Respiration During Exercise Flashcards
Function of Respiratory System
Exchange gasses between external environment and body
- Replacing O2
- Removing CO2
- Regulation of acid-base balance
Ventilation
Mechanical process of moving air into and out of lungs
Perfusion
Blood flow to the lungs
Diffusion
- Random movement of molecules
- High concentration → lower concentration
4 Stages of Respiration
- Pulmonary ventilation (breathing)
► Movement of air in and out of lung - Pulmonary diffusion
►O2 ↔ CO2 between lungs and blood
►Occurs at the level of the alveoli - Transport of O2 and CO2 in blood
►Hemoglobin and plasma - Gas exchange in tissues
►Cellular exchange of O2 and CO2
- 1 is EXTERNAL
- 2 – 4 are INTERNAL
Upper vs Lower respiratory tract (Structurally different)
Upper respiratory system contains the nose, pharynx, and
associated structures
The lower respiratory system consists of larynx, trachea, bronchi,
and lungs
Upper vs Lower respiratory tract (Functionally different)
Upper respiratory system will filter, warm, and moisten air and
conduct it into the lungs
The lower respiratory system is where gas exchange occurs
between air and blood
The Lung and Pulmonary Diffusion (Structure)
Located above diaphragm, enclosed by pleural membranes
- Visceral
- Parietal
- Intermembrane space
The Lung and Pulmonary Diffusion (Pressure)
Intrapleural pressure is less than atmospheric pressure
- ↓ further below atmospheric by contraction of diaphragm
- ↑ above atmospheric by relaxation of diaphragm
- These pressure changes drive “bulk flow”
Bulk Flow
Mass movement of molecules from an area of high pressure to an area of lower pressure
The movement of molecules due to pressure differences between two ends of a passageway
Atmospheric pressure is:
760 mmHG
- Reduced at high altitude (everest expeditions)
The conducting zone
which includes everything from the nose to the smallest
bronchioles, moves air into and out of the lungs (Heat, Humidify and Filter.)
The respiratory zone
includes the respiratory bronchioles and alveoli and moves the
respiratory gasses, that is oxygen and carbon dioxide, in and out of the blood
(Macrophages.)
Bronchial Tree (Defined, functions)
The collective term used for these
multiple-branched bronchi
- The main function of the bronchi, like other conducting zone structures, is to provide a passageway for air to move into and out of each lung
- In addition, the mucous membrane traps debris and pathogens
Alveolar Gas Exchange
Pulmonary capillaries form baskets around alveoli
occurs through a process called diffusion, which is the movement of gases from an area of high concentration to an area of low concentration. In the lungs, oxygen-rich air is breathed in and fills the alveoli, which have a high concentration of oxygen. At the same time, carbon dioxide-rich blood from the body flows into the capillaries surrounding the alveoli, which have a high concentration of carbon dioxide. Oxygen and carbon dioxide then diffuse across the thin walls of the alveoli and capillaries, allowing for the exchange of gases between the air and blood. The oxygen then binds to red blood cells, which transport it to the body’s tissues, while the carbon dioxide is carried back to the lungs and exhaled.
Structure optimizes deoxygenated → oxygenated
Alveoli and Respiratory Membrane (What are they and how they connect)
- Capillaries form dense network around each alveolus
- Blood gasses must cross “respiratory membrane”
- Barrier that is 1 cell thick to minimize resistance
Alevoli
Microscopic air sacs located in the lung where gas exchange occurs between respiratory gasses and the blood
Respiration
External respiration is the exchange of oxygen and carbon dioxide between the lungs and the environment; internal respiration describes the use of oxygen by the cell (Mitochondria)
Type II Alveolar Cells
- Generate surfactant
- ↓ Surface tension of alveolar bubbles
- Greatly facilitates pulmonary diffusion
- By ↓ resistance to incoming air
Inspiration
- When intrapulmonary pressure < atmospheric
- Due to respiratory muscles contraction
- Decreases intrapleural pressure
- Allows lungs to expand with incoming air
- Active process (diaphragm needs to contract)
Expiration
- When intrapulmonary pressure > atmospheric
- Due to respiratory muscles relaxation (recoil)
- Increases intrapleural pressure
- Expels air from lungs into atmosphere
- Mostly passive process (except for ↑ VE)
Diaphragm
Diaphragm is a very thin and dome shaped skeletal muscle
- Continuously active though lifespan upon birth
Attached to bottom of rib cage; innervated by phrenic nerve
- FLATTENED when it contracts; DOMED when it relaxes
- Does most ventilatory work at rest
Accessory Muscles during exercise that contribute
- External intercostals
- Pectoralis minor
- Scalenes
- Sternocleidomastoid
^(All help diaphragm to decrease intrapulmonary pressure)^
Muscles during expiration (Exercise)
Expiration is passive at rest but active during exercise
- Rectus abdominis
- Internal oblique
^(Draws ribs inward and downward to increase pressure)^
What is the O2 cost of ventilation?
Rest < 1%
Submaximal exercise 1 - 2%
Maximal exercise 5 - 10%
Supramaximal exercise 10 - 15%
Do respiratory muscles fatigue during exercise?
Historically believed that respiratory muscles do not fatigue
Current evidence suggests that respiratory muscles do fatigue
During prolonged exercise (>120 minutes) | During high-intensity exercise (90 – 100%
VO2 max)
Do respiratory muscles adapt to training?
YES
- Increased oxidative capacity of diaphragm fibers
- Increased fatigue resistance
- Upper airway more relaxed?
- Reduced work of breathing
Pulmonary Ventilation
The amount of air moved in or out of the lungs (VE)
- Per minute (L min-1)
- VE = VT x f
- Resting and exercise volumes
Tidal Volume (VT)
- Amount of air moved per breath
Breathing frequency (f)
of breaths per minutes
Typical VE at rest:
~ 7.5 L min-1
- 0.5 L min-1 x 15 breaths min-1
Typical VE during maximal exercise:
~ 120 L min-1
- 2.0 L min-1 x 60 breaths min-1
Components of PV (3 names plus defined)
Pulmonary ventilation
- The sum of VA + VD
Alveolar ventilation (VA)
- Volume of air that reaches the respiratory zone
Dead-space ventilation (VD)
- Volume of air not participating in gas exchange
- it is air remaining in conduction zone
- Does not reach alveolus
- Due to anatomical “dead space”
(Airway resistance) Airflow depends on:
Pressure difference between two ends of airway
- P1-P2
- Resistance of airways (diameter of bronchioles)
Airflow = (P1 - P2)/Resistance
Airway Resistance depends on
Airway resistance depends on diameter
- Chronic obstructive lung disease
- Asthma and exercise-induced asthma
Diffusing Capacity of Lung
Quantifies the ability of the lung to exchange gasses
Gas Flow across lungs depends on:
- Partial Pressures (Dalton’s Law)
- Properties of gasses (Henry’s Law)
- Respiratory Zone properties
Exchange of O2 and CO2 across lung depends upon:
- Partial pressures of each gas: The PO2 and PCO2
- Between alveoli and pulmonary capillary
These partial pressure differences determine:
- Which way each gas flows
- How fast each gas flows
Dalton’s Law
Relationship between partial pressures and total pressures of any gas
- Total pressure of a gas mixture is equal to: The sum of the pressure that each
gas exerts independently
P-atmosphere = PO2 + PCO2 + PN2
- Trace gasses are ignored
Henry’s Law
Gasses dissolve in liquids in proportion to:
- Solubility of gasses in blood (O2 and CO2)
- Temperature (homeostasis)
- Partial pressures of gasses in blood
Some factors are constant
- Solubility of gasses in blood
- Temperature
Some factors change with exercise
- Partial pressures of gasses in blood
Fick’s Law of Diffusion
The rate of gas transfer is proportional to:
- Tissue (surface) area
- Diffusion coefficient of the gas
- Difference in the partial pressure of the gas across tissue
The rate of gas transfer is inversely proportional to:
- Thickness of tissue
V gas = A/T x D x (P1 - P2)
V gas = rate of diffusion
A = tissue area
T = tissue thickness
D = diffusion coefficient of gas
P1 – P2 = difference in partial pressure
How does CO2 leave the body when ▲P is small ?
CO2 diffuses 20X better than does
O2
The Ventilation to Perfusion Ratio
- Matching of blood flow to ventilation in lung
- Gas transfer greatest when ratio is ~ 1:1
Regional V:Q varies greatly from 1:1 - Apex of lung (standing) * Under perfused relative to air supply * V:Q ratio > 1.0
- Base of lung (standing) * Over perfused relative to air supply * V:Q ratio < 1.0
^Changes with exercise (see Figure 10.15)^ - Blood flow not perfectly matched with ventilation at rest, rates become
closer during exercise
CO2 and pH buffering
Hemoglobin gives up H+ as long as we can “vent” CO2
this mechanism manages blood pH
Ventilation (VE) and Exercise
Rest to Submaximal:
VE at rest is ~ 5 L per min § the VE to VO2 ratio is ~ 17 to 1 (i.e., 5000 / 250)
Submaximal exercise range: 20 - 100 L min -1
during submaximal exercise, VE ↑ parallels VO2 ↑
The VE to VO2 ratio is constant (i.e., we ↑ VE to ↑ VO2)
Submaximal to Maximal:
VE with maximal exercise from 100 - 200 L min -1
above submaximal exercise, VE ↑ more than VO2!
The VE to VO2 ratio gets much bigger (30 to 1!)
the extra ventilation is “geared” to VCO2 and not VO2!
This is hyperventilation; the VE to VO2 ratio is not constant
Dyspnea:
ventilation at a rate required for normal function
VE ≈ VO2
applies to submaximal exercise
below Lactate Threshold
Hyperventilation
ventilation exceeds that necessary for normal function
VE ≠ VO2
applies to maximal exercise
above Lactate Threshold
Submax increases linearly until reaching
until reaching max (VENTILATORY BREAKPOINT)
Respiratory acidosis vs respiratory alkalosis
We need to ↑ VE during progressive exercise
to keep pace with production of non-metabolic CO2
maintains blood pH
this is respiratory alkalosis
When VE is insufficient during progressive exercise
relative to the production of non-metabolic CO2
does not maintain blood pH (↓)
this is respiratory acidosis
Explains why VE is an index of lactate threshold
occurs at the same intensity
Explains danger of pulmonary disease
chronic obstructive pulmonary diseases
insufficient VE at rest can cause death!
Control of Ventilation
Respiratory control centre = Feed-forward
Peripheral receptors = Feed-back
The Respiratory Center
Autonomic respiratory centres
medulla oblongata
pons
Establish breathing frequency and tidal volume
inspiratory centre
expiratory centre
send neural signals to respiratory muscles
Control ventilation at rest and during exercise
via “feed-forward”
via “feed-back”
Fast Phase: “feed forward”
Provides anticipatory increase in VE
arises from proprioceptors?
arises from the motor cortex ?
Signals stimulate Respiratory Center
to increase ventilation
before blood chemistry changes (e.g., pCO2, pH)
Rapid response helps blunt disruptions to homeostasis
Chemoreceptors: Providing Feedback
A cell or group of cells
detect chemical changes (PCO2 and PO2)
relays to respiratory centre
Central
located in brain
Peripheral
located in 1. aortic arch + 2. carotid artery
Provide chemically based feedback
fine tunes ventilation to
minimize disturbance to homeostasis * e.g., hyperventilation & respiratory alkalosis
Chemoreceptors located in medulla oblongata (central chemoreceptor)
Stimulus:
increased PCO2
An increase in arterial PCO2 results in diffusion of CO2 from the blood into the brain = lower pH → stimulates the central chemoreceptor to send signals to the RCC → increased breathing = increased alveolar ventilation
Carotid body (peripheral chemoreceptor)
Stimulus:
increased PCO2
decreased pH or PO2
Increase in arterial PCO2 → stimulates the carotid bodies to send signals to RCC = increased breathing
A decrease in arterial pH and/or PO2 → carotid bodies sending signals to the RCC = increased ventilation
Aortic body (peripheral chemoreceptor)
Stimulus:
increased PCO2
decreased pH
Increased arterial PCO2 / Decrease in blood pH → Aortic body sending signals RCC = increased breathing
Muscle mechanoreceptors
Stimulus:
increased muscle contractile activity
Muscle contractile activity stimulates its receptors to send neural signals to the RCC → to increased breathing (in direct proportion to the exercise intensity!)
Muscle chemoreceptors (also called muscle metaboreceptors)
Stimulus:
increased Potassium
decreased pH
Exercise → decreased muscle pH + increased extracellular potassium concentrations = stimulates these chemoreceptors to send neural signals to RCC = increased breathing
Training Reduces Ventilatory Response to Exercise
No major effects on lung structure or function
lead to the idea that the “normal lung” was “over built”
to meet demands of gas exchange
during even maximal exercise
Pulmonary adaptations not required?
for lung to maintain blood-gas homeostasis
at intensities below or over the lactate threshold
What is evidence for this?
VE can always be increased volitionally
represents a “ventilatory reserve?”
Reduction in submaximal VE with training? (10.2!)
due to ↑ aerobic fitness
↓ need to buffer lactic acid
What limits VO2 Max?
Cardiac output or peripheral extraction of O2 is a limiting factor in the vast majority of people
(i.e. [HR x SV] x A-V O2 difference)
Pulmonary diffusion does NOT limit VO2 Max in most people
Does pulmonary diffusion ever limit performance?
Transit times of RBCs through pulmonary capillaries
- 1 to 2 seconds at cardiac outputs producing VO2 Max
- not problematic as long as pulmonary PO2 > 80-90 mmHg
- due to shape of oxyhemoglobin dissociation curve
- SaO2 of haemoglobin ~ 98%!
Ventilation and Maximal exercise: Normal people
For most healthy/fit people
- pulmonary diffusion not rate limiting for VO2 Max
- limitation is O2 delivery or extraction in CV system
Small declines in PO2 do not reduce arterial SaO2
- recall oxyhemoglobin dissociation curve
- SaO2 of blood leaving pulmonary capillary remains high
- > 98%
Transit time of RBCs through pulmonary capillary
- long enough to equilibrate with alveoli
For this population the lung does not limit
- thus, the A-V O2 difference remains high
- confirms the lung is “overbuilt” for exercise
Ventilation and Maximal exercise: Elite athletes
For a small % of elite endurance athletes
- pulmonary diffusion is rate limiting for VO2 Max
- not O2 delivery or extraction in CV system
~ 33% of ♂ ♀ elite endurance athletes display hypoxemia
- PO2 ~ 70 mmHg in pulmonary capillaries (SaO2 ~ 90%)
Occurs because of very high pulmonary cardiac outputs
- transit time of red blood cells may be < ½ sec!
- may limit O2 loading onto RBCs
In this subset of high-performance athletes
- reductions in A-V O2 difference may limit VO2 Max! Why?
↑ Cardiac output & pulmonary perfusion so high
- that a new weak link is produced
- confirms lungs are not as adaptable as the CV system? and that high performance athletes are built differently?
Partial Pressures of O2 and CO2 | Gas Exchange
Difference between PaO2 & PvO2 = A-V O2 difference
PO2 : ↓ 10 mmHg
PCO2: ↑ 75 mmHg
A-V O2 difference is critically dependent on red blood cells and hemoglobin
Red Blood Cells
Produced in bone marrow via erythropoiesis
- each RBC survives ~ 120 days q
Production stimulated by erythropoietin (EPO)
Have no nucleus or mitochondria
Adults have ~ 2.5 x 10 RBC
- hematocrit can ↑ or ↓ volume
- Independently of plasma volume
- Athletes have in fact an increased total mass of red blood cells and hemoglobin in circulation relative to sedentary individuals
Gender differences
♀ = 4 - 5 million RBC per µL
♂ = 5 - 6 million RBC per µL
1 ml blood has ~ 5 billion RBCs!
RBC diameter is 6 – 8 microns
size & shape optimises exchange
of either O2 or CO2
Frisbee like and flexible
squeeze through small capillaries
draft through capillaries
O2 transport by haemoglobin
RBC contains ~ 270 million haemoglobin molecules
- each RBC is ~ 97% haemoglobin by dry weight
Haemoglobin contains heme group
- where does heme come from?
Heme group binds O2
- according to the plasma PO2
- Oxy-Hb dissociation curve
99% of O2 transported in blood is bound to haemoglobin
- Thus, O2 content of blood depends critically on [Haemoglobin]
1% of O2 transported in blood is dissolved in plasma
- not even enough to support resting VO2 * if 3.5 ml kg-1 min-1 (< 300 ml O2)
Hemoglobin: two species
Oxyhemoglobin - O2 bound
Deoxyhemoglobin - not O2 bound
- Saturation with O2 (SaO2) varies with: PO2, PCO2, pH, temperature
SaO2
The percentage of available binding sites on hemoglobin that are bound with oxygen in arterial blood
Hemoglobin: Attributes
Each hemoglobin molecule has 4 iron molecules
- each iron molecule binds 1 O2 molecule
- at “heme” group
Each hemoglobin molecule can carry up to 4 O2 molecules
- when 100% saturated
- O2 binding to Hb displays cooperativity
Amount of O2 carried by blood depends on both:
Hb concentration
% saturation of Hb
Hb concentration is
130-150 grams per litre of blood
Range due to male-female differences
Inter- and intra-individual differences (genetics, endurance training, etc)
Men have more RBC and thus a greater hemoglobin content than women
12 to 14 grams Hb per 100 ml blood (WOMEN)
14 to 16 grams Hb per 100 ml blood (MEN)
Gender Differences in O2 Transport by Hemoglobin
Each gram of Hb carries up to 1.34 ml O2 of Hb when 100% saturated
1.34 ml O2 per gram Hb x 130 grams Hb per litre of blood (Assuming 100% SaO2)
= 174 ml O2 per litre of blood or (17.4 ml O2 per 100 mL of blood) (WOMEN)
1.34 ml O2 per gram Hb x 150 grams Hb per litre of blood (Assuming 100% SaO2)
= 201 ml O2 per litre of blood or (20.1 ml O2 per 100 mL of blood) (MEN)
20 ml O2 per 100 ml - Males
17.4 ml O2 per 100 ml - Females
Thus, the maximal A-V O2 difference is greater for ♂ than for ♀
Deoxyhemoglobin + O2 <->Oxyhemoglobin
Direction of reaction depends on PO2 of the blood (remember these numbers!)
At lung
- high PO2 = oxyhemoglobin
- O2 transport
At tissues
- low PO2 = deoxyhemoglobin
- release of O2
Oxygen-Hemoglobin Dissociation Curve
Describes the relationship between plasma PO2
- and percent of O2 binding sites on Hb occupied with O2
Relationship between plasma PO2 & % saturation of Hb
- Sigmoidal curve
- reflects O2 binding properties of Hb
- at different PO2 extant through system
The PO2 and SaO2 are very high on arterial side
- Range: largely exercise independent
The PO2 and SaO2 are very low in tissues and in veins
- Range: very exercise dependent
Curve is flat when PO2 is high (> 80 mmHG)
Curve is steep when PO2 is 20 - 80 mmHg
Curve is flat when PO2 is < 20 mmHg
Oxyhemoglobin Dissociation Curve: Effect of exercise
Normal curve:
- pH at 7.4
- temp 37 C
- PCO2 at 40
With exercise:
- pH declines
- temp increases
- PCO2 increases
Summary: Exercise & Oxyhemoglobin Dissociation Curve
BOHR EFFECT
PCO2 ↑
pH ↓
Core temperature ↑
Shifts curve to right (→ )
Largest effect when PO2 < 60 mmHg
This ↑ O2 delivery at tissue level
Thus increasing ↑ the A-V O2 difference!
Myoglobin and O2 Transport in Muscle
Myoglobin is similar to hemoglobin in structure
- does a similar job but has different properties
Myoglobin shuttles O2 within cytosol of fibers
- from membrane to mitochondria
Myoglobin has a higher affinity for O2 than hemoglobin
- @ low PO2 Mb stores O2
- retains O2 until very low PO2 (1-2 mmHG)
Type I > Type IIa > Type IIX
- gives muscle a distinct red colour
- accounts for dark vs white meat
Myoglobin:
Stores O2 when the PO2 > 10 mmHg
Releases O2 when PO2 < 10 mmHg
Carbon Dioxide Transport : Metabolic CO2 transported to the lungs in one of 3 ways:
- Dissolved in plasma (~ 10 %)
- Bound to Hb (~ 20 %)
- Via bicarbonate (~ 70 %)
Carbon Dioxide Transport : Dissolved in Plasma
Amount of CO2 carried by plasma is small but ↑ with PCO2:
- 46 vs 40 mmHg (at rest) (veins vs arteries)
- 75 vs 46 mmHG (exercise) (veins only)
This ↑ in plasma PCO2 ↑ the SaCO2 of hemoglobin
Carbon Dioxide Transport : Bound to Hemoglobin
↑ in plasma PCO2 creates ↑ carbaminohemoglobin (HbCO2)
- CO2 doesn’t bind at same site O2 q
But O2 binding influences CO2 binding (due to cooperativity)
- the higher the SaO2 the lower the SaCO2 (and vice versa)
- deoxyhemoglobin binds more CO2 than oxyhemoglobin
Carbon Dioxide Transport : As Bicarbonate
Most CO2 reacts with H2O to form H2CO3
- carbonic acid
Catalyzed by carbonic anhydrase enzyme (CA)
- a REVERSIBLE reaction
CO2 + H2O = H2CO3 <-> H+ + HCO3 –
= is Carbonic Anhydrase
- Happens in capillaries or venules
In the lung, the reaction reverses (<->) direction due to ↓ PCO2
Summary: CO2 Transport
At the tissue:
- H+ binds to Hb
- HCO3 – diffuses out of RBC into plasma
- Cl– diffuses into RBC (chloride shift)
At the lung:
- O2 binds to Hb (drives off H+)
- Reaction reverses to release CO2 (and make water)
- Cl– diffuses out of RBC (reverses chloride shift)
