Respiratory adaptations in response to exercise , high altitude

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					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 O2 is 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


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.

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-VO2 difference
     - Muscle capillarisation
     - Greater oxygen extraction by muscles


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
O2 and CO2 diffuse down the pressure gradient
PO2 returning from muscle tissue following heavy exercise, only 16mm Hg
increased driving pressure of O2 from arterial blood into muscle
tissues with high aerobic needs are more vascularized greater surface
area for exchange

Arterial PO2 & PCO2 during exercise

► Remarkably, mean values for arterial PO2 & PCO2 do not change during
► 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 O2 entering the blood increases from 250ml/min at
rest to about 4000ml/min.
► The PO2 of blood entering the lungs is reduced which increases the
pressure difference b/w blood and alveolar PO2 leading to increased O2
diffusion 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 O2 entering the lungs increases from 250ml/min at
rest to about 4000ml/min.
► Similarly CO2 removal 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
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 O2 consumption to a greater extent than
untrained person.

So O2 dept in athletes is less.
Adaptation to high altitude

►The respiratory responses to high altitude are the adaptive adjustments a
person must make to the decreased PO2 in 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

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 PO2 is 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 PCO2 decreases, 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

►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

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 O2 carrying capacity, which
increases the total O2 content of blood in spite of arterial PO2 being

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

►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

Changes in cell in response to adaptation to high
Compensatory changes also occur in the tissues:

The mitochondria (site of oxidative reactions) increase in number and
myoglobin increases which facilitates the movement of O2 in the tissues.

The tissue content of cytochrome oxidase also increases.

►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 P50.

►The decrease in O2 affinity makes more O2 available to the tissue

►However ,the value of the increase in P50 is 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.
►Submersion in Water
      Exposure to hyperbaric conditions -volume decreases when pressure

►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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