Exercise Physiology Exam 2: Chapter 9

What are the four processes of respiration?

1. Pulmonary ventilation - air moves iinto and out of lungs: atmospheric air enters the nose and mouth goes to the alveoli - fails in asthma

2. External respiration - exchange of gases between the lungs and blood: alveoli of lungs exchange O2 and CO2 with the pulmonary capillary blood - fails in pulmonary oedema

Transport (not one of the four) - fail in anaemia

3. Internal respriation- the exchange of gases between the blood and the tissues at the cellular level: systemic capillary blood exchanges O2 and CO2 with the muscle cells - fails in carbon monoxide

4. Cellular respiration- the utilization of oxygen by the muscle cells to produce energy through aerobic metabolism —> yields ATP - fails in cyanide

Conductive zone

Function: moves air and exchanges nothing - transports air, warms it to 37 C, humidifies it to 99.5% saturated, filters it

No gas exchange occurs here —> anatomical dead space

comprised of: nose and mouth to the terminal bronchioles

Respiratory zone

comprised of: respiratory bronchioles, alveolar ducts, alveolar sacs

every gas exchange in the lungs happens here

The path from the nose to the alveolus

1. Nose and mouth —> pharynx —> larynx —> trachea

2. trachea divides into left and right primary bronchi

3. bronchi branch to secondary and tertirary —> bronchioles

4. Respiratory bronchioles —> alveolar ducts —> alveolar sacs

each generation is narrower and there is far more of them

Inspiration

always requires muscle

diaphragm contracts and flattens, ribs lift outward

thoracic volume increases

intrapulmonary pressure falls below atmospheric

air flows in

Expiration

Passive at rest: the diaphragm relaxes, ribs fall, lung recoils elastically

thoracic volume decrease s

intrapulmonary pressure rises above atmospheric

air flows out

In exercise: ACTIVE - abdominals and internal intercostals drive it

What is the airflow equation?

V = ΔP/R

V is airflow, in litres per second

ΔP is the pressure gradient, P1 - P2 in mmHg 

R is resistance, in mmHg per litre per second

A bigger gradient gives more flow. More resistance gives less flow 

• Resistance rises steeply as airway radius falls

Ventilation and pefusion relationship

They are matched, but not evenly

the ideal V/Q (ventilation/perfusion) ratio is 1.0

apex: relatively underperfused, V/Q above 1.0

base: relatively overperfused, V/Q below 1.0

the best-perfused region is also the best ventilated

What is the effect of light exercise on ventilation and perfusion?

light exercise improves matching of ventilation and perfusion

What is the effect of heavy exercise on ventilation and perfusion?

reintroduces inequality in matching

coordination of cardio and respiratory systems becomes very important- can be done with focus

it is more efficient to take more deep breaths than shallow ones because they have a higher concentration of oxygen and more surface area for gas exchange

Inspiratory reserve volume (IRV)

the greatest amount of air that can be inspired at the end of a normal inspiration

Tidal volume (Vt)

the amount of air that is inspired or expired in a normal breath

Expiratory reserve volume (ERV)

the greatest amount of air that can be expired at the end of a normal expiration

Residual volume (RV)

the amount of air that is left in the lungs following maximal exhalation

Inspiratory Capacity (IC)

the greatest amount of air that can be inspired from a resting expiratory level

IC= IRV + Vt

Vital capacity (VC)

the greatest amount of air that can be exhaled following a maximal inhalation

VC= IRV + Vt +ERV

Functional residual capacity (FRC)

the amount of air left in the lungs at the end of a normal expiration

FRC = ERV +RV

Total lung capacity (TLC)

the greatest amount of air that can be contained in the lungs

TLC = VC + RV

= IC +FRC

= IRV + Vt + ERV + RV

Spirometry

the volume and flow of air inhaled or exhaled

cannot measure residual volume because the air remaining after maximal expiration is not exhaled into the instrument —> the residual volume

therefore spirometry can’t directly measure functional residual capacity and total lung capacity because they both require residual volume

FEV1

forced expiratory volume for one second

can be used to predict all-cause mortaility in the general population

FVC

forced vital capacity

the total volume of air that can be forcefully exhaled after a maximal inspiration

FEV1/FVC

the proportion of the forced vital capacity exhaled during the first econd

Spirometry notation guide:

• Capital letter is the variable: V volume, P pressure, S saturation, F fraction 

• Capital subscript is the gas phase: A alveolar, I inspired, E expired, T tidal, D dead space 

• Lowercase subscript is the blood phase: a arterial, v venous, c capillary 

• A volume per unit time is a flow, so VO2max is a flow rate in mL/min

• A bar means a mean so v (with bar) is MIXED venous, the average of all venous return 

• A dot above means per unit time

• Lowercase f standing alone is frequency, breaths per minute, not the F above 

• So PAO2 is alveolar, and PaO2 is arterial

Minute ventilation

what moved - total amount of air breathed in or out each minute

• VE = VT x f 

• At rest: 12 breaths/min x 0.5 L = 6.0 L/min

• Counts every litre that moved, included the wasted ones

VT= tidal volume in liters per breath

f = breathing frequency in breaths per minute

Alveolar ventilation

what you used - the volume of air reaching the alveoli each minute

• VA = (VT - VD) x f 

• At rest: 12 x (0.5-0.15)L = 4.2 L/min

• Counts only the litres that reached an alveolus 

VD = dead-space volume

Relationship between minute ventilation and alveolar ventilation

they do not always equal each other

Breathing pattern

generated in the medulla and smoothed by the pons

Breathing pattern: Higher brain centers

Hypothalamus: sympathetic drive, pain, strong emotion, cold water emersion

cerebral cortex: conscious control for speech, singing, lifting, swimming —> can bypass the medulla and directly innervate inspiratory muscles

send signlas to the medulla (dorsal and ventral respiratory group) where rhythm is made

breathing pattern: mechanical receptors

Lung stretch: the Hering-Bruer reflex- cuts off an over-deep breath

Irritant: cough and bronchoconstriction

muscle and joing: movement signals the centers

send signals to the medulla (dorsal integrates, ventral generates rhythm)- sends signals to inspiratory and expiratory muscles

breathing pattern: chemoreceptors

central in the medulla: respond to CO2 and falling pH

peripheral, carotid and aortic bodies: falling O2, increased CO2, decreased H+, and rising K+

what is exercise hyperpnea and what drives it?

increase in ventilation that accompanies exercise to meet the body’s increased gas-exchange needs

What drives it: low pH (by way of CO2 and lactate), potassium released from working muscle, muscle and joint mechanoreceptors, central command feeding forward

what does not drive exercise hyperpnea: PaO2, PaCO2, Hering-Breuer reflex, minimal even in exercise

shallow-water blackout

hyperventilation extends breath-hold time by lowering CO2, not by adding oxygen

it removes the warning without adding the reverse and causes loss of consciousness

1. person voluntarily hyperventilates before submerging

2. hyperventilation lowers arterial CO2

3. The reduced CO2 delays the urge to breathe

4. oxygen continues to be consumed with the person holds their breath

5. oxygen levels fall critically low before the urge to breathe becomes overwhelming

6. loss of consciousness

Masks during exercise

cost you comfort, but not performance

affect percieved breathing effort and produce moisture around the face

Fick’s law of diffusion

Vgas = (A * D *𝚫P)/ T

A- area

D- diffusion coefficient which rises with solubility

𝚫P - the pressure gradient

T - thickness of barrier

governs how fast a gas crosses the alveolar membrane

rate of gas diffusion depends on the pressure gradient, surface area, diffusion properties of gas, thickness of barrier (solubility of gas in barrier liquid - dependent on surfactant)

Answers: why does oxygen get into the blood at all

Fick’s law of diffusion applied to the lungs

alveoli provide a large surface area

alveolar walls and pulmonary capillary walls are extremely thin

Alveolar PO2 is higher than the PO2 of incoming mixed venous blood

mixed venous blood PCO2 is higher than alveolar PCO2

O2 diffuses from alveoli into blood, CO2 diffuses from blood into alveoli

Partial pressure gradients and movement of gases: O2

gases diffuse passively from an area of high partial pressure to an area of low

In the lungs: PAO2 (alveolar oxygen partial pressure) is high (100mmHg(

in the blood: PvO2 is low (40 mmHg)

forces O2 into the blood to be delivered to the tissues

Partial pressure gradients and movement of gases: CO2

Venous blood: PvCO2 45mmHg

alveoli: PACO2 40 mmHg

CO2 diffuses into alveoli to be exhaled out

what is A-vO2 diff

how much oxygen the tissues actually took

= arterial O2 content - venous O2 content

• At rest: 19.79 - 15.2 = 4.59 mL/dL

• Only about 25% of the oxygen carried, extracted in one pass 

• The other 75% returns to the lungs unused 

• Represented in the shaded band

Effect of exercise on extraction: Arterial and venous O2 content

• At rest 

  • Arterial O2 content: 19.79 mL/dL

  • Venous O2 content: 15.20 mL/dL

  • a-VO2diff = 19.79 -15.20 = 4.59 mL/dL, 25% extracted 

• During heavy exercise 

  • Arterial O2 content: 19.79mL/dL, essentially unchanged 

    • Why? Arterial content is the same because the perfusion is matched with ventilation

    • Venous O2 content: about 10.00 mL/dL

    • a-VO2diff = 19.79 - 10.00 = 9.79 mL/dL, more than double 

Oxygen Content (CO2)

the total amount of oxygen carried in a given volume of blood

either bound to hemoglobin or dissolved in plasma

oxygen dissociation curve

Partial pressure of oxygen and percentage of hemoglobin binding sites occupied

s shape creates a safety margin on top and a delivery zone at the bottom: binding one O2 molecule makes it easier for additional O2 to bind

flat above 60mmHg: big dips in PO2 cost little saturation - loading safety margin

steep below 40mmHg: small dips in PO2 release a lot of O2 - unloading zone at the working tissue - when muscles need oxygen during exercise, PO2 decreases as they consume more, encouraging more hemoglobin to unload it

load at the lungs, unload at the tissues

3 factors that cause a right shift of the curve

1. decreased pH - lowers Hb-O2 affinity, favors offloading O2 to the tissues, Bohr effect

2. increased temperature - lowers Hb-O2 affinity, a working muscle is warm so it unloads more

3. increased 2,3-DPG, a byproduct of glycolysis in the red cell, rises at altitude, not a major cause during exercise

from anatomy: CADET (CO2, Acid, DPG, Exercise, Temperature)

Factors that cause a left shift of the curve

1. Fetal Hb

2. inactivity

3. basic pH (high)

4. decreased temperature

from anatomy: FIBB

Myoglobin

the carrier of oxygen in muscle cells

has a higher affinity for O2 than hemoglobin

accepts O2 at low PO2 inside the cell and shuttles it to mitochondria

carbon dioxide transport

1. Dissolved (5-10%) - in plasma, sets the partial pressure of CO2, read by chemoreceptors

2. Carbamino (20%) - binds to the GLOBIN portion, not the heme so it doesn’t compete with O2 for a binding site, but deoxygenated Hb carries more CO2

3. Bicarbonate (70-75%) - CO2 + H2O —> H2CO3 (via carbonic anhydrase) H2CO3 —> H+ + HCO3- HCO3- leaves the cell, Cl- enters: chloride shift

respiratory acidosis

caused by hypercapnia- not get riding of enough CO2, thus making more H+

CO2 + H2O —> H2CO3 —> H+ + HCO3-

equation moves forward and causes accumulation of H+

due to inadequate alveolar ventilation

respiratory alkalosis

breathing out more CO2 than you are creating causing pH to become alkaline

excessive alveolar ventilation

respiratory vs renal compensation

respiratory compensation acts within 1 to 3 minutes

renal compensation handles HCO3- and H+ over hours to days