Exercise & the Respiratory System

Topics: Pulmonary Exercise Physiology; Lung Volumes and Exercise; Pulmonary Ventilation; Gas Exchange during Exercise; Regulation of Exercise; Respiration and Exercise

Why is it important?

Respiration is a way of getting air into the lungs to provide oxygen for our working muscle.

What does the heart do?

Pumps oxygen to working muscles.

What do the lungs do?

Bring oxygen into the body, which is required to produce energy for exercise. They also help remove carbon dioxide, a byproduct of metabolism, from the bloodstream.

What occurs during exercise?

More oxygen is needed to keep up with energy demands. More CO2 is produced due to higher energy production. Respiration rate and minute ventilation increases (up to 100L). Increased blood flow to the muscles enhances oxygen delivery.

Assessing Ventilation (respiratory status)

Lung volumes (classified as either static or dynamic lung volumes / capacities).

Static Lung Volumes / Capacities

Are not dependent on the speed of airflow into or out of the lungs. Describes an individuals lung capacity.

Dynamic Volume / Capacities

Describes the speed in which air flows into or out of the lungs. Grants ability to access issues with breathing or lung conditions.

Static Lung Volumes

Tidal Volume (TV) & Inspiratory Reserve Volume (IRV)

Tidal Volume

Volume of air moving in and out of the lungs, approximately 500ml of air (average healthy adult).

Inspiratory Reserve Volume

Amount of additional air that can be inhaled over and above the tidal volume. Deep breath. Is approximately 3100mL (average healthy adult).

What is a Respiratory Volume?

The volumes of air that provides information about inhaled air or air left over after exhale.

There are two: Expiratory Reserve Volume (ERV) and Residual Volume (RV).

Expiratory Reserve Volume

Amount of air that is able to be forcibly expelled from the lungs.

Approximately 1-1.2L (average healthy adult)

Residual Volume

Amount of air that always remains in the lungs to keep the alveoli open. Is approximately 1.2L (average, healthy adult).

Static Respiratory Capacities

Found by combining 2 or more respiratory volumes.

Inspiratory Capacity (IC); Functional Residual Capacity (FRC); Vital Capacity; Total Lung Capacity (TLC).

Inspiratory Capacity

Capacity of lungs for inspiration.

Tidal volume + Inspiratory Reserve Volume

Dynamic Lung Volumes

Describes the rate of flow of air into and out of the lungs.

Comprised of: Forced Vital Capacity (FVC); Forced Expiratory Volume (FEV).

Forced Expiratory Volume

Amount of air forcibly expelled in the first second of exhalation. 80% of FVC in average, healthy adult.

Can tell us if there is an obstruction in lungs (less than 80%).

Can tell us if there is a restriction to breathing (80% or more due to compensation).

Pulmonary Function Tests

Measures dynamic lung volumes as tests are designed to measure the rate of air movement.

Spirometry equipment used and generates a flow-volume loop.

Can see where peak expiratory flow rate is measured (fastest air has flowed out of lungs); can also measure the FEV in 1s (approx 4.5L on volume axis).

Purpose of spirometry

Distinguishes between people who might have obstructive pulmonary disease or restrictive disease.

Only performed when an individual is suspected to have a lung disease.

Obstructive Pulmonary Disease

Increased airway resistance; harder to get the air out (bronchitis). FEV in 1s decreased as obstruction = slower expiration.

Restrictive Disease

Reduced lung capacity (tuberculosis of fibrosis of lungs - exposure to environmental agents).

Performing a Pulmonary Test

• Person sits with mouthpiece at rest

• Breathe steadily, then asked to take a  big inhalation and fill their lungs w air. 

• As soon as their lungs are full with air, they are asked to exhale as hard and fast as they can 

• In initial exhalation, the flow of air increases (speed of which air flows out of the lungs)

• Eventually as you empty your lungs, the flow decreases 

Maximal Voluntary Ventilation (MVV)

Also known as maximum breathing capacity.

Referring to the maximum minute ventilation that a person can maintain for 12-15s.

MVV = approximately 15-20 * resting minute volume (resting breaths per min).

Correlates well with Subjective dyspnea (feelings of breathlessness).

Useful to evaluate an individuals exercise tolerance.

Measuring Maximal Voluntary Ventilation

Subjects must breath rapidly and deeply for between 15-30s. Record ventilatory volumes.

The maximum volume achieved over 15s is expressed in L/min.

Breathing Reserve

Additional breathing during exercise.

Calculated as the ratio of MVV at rest compared to maximal exercise ventilation (MEV) during exercise test.

(MVV - VE / MVV) * 100 = BR

Healthy subjects MEV = 60-80% of MVV at rest (there is a breathing reserve). Maximum Ventilation does not usually exceed 80% of MVV.

There is a substantial ventilatory reserve at peak exercise.

Changes during Exercise

TV increases; Respiratory Rate increases (for ventilation to increase); MVV is not usually reached (healthy people have a reserve).

Pulmonary Ventilation

Alveolar Ventilation - Volume of air that ventilates only the alveolar chambers each minute.

Minute Ventilation - Volume of air moved into and out of the total respiratory tract each minute.

Exercise makes both AVR and MV increase to increase oxygen in the lungs.

Alveolar Ventilation (AVR)

AVR (ml/min) = (Tidal Volume - dead space volume (ml/breath) * Breathing Rate.

Flow of gases into and out of alveoli (ventilation) during a particular time, taking part in gas exchange. Effective ventilation = get air to alveoli.

Dead space = volume of air that enters the lungs and doesn’t take part in gas exchange (trapped in lung structures).

• Usually areas conducting air to alveoli (pharynx, trachea, bronchi, bronchioles).

Increased TV causes an increase in AVR; Fast but shallow breathing can decrease AVR (air not entering low gas exchange area of lungs - stuck in conducting spaces).

Hyperpnea

When ventilation increases during exercise in response to metabolic needs. massive increase in volume (10-20 fold) entering the lungs per minute to ensure enough oxygen.

Provides extra oxygen and eliminates some heat and CO2.

Respiratory Adjustments during Exercise

Rest: normal breathing rate (aprox 12 bpm); normal TV = 500ml; minute ventilation = 6L/min (TV*BR=MVR).

Moderate Exercise: big increase in BR, TV and MVR.

Intense Exercise: Big increase in BR (almost doubling MVR); small change in TV.

NOTE: TV only accounts for 60-70% of vital capacity during exercise.

Change in Ventilation with Increasing Exercise Intensity

1. Initial increase (light to moderate exercise)

• Ventilation increases linearly with exercise intensity.

• Driven mainly by increases in tidal volume.

2. Ventilatory threshold (mod.-high intensity)
   At a certain point (around 50–75% of VO₂ max), ventilation increases more steeply.

• This point is called the ventilatory threshold or anaerobic threshold.

• Caused by rising CO₂ and H⁺ (acid) from increased anaerobic metabolism.

3. Steep increase (near maximal intensity)

• Ventilation increases disproportionately to oxygen consumption.

• Driven by increased respiratory rate more than tidal volume.

TV increases up to approx. 60-70% of the vital capacity after which, ventilation also increases at higher intensities of exercise.

Partial Pressures of O2, CO2 & H2O in alveoli

O2 = 20.9% of air, 159mmHg

• 13.7%, 104mmHh

CO2 = 0.04%, 0.3mmHg

• 5.2%, 40mmHg

H2O = water vapour in the lungs (air saturated with water in lungs)

• 0.46%, 3.7mmHg

• 6.2%, 47mmHg

Dead Space:

Volume of air not taking part in gas exchange.

Anatomic Dead Space - does not contribute to gas exchange. (150ml out of 500ml TV). No air flow

Alveolar Dead Space - space occupied by nonfunctional alveoli (lack of blood flow). no blood flow

Ventilation (V), Perfusion (Q), Coupling

Ventilation = amount of air reaching alveoli.

Perfusion (Q) = amount of blood that reaches alveoli per minute.

Gas exchange requires air ventilation in lungs. Also requires ventilation to be reasonably matched with blood flow (to infuse blood with oxygen to travel around body).

Ventilation-Perfusion (V/Q) Ratio

Provides an indication of whether efficient gas exchange is taking place.

V/Q ratio in healthy adults is approx 0.8.

Less than 0.8 = Shunt Perfusion. (no ventilation, but perfusion is occurring).

Greater than 0.8 = Deadspace Ventilation (is ventilation, but no purfusion occurring).

Exercise = increase in ventilation due to increased TV and Respiratory Rate. Increased ventilation must be matched with increased perfusion to ensure efficient gas exchange across lungs.

Pulmonary Circulation at Rest

Functional state: Pulmonary Vascular Resistance = (mean pulmonary artery pressure - left atrial pressure) / (pulmonary blood flow / cardiac output).

An increase in PVR can be achieved by:

• Increasing the pressure gradient between flowing and outflowing blood. Up pulmonary artery pressure to make it harder for blood to flow out of the lungs.

• Decreasing pulmonary blood flow (Down Q)

A decrease in PVR can be achieved by:

• Reduction in the pressure gradient between the inflow and outflowing blood (Down Pap).

• Increased pulmonary blood flow (Up Q)

• Combination of both

Pulmonary Vascular Resistance

Determines the amount of blood that flows through the lungs.

Pulmonary Artery Pressure

Pressure/drive of incoming blood; pressure generated from left ventricle.

Left Atrial Pressure

Outflow pressure; difference between Pap and Pla creases a mean pressure gradient that changes the influence of the flow of blood in the lungs.

Pulmonary Blood Flow/ Cardiac Output

overall amount of blood flowing in pulmonary circulation. Amount of blood arised from CO.

Lung Zones with Perfusion

Regional difference occur mainly due to weight of lung and influence of gravity. Decreases as you move up from base of lung.

Zone 1 = Little perfusion because the arterial pressure is less than the pressure in the alveoli, but it is greater than the venous pressure 

Zone 2 = Alveolar pressure is less than arterial pressure, but greater than the venous pressure

Zone 3 = Has the highest blood flow. Venous pressure is less than the arterial pressure, but greater than the alveolar pressure 

• Contributes to greater blood flow through this area of the lung 

Ventilation Differences in Lung Zones

The lower zone of the lung (base) has the highest ventilation; The upper zone (top) has the least.

Pulmonary Ventilation and Perfusion during Exercise

V/Q ratio relatively constant at 0.8 as ventilation is fairly well matched by perfusion.

Blood flow through lungs increases to accommodate increased ventilation.

Pulmonary Circulation - Exercise

Directly related to the mean of the pressure gradient between pulmonary artery and left atrial pressures.

Inversely related to pulmonary blood flow.

Cardiac Output increases from % L/min (rest) to 25 L/min (high intensity).

Pulmonary Blood Flow increases approx 4-7x compared to rest. Base of lungs increases 2-3x. Apex of lung increases 8x.

Overall lung = better perfused to match increase in ventilation.

Recruitment

• May participate in the process of continuing exercise along with distension

Major mechanism responsible for the drop in PVR that occurs with an initial rise in pulmonary artery pressure (PAP).

Initially, as Pap increases from low levels, some capillaries that were earlier closed/open with no blood flow start to conduct blood - thus lowering overall resistance to blood flow.

Decreases dead space volume.

As CO further increases, widening of individual capillary segments also occurs.

Distension

• Predominant mechanism responsible for fall in PVR at high vascular pressures.

Thin muscle membrane around capillaries makes them highly dispensable (diameter can increase/widen to accommodate a volume flowing through them.

The distension of capillaries happens due to the presence of the thin membrane separating the capillary from the alveolar space.

Most likely the mechanism as to how PVR decreases.

Blood Gases at Rest

• Partial pressures (gases between lungs and blood) ensure adequate diffusion of gases into blood for deliver to muscles.

• Deoxygenated blood arrives at lungs with partial pressure (PP) gradient between alveoli and arterial blood ensures exchange of: O₂ from lungs → arterial blood; CO₂ from blood → Lungs.

• After gas exchange, blood returning to ♡ from lungs has O₂ PP of approx 95mmHg and CO₂ PP of approx 40mmHg

Blood Gasses during Exercise

After returning from the heart, blood gets pumped to rest of body.

At skeletal muscle, O2 extracted from blood; CO2 removed from muscle into blood. Low O2 extraction at rest.

Partial pressure of venous blood (going back to heart) decreases to approx 40mmHg.

Partial pressure of CO2 increases to approx 46mmHg

Arterial partial pressure of O2 and CO2 at skeletal muscle remain constant in steady-state exercise.

Increased ventilation ensures maintenance of gas concentrations.

Partial pressure of O2 in blood decreases due to muscle O2 uptake.

(a-v) O2 Difference at Skeletal Muscle - Rest

O2 content difference is approx 50ml of O2 per L of blood.

Systemic circulation: arteries carry O2 blood away from heart, Veins carry deoxygenated blood from lungs to heart.

Arterial vs Venous blood

Arterial = away from heart

Venous = towards heart

(a-v) O2 Difference at Skeletal Muscle - Exercise

Arterial O2 difference increases due to muscle uptake.

Causing decrease in mixed venous O2 content returning to heart.

Pulmonary system ensures adequate gas exchange (lungs) & cardiovascular (O2 delivery), keeping arterial content relatively stable.

FICK Principle

VO2 = HR x SV x (a-v) O2 diff

Effort of cardiopulmonary system to ensure O2 delivery, uptake and usage.

Related to product of Cardiac Output and arterial venous difference.

Bohr Effect

Describes red blood cells ability to adapt to changes in the biochemical environment, maximising haemoglobin O2 binding capacity in lungs while simultaneously optimising O2 delivery to tissues with the greatest demand.

Is apart of gas exchange, involves transportation of O2 to skeletal muscle and diffusion of gas into tissue.

Factors influencing saturation of haemoglobin with O2:

UP temperature, H+ and PCO2 (structure modification)

• Causing: decrease in haemoglobin’s affinity for O2 in systemic capilaries.

• This enhances O2 unloading —> shift in O2 hemoglobin dissociation (right curve).

Decrease in temp, H+ and PCO2 cause left shift on curve and a decrease in O2 unloading from blood.

Haemoglobin curve

Normal body temp = approx 38 degrees

Increase = right curve (less O2 Hb saturation);

Blood PH = increase PP CO2 = right curve (less O2 Hb saturation).

O2 Haemoglobin Dissociation Curve

Right shift with exercise as core body temp increases (exercise) and PCO2 increases (metabolic waste increases).

Results in decreased O2 binding affinity to Hb

Myoglobin

Protein primarily in striated muscles of vertebrates.

One polypeptide chain with one O2 binding side.

• binds to O2 non-cooperatively (ligand binding doesn’t effect affinity of 2nd ligand site.

• saturation curve = hyperbolic

• higher O2 affinity, efficient O2 blood extraction

Higher than Hb % saturation in relatively low O2 partial pressures.

Haemoglobin

Protein in blood that cooperatively binds to O2 resulting in a sigmoid shaped curve .

Carbon Dioxide Transport

• 10% = dissolved in plasma

• 20% binds to carbaminohaemoglobin (globin in haemoglobin)

• 70% transported as bicarbonate ions in plasma

Ventilation changes in steady state

Phase one = immediate increase in ventilation at onset of exercise with time constant (few secs).

Phase two = slow exponential rise in ventilation with time constant (approx 1 min)

Phase three = by min 3 ventilation reaches steady state

Regulation of ventilation

Peripheral chemoreceptors (aortic arch + carotid arteries) detect chemical changes in blood and initiate an appropriate respiratory response.

Responses = changes in blood gas PP of O2 and CO2.

• decrease way below 30mmHg in PP O2 = corresponding increase in ventilation. (high altitudes, chronic pulmonary disease). RARE occurance, PP O2 in exercise = approx 95mmHg

What Else Controls Ventilation?

Decrease in plasma pH caused by:

• detected increase in hydrogen ions by peripheral chemoreceptors)

• Increase in partial pressure of CO2

Purpose of Increased Ventilation

Removal of excess CO2 and the formation of a section of the respiratory buffering system

Regulation of Ventilation During Steady-state

Chemoreceptors thought to regulate by sensing O2 and CO2 changes - not fully accurate. PP of O2 and CO2 remain relatively stable during exercise causing there to be a too small change to be detected by chemoreceptors.

Body lacks direct sensors for muscle metabolic activity. Due to chemoreceptor peripheral and central location, cannot directly detect muscle metabolism.

Ventilation rises immediately and proportionately with metabolic rate, preventing hypercapnia and maintaining blood homeostasis.

Respiratory system has feedforward control and is efficient as no major changes in CO2 levels.

Hypercapnia

Immediate increase in ventilation proportionate to metabolic rate to maintain arterial blood, gas, homeostasis.

To Prevent: PP of CO2 does not change in order to produce a reflex ventilatory response.

Respiratory Adjustments During Exercise Phases

Neural and Humoral mechanisms control hypernea similar to responses in anticipation of exercise.

Phase 1 = Central command stimulates an immediate increase in ventilation

Phase 2 = Ventilation is gradually increased due to input from skeletal muscle and the respiratory centres to the cortex causing an exponential increase in ventilation.

Phase 3 = Ventilation regulated through input from peripheral chemoreceptors in the blood vessels and skeletal muscles 

NOTE: Assumption only neural feedback/forward mechanisms can account for its speed. BUT only a humoral mechanism would work as an effective metabolic rate sensor (explains characteristic phases of phase 2 and 3 of hyperpnea) 

Respiratory changes with Exercise Cessation

• Sudden decline of ventilation (central command removal).

• Gradual decline of ventilation to baseline (due to decline in CO₂ after exercise ends).

• Increased respiratory drive causing decreased arterial PP or CO2 due to better perfusion of under-perfused lung areas at rest (decreased deadspace).

• More CO2 diffused across lungs than at rest.

• Rapid alveolar ventilation increase ahead of CO2 build-up.

Heavy/non-steady-state Exercise

• Ventilation increase until cessation/exhaustion

• O2 consumption and CO2 production fail to reach steady-state.

• Ventilation can increase over 150L/min (normal A), over 200L/min (elite). Intensity maximum = 2 mins.

• Ventilation increases non linearly in relation to O2 consumption.

Hyperventilation

Simultaneous metabolic acidosis resulting in stimulation of peripheral chemoreceptors, providing extra drive to breath to compensate for reduction in arterial pH.

• Debates that other mechanisms also significantly contribute to hyperventilation (fatigue).

Muscle Metabolism (Non-Steady State)

Accumulation of H+ ions at start of electron transport chain.

Pyruvate combines with excess H+ ions via enzyme lactate dehydrogenase to regenerate electron transporter NAD+.

Lactate is produced and blood lactate levels rise when anaerobic threshold has been reached.

Lactate transported (via blood) to liver to be converted back into glucose (energy).

Cori Cycle

Process of lactate leaving skeletal muscle and going to the liver to be converted back to glucose

Effect of Lactate Production

Increase in plasma H+ ion concentration causing reduction in blood pH.

Body compensates for reduction by buffering H+ in blood (bicarbonate buffering system).

H+ combines with Bicarbonate creating carbonic acid, which is carried through red blood cells.

In lungs, carbonic acid dissociates into CO2 and H2O.

Effect of Lactate Production on RER

Increased lactate increases VCO2 and increases the overall ratio of RER (VCO2/VO2).

RER often 1 or higher. Means high intensity exercise is occuring.

Measurement of Ventilatory Threshold

(ml/O2 or L/O2)

Estimator of onset of metabolic acidosis caused predominantly by the increased rise of arterial lactate during exercise.

Functions:

1. sensitive marker for aerobic training status (higher VT = fitter).

2. Good predictor of endurance performance

3. Established effective training intensity based on active muscles aerobic metabolic dynamics