18) **** Respiratory Responses to Acute Exercise **** Flashcards
What are two roles of the respiratory system?
Role of the respiratory system:
(1) Gas exchange between the environment and the body
(2) Regulation of acid base-balance during exercise (bicarbonate system)
* CO2 + H2O ↔ H2CO3 ↔ HCO3- + H+
Respiration → exchange of gas molecules through a membrane or liquid
* Pulmonary respiration → exchange of gases (O2 and CO2) in the lungs (across capillary wall/alveolar wall); in the lungs
* Cellular respiration → exchange of O2 and CO2 in individual cells (across capillary wall/cell membrane); at tissue/organ level
Define Respiration, Pulmonary Resp, Cellular Resp
Respiration → exchange of gas molecules through a membrane or liquid
Pulmonary respiration → exchange of gases (O2 and CO2) in the lungs (across capillary wall/alveolar wall); in the lungs
Cellular respiration → exchange of O2 and CO2 in individual cells (across capillary wall/cell membrane); at tissue/organ level
How is Minute (total) ventilation calculated?
Does it change during exercise?
Minute (total) Ventilation = tidal volume (TV) x Breathing Frequency
- Increases during exercise
- FYI: Minute ventilation (rest) = 0.5 L x 12 breaths/min
= 6.0 L/min
Minute ventilation (exercise) = 2 L x 70 breaths/min (TV x Breathing freq)
= 140 L/min (huge increase in respiratory activity)
What is Alveolar ventilation?
Alveolar ventilation
* The portion of minute ventilation that *mixes with the air in the alveolar chambers *
* Breathing rate and depth change with exercise to maintain alveolar ventilation
* Moderate exercise (trained) – increase TV and minimally increase breathing rate
Amount of air that ventilates alveoli
More trained individuals TV increases»_space;> Breathing rate
Increasing Tidal Volume during exercise results from:
Increasing Tidal Volume during exercise results from encroachment on IRV and a lesser decrease in ERV
- TV plateaus at about 60% Vital capacity (VC) (VC = TV + IRV + ERV)
- Further increases in minute ventilation come from increasing Breathing Rate
IRV = Inspiratory reserve volume
- add’nal volume of air that can be forcibly inhaled (max possible inspiration)
ERV: Expiratory reserve volume
- add’nal vol of air that can be forcibly exhaled following normal expiration (Max voluntary expiration)
Vital Capacity: VC = TV + IRV + ERV
What is Entrainment?
Entrainment → breathing pattern whereby an individual that performs rhythmical physical activity synchronizes breathing frequency with limb movements
Each individual develops a style of breathing by adjusting TV and breathing rate
* Conscious attempts to modify breathing during physical activities do not benefit exercise performance
Oxyhemoglobin Dissociation Curve
- At the lungs
- At the tissues
Oxyhemoglobin Dissociation Curve
At the lungs (low slope)
- High PO2 = hemoglobin high affinity for O2 (prevents dissociation)
- Mostly oxyhemoglobin
At the tissues (high slope)
- Low PO2 = Hemoglobin lower affinity for O2 = O2 dissociates
- Mostly deoxyhemoglobin
- At lower pressures O2, small changes in PO2 result in release of large amounts of O2 (important during exercise - high o2 consumption)
Shift Right = High affinity Hb + O2 = Loading
Move Left = Low affinity = Unloading
O2 Unloading to Muscle
What causes the rapid decrease in Hb-O2 affinity at capillaries in exercising muscle?
Rapid decrease in Hb-O2 affinity:
- Decreased pH: Release of H+, CO2 and lactate into blood capillaries → ↓ affinity
- Higher Temperature in working mm → ↓ affinity
Rightward shift in curve → ↓ affinity → unloading of O2
What is required to increase O2 unloading, given that hemoglobin has an intrinsically high O2 affinity?
Increased demand for O2 during exercise is met by increased blood flow and increased O2 unloading
* Intrinsic O2-affinity of hemoglobin (HB) is very high
Allosteric effectors are required that decrease Hb-O2 affinity, allowing unloading of O2 from the Hb
* 2,3-DPG: product of glycolysis converted to DPG binds to hemoglobin and reduces affinity for O2
- ATP,
- H+
- CO2,
- temperature,
- Cl− (small effect)
- lactate
Hb-O2 affinity is low while RBCs pass through tissues with a high O2 demand and increased when RBCs return to the lung (↑aerobic exercise→↑erythropoeisis → new RBC → high DPG)
* Differences in pH, CO2 and temperature exist between the lung and capillaries in working muscles
Oxygen Transport Capacity:
Can oxygen transport capacity be changed?
Increasing amount of Hb increases the amount of O2 that can be delivered to the tissues:
-O2 transport capacity correlates directly with aerobic performance
* Increased performance after infusion of RBCs
* Strong correlation between total Hb and maximal O2 uptake (VO2max) in athletes
* Means to increase aerobic capacity such as blood and erythropoietin (EPO) doping
Gas exchange at the muscles:
What is (a-ṽ)O2 difference and what does it reflect about gas exchange at the muscles?
(a-ṽ)O2 difference: Arterial-venous O2 Difference
* Difference between arterial and venous O2
* Reflects amount of O2 extracted by the tissue
* As extraction of O2 ↑ (rate of O2 use ↑) → ↓ amount of O2 in venous blood → ↑ (a-v)O2 difference
Oxygen Transport in MM
What happens to oxygen once it is unloaded to the muscle cell
Myoglobin shuttles O2 from the cell membrane to inside the cell (to low O2 area)
- Most O2 used by MIT to generate ATP (maintains O2 gradient)
Myoglobin has higher affinity for O2 at low PO2 than Hb
- O2 reserve for mm -> allows myoglobin to store O2
Myoglobin levels: Slow twitch (type 1)»_space; Fast twitch (type II) // type IIa have some myoglobin, type IIx have very little if any
Why does (a-ṽ)O2 difference increase as exercise increases?
(a-ṽ)O2 difference increases with increasing rate of oxygen use during increasing exercise
* Difference represents decreasing venous content
* More oxygen unloaded into muscle during intense exercise as PO2 exercising muscle «_space;arterial blood
* As activity Increases -> Increase O2 extraction
How does Hematocrit change during exercise?
Hematocrit (%Volume RBC in plasma) increases during exercise due decrease in plasma volume:
(1) Water shifts from plasma volume to interstitial and intracellular spaces
- due to Increases in osmotic pressure from metabolic byproducts (osmotic factors)
(2) Increased Blood Pressure increases hydrostatic pressure
(3) Sweating
Hematocrit increases because plasma volume decreases, NOT due to INCREASING RBC #
Factors influencing O2 delivery and uptake:
Rates of Oxygen uptake and delivery depend on:
(1) Oxygen Content in blood
- Arterial blood (hemoglobin) normally 95% saturated
- Factors impacting Hb will impact O2sat
(2) Blood flow
- Increase CO -> extract less O2/100mL blood
(3) Local Conditions
- pH
- Temperature
- Allosteric factors causing a rightward shift to oxyhemoglobin curve -> increase unloading
Gas exchange at the muscles;
What happens to CO2 produced by working muscles?
CO2 has a major impact on ventilation
-Generated through oxidative metabolism (CAC)
-Exits cells through simple diffusion
- Driven by PCO2 levels (all gases move based on pressure gradients)
- High PCO2 in muscle
- Low PCO2 in capillary blood
CO2 leaves the muscle and enters blood to be exhaled at the lungs
CO2 is carried in the blood in 3 forms:
* Bicarbonate (HCO3-; 60 - 65 %)
* Carbamino compounds (25 - 30 %; bound to hemoglobin)
* Dissolved (5 %)
How is acid-base balance buffered by bicarbonate?
Bicarbonate buffer system converts H+ to H2O (easier for body to handle)
CO2 and protons produced by mm enter RBC: CO2 + H2O → H2CO3 → H+ + HCO3-
At Lungs: CO2 is expelled
H20 is expelled or recylced
Ventilatory Control During Rest:
Neural factors:
The body regulates the rate and depth of breathing in response to metabolic needs
Neural factors:
* The normal respiratory cycle comes from inherent, automatic activity of inspiratory neurons whose cell bodies reside in the medulla
* Neurons activate the diaphragm and intercostal muscles to inflate lungs
* Expiration occurs when muscles of inspiration relax
Humoral factors:
-Plasma PO2 and chemoreceptors
* Hypoxic threshold → point at which arterial PO2 stimulates ventilation (60 – 70 mmHg)
-Plasma PCO2 and H+ concentration:
* CO2 pressure in arterial plasma provides the most important respiratory stimulus at rest → Small changes in PCO2 stimulate large increases in minute ventilation
* Increased [H+] (varies directly with CO2) stimulates ventilation
H+ + HCO3- → H2CO3 → CO2 + H2O
Ventilatory Control During Rest:
Humoral factors:
The body regulates the rate and depth of breathing in response to metabolic needs
Humoral factors:
-Plasma PO2 and chemoreceptors
* Hypoxic threshold → point at which arterial PO2 stimulates ventilation (60 – 70 mmHg)
-Plasma PCO2 and H+ concentration:
* CO2 pressure in arterial plasma provides the most important respiratory stimulus at rest → Small changes in PCO2 stimulate large increases in minute ventilation
* Increased [H+] (varies directly with CO2) stimulates ventilation
H+ + HCO3- → H2CO3 → CO2 + H2O
CO2 is MOST IMPORTANT FACTOR IN CHANGING VENTILATION
Neural factors:
* The normal respiratory cycle comes from inherent, automatic activity of inspiratory neurons whose cell bodies reside in the medulla
* Neurons activate the diaphragm and intercostal muscles to inflate lungs
* Expiration occurs when muscles of inspiration relax
Cardiorespiratory control center during exercise
The Cardiorespiratory Control Centre receives input from which three receptors/sites?
Cardiorespiratory control center → brainstem; receives input from:
(1) Central command – the signal sent from the motor cortex to the cardiorespiratory control centers
* Higher brain centers tell lower brain centers you are trying to move (immediate)
(2) Chemoreceptors – sensory neurons that detect changes in chemical concentrations
* Central chemoreceptors – medulla; detects changes in CSF; most sensitive to PCO2 and H+ (CO2 reacts with water to produce H+)
* Peripheral chemoreceptors – aortic arch (aortic bodies), carotid arteries (carotid bodies), skeletal muscles; sensitive to PO2, PCO2, H+, blood K+
(3) Mechanoreceptors – sensory neurons that detect mechanical changes (ie. tension, shape of tissue)
* Aortic arch and carotid sinus baroreceptors, skeletal muscle
Ventilatory Control During Submaximal Steady-state Exercise
Rate of ventilation during submaximal steady-state exercise is primarily drive by ?
- Linear increases with O2 consumption and CO2 production occurs through ?
- Other factors?
Submaximal steady-state exercise
* Primarily driven by higher brain centers: central command
* Ventilation increases linearly with O2 consumption and CO2 production; occurs primarily through increased tidal volume
* Fine tuned by peripheral receptor feedback
* Other factors which increase ventilation: ↑ blood
K+, body temperature, blood catecholamines (Modify higher brain centers)
Strenuous exercise
* Non-linear increase in VE after ventilatory threshold
* Rate of breathing increases and minute ventilation rises disproportionately to the increase in O2 consumption
* Ventilatory threshold → inflection point where VE increases exponentially
Ventilatory Control During Strenuous Exercise
What is the Ventilatory Threshold?
How is ventilation changed during strenuous exercise?
Strenuous exercise
* Non-linear increase in VE after ventilatory threshold
* Rate of breathing increases and minute ventilation rises disproportionately to the increase in O2 consumption
Ventilatory threshold → inflection point where Ventilation increases exponentially
- Breathing in more O2 than required (Above O2 consumption)
What causes the Ventilatory threshold?
Ventilatory threshold → ventilation increases disproportionately to the increase in O2 consumption
Caused by a person using bicarbonate to reduce acidity of blood by expelling additional CO2
H+ + HCO3- → H2CO3 → CO2 + H2O
Respiratory compensation → lactate is rapidly increasing with intensity; represents hyperventilation even relative to the extra CO2 that is being produced
* Represents the point at which blowing off the CO2 can no longer buffer the increase in acidity that is occurring with progressively intense exercise
* More H+ -> some exhaled, others stimulate peripheral chemoreceptors -> increase breathing
Ventilatory threshold → inflection point where Ventilation increases exponentially
- Breathing in more O2 than required (Above O2 consumption)
- To remove excess CO2
Incremental Exercise
Ventilation and Blood PO2 in Untrained vs Trained
Untrained:
* Blood PO2: Maintained within 10 – 12 mmHg of resting value
* Ventilation (VE): Linear increase up to ~ 50 – 75%
VO2max // H+ ions/CO2 decrease pH to decrease Hb-O2 affinity
Trained:
*Blood PO2: Decreases 30 – 40 mmHg at near-
maximal work
* Hypoxemia (very elite): Due to short RBC transit time in pulmonary capillary; reduced arterial PO2
* Ventilation/perfusion mismatch – because high CO
*Ventilation (VE)
* Occurs at higher VO2max (75%)
* Delayed pH drop
What is the effect of Arterial PCO2 and PO2 on Ventilation?
An increase in arterial PCO2 causes a linear increase in VE
A decrease in arterial PO2 causes an increase in VE
* Small increase only
* VE is more regulated by PCO2 than PO2
What is the effect of Training on the Ventilatory Response to Exercise?
Training does change exercise ventilation (Reduces the Ventilatory Response)
* 20 – 30% decrease in ventilation at same submaximal exercise
* Decreased slope
* Increased skeletal muscle efficiency: Less H+ produced → stimulant for ventilation
Training has no measurable effect on lung structure and function
* Lungs in exercise trained individuals are not significantly different from the lungs in a sedentary individual
