodate

memorize: what is the resting Q(CO)?

5 L/Min

memorize: what is the untrained Qmax?

20-25 L/min

list the 5 steps of how Plasma volume(PV) increases VO2max?

Increased PV->Increased VR-> Increased EDV->Increased Qmax-> Increased VO2max

if larger individuals have more blood volume, how does this affect their plasma volume and left ventricles?

Increased PV

Increased Left Ventricles

if the MAP is increasing, what must happen to TPR during exercise to achieve steady state? [MAP = (HRxSV)xTPR, be careful and consider the variables]

decrease until steady state

does an decreased TPR aid in increasing muscle blood flow?

YES

allows the heart to beat faster and push more volume out since there is decreased pressure against it

what factor of MAP has the biggest effect on BP during resistance training?(MAP=1/3 SBP x 2/3 DBP)

2/3 DBP

massive driving force for increased bP

how does the valsalva maneuver increase BP?

prolonged use causes decreased preload, decreased CO and decreased MAP which can lead to syncope

what are the 3 biggest differences between CV adjustments to exercise for lower body exercise(LE) vs upper body exercise(UE)

1. VO2max is 20-30% lower during UE

2. HRmax and Vemax are lower during UE

3. during submax, UE elicits higher relativbe BP, HR, RPE, Ve, and VO2

what are the 5 mechanisms for differences between CV adjustments to exercise for lower body exercise(LE) vs upper body exercise(UE)

1. smaller muscle mass=less VR and SV

2. increased feedforward stimulation to CCC(cardiac command center

3. increased feedback to medulla from peripheral receptors in active tissue(groups 3/4 stimulation)

4. narrowed blood vessels and shorter vessel length in UE= increased BF resistance leading to increased BPs

5. energy demands of trunk stabilization impairing mechanical efficiency

what will eating a large meal do to blood going to metabolically active tissue?

decrease blood flow since it has to route blood to the GI

what two factors will worsen the competition for blood?

dehydration and heat

what is the Po2 during exercise, specifcally at metabolically active tissue?

0

due to the tissue taking all available O2

what is the Po2 during max exercise in general, more importantly, why?

16- 17 mmHg

mixing with venous blood from none metabolically active tissues

what 3 pressures affect capillary fluid into and out of a tissue(think about what is blood made of and the pressure associate with those)?

Hydrostatic (SBP and DBP)

Oncotic pressure (Proteins)

Osmotic Pressure (Electrolytes)

what occurs to plasma volume during upright exercise and what causes this via what 3 functions?

Decreased PV: due to intensity

1. increased MAP -> Increased capillary hydrostatic pressure

2. Metabolite buildup in muscle-> increases tissue osmotic pressure

3. sweating further will decrease plasma volume

what are 4 net effects of decreasing PV(think about thick blood)?

RBC concentration increases

Hb concentration increases

O2-carrying capacity increases

Increased blood viscosity->increased HR

big point: what is the central command theory, and where are effects seen?

Higher brain centers co-activate motor and CV centers( neuronal spillage) in a feedforward fashion

-1 AP could signal 2 tissues

effects can be seen in skeletal m., heart, lungs, and group 3/4

does the CCC(cardiac command center) use negative or positive feedback, what 2 receptors provide this information and what does it do with these responses?

1. negative.

-why the hell would it use positive, its not giving birth.

2. Central and peripheral receptors

3. used to fine tune CV responses for MAP regulation

Big Point: T/F humans will NOT prioritize MAP above other physiologic needs.

the biggest FALSE ever

-it will always come before every need because without it we cant do those other needs.

describe the 3 phases of minute ventilation(VE) during exercise

Phase 1: immediate increase in VE

-can occur before or at onset of exercise from the neural system

-anticipatory response from central command group 3/4 muscle afferents

Phase 2: gradual increase in VE

-driven by hormonal and chemical changes(increase CO2, K+ and H+) in arterial blood sensed by peripheral chemoreceptors

Phase 3: VE achieves steady state

-via peripheral and central feedback

what feedback comes from right atrial stretch receptors?

An increase in VE is proportional to increase in Cardiac Output

Ventilation will increase proportionally to metabolic demand. At low exercises, what respiratory volume will be the main cause of an increase in VE?

Tidal Volume

what occurs to Tidal Volume and respiratory rate during >60% VO2 max, and how does this affect VE?

Tidal volume: will slowly plateau but never entirely, VE will be sustained from this

Respiratory Rate: increase accordingly, driving VE up

Big Point: tidal volume is similar to SV(he said to write this down so)

Synthesis point: why does VE remain high during post exercise?

it will help in oxidizing lactate, removal of metabolites, cori cycle, lactate shuttle

what are the 3 regulatory process of post-exercise breathing?

1. Acid-base balance (blood pH)

2. restoration of Pco2

3. return of blood temperature

Dyspnea is classified as ?

a shortness of breath

-caused by an inability to adjust high blood Pco2 and H+

hyperventilation is classified as ?

what occurs to the PaCO2 and PAO2 (partial pressure of CO2 and O2 in arteries and alveoli)?

excessive ventilation:breathing in a bag does have a physiological explanation

-respiratory alkalosis, often created by anxiety or anticipation about exercise

-decreasing PaCO2 will increase PAO2 (alveolar

-decreasing PaCO2 -> increased blood pH-> decrease drive to breath

(often syncope(fainting) occurs)

Big point: what is Ventilatory Equivalent and what does it represent?

-Ventilatory Equivalent= Ve/VO2 (L air breathed / L O2 consumed /(per) min)

-represents and index of how well the control of breathing is matched to the bodys demand for oxygen

BIG POINT: what is Ventilatory Threshold (Vt) and what does it represent?

-it is a point where Ve increases disproportionately to L O2 consumed

-indicates a shift towards increasing anaerobic metabolism, increasing VCO2 stimulates respiration

when will Vt (as a percent of VO2 max) in untrained and trained individuals?

55-70% from untrained to trained

Big point: T/F Lactic Acid and CO2 WILL accumulate simultaneously.

TRUE

-RER will increase while this happens to above 1 due to alot of factors but the buffers become overwhelmed and cannot remove H+ so they move away from Oxidative metabolism.

what are 3 ways you can increase your bicarbonate reserve?

training

supplements

nutrition

BIG POINT: what is the ventilatory equivalents method, when does it occur and what are the steps to determine Vt?

1. Ventilatory threshold reflects the disproportionate increase in VE (to remove CO2) relative to VO2

2. theres in increase in Ve/VO2(ventilatory equivalent of Oxygen) WITHOUT an increase in Ve/VCO2(ventilatory equivalent of Carbon Dioxide)

3.

step one: find the lowest point of Ve/VO2 curve just before an increase(should happen first)

step two: find the plateau of Ve/VCO2 curve

(possible)Exam Question: identify the workload that the VT occurs at from the graph

occurs around 175 watts

use the steps listed: of course he wont give us the Vt

step one: find the lowest point of Ve/VO2 curve just before an increase(should happen first)

step two: find the plateau of Ve/VCO2 curve

what is the RCP and what does this represent?

-the point on the ventilatory equivalents graph where Ve/VO2 and Ve/VCO2 both increase

-uncoupling of PCO2 control of VE, indicates the Bicarb Buffering system has been surpassed.

what is V-slope method used for?

determining anaerobic threshold

BIG POINT: What is Exercise-induced arterial hypoxemia and who is mainly affected?

1. it is a pulmonary diffusion limitation, essentially the ventilation and cardiac output is way too fast for the blood to become saturated with Hb

2. only affects super elite athletes, not regular people

Big point: what is the best way for quicker reduction in blood lactate levels during active recovery and what 2 mechanisms support this?

1. keeping the blood circulating, just keep moving and dont sit down or stop moving

2.

-respiratory/renal removal of excess CO2 via bicarbonate buffering system

-lactate removal by muscles, liver and heart(cori cycle, lactate shuttle)