RESPIRATORY ADAPTATIONS IN RESPONSE TO EXERCISE HIGH ALTITUDE

1 NEONATAL RESPIRATORY DISTRESS INCLUDING CPAP CLINICAL LEARNING RESOURCE
17 TABLE 1 COMMON MICROBIOTA OF THE RESPIRATORY TRACT
20 PREVENTION OF RESPIRATORY INSUFFICIENCY AFTER SURGICAL MANAGEMENT (PRISM)

21 NCAC 46 2610 MEDICAL GAS OXYGEN AND RESPIRATORY
49714 §497—SCHEDULE OF RATINGS–RESPIRATORY SYSTEM 49714 §497 SCHEDULE OF
AIRSTREAM MECHANISMS PULMONIC MOVEMENT OF LUNG AIR BY RESPIRATORY

Respiratory adaptations in response to exercise , high altitude and deep sea diving

Learning objectives

At the end of lecture , the student should be able to:

1. Understand the respiratory responses in relation to exercise

2. Changes occurring in the muscles during exercise

3. The response of Oxygen hemoglobin dissociation curve during exercise

4. Oxygen debt and its importance

5. How does the respiratory system adapt to high altitude pressures

6. Changes occurring in the body at high altitudes

7. Acclimitization and its importance

8. Under water diving and changes in the body

9. Decompression sickness and its consequences

Lecture outline

Response of respiratory system to Exercise

The respiratory and cardiovascular systems make adjustments in response to both intensity and duration of exercise

The response of respiratory system to exercise is remarkable

As the body’s demand for O₂ increases more O₂is supplied by increasing the ventilation rate.

Excellent matching occurs b/w O₂ consumption, CO₂ production and the ventilation rate

Respiratory adaptations

Increased lung ventilation
Increased oxygen uptake
Increased anaerobic or lactate threshold

INCREASED LUNG VENTILATION

Aerobic training results in a more efficient and improved lung ventilation.

At REST and during SUB MAX. work ventilation may be decreased due to improved oxygen extraction (pulmonary diffusion), however during MAX. work ventilation is increased because of increased tidal volume and respiratory frequency.

INCREASED MAXIMUM OXYGEN UPTAKE (VO₂ MAX)

VO₂ max is improved as a result of aerobic training – it can be improved between 5 to 30 %.

Improvements are a result of:

- Increases in cardiac output

- red blood cell numbers

- a-VO₂difference

- Muscle capillarisation

- Greater oxygen extraction by muscles

INCREASED ANAEROBIC OR LACTATE THRESHOLD

Lactate Threshold

As stages continue to increase, a point is reached at which blood lactate concentration suddenly increases

Lower work rates, lactate metabolized as fast as it is produced

Lactate threshold changes as a result of endurance training

As a result of improved O₂ delivery & utilization , a higher lactate threshold (the point where O₂ supply cannot keep up with O₂ demand) is developed.

Changes in the Muscle tissue

The following tissue changes occur:

Increased O₂ utilization
increased size and number of mitochondria
Increased myoglobin stores
Increased muscular fuel stores
Increased oxidation of glucose and fats
Decreased utilization of the anaerobic glycolysis (LA) system
Muscle fiber type adaptations

Exercise and rate of diffusion

Pulmonary diffusion

humans : 4-5 fold increase in pulmonary blood flow; expanding capillary blood volume 3 times

Tissue diffusion

O₂and CO₂diffuse down the pressure gradient

PO₂ returning from muscle tissue following heavy exercise, only 16mm Hg

increased driving pressure of O₂from arterial blood into muscle

tissues with high aerobic needs are more vascularized greater surface area for exchange

Arterial PO₂& PCO₂during exercise

Remarkably, mean values for arterial PO₂& PCO₂ do not change during exercise.
An increased ventilation rate and increased efficiency of gas exchange ensure that there is neither a decrease in arterial PO₂ nor an increase in arterial PCO₂.
The total amount of O₂entering the blood increases from 250ml/min at rest to about 4000ml/min.
The PO₂of blood entering the lungs is reduced which increases the pressure difference b/w blood and alveolar PO₂leading to increased O₂diffusion into the blood from alveoli.

Changes during Exercise

Blood flow/min is increased from 5L/min to about 25-30L/min.
The total amount of O₂entering the lungs increases from 250ml/min at rest to about 4000ml/min.
Similarly CO₂removal increases from 200ml/min to about 8000ml/min.

Oxygen diffusion at rest and exercise

Oxygen Diffusion at rest

Air--> alveoli-->arteriolar blood--> cells
(159) (100) (100) (40)

Oxygen Diffusion during exercise

Air--> alveoli-->arteriolar blood--> cells
(159) (100) (100) (20)

CO2 diffusion at rest and exercise

CO₂ Diffusion during rest

Air<-- alveoli <--venous blood <-- cells
(.3) (40) (46) (46)

CO₂ Diffusion during exercise

Air<-- alveoli <--venous blood <-- cells
(.3) (40) (55) (55)

O₂ – Hb dissociation curve

During exercise the O₂– Hb dissociation curve shifts to the right.

This right shift is due to multiple reasons including :

Increased tissue PCO₂
Decreased tissue pH
Increased temperature
Increased 2,3- BPG

RESPIRATORY ADAPTATIONS IN RESPONSE TO EXERCISE HIGH ALTITUDE

Oxygen debt

The oxygen dept is the amount of air that is consumed after the exercise is over until a constant, basal condition is reached.

The trained athletes can increase the O₂consumption to a greater extent than untrained person.

So O₂dept in athletes is less.

RESPIRATORY ADAPTATIONS IN RESPONSE TO EXERCISE HIGH ALTITUDE

Adaptation to high altitude

The respiratory responses to high altitude are the adaptive adjustments a person must make to the decreased PO₂in inspired and alveolar air.

At high altitude the decrease in PO₂ is due to:

At sea level, the barometric pressure is 760mmHg.

At 18,000 feet above sea level, the barometric pressure is one half that value or 380 mmHg

To calculate the PO₂ of humidified inspired air at 18000 feet above sea level, correct the barometric pressure of dry air by the water vapor pressure of 47 mmHg, then multiply by the fractional concentration of O₂, which is 21%.

Thus ,at 18,000 feet, PO₂=70mmHg (360 – 47mmHg) x 0.21 = 70 mmHg

The pressure at the peak of Mount Everest yields a PO₂ of inspired air of only 47 mmHg.

Pressures at high Altitude

Altitude Pb PO₂ Alveolar PO₂
sea level 760 159 104
10,000ft 523 110 67
20,000ft 349 73 40

Despite severe reductions in the PO₂ of both inspired and alveolar air, it is possible to live at high altitude ,if the following adaptive responses occur:

Hyperventilation : the most significant response to high altitude is hyperventilation (increase in ventilation rate).

For example if the alveolar PO₂ is 70mmHg, then the arterial blood which is almost perfectly equilibrated, also will have a PO₂ of 70 mmHg , which will not stimulate peripheral chemoreceptor.

However, if alveolar PO₂is 60mmHg then arterial blood will have a PO₂ of 60 mmHg, in which the hypoxemia is severe enough to stimulate peripheral chemoreceptors in the carotid and aortic bodies.

In turn, the chemoreceptors instruct the medullary inspiratory center to increase the breathing rate.

A consequence of hyperventilation is that extra CO₂ is expired by the lungs and arterial PCO₂decreases, producing respiratory alkalosis

However, the decrease in PCO₂ and resulting increase in pH will inhibit central and peripheral chemoreceptors and offset the increase in ventilation rate

These offsetting effects of CO₂ and pH occur initially, but within several days HCO₃^-excretion increases.

HCO₃^-leaves the CSF, and the pH of CSF decreases toward normal

Thus, within a few days, the offsetting effects are reduced and hyperventilation resumes.

The respiratory alkalosis that occurs as a result of ascent to high altitude can be treated with carbonic anhydrates inhibitors (acetazolamide).

These drugs increase HCO₃^-excretion, creating a mild compensatory metabolic acidosis.

Other changes in response to Adaptation to high altitude

Polycythemia: ascent to high altitude produce an increase in red cell conc. and as a consequence increase in in Hb conc.

The increase in Hb conc. In turn increase the O₂carrying capacity, which increases the total O₂content of blood in spite of arterial PO₂being decreased.

O₂- hemoglobin dissociation curve

The most interesting feature of body adaptation to high altitude is an increase synthesis of 2,3- DPG by red blood cells.

This increase 2,3- DPG causes shift of O₂-Hb curve to the right.

This right shift is advantageous to the tissues, b/c it is associated with increased P₅₀, decreased affinity, and increased unloading of O₂ to the tissues.

This right shift is disadvantageous in the lungs b/c it becomes more difficult to load the pulmonary capillary blood with O₂.

Pulmonary vasoconstriction:

At high altitude ,alveolar gas has a low PO₂, which has a direct vasoconstriction effect on pulmonary vasculature (hypoxic vasoconstriction).

Changes in cell in response to adaptation to high altitude

Compensatory changes also occur in the tissues:

The mitochondria (site of oxidative reactions) increase in number and myoglobin increases which facilitates the movement of O₂in the tissues.

The tissue content of cytochrome oxidase also increases.

Acclimatization

If a person remains on high altitude for a week, month or year then he becomes more acclimatized and the effects of hypoxia are faded, this is called acclimatization

Acclimatization to altitude is due to the operation of a variety of compensatory mechanism.

The respiratory alkalosis produced by the hyperventilation shift the O₂- Hb dissociation curve to the left, but a concomitant increase in red cell ,2,3-DPG tends to decrease the O₂ affinity of Hb.

The net effect is a small increase in P_50.

The decrease in O₂ affinity makes more O₂available to the tissue

However ,the value of the increase in P₅₀is limited b/c when the arterial PO₂ is markedly reduced, the decrease O₂ affinity also interferes with O₂ uptake by Hb in the lungs.

The initial ventilatory response to increase altitude is relatively small, b/c alkalosis tends to counteract the stimulating effect of hypoxia

However ventilation slowly increases over next 4 days b/c the active transport of H⁺into CSF, causes a fall in CSF pH that increases the response to hypoxia.

RESPIRATORY ADAPTATIONS IN RESPONSE TO EXERCISE HIGH ALTITUDE

HYPERBARIC CONDITIONS - EXERCISING UNDERWATER

Submersion in Water

Exposure to hyperbaric conditions -volume decreases when pressure increases.

More molecules of gas are forced into solution, with rapid ascent, they come out of solution and can form bubbles - emboli develop, block major vessels, extensive tissue damage.

Resting HEART RATE DECREASES by 5 - 8 beats per minute (facilitation blood return to the heart) diving in cold water - greater bradycardia, higher incidence of arrhythmias

During diving under water, the pressure increases by one atmosphere (760mmHg) for every 10 meters or 33 feet descent.

The density of gas increases in depth leads to increase work of breathing.

During diving due to high atmospheric pressure the air filled cavities are compressed as they failed to communicate with external air

As the person ascends these air filled cavities over expand.

The increased pressure (hyperbarism) do not affect the solid tissue or liquids of the body but only the gas filled cavities are affected.

During diving at high pressure the nitrogen (which is poorly soluble in blood) enters into the body

Nitrogen is relatively soluble in fats.

During descent nitrogen diffuses slowly into the tissues.

During ascend it slowly removed from the tissues b/c decompression occur due to decrease in pressure from deeper to upper levels in water.

Decompression sickness can be avoided if the divers are trained to ascends slowly, which prevents increase in size of oxygen bubbles.

The divers ascend in stages (at intervals) and spend some time at different depth to avoid nitrogen toxicity.

Weightlessness in space

Physiological consequences of prolonged periods in space are following:

Decreased blood volume
Decreased red cell mass
Decreased muscle strength & work capacity
Decreased maximum cardiac output
Loss of calcium and phosphate from bones and loss of bone mass

Physiological problems with Weightlessness:

Motion sickness during the first few days of travel.
Translocation of fluids in the body b/c of failure of gravity to cause hydrostatic pressure.
Diminished physical activity b/c no strength of muscle contraction is required to oppose the force of gravity.

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