Exercise Physiology- physiological changes at altitude and altitude disorders.

1. Immediate Physical
Response at Altitude
Dr. Usha (PT)
Assistant Professor

2. IMMEDIATE ADJUSTMENTS
At elevations above 2300 m (7546 ft), rapid
physiologic adjustments compensate for the
thinner air and reduced alveolar oxygen
pressure. The most important of these responses
include:
Hyperventilation triggered by increased
respiratory drive
Increased blood flow (cardiac output) during
rest and submaximal exercise

3. 1. Hyperventilation triggered by increased
respiratory drive:
Hyperventilation represents the immediate
first line of defence to altitude exposure.
Chemoreceptors located in the aortic arch
and branching of the carotid arteries in the
neck detect reductions in arterial PO2.

4. • Chemoreceptor stimulation increases
ventilation, raising alveolar oxygen
concentration toward the level in ambient
air.
• Any increase in alveolar PO2 with
hyperventilation facilitates oxygen loading
in the lungs.

5. 2. Increased blood flow (cardiac output)
during rest and submaximal exercise:
Submaximal heart rate and cardiac output
increase 50% above sea level values in the early
stages of altitude acclimatization, but the heart’s
stroke volume remains essentially unchanged.
Sea level and altitude exercise oxygen uptake
remain similar, but increased submaximal
exercise blood flow at altitude compensates for
the reduced arterial oxygen content.

6. In contrast, the circulatory adjustments to
acute altitude exposure with maximal
exercise cannot compensate for the lower
oxygen content of arterial blood dramatically
decreasing VO2max and exercise capacity.

7. FLUID LOSS
A depressed thirst sensation at altitude
negatively affects body fluid balance.
The cool, dry air in mountainous regions also
causes considerable body water to evaporate
as air warms and moistens the respiratory
passages.

8.  Respiratory fluid loss often leads to moderate
dehydration and accompanying symptoms of
dryness of the lips, mouth, and throat,
particularly for physically active people with
relatively large daily pulmonary ventilations and
exercise- related sweat loss.
 For these active people, body weight should be
checked frequently augmented with unlimited fluid
availability to ensure against dehydration

10. LONGER TERM
ADJUSTMENTS
 Hyperventilation and increased submaximal cardiac
output provide a rapid, effective counter to the
acute altitude challenge. Other slower acting
physiologic adjustments commence during a
prolonged altitude stay. The three most important
longer term adjustments include:
1. Acid–base adjustment
2. Hematologic changes
3. Cellular adaptations

11. 1. ACID–BASE ADJUSTMENT:
 Hyperventilation at altitude favourably increases
alveolar oxygen concentration, while carbon dioxide
concentration decreases.
 The ambient air contains essentially no carbon dioxide,
so increased alveolar ventilation at altitude washes out
(dilutes) carbon dioxide in the alveoli.
 This creates a larger than normal gradient for carbon
dioxide diffusion from blood into the lungs, reducing
arterial carbon dioxide considerably.

12. During prolonged high-altitude exposure,
alveolar carbon dioxide pressure can
decrease to 10 mm Hg compared with the
sea level value of 40 mm Hg.
Carbon dioxide loss from body fluids causes
pH to increase as the blood becomes more
alkaline. The carbonic acid transports the
largest amount of the body’s carbon dioxide.

13.  Control of respiratory alkalosis produced by
hyperventilation occurs in the kidneys, which slowly
excrete base (HCO3) through the renal tubules.
 The establishment of acid–base equilibrium with
acclimatization occurs with a loss of alkaline reserve.
Altitude does not affect anaerobic metabolic pathways
per se, but blood’s buffering capacity for acids
gradually decreases, reducing the critical level for
accumulation of acid metabolites such as lactic acid.

14. 2. HEMATOLOGIC CHANGES:
 An increase in the blood’s oxygen-carrying capacity
provides the most important long-term adaptation to
altitude.
 Two factors account for this adaptation:
a) Initial decrease in plasma volume
b) Increase in erythrocytes and haemoglobin
synthesis

15.  A rapid decrease in plasma volume increases red
blood cell (RBC) concentration during the first few
days at altitude.
 This response causes arterial blood’s oxygen
concentration to increase above values observed on
immediate ascent to altitude.
 The reduced arterial PO2 stimulates a concurrent
increase in RBC mass, a response termed
polycythemia that directly increases the blood’s
capacity to transport oxygen.

16. The kidneys release the erythrocyte-
stimulating hormone erythropoietin within
15 hours after altitude ascent. In the weeks
that follow, RBC production in the marrow
of the long bones increases and remains
elevated. For example, the oxygen-carrying
capacity of blood for high-altitude residents
of Peru averages 28% above sea-level
natives.

17.  For well-acclimatized mountaineers, oxygen transport
capacity for each dL (100 mL) of blood (at sea level
PO2) ranges between 25 and 31 mL compared with
about 20 mL for lowland residents.
 Even with haemoglobin's reduced oxygen saturation at
altitude, the actual quantity of oxygen in arterial blood
of elite mountaineers at altitude nearly equals sea-level
values.

18.  The general trend for increased haemoglobin and
haematocrit during altitude acclimatization for eight
young women at the University of Missouri
(altitude, 213 m) who lived and worked for 10
weeks at the 4267-m summit of Pikes Peak.

19.  Upon reaching Pikes Peak, their RBC
concentrations increased rapidly because of a
reduced plasma volume during the first 24 hours.
 Over the following month, haemoglobin
concentration and haematocrit continued to increase
and then stabilized for the remainder of the stay.
Two weeks after the women returned to Missouri,
their haemoglobin and haematocrit levels returned
to pre-altitude values.

20. 3. CELLULAR ADAPTATIONS:
 Long-term acclimatization initiates peripheral changes that
facilitate aerobic metabolism. Three important adaptive changes
are as follows:
i. Increased capillary concentration in skeletal
muscle, thus reducing the distance for oxygen
diffusion between blood and tissues
ii. Formation of additional mitochondria and an
increase in aerobic enzyme concentration
iii. Expanded oxygen storage within specific muscle
fibers via increase myoglobin, which facilitates
intracellular oxygen delivery and utilization,
particularly at low tissue PO2

22. System Acute hypoxic effect at rest Acute hypoxic effect at a given
submaximal exercise intensity
Respiratory
and
oxygen
transport
• Immediate increase in
ventilation (increased
frequency > increased tidal
volume)
• Decreased 2,3-DPG
concentration
• Leftward shift in the
oxyhemoglobin dissociation
curve
• Stimulation of peripheral
chemoreceptors
• Respiratory alkalosis
Increased ventilation
Cardiovascular • Decreased plasma volume
• Increased heart rate
• Decreased stroke volume
• Increased cardiac output
• Increased blood pressure
• Increased heart rate
• Decreased stroke volume (due
to decreased plasma volume)
• Increased cardiac output
• Increased VO2

23. System Acute hypoxic effect at rest Acute hypoxic effect at
a given submaximal
exercise intensity
Metabolic • Increased basal metabolic
rate
• Decreased (a-v )O2
difference
• Greater utilization of
carbohydrates for
energy
• Increased lactate
production initially,
then lower
• Decreased blood pH
Renal • Diuresis
• Excretion of bicarbonate
ions
• Increased release of
erythropoietin
-

24. DISORDERS AT ALTITUDE
 Natives who live and work at high altitudes and newcomers to
high altitudes encounter medical problems associated with
reduced ambient PO2.
 Some mild problems dissipate within hours or several days,
depending on the rapidity of ascent and degree of exposure,
but other medical complications become severe and
compromise overall health and safety.
 Four medical conditions are associated with high-altitude
exposure:

25. ACUTE MOUNTAIN SICKNESS
 AMS is a relatively benign condition that becomes
exacerbated by exercise in the first few hours of exposure. I
occurs most often in people who ascend rapidly to high
altitude (10,000 ft.; 3000 m) without benefitting from gradual
and progressive acclimatization to lower altitudes.
 Symptoms begin within 4 to 12 hours after exposure and
dissipate within 1 week.
 Treatment usually involves rest and gradual acclimatization.

26. HIGH-ALTITUDE PULMONARY EDEMA
 (HAPE) is a life-threatening condition that includes fluid
accumulation in the brain and lungs. Predisposing factors
include high altitude, rate of ascent, and individual
susceptibility.
 Symptoms usually manifest within 24 to 96 hours after a
rapid ascent.
 Preventing severe disability or death requires immediate
descent to a lower altitude on a stretcher or being flown to
safety.
 Any physical activity potentiates complications.
 Supplemental oxygen is helpful during descent.

27. HIGH-ALTITUDE CEREBRAL
EDEMA
 (HACE) is a potentially fatal neurologic syndrome that
develops within hours or days in people with AMS.
 It usually occurs in people exposed to altitudes above 9000 ft
(2700 m).
 Cerebral edema results from cerebral vasodilation and
elevation in capillary hydrostatic pressures, causing
movement of fluid and protein from the vascular
compartment across the blood–brain barrier.
 Early symptoms similar to those of AMS and HAPE include
headache, severe fatigue, and altered mental state. Immediate
descent to a lower altitude is required along with
supplemental oxygen adminstration.

28. HIGH-ALTITUDE RETINAL
HEMORRHAGE
 (HARH) includes hemorrhage in the macula of the eye that
produces irreversible visual defects.
 Retinal bleeding probably results from surges in blood
pressure with exercise that cause blood vessels in the eye to
dilate and rupture from increased cerebral blood flow.
 Immediate descent to a lower elevation with supplemental
oxygen or use of a hyperbaric chamber is the mandatory
treatment.