C
H A P T E R
24
Exercise at
Medium and
High Altitude
Chapter Objectives
• Outline the effects of increasingly higher altitudes on
(1) partial pressure of oxygen in ambient air, (2) oxygen saturation
of hemoglobin in pulmonary capillar•
ies, and (3) VO2max
• Describe and quantify the oxygen transport cascade
at sea level and at 4300 m
• Discuss immediate and longer-term physiologic adjustments to altitude exposure
• Give symptoms, possible causes, and treatment for
acute mountain sickness, high-altitude pulmonary
edema, and high-altitude cerebral edema
• Describe the “lactate paradox” and possible causes
for its occurrence
602
• Summarize factors that affect the time course for altitude acclimatization
•
• Graph the relation between the decrease in VO2max
(% sea-level value) with increasing altitude or simulated altitude exposure
• Discuss alterations in circulatory function that offset
the benefits of altitude acclimatization on oxygen
transport capacity
• Discuss whether altitude training produces greater
improvement than sea-level training on sea-level exercise performance
• Describe the training concept “living high, training
low”
CHAPTER 24
More than 40 million people live, work, and recreate at terrestrial elevations between 3048 m (10,000 ft) and 5486 m
(18,000 ft) above sea level. In terms of the earth’s topography,
these elevations encompass the range generally considered
high altitude. High-altitude natives inhabit permanent settlements as high as 5486 m in the Andes and Himalayas. However, prolonged exposure of an unacclimatized person to this
altitude can cause death from the ambient air’s subnormal
oxygen pressure (hypoxia), even if the person remains inactive. The physiologic challenge of even medium altitude becomes readily apparent during physical activity. In the United
States, close to 1 million people a year ascend Pikes Peak,
Colorado (4300 m) by train, car, or railroad, and thousands of
others do so by climbing, cycling, and even running. Millions
more throughout the world ascend to high altitudes for mountaineering, trekking, tourism, business, and scientific and military excursions. Whatever the purpose, many newcomers to
altitude do not take sufficient time to acclimatize to the physiologic challenge of the reduced partial pressure of oxygen
(PO2) in ambient air.
75
50
603
THE STRESS OF ALTITUDE
Altitude’s challenge comes directly from the decreased ambient PO2, not from the reduced total barometric pressure per se
or any change in the relative concentrations (percentages) of
gases in inspired (ambient) air. Figure 24.1 illustrates the
barometric pressure, the pressures of the respired gases, and
the percentage saturation of hemoglobin at various terrestrial
elevations. Figure 24.2 shows changes that occur in oxygen
availability (reflected by PO2) in ambient air, alveolar air, and
arterial and mixed-venous blood as one ascends from sea
level to Pikes Peak. The progressive change in the environment’s oxygen pressure and in various body areas is termed
the oxygen transport cascade.
Air density decreases progressively as one ascends
above sea level. For example, the barometric pressure at sea
level averages 760 mm Hg, and at 3048 m the barometer
reads 510 mm Hg; at an elevation of 5486 m, the pressure of
a column of air at the earth’s surface equals about one-half its
pressure at sea level. Although dry ambient air at sea level and
Hb saturation (percent)
100
• Exercise at Medium and High Altitude
Paco2 (mm Hg)
25
50
0
226
30
Pio2
9
Mt. Everest
e
Sao2
Pao2
25
Paco2
d
349
Upper limit for permanent residence
Quilcha, Chile
429
Morococha, Peru
Peru
c
Mt. Evans,
Pikes Peak,
Peak, CO
b
523
Leadville,
Leadv ille, CO
632
Mexico City
a
Denver,
Denver, CO
Altitude
m
ft
0
0
1,000 3,280
1,500 4,920
2,000 6,560
3,000 9,840
4,000 13,120
5,000 16,400
6,000 19,690
7,000 22,970
8,000 26,250
9,000 29,530
Ambient
pressure
mm Hg
760
674
634
596
526
462
405
354
308
267
230
Ambient
Po2
mm Hg
159
141
133
125
110
97
85
74
64
56
48 20
15
10
5
3
Altitude (meters x 103)
7
Altitude (feet x 103)
Barometric pressure (mm Hg)
282
5
1
0
760
150
100
50
0
Pao2 and Pio2 (mm Hg)
a) Lightheadedness, headache b) Insomnia, nausea, vomiting, pulmonary discomfort
c) Dyspnea, anorexia, GI disturbances d) Lethargy, general weakness e) Impending collapse
FIGURE 24.1 • Changes in environmental and physiologic variables with progressive elevations in altitude (PaO2, partial pressure of arterial oxygen; PaCO2, partial pressure of arterial carbon dioxide; PiO2, partial pressure of oxygen in inspired air; SaO2, oxygen saturation of hemoglobin).
604
• Exercise Performance and Environmental Stress
SECTION 5
150
Po2 (torr)
110
70
30
0
Inspired
air
Sea level
Alveolar
gas
Arterial
blood
Mixed
venous
blood
4300 m
FIGURE 24.2 • Oxygen transport cascade from sea level to 4,300 m
(14,108 ft).
altitude contains 20.93% oxygen, the PO2 (density of the oxygen molecules) of air decreases directly with the fall in barometric pressure upon ascending to higher elevations (PO2 ⫽
0.2093 ⫻ barometric pressure). Thus, ambient PO2 at sea
level averages about 150 mm Hg, but only 107 mm Hg at
3048 m. At the summit of Mt. Everest (8848 m; 29,028 ft)
ambient air pressure on a day climbers usually ascend to the
summit ranges between 251 and 253 mm Hg, with a concomitant alveolar PO2 of about 25 mm Hg (ambient air PO2 between 42 and 43 mm Hg).104 This equals only about 30% of
the oxygen available in air at sea level. The reduction in PO2,
and accompanying arterial hypoxia, precipitates the immediate physiologic adjustments to altitude and longer-term acclimatization. Acclimatization refers to adaptations produced
by a change in the natural environment, whether a change in
season or place or residence. In contrast, acclimation refers
to adaptation produced in a controlled laboratory environment
as in chambers that can simulate high altitude or microgravity, hypoxic environments, and extremes of thermal stress.
Oxygen Loading at Altitude
The oxyhemoglobin dissociation curve is S-shaped (see
Chapter 13, Fig. 13.3), and only a small change occurs in hemoglobin’s percentage saturation with oxygen until an altitude of about 3048 m. At 1981 m (6500 ft), for example, alveolar PO2 decreases from its sea level value of 100 mm Hg to
78 mm Hg, yet hemoglobin remains 90% saturated with oxy-
gen. This relatively small arterial desaturation exerts little effect on a person during rest or even mild exercise, but performance in vigorous aerobic activities deteriorates. The relatively poor performances of men and women in middledistance and distance running and swimming during the 1968
Olympics in Mexico City (altitude 2300 m; 7546 ft) resulted
from the small reduction in oxygen transport at this altitude.18
No world records emerged in events lasting longer than 2.5
minutes. Altitude does not impair the short-term anaerobic
energy system at moderate altitude (e.g., glycogen storage,
pathways of glycolysis and corresponding phosphorylase and
phosphofructokinase enzyme activity, although maximal lactate accumulation becomes depressed at extreme elevation
[see page 612]) or success in sprint–power activities such as
sprint running, speed skating, track cycling, jumping, and discus.27,30 However, impaired performance has been reported
for reported for repeated interval sets of short-term power
output (15-s training intervals) in elite athletes.12 Performance
in single bouts of such activities often improves because of
lower air density (air resistance or drag force) at altitude than
at sea level. In addition the lessened air resistance from a 24%
reduction in air density at 2300 m should improve performance in the shot put (⫹6 cm), hammer throw (⫹53 cm), and
javelin (⫹162 cm).22 The oxygen cost for stationary cycling
remains unaltered during altitude exposure.
In the transition from moderate altitude to higher elevations, values for alveolar (arterial) PO2 are on the steep part of
the oxyhemoglobin dissociation curve. This dramatically reduces hemoglobin oxygenation and oxygen transport capacity
and negatively affects even mild aerobic activities. At high elevations in the Andes and Himalayas, oxygen loading of hemoglobin decreases dramatically, and physical activity becomes difficult to sustain. A small change in inspired PO2 (i.e.,
barometric pressure) greatly affects aerobic capacity at the
summit of Mt. Everest. For well-acclimatized mountain
climbers, for example, breathing ambient air with a PO2 of
•
48.5 mm Hg produces a VO2max of 1450 mL ⭈ min⫺1. This declines to 1070 mL ⭈ min⫺1 with only a 6–mm Hg decrease in
•
inspired PO2–a decrease of 63 mL O2 ⭈ min⫺1 in VO2max for
each 1 mm Hg drop in inspired PO2.103,104
Sudden exposure to 4300 m, for example, causes a
32% reduction in aerobic capacity compared with sea-level
values.110 At altitudes above 5182 m (17,000 ft), permanent
living becomes nearly impossible, and mountain climbing
frequently requires the aid of hyperoxic breathing mixtures.74 At 5486 m (18,000 ft), arterial PO2 averages 38 mm
Hg and hemoglobin maintains only 73% oxygen saturation. Amazingly, however, reports describe acclimatized
mountaineers who lived for weeks at 6706 m (22,000 ft)
breathing only ambient air.42 In fact, members of two
Swiss expeditions to Mt. Everest remained at the summit
for 2 hours without using breathing equipment!73 This represents an impressive feat considering that arterial PO2 averages only 25 mm Hg, with a corresponding arterial blood
oxygen saturation of 58%. An unacclimatized person becomes unconscious within 30 seconds under these conditions.106 For acclimatized men at simulated extreme alti-
CHAPTER 24
•
tudes that approach the summit of Mt. Everest, VO2max
decreases by 70% from 4.13 L ⭈ min⫺1 to 1.17 L ⭈ min⫺1,
or from 49.1 mL ⭈ kg⫺1 ⭈ min⫺1 to 15.3 mL ⭈ kg⫺1 ⭈
min⫺1.34 These low values reflect the sea-level aerobic capacity of a sedentary 80-year-old man. Despite the significant physiologic strain imposed by high altitude, mountaineer Tom Whittaker, age 50, became the first amputee to
reach Mt. Everest’s summit (third attempt) on May 27,
1998. Although remarkable performances at high altitude
reflect exceptions and not the rule, they demonstrate the
605
enormous adaptive capability of humans to survive and
even work without external support at extreme terrestrial
elevations (see “Focus on Research”).
INTEGRATIVE QUESTION
Respond to this question: “If altitude has such negative effects on the body, how come certain track
and field records are broken during competition at
higher elevations?”
High Altitude: A Hostile Environment
Pugh LGCE, et al. Muscular exercise at great altitudes. J
Appl Physiol 1964;19:431.
➤ Since the first ascent of Mt. Everest (8848 m; 29,028 ft)
in 1953 by Sir Edmund Hillary and Tenzig Norgay, scientists
have studied relationships between terrestrial elevation, partial pressure of oxygen in ambient air, arterial hemoglobin
oxygen loading, and cardiovascular function to explain reduced exercise capacity at altitude. Early experiments at
high altitude posed enormous scientific challenges owing to
equipment limitations and lack of trained personnel with
mountaineering experience. The experiments, carried out by
the Himalayan Scientific and Mountaineering Expedition of
1960–1961 (sponsored by the publishers of World Book Encyclopedia, Chicago, IL, and the Medical Research Council,
London, England), represent “classic” experiments in environmental physiology. Discoveries from this legendary scientific expedition provided the underpinnings to current understanding about physical work at high altitude. The
research by L. G. C. E. Pugh and coworkers was part of the
first series of studies to demonstrate that lung diffusion capacity, cardiac output, and the oxygen cost of extreme pulmonary ventilation limit exercise capacity at altitudes above
5800 m (19,000 ft).
The researchers used bicycle ergometer exercise to assess physical working capacity at sea level and at altitudes
ranging from 4650 m to 7440 m (barometric pressure of
440 to 300 mm Hg). They established a base station at 4650
m but used a prefabricated laboratory hut at 5800 m (barometric pressure of 380 mm Hg) to conduct most of the
research.
Subjects included eight men—six experienced mountaineers and one “sportsman,” all acclimatized to high altitude, and one high-altitude Sherpa guide. The scientists with
the Himalayan Scientific Expedition were five of the seven
“lowland” subjects. The Sherpa guide carried the bicycle ergometer (20 kg) to the laboratory hut. Subjects pedaled at
50 RPM, with expired air collected by the Douglas bag
method. A dry-gas meter measured expired air volumes
with respiratory gas concentrations analyzed with a LloydHaldane chemical analyzer. The exercise protocol (preceded
by a 10-min warm-up) included 6 minutes of exercise (12
min at sea level) starting at 300 kg-m ⭈ min⫺1 with increments of 300 kg-m ⭈ min⫺1. The test terminated when the
subject would not exercise for at least 2 minutes at a given
intensity. Oxygen consumption, pulmonary ventilation, heart
rate, respiratory exchange ratio, and venous blood samples
(not secured from all subjects) were obtained during the last
2 minutes at each exercise level.
•
Figure 1 presents the researchers’ original plot of VO2max
•
in relation to terrestrial elevation. Clearly, VO2max decreased
from sea level upward and declined steeply above 6000 m,
to reach an average of 1.42 L ⭈ min⫺1 at 7440 m.
(continued)
S.L.
60
5
1
10
2
3
15
4
20
5
6
25 x 1,000 ft
7
8 km
50
O2 intake (ml . kg . min)
Focus on Research
• Exercise at Medium and High Altitude
40
30
20
10
0
S.L. 700
600
500
400
300
200
Atmospheric pressure (mm Hg)
Normal climbing
Everest data (max exercise)
Himalayan expd. 1960/61 (max exercise)
Figure 1. Oxygen consumption during submaximal (purple symbols;
men climbing at their typical pace) and maximal (yellow and orange
symbols) exercise in relation to ambient barometric pressure and
terrestrial elevation. S.L., sea level.
606
• Exercise Performance and Environmental Stress
SECTION 5
Focus on Research
High Altitude: A Hostile Environment
200
160
120
exercise ventilation. Heart rates remained elevated during
submaximal exercise at altitude.
Figure 3 shows a tendency for a higher respiratory exchange ratio (R) at all exercise levels at 5800 m than at sea
•
level. At VO2s above 2.0 L ⭈ min⫺1, R increased nearly vertically,
a response consistent with the extreme hyperventilation at
high altitude. Altitude exposure increased exercise blood lactate (not shown), which also contributed to exercise hyperventilation. Finally, comparisons of data for the Sherpa guide
with those of the other subjects showed his superior work capacity, attributable to economy of ventilation with preservation
of a normal blood pH and maintenance of a relatively higher arterial PO2. The guide also maintained a high pulmonary diffusing capacity for oxygen and a high cardiac output relative to
work intensity (measured in a separate experiment).
These pioneering studies demonstrated physiologic
links to exercise limitations at high altitude and formed the
foundation for expanding knowledge of human physical
working capacity at extreme terrestrial elevations.
80
40
1.30
200
160
1.20
120
Respiratory exchange ratio
Ventilation (L/min S.T.P.D.)
Ventilation (L/min B.T.P.S.)
Heart rate (beats/min)
Figure 2 shows pulmonary ventilation (STPD and BTPS)
•
and heart rate in response to VO2 during exercise at different
altitudes. The curves for pulmonary ventilation shift to the
left and increase in slope during exercise at higher elevations, with submaximal effort requiring the greatest ventilation at the highest altitude. This altitude-related hyperventilation reflects the experience of mountain climbers at great
altitude; any slight increase in mountain slope or snow conditions brings them to a halt with breathlessness. Only the
highest altitude produced apparent impairment of maximum
80
40
0
160
120
80
1.10
1.00
0.90
0.80
40
0
S.L.
0
1.0
2.0
3.0
4.0
0.70
0
Oxygen intake (L/min)
4600 m
5800 m 6400 m
1.0
2.0
3.0
4.0
Oxygen intake (L/min)
7400 m
Figure 2. Pulmonary minute ventilation (BTPS, STPD) and heart rate
in relation to oxygen consumption at sea level and altitudes up to
7400 m (24,440 ft). S.L., sea level.
Sea level
5800 m
Figure 3. Respiratory exchange ratio during graded exercise at sea
level and 5800 m (19,000 ft).
CHAPTER 24
• Exercise at Medium and High Altitude
607
ACCLIMATIZATION
Hyperventilation
During the many years that mountaineers attempted to climb
the world’s highest peaks, they knew that it required weeks to
adjust to successively higher elevations. The term altitude acclimatization broadly describes adaptive responses in physiology and metabolism that improve tolerance to altitude hypoxia. Each adjustment to a higher elevation proceeds
progressively, and full acclimatization requires time. Successful adjustment to medium altitude affords only partial adjustment to a higher elevation. Residents of moderate altitudes,
however, do show less decrement in physiologic capacity and
exercise performance than lowlanders when both groups
travel to a higher altitude.63
Table 24.1 indicates that compensatory responses to altitude occur almost immediately, while other adaptations take
weeks or even months. The rapidity of the body’s response remains largely altitude dependent, although considerable individual variability exists for both the rate and success of acclimatization.71,75 A person can retain many of the beneficial
submaximal exercise responses associated with 16 days of acclimatization at 4300 m despite intermittent sojourns to sea
level for up to 8 days.8 This suggests that certain aspects of
acclimatization regress more slowly than they are acquired.
Hyperventilation from reduced arterial PO2 is the most important and clear-cut immediate response of the native lowlander
to altitude exposure.21,44,91 Once initiated, this “hypoxic drive”
increases during the first few weeks and can remain elevated
for a year or longer during prolonged altitude residence.52
The aortic arch and branching of the carotid arteries in the
neck contain peripheral chemoreceptors sensitive to reduced
oxygen pressure. A significant reduction in arterial PO2, which
occurs at altitudes above 2000 m, progressively stimulates these
receptors. This modifies inspiratory activity to increase alveolar
ventilation and cause alveolar PO2 to rise toward the level in ambient air. Increases in alveolar PO2 with hyperventilation facilitate oxygen loading in the lungs and provide the rapid first line
of defense against reduced ambient PO2 at altitude. For females,
variations in menstrual cycle phase do not affect ventilatory responses and exercise performance decrements during acute altitude exposure compared with those at sea level.9 Mountaineers
who respond with a strong, hypoxic ventilatory drive to sudden
altitude exposure perform exercise tasks at extreme altitudes
more effectively (and reach higher altitude) than climbers with
a blunted hypoxic ventilatory response.91
INTEGRATIVE QUESTION
Immediate Responses to Altitude
Arrival at elevations of 2300 m and higher initiates rapid
physiologic adjustments to compensate for the thinner air and
accompanying reduction in alveolar PO2. The two more important responses include:
• Increase in the respiratory drive to produce hyperventilation
• Increase in blood flow during rest and submaximal
exercise
From a physiologic perspective, what represents a
safe altitude for flight in an airplane with a nonpressurized cabin?
Increased Cardiovascular Response
Resting systemic blood pressure increases in the early stages
of altitude adaptation.44 In addition, submaximal exercise
heart rate and cardiac output rise as much as 50% above sea
level values, while the heart’s stroke volume remains un-
➤ IMMEDIATE AND LONGER-TERM ADJUSTMENTS TO ALTITUDE HYPOXIA
IMMEDIATE
LONGER-TERM
Pulmonary acid–base
Hyperventilation
Hyperventilation
Bodily fluids become more alkaline due to reExcretion of base (HCO3⫺) via the kidneys and concomitant
reduction in alkaline reserve
duction in CO2 (H2CO3) with hyperventilation
Cardiovascular
Increase in submaximal heart rate
Submaximal heart rate remains elevated
Increase in submaximal cardiac output
Submaximal cardiac output falls to or below sea-level values
Stroke volume remains the same or decreases
Stroke volume decreases
slightly
Maximum cardiac output remains the same or
Maximum cardiac output decreases
decreases slightly
Hematologic
Decreased plasma volume
Increased hematocrit
Increased hemoglobin concentration
Increased total number of red blood cells
Local
Possible increased capillarization of skeletal muscle
Increased red-blood-cell 2,3-DPG
Increased mitochondrial density
Increased aerobic enzymes in muscle
Loss of body weight and lean body mass
TABLE 24.1
SYSTEM
SECTION 5
• Exercise Performance and Environmental Stress
Oxygen consumption (L . min-1)
5.0
4.0
VO2max
3.0
2.0 L . min-1
2.0
50%
VO2max
1.0
0
Sea level
70%
VO2max
High altitude
4300 m
Steady-rate VO2 at 100-W power output
FIGURE 24.3 • Comparison of oxygen cost and relative strenuousness of submaximal exercise at sea level and high altitude.
changed.49 The increased submaximal exercise blood flow at
altitude largely compensates for arterial desaturation. For example, a 10% increase in cardiac output during rest or moderate exercise offsets a 10% reduction in arterial oxygen saturation, at least in terms of total oxygen transported through
the body. Figure 24.3 shows that while the oxygen cost of
submaximal exercise at 100 watts on a bicycle ergometer
at sea level and high altitude remains unchanged at about
2.0 L ⭈ min⫺1, the relative strenuousness of the effort increases dramatically at altitude. In this example, submaximal
•
exercise representing 50% of sea-level VO2max equals 70% of
•
VO2max at 4300 m.
Catecholamine Response
Norepinephrine activity progressively increases over time during rest and exercise with altitude exposure.67,68 Increased
blood pressure and heart rate at altitude coincide with the
steady rise in plasma levels and excretion rates of norepinephrine. Norepinephrine levels peak in women and men after
6 days of high-altitude exposure and then remain stable.65,66,107
In addition to affecting heart rate and blood pressure, increased
sympathoadrenal activity contributes to regulation of stroke
volume, vascular resistance, and substrate use during shortand long-term hypobaric exposures. Figure 24.4 shows the 24hour urinary excretion of norepinephrine and epinephrine during control (sea level) measurements and following exposure
to 4300-m altitude for 7 days. Epinephrine showed little
change, but norepinephrine excretion increased significantly
by the fourth day. Urinary norepinephrine levels remain elevated for approximately 1 week following return to sea level.96
Table 24.2 shows metabolic and cardiorespiratory responses to moderate and maximal cycling exercise in young
men at sea level and during brief exposure to simulated altitude of 4000 m.94 Despite the increase in pulmonary ventilation during submaximal exercise at “altitude,” arterial
oxygen saturation decreased from 96% at sea level to 70%
during all exercise intensities. In submaximal exercise, increased cardiac output entirely compensated for the blood’s
reduced oxygen content. Augmented blood flow resulted
from the higher heart rate because the heart’s stroke volume
remained unchanged during short-term altitude exposure.
With an increase in cardiac output, submaximal exercise
oxygen consumption remained essentially identical at sea
level and altitude. The greatest altitude effect on aerobic me•
tabolism emerged during maximal exercise when VO2max decreased to 72% of the sea level value.
With maximal exercise during short-term altitude exposure (ⱕ7d), ventilatory and circulatory adjustments fail to compensate for the depressed arterial oxygen content. Figure 24.5
illustrates the relationship between pulmonary ventilation and
oxygen consumption up to maximum during bicycle ergometer exercise at sea level and simulated altitudes from 1000 to
4000 m. Each 1000-m increase in altitude caused a proportionate increase in exercise ventilation volume. However,
when exercise oxygen consumption exceeded 2.0 L ⭈ min⫺1,
pulmonary ventilation increased disproportionately at progressively higher elevations.
µg per 24 h
608
120
110
100
90
80
70
60
50
40
30
20
10
0
1
2
3
1
2
3
Pre-altitude
(50 m)
4
5
6
7
Altitude
(4300 m)
Days
Norepinephrine
Epinephrine
FIGURE 24.4 • Effects of a 7-day stay at 4300-m (14,108-ft) on urinary norepinephrine and epinephrine in eight male sea-level residents.
(Modified from Surks MJ, et al. Changes in plasma thyroxine concentration and metabolism, catecholamine excretion and basal oxygen
uptake during acute exposure to high altitude (14,100 ft). J Clin Invest
1966;45:1442.)
CHAPTER 24
TABLE 24.2
• Exercise at Medium and High Altitude
609
➤ CARDIORESPIRATORY AND METABOLIC RESPONSE DURING SUBMAXIMAL AND MAXIMAL
EXERCISE AT SEA LEVEL AND SIMULATED ALTITUDE OF 4000 M (13,115 FT)
•
Altitude, m
600 kg-m ⭈ min⫺1
900 kg-m ⭈ min⫺1
Maximum
600 kg-m ⭈ min⫺1
900 kg-m ⭈ min⫺1
Maximum
VE (L ⭈ MIN⫺1 BTPS)
ARTERIAL SATURATION (%)
0
4000
0
4000
0
4000
1.50
2.17
3.46
1.56
2.23
2.50
39.6
59.0
123.5
53.7
93.7
118.0
96
95
94
71
69
70
•
Q (L ⭈ MIN⫺1)
EXERCISE LEVEL
Altitude, m
•
VO2 (L ⭈ MIN⫺1)
EXERCISE LEVEL
H R (B ⭈ MIN⫺1)
A-V
苶 O2 DIFF
(ML O2 ⭈ dL⫺1)
S V (ML)
0
4000
0
4000
0
4000
0
4000
13.0
19.2
23.7
16.7
21.6
23.2
115
154
186
148
176
184
122
125
127
113
123
126
10.8
11.4
14.6
9.4
10.4
10.8
From Sternberg J, et al. Hemodynamic response to work at simulated altitude 4000 m. J Appl Physiol 1966;21:1589.
•
Q⫽ cardiac output
Fluid Loss
Because ambient air in mountainous regions remains cool and
dry, considerable body water evaporates as inspired air becomes warmed and moistened in the respiratory passages. This
fluid loss often leads to moderate dehydration and accompany-
ing symptoms of dryness of the lips, mouth, and throat. Fluid
loss becomes pronounced for physically active people because
of large daily total sweat loss and exercise pulmonary ventilation volumes (and hence water loss). Physically active individuals should have access to water at all times.
Exercise intensity (W)
35
100
165
230
295
Pulmonary minute ventilation (L . min-1)
180
160
140
120
100
80
60
40
20
2.0
3.0
4.0
5.0
Oxygen consumption (L . min-1)
Tracheal Po2 (mm Hg)
Sea level (149)
1000 m (131)
2000 m (115)
3000 m
(100)
4000 m (87)
FIGURE 24.5 • Effects of a progressive increase in simulated altitude
from sea level (tracheal PO2 ⫽ 149
mm Hg) to 4000 m (tracheal PO2 ⫽
87 mm Hg) on the relationship between pulmonary ventilation and oxygen consumption during cycle ergometry. (Modified from Åstrand PO.
The respiratory activity in man exposed to prolonged hypoxia. Acta
Physiol Scand 1954;30:343.)
610
SECTION 5
• Exercise Performance and Environmental Stress
IN A PRACTICAL SENSE
➤➤ IDENTIFICATION AND TREATMENT OF
ALTITUDE-RELATED MEDICAL PROBLEMS
Natives who live and work at high altitudes as well as newcomers risk a variety of medical problems associated with
reduced arterial PO2. These problems usually remain mild
and dissipate within several days, depending on the rapidity
of the ascent and degree of exposure. Other medical complications significantly compromise overall health and
safety. Three medical conditions threaten those who ascend
to high altitude:
tional 600 to 900 m climbed. Abrupt increases of more
than 600 m in the altitude for sleeping should be avoided
at 2500 m or higher (“climb high–sleep low”). If acclimatization proves ineffective, a 300-m descent usually alleviates symptoms; supplemental oxygen and the drug acetazolamide (Diamox) facilitate recovery.
1. Acute mountain sickness (AMS), the most common malady
2. High-altitude pulmonary edema (HAPE), which reverses if the person returns quickly to a lower altitude
3. High-altitude cerebral edema (HACE), a potentially fatal condition if not diagnosed and treated
immediately
For unknown reasons, about 2% of sojourners to altitudes
above 3000 m experience HAPE. Symptoms (Table 1) usually manifest within 12 to 96 hours following rapid ascent.
Major predisposing factors for HAPE include level of altitude, rate of ascent, and individual susceptibility.6 Fluid accumulates in the brain and lungs in this life-threatening condition.3,79 At first, symptoms do not seem severe, but the
syndrome progresses to pulmonary edema and fluid retention by the kidneys. Chest examination reveals wheezy,
raspy sounds known as rales. Even in well-acclimatized individuals, HAPE can develop with severe exertion at elevations above 5486 m (18,000 ft), probably the result of increased pulmonary artery pressure with damage to the
blood-gas barrier.105
Table 2 lists appropriate methods to avoid and treat
HAPE. Treatment to prevent severe disability or even death
requires immediate descent to lower altitude on a stretcher
(or flown to safety), because physical activity from walking
potentiates complications. With proper treatment, symptoms decrease within hours, with complete clinical recovery
within days. HAPE poses no problem for healthy individuals
who journey to and recreate without acclimatization at altitudes below 1676 m.
Acute Mountain Sickness
Most people experience the discomfort of AMS during the
first few days at altitudes of 2500 m and above. This relatively benign condition, which becomes exacerbated by exercise in the first few hours of exposure,80 possibly results
from acute reduction in cerebral oxygen saturation.85 It occurs most frequently in those who ascend rapidly to a high
altitude without benefiting from gradual and progressive
acclimatization to lower altitudes. Symptoms (Table 1) usually begin within 4 to 12 hours and dissipate within the first
week.35,39,54 Headache, the most frequent symptom, probably results from increased cerebral hemodynamics from
short-term hyperventilation.45 Most symptoms become
prevalent above 3000 m. Rapid ascent to 4200 m almost
guarantees some form of AMS.61
Decreased thirst sensation and severe appetite suppression can occur during the early stages, often resulting in
a 40% reduction in energy intake and consequent body
mass loss. Diets low in salt and high in carbohydrates are
well tolerated during the early stay at high altitude. A potential benefit of maintaining carbohydrate reserves through dietary intake lies in the liberation of more energy per unit oxygen with carbohydrate oxidation than with fat (5.0 kcal vs.
4.7 kcal per L of O2). Also, high blood lipid levels following a
high-fat meal may reduce arterial oxygen saturation. Benefits of maintaining a high-carbohydrate diet include:
1. Enhanced altitude tolerance
2. Reduced severity of mountain sickness
3. Lessened physical performance decrements during the early stages of altitude exposure
Even moderate exercise becomes intolerable for persons suffering the effects of AMS. Symptoms subside and
often disappear as acclimatization progresses. Acclimatizing slowly to moderate altitudes below 3048 m followed
by a gradual progression to higher elevations (termed
staged ascent) usually prevents AMS. Climbers should
spend several nights at 2500 to 3000 m before going
higher, and an extra night should be added for each addi-
High-Altitude Pulmonary Edema
TABLE 1. IMPORTANT ALTITUDE-RELATED MEDICAL CONDITIONS
CONDITION
Acute mountain
sickness (AMS)
High-altitude
pulmonary
edema (HAPE)
High-altitude
cerebral edema
(HACE)
SYMPTOMS
Severe headache, fatigue, irritability, nausea,
vomiting, loss of appetite, indigestion, flatulence, generalized weakness, constipation, decreased urine output with normal
hydration, sleep disturbance
Debilitating headache and severe fatigue; excessively rapid breathing and heart rate;
rales;a cough producing pink frothy sputum; bluish skin color (from low blood
PO2); disruption of vision, bladder, and
bowel functions; poor reflexes; loss of coordination of trunk muscles; paralysis on
one side of the body
Staggered gait, dyspnea upon exertion, severe weakness/fatigue, persistent cough
with pulmonary infection, pain or pressure
in substernal area, confusion, impaired
mental processing, drowsiness, ashen skin
color, loss of consciousness
a
Excess mucus in the lungs diagnosed as clicking sounds heard through a
stethoscope.
CHAPTER 24
• Exercise at Medium and High Altitude
611
IN A PRACTICAL SENSE
➤➤ IDENTIFICATION AND TREATMENT OF
ALTITUDE-RELATED MEDICAL PROBLEMS—cont’d
TABLE 2. PREVENTION AND TREATMENT OF HIGH-ALTITUDE
PULMONARY EDEMA
Prevention
1. Slow ascent for susceptible individuals (average increase in
sleeping altitude of 300–350 m ⭈ d⫺1 above 2500 m)
2. No ascent to higher altitude with symptoms of AMS
3. Descent when AMS symptoms do not improve after a day
of rest
4. Under circumstances of high risk: avoid vigorous exercise
when not acclimatized
5. Nifedipine: 20 mg slow-release formulation every 6 hours (or
30–60 mg sustained-release formulation once daily) for susceptible individuals when slow ascent is impossible
Treatment
1. Descent by at least 1000 m (primary choice in mountaineering)
2. Supplemental oxygen: 2–4 L ⭈ min⫺1 (primary choice in areas
with medical facilities)
3. When 1 and/or 2 not possible:
• Administer 20 mg nifedipine slow-release formulation
every 6 hours
• Use portable hyperbaric chamber (see Fig. 26.10)
• Descend to low altitude as soon as possible
High-Altitude Cerebral Edema
HACE is a potentially fatal neurologic syndrome that develops within hours or days in individuals with AMS. HACE
occurs in about 1% of people exposed to altitudes above
2700 m; it involves increased intracranial pressure that
causes coma and death if left untreated. The early symptoms (Table 1), similar to those of AMS and HAPE, progres-
SENSORY FUNCTIONS. Figure 24.6 shows deterioration in a
variety of sensory and mental functions with the decrease in
arterial oxygen saturation at altitude. Neurologic alterations
range from a 5% decrease in sensitivity to light at 1524 m
to a further 25% decrease in light sensitivity and 30% decrease in visual acuity when elevation doubles to 3048 m,
and a 25% deterioration in coding task performance and
simple reaction time at 6096 m.
MYOCARDIAL FUNCTION. Individuals with normal electrocardiograms at sea level including patients with stable chronic
heart failure generally show no adverse changes to indicate
myocardial ischemia (e.g., arrythmias, angina, ECG abnormalities) at simulated high altitudes, even during maximal exercise.2,82,95 Even on Mt. Everest, contractile function of the
heart remains stable despite the considerable chronic hypoxia.77 Because little information exists about the effects of
altitude on individuals with coronary artery disease and with
sively worsen as the altitude stay progresses. Cerebral
edema probably results from cerebral vasodilation and elevations in capillary hydrostatic pressure that cause movement of fluid and protein from the vascular compartment
across the blood–brain barrier.36 An enlarged cerebral fluid
volume eventually distorts brain structures, particularly the
white matter, which exacerbates symptoms and increases
sympathetic nervous system activity. Tissue hypoxia caused
by high-altitude exposure may also initiate a series of local
events that stimulate angiogenesis (new capillary vessel
growth) in brain tissue.108 Because of the difficulty in adequately diagnosing HACE at high altitude, immediate descent to a lower elevation is mandatory.
OTHER CONDITIONS
Chronic mountain sickness (CMS), prevalent in a small
number of altitude natives, can develop after months and
years at altitude. CMS relates to excessive polycythemia,
perhaps the result of a genetically linked variation in the
EPO response to hypoxic stress.72 CMS symptoms include
lethargy, weakness, sleep disturbance, bluish skin coloring
(cyanosis), and change in mental status. High-altitude retinal hemorrhage (HARH) affects virtually all climbers at altitudes above 6700 m (21,982 ft). HARH usually progresses
unnoticed with no specific treatment or means for prevention. Hemorrhage in the macula of the eye—the oval “yellow spot” region in the back of the eyeball close to the optic disc—can produce 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.97
congestive heart failure, these patients should avoid highaltitude exposure altogether.61
Longer-Term Adjustments to Altitude
Hyperventilation and increased submaximal exercise cardiac
output provide a rapid and relatively effective counter to the
acute challenge of altitude exposure. Concurrently, other
slower-acting adjustments occur during a prolonged altitude
stay. The most important longer-term adjustments involve:
• Regulation of acid–base balance of body fluids altered by hyperventilation
• Synthesis of hemoglobin and red blood cells and accompanying changes in local circulation and aerobic
cellular function
• Elevated sympathetic neurohumoral activity as reflected by a significant increase in norepinephrine
that peaks within 1 week at altitude.
612
SECTION 5
• Exercise Performance and Environmental Stress
Pio2 (torr)
FIGURE 24.6 • Arterial saturation as
a function of increasing altitude and
the corresponding impairment ( ▼ ) in
diverse sensory and mental functions. (Modified from Fulco CS,
Cymerman A. Human performance
and acute hypoxia. In: Pandolf KB, et
al., eds. Human performance physiology and environmental medicine at
terrestrial extremes. Carmel, IN:
Cooper Publishing Group, 1988.)
Arterial oxygen saturation (%)
100
126
100
80
63
49
25% light
sensitivity
90
25%
attention
5% light
sensitivity
30%
visual
acuity
80
15%
cognition
33%
postural
stability
70
20%
recall
25%
pursuit
tracking
25% reaction
time
25%
coding
60
0
1524
3048
4572
6096
7620
Altitude (m)
Each of these acclimatization components improves tolerance to the relative hypoxia of medium and high altitudes.
Acid–Base Readjustment
The beneficial effect of hyperventilation at altitude to increase
alveolar PO2 produces the opposite effect on the body’s carbon
dioxide level. Because ambient air contains essentially no carbon dioxide, the increased breathing volumes at altitude dilute
normal alveolar carbon dioxide concentrations. This creates a
larger-than-normal gradient for diffusion (“wash out”) of carbon dioxide from the blood to the lungs, causing arterial PCO2
to decrease considerably. With exposure to 3048 m, for example, alveolar PCO2 drops to about 24 mm Hg, in contrast to its
usual 40 mm Hg value at sea level. Alveolar PCO2 drops as low
as 10 mm Hg during a prolonged stay at high altitude.
Carbon dioxide loss from the bodily fluids in a hypoxic
environment creates a physiologic disequilibrium. We pointed
out in Chapter 13 that carbonic acid (H2CO3) normally carries
the largest quantity of carbon dioxide in the body. This relatively weak acid readily dissociates into H⫹ and HCO3⫺,
which move to the lungs in the venous circulation. H⫹ and
HCO3⫺ recombine in the pulmonary capillaries to form
H2CO3, which in turn forms carbon dioxide and water; carbon
dioxide diffuses from the blood into the alveoli and leaves the
body. A decrease in carbon dioxide level with hyperventilation increases the pH from loss of carbonic acid, and bodily
fluids become more alkaline.
Because hyperventilation represents a sustained and beneficial response to altitude exposure, adjustments proceed during
acclimatization to minimize the accompanying negative disruption in acid–base balance. Control of ventilatory-induced alkalosis advances slowly as the kidneys excrete base (HCO3⫺)
through the renal tubules. In turn, restoration of normal pH increases the respiratory center’s responsiveness, thus enabling
even greater hyperventilation in response to altitude hypoxia.
REDUCED BUFFERING CAPACITY AND THE “LACTATE PARADOX.” Establishing acid–base equilibrium with acclimatization occurs
at the expense of a loss of absolute alkaline reserve. Thus, although the pathways of anaerobic metabolism remain unaffected at altitude, the blood’s capacity for buffering acid gradually decreases, and the critical level lowers for acid
metabolite accumulation. A general depression in maximum
lactate concentrations becomes apparent in maximal exercise
above 4000 m.76
On immediate ascent to high altitude, a given submaximal exercise load increases blood lactate concentration compared with sea level values. Presumably, increased lactate accumulation results from greater reliance on anaerobic
glycolysis with altitude hypoxia. Surprisingly, the same submaximal and maximal exercise with large muscle groups after
several weeks of hypoxic exposure produces lower lactate lev•
els, despite a lack of increase in either VO2max or regional blood
flow in active tissues. The question arises concerning this apparent physiologic contradiction, termed the lactate paradox,
“How is lactate accumulation reduced without a concomitant
increase in tissue oxygenation, when the hypoxemia associated with high altitude should promote lactate accumulation?”
Research to resolve the lactate paradox points to reduced
output of the glucose-mobilizing hormone epinephrine during
chronic high-altitude exposure.10 Because glucose and glycogen are the only macronutrient sources for anaerobic energy
(and lactate formation), reduced glucose mobilization blunts
the capacity for lactate formation. Reductions in intracellular
ADP during long-term altitude exposure may also inhibit activation of the glycolytic pathway. In addition, depressed lactate formation during maximal exercise may partly reflect an
overall reduced central nervous system drive, which would
blunt capacity for all-out physical effort.48,64 Reduced blood
lactate accumulation at high altitude is apparently not related
to the decreased buffering capacity that accompanies highaltitude acclimatization.47
• Exercise at Medium and High Altitude
CHAPTER 24
PLASMA VOLUME DECREASE. During the first several days of al-
titude exposure, the body’s fluid balance changes in a direction
that shifts fluid from the intravascular space to the interstitial
and intracellular spaces. The decrease in plasma volume that
occurs within several hours of altitude exposure increases red
blood cell concentration.90 After a week at 2300 m, for example, the plasma volume decreases by about 8%, whereas the
concentration of red blood cells (hematocrit) increases 4% and
hemoglobin, 10%. A 1-week stay at 4300 m decreases plasma
volume 16 to 25% with concomitant increases in hematocrit
(6%) and hemoglobin (20%).37 The rapid reduction in plasma
volume (and accompanying hemoconcentration) increases the
oxygen content of arterial blood significantly above values observed on arrival at altitude. Diuresis (increased urine output)
accompanies the shift in fluid from the plasma during acclimatization, which maintains balance in the fluid compartments at a lower total body water content.
RED BLOOD CELL MASS INCREASE. Reduced arterial PO2 at altitude
stimulates an increase in the total number of red blood cells, a
condition termed polycythemia. The erythrocyte-stimulating
hormone erythropoietin (EPO), synthesized and released
primarily from the kidneys in response to localized arterial
hypoxia, initiates red blood cell formation within 15 hours after altitude ascent. In the weeks that follow, erythrocyte production in the marrow of the long bones increases considerably and remains elevated throughout the altitude stay.34 The
blood of a typical miner in the Andes contains 38% more erythrocytes than the blood of a lowlander. In some apparently
healthy high-altitude natives, red cell count may reach levels
50% above normal—8 million cells per mm3 compared with
5.3 million for the native lowlander!62 Climbers acclimatized
at 6500 m during a 1973 Mt. Everest expedition showed a
40% increase in hemoglobin concentration and a 66% increase in hematocrit.16 This probably approaches the upper
limit for a beneficial hematologic response. Any further erythrocyte packing increases blood viscosity and restricts blood
flow and oxygen diffusion to the tissues.
Hb (g .100dL-1) Hct ratio (%)
An increase in the blood’s oxygen-carrying capacity is the
most important longer-term adjustment to altitude exposure.
Two factors account for this adaptation: (1) an initial decrease
in plasma volume, followed by (2) increased synthesis of erythrocytes and hemoglobin.
carrying capacity of blood in high-altitude residents of Peru averages 28% above sea-level values.43 In well-acclimatized
mountaineers, the blood carries 25 to 31 mL of oxygen per dL
of blood, compared with 20 mL for lowland residents.74 Thus,
despite reduced hemoglobin oxygen saturation at altitude, the
quantity of oxygen in arterial blood may approach or even
equal sea-level values.
Figure 24.7A illustrates the general trend for hemoglobin
and hematocrit increases during acclimatization. For eight
young women who lived and worked for 10 weeks at the
4267-m summit of Pikes Peak. Because the researchers’ previous work showed significantly fewer hematologic changes
during acclimatization in women than in men (possibly because of inadequate iron intake), each woman received iron
supplementation prior to, during, and on return from altitude.
52
50
48
46
44
42
17
16
15
14
13
12
Pre- 0
altitude
10
20
30
40
50
60
Days at Pikes Peak
A
50
48
Hct ratio (%)
Hematologic Changes
613
46
44
42
40
0
B
Pre-
altitude
0
10
20
30
60
70
Days at Pikes Peak
INTEGRATIVE QUESTION
For their assault on Mt. Everest, elite mountaineers
spend a total of 3 months at camps at 16,600 feet,
19,500 feet, 21,300 feet, 24,000 feet, and 26,000
feet before their final ascent. Explain the physiologic rationale for a “stage ascent” approach to
mountaineering.
Polycythemia translates directly to an increase in the
blood’s capacity to transport oxygen. For example, the oxygen-
Men
Women (+Fe)
Women
FIGURE 24.7 • A. Effects of altitude on hemoglobin (Hb; yellow line)
and hematocrit (Hct; red line) levels of 8 young women from the University of Missouri (213 m) prior to, during, and 2 weeks after exposure to 4267 m at Pikes Peak, Colorado. (From Hannon JP, et al. Effects of altitude acclimatization on blood composition of women. J
Appl Physiol 1968; 26: 540.) B. Hematocrit response of young women
receiving supplemental iron (⫹Fe) prior to and during altitude exposure compared to groups of male and female subjects receiving no
supplemental iron. (Courtesy of Dr. J. P. Hannon.)
614
SECTION 5
• Exercise Performance and Environmental Stress
Red blood cell concentration increased rapidly upon reaching
Pikes Peak. Hemoconcentration resulted from a reduction in
plasma volume within the first 24 hours at altitude. Hemoglobin concentration and hematocrit continued to rise in the
month that followed and then stabilized for the remainder of
the stay. Prealtitude values reestablished within 2 weeks after
the women returned to Missouri.
Figure 24.7B shows that iron supplementation increased
the prealtitude values for hematocrit and hemoglobin. One
might anticipate this finding, as young women frequently suffer from mild dietary iron insufficiency with depressed iron
reserves (see Chapter 2). Comparison of the acclimatization
curve for the iron-supplemented women with another group
of women not given additional iron showed a greater hematocrit increase in the supplemented group. Iron supplementation enhanced hematocrit increases at altitude to a level
equivalent to that of men at the same location. These findings
indicate that athletes with borderline iron stores may not respond to acclimatization as effectively as individuals who arrive at altitude with iron reserves adequate to sustain an increase in erythrocyte production.
Cellular Adaptations
A topic of considerable debate concerns whether extreme terrestrial hypoxia stimulates vascular and cellular adaptations
in humans that improve local oxygen extraction and maximize oxidative functions.30,40,69,99 Any improvement in the energy state of the muscle with acclimatization probably does
not result from a reorginazation of metabolic pathways.31 Animals born and raised at high altitude showed more concentrated capillarization of skeletal muscle (number per mm2)
than sea-level counterparts.100 Chronic hypoxia may also initiate remodeling of capillary diameter and length and the formation of new capillaries to significantly increase oxygen
conductance to neural tissues.
Human residents of sea level also show increased tissue
capillarization during an altitude stay.71 A more prolific microcirculation reduces the oxygen diffusion distance between
the blood and tissues to optimize tissue oxygenation at
altitude when arterial PO2 decreases. Furthermore, muscle
biopsy specimens from humans living at altitude indicate that
myoglobin increases up to 16% after acclimatization.78 Additional myoglobin augments oxygen “storage” in specific
fibers and facilitates intracellular oxygen release and delivery
at a low tissue PO2. Whether the small increase in mitochondrial number and concentration of aerobic energy transfer enzymes with prolonged exposure59 (or when training under
normobaric hypoxic versus normoxic conditions69) reflects
exercise training effects or the hypoxic environment remains
unclear.41,88
High-altitude natives benefit from the slight shift to the
right of the oxyhemoglobin dissociation curve at altitude.
This effect decreases hemoglobin’s affinity for oxygen to favor more oxygen release to tissues for a given drop in cellular PO2. Facilitated oxygen release from hemoglobin with
long-term altitude exposure occurs from an increased concen-
tration of red blood cell 2,3-diphosphoglycerate (2,3-DPG;
see Chapter 13).55 Increased 2,3-DPG coupled with more circulating hemoglobin (and red blood cells) favorably affects
the long-term resident’s capacity to supply oxygen to active
tissue during physical activity.
Changes in Body Mass and Body Composition
Prolonged high-altitude exposure significantly reduces lean
body mass (muscle fibers atrophy up to 20%) and body fat,
with the magnitude of weight loss directly related to terrestrial elevation. Six men participated in a 40-day progressive
decompression to an ambient pressure of 249 mm Hg in a hyperbaric chamber to simulate an ascent of Mt. Everest.84 Daily
caloric intake from a depressed appetite decreased by 43%
during the exposure period. Reduced energy intake reduced
body mass 7.4 kg, predominantly from the muscle component
of the fat-free body mass. In addition to depressed appetite
and food intake during high-altitude exposure, intestinal absorption efficiency decreases to compound the difficulty in
maintaining body weight.13,23,101 The basal metabolic rate also
increases significantly upon arrival at altitude, which further
affects the tendency to lose weight. To some extent, one can
override an accelerated metabolic rate and minimize weight
loss by consciously increasing energy intake while at altitude.
Time Required for Acclimatization
The time required to acclimatize to altitude depends on terrestrial elevation. Acclimation to one altitude ensures only
partial adjustment to a higher elevation. As a broad guideline,
it takes about 2 weeks to adapt to altitudes up to 2300 m.
Thereafter, each 610-m altitude increase requires an additional week to fully acclimatize, up to 4600 m. Athletes desiring to compete at altitude should begin intense training as
soon as possible during acclimatization. Rapid initiation of
training minimizes detraining effects brought about by the
normal tendency to reduce physical activity in the first few
days at altitude.53 Acclimatization adaptations dissipate
within 2 or 3 weeks after returning to sea level.
METABOLIC, PHYSIOLOGIC, AND EXERCISE
CAPACITIES AT ALTITUDE
The stress of high altitude significantly restricts work capacity
and physiologic function. Even at lower altitudes, the physiologic and metabolic adjustments do not fully compensate for
the reduced ambient oxygen pressure, and exercise performance deteriorates. Certain circulatory parameters, particularly
stroke volume and maximum heart rate, acclimatize in a direc•
tion that reduces oxygen transport capacity and VO2max.26,29,87
Maximal Oxygen Consumption
Figure 24.8A depicts the relationship between the decrease in
•
VO2max (% of sea-level value) and increasing altitude or simulated exposures (i.e., hypobaric chambers or normobaric hy-
CHAPTER 24
• Exercise at Medium and High Altitude
615
5
Percent decline in VO2max from sea level
0
-5
-10
-15
-20
-25
-30
-35
-40
-45
-50
-55
-60
-65
-70
-75
-80
A
0
1000
2000
3000
4000
5000
7000
8000
9000
Altitude (m)
130
Percent of sea level race times
6000
125
120
115
110
105
100
95
0
1000
B
2000
3000
4000
5000
Altitude (m)
Race duration:
<2 min
2 to 5 min
20 to 30 min
poxic gas breathing) as reported in diverse civilian and military
studies.27 Variation in points about the orange line depicting the
relationship most likely result from disparities in experimental
design and procedures and physiologic differences among sub•
jects. The figure indicates that small declines in VO2max become
2 to 3 h
FIGURE 24.8 • A. Reduction in
•
VO2max as a percentage of the sealevel value in relation to altitude exposure, derived from 146 average
data points from 67 different civilian
and military investigations conducted
at altitudes from 580 m (1902 ft) to
8848 m (29,021 ft). “Altitudes” represent data from actual terrestrial elevations or simulated elevations with
hypoxic chambers or hypoxic gas
breathing. The orange curvilinear line
is a database regression line drawn
using the 146 points. B. Generalized
trend in performance decrements in
relation to altitude exposure for runners and swimmers, primarily during
competition. (Modified from Fulco
CS, et al. Maximal and submaximal
exercise performance at altitude.
Aviat Space Environ Med 1998;69:
793.)
noticeable beginning at an altitude of 589 m. Thereafter, arter•
ial desaturation causes the VO2max of men and women to decrease at a rate of 7 to 9% per 1000-m altitude increase up to
6300 m, where aerobic capacity declines at a more rapid, nonlinear rate.19,75,86 For example, aerobic capacity at 4000 m av-
616
SECTION 5
• Exercise Performance and Environmental Stress
•
erages 75% of the sea-level value. At 7000 m, VO2max averages
•
one-half the sea-level value; the VO2max of a relatively fit man
atop Mt. Everest is about 1000 mL ⭈ min⫺1, which corresponds
to an exercise power output of only 50 watts on a bicycle
ergometer.73
Physical conditioning prior to altitude exposure offers
little protection because the endurance athlete experiences a
•
slightly greater percentage reduction in VO2max than does an
untrained person. In addition, large variability exists among
•
individuals in the decrement in VO2max with altitude exposure.
Men experience the largest decrease, particularly those with a
large lean body mass, a large sea-level aerobic capacity, and a
low sea-level lactate threshold.81 To some extent, arterial de•
saturation and decrease in VO2max are more pronounced in individuals with a blunted hyperventilation response to exercise
in a hypoxic environment.28 Despite any unique effects of altitude exposure on aerobically fit individuals, a standard exercise task at altitude still provides relatively less stress for
well-conditioned women and men because they perform it at
•
a lower percentage of VO2max.
Circulatory Factors
Even after several months of acclimatization to hypoxia,
•
VO2max remains significantly below sea-level values, despite
relatively rapid and pronounced increases in hemoglobin concentration. This occurs because reduced circulatory capacity—
combined effect of lowered maximum heart and stroke volume—offsets the hematologic benefits of acclimatization.29,50
Submaximal Exercise
The immediate altitude response to exercise increases submaximal cardiac output (Table 24.2), but this response diminishes as acclimatization progresses and does not improve with
prolonged exposure.49 Reduced exercise cardiac output results mainly from a progressive decrease in the heart’s stroke
volume (associated with diminished plasma volume) as the
altitude stay progresses. Despite the reduced cardiac output,
submaximal oxygen consumption remains stable through an
expanded a-v
苶 O2 difference. To some extent, an increased
submaximal heart rate offsets the decrease in stroke volume
during submaximal exercise.
Maximal Exercise
Maximum cardiac output decreases after about a week
above 3048 m and remains lower throughout one’s stay.33,75
Reduced blood flow during maximal exercise results from
the combined effect of decreases in maximum heart rate and
stroke volume, both of which continue to decrease with the
length and magnitude of altitude exposure.49–52,86,89 This
blunted cardiac response does not result from myocardial
hypoxia, at least as reflected by electrocardiographic and
coronary blood flow measurements during vigorous exercise at high altitudes.38,87 Decreased plasma volume and increased total peripheral vascular resistance contribute to the
reduced maximum stroke volume. Enhanced parasympathetic tone induced by prolonged altitude exposure probably reduces the maximum heart rate.89
INTEGRATIVE QUESTION
If altitude acclimatization improves endurance exercise performance at altitude, why does it not improve similar performance immediately upon return
to sea level?
Performance Measures
Figure 24.8B illustrates the generalized trend in exercise performance decrements, primarily during competition for athletes at different altitude exposures. Altitude exerts no adverse
effect on events lasting less than 2 minutes. For longer-duration events, performance times are longer (poorer performance) at higher elevations than at sea level. The threshold for
decrements occurs at about 1600 m for events with a duration
of 2 to 5 minutes, while only a 600- to 700-m altitude induces
poorer performance in events lasting longer than 20 minutes.
For the 1- and 3-mile runs, medium altitude (2300 m) causes
a 2 to 13% performance decrement for fit subjects.25 This coincides with the 7.2% increase in 2-mile run times for highly
trained middle-distance runners at the same altitude.1 Even after 29 days of acclimatization, high-altitude exposure significantly increases 3-mile run time, compared with times for the
same run near sea level.76 The small improvement in endurance performance during acclimatization, despite lack of
•
concomitant increase in VO2max, relates to three factors: (1) increased minute pulmonary ventilation (ventilatory acclimatization), (2) increased arterial oxygen saturation and cellular
aerobic functions, and (3) blunting of the blood lactate response in exercise (see “lactate paradox,” page 612).
AEROBIC CAPACITY ON RETURN
TO SEA LEVEL
Sea-level exercise performance does not significantly improve
•
after living at altitude when VO2max serves as the improvement
46,56,70
criterion.
An 18-day stay at 3100 m produced no significant change in the altitude-induced 25% reduction in aerobic
•
capacity in young runners.33 Furthermore, VO2max was about
the same as the prealtitude measure on return to sea level.
•
Even in studies showing small improvements in either VO2max
or exercise performance at altitude and on return to sea level,
the change often relates to an increase in physical activity
(i.e., the effects of training and/or repeated testing) during altitude exposure.20,51
Possible Negative Effects
Several physiologic changes during prolonged altitude exposure negate adaptations that could improve exercise performance on return to sea level. For example, the residual effects
of a loss of muscle mass and a reduced maximum heart rate
• Exercise at Medium and High Altitude
CHAPTER 24
617
training at sea level.1 Six middle-distance runners trained at
•
sea level for 3 weeks at 75% of their sea-level VO2max. Another group of six runners trained an equivalent distance at
•
the same percentage VO2max measured at 2300 m. The groups
then exchanged training sites and continued to train for 3
weeks at the same relative intensity as the preceding group.
Initially, 2-mile run times were 7.2% slower at altitude, compared with those at sea level. Run times improved 2.0% for
both groups during altitude training, but postaltitude performance at sea level remained the same as the prealtitude sealevel runs. Figure 24.9 shows that short-term altitude expo•
sure decreased VO2max 17.4% for both groups; it improved
only slightly after 20 days of altitude training. When the runners returned to sea level after altitude training, aerobic capacity remained 2.8% below prealtitude sea-level values.
Clearly, for these well-conditioned middle-distance runners,
no synergistic effect emerged from combining aerobic training at medium altitude compared with equivalent sea-level
training.
•
Others have duplicated these observations for VO2max and
endurance performance at both moderate and higher altitudes.24,53 Highly trained male track athletes flew to Nunoa,
Peru (altitude 4000 m), where they continued to train and ac•
climatize for 40 to 57 days. VO2max decreased 29% below sealevel values after the initial 3 days at altitude; after 48 days it
still remained 26% lower. The 440-yard, 880-yard, and 1- and
2-mile runs during a “track meet” with the altitude natives
measured running performance after acclimatization. The
times after acclimatization remained considerably slower than
prealtitude, sea-level times, particularly for the longer runs.
•
Furthermore, when the athletes returned to sea level, VO2max
and running performance generally did not differ from prealtitude measures. On no occasion did a runner improve his
previous prealtitude run time. In fact, running times in the
longer events averaged 5% below prealtitude trials. In other
studies, training in a hypobaric chamber provided no additional benefit to sea-level performance compared with similar training (albeit at a higher absolute exercise level) at sea
and stroke volume would not enhance sea-level performance.
Any reduction in maximum cardiac output at altitude offsets
benefits from an increase in the blood’s oxygen-carrying capacity. Although a blunted circulatory capacity returns to normal after a few weeks at sea level, so also do potentially positive hematologic adaptations.37 Within a physiologic context,
the controversial use of blood doping (see Chapter 23) mimics the hematologic benefits of altitude exposure without the
potential negative effects on maximum cardiovascular dynamics and body composition.
ALTITUDE TRAINING AND SEA-LEVEL
PERFORMANCE
Most research does not support endurance training at altitude
to improve subsequent sea-level exercise performance. Altitude acclimatization improves capacity for exercise at altitude, particularly high altitude. However, the effect of altitude
training on aerobic capacity and endurance performance immediately on return to sea level remains unclear. As discussed
above, altitude adaptations in local circulation and cellular
metabolism, combined with compensatory increases in the
blood’s oxygen-carrying capacity, should theoretically improve subsequent sea-level performance. Also, positive pulmonary adaptations and responses during prolonged hypoxic
exposure do not regress immediately upon descent from altitude.92 Furthermore, if tissue hypoxia provides an important
training stimulus, altitude plus training should act synergistically, and the total effect should exceed similar training at sea
level. Unfortunately, much of the exercise training–altitude
exposure research contains experimental design flaws that
limit evaluation of this possibility. Poor control over subjects’
physical activity at altitude makes it difficult to discern
•
whether any improved VO2max or performance score on return
to sea level represents a training effect, an altitude effect, or
synergism between altitude and training.
Researchers used equivalent groups to compare the effectiveness of altitude training (2300 m) and equivalent
4.8
4.6
FIGURE 24.9 • Maximal oxygen con-
4.4
4.2
3.8
3.6
0
5
Pre-experiment
Group 1 (sea level-altitude)
10
15
20
change
4.0
change
VO2 max (L . min–1)
5.0
25
30
35
40
45
Experiment day
Group 2 (altitude-sea level)
sumption of two equivalent groups
during training for 3 weeks at altitude
and 3 weeks at sea level. Group 1
trained first at sea level and continued
training for 3 weeks at altitude. For
Group 2, the procedure reversed, and
they trained first at altitude and then
at sea level. Green arrows in figure indicate change in training site. (From
Adams WC, et al. Effects of equivalent sea-level and altitude training on
•
VO2max and running performance. J
Appl Physiol 1975;39:262.)
618
SECTION 5
• Exercise Performance and Environmental Stress
•
TABLE 24.3
➤ EFFECT OF ALTITUDE ON TRAINING
INTENSITY FOR SIX COLLEGIATE
ATHLETES
ALTITUDE (M)
Intensity of workout
•
(%VO2max at 200 m)
300
2300
3100
4000
78
60
56
39
From Kollias J, Buskirk ER. Exercise and altitude. In Science and medicine
of exercise and sports. 2nd ed. Johnson WR, ER Buskirk, eds. New York:
Harper & Row. 1974: .
level. As expected, the “altitude”-trained group eventually
showed significantly better exercise performance at simulated altitude than sea-level residents.98
INTEGRATIVE QUESTION
Give your opinion (and rationale) about what effects a 2-week exposure to an altitude of 3000 m
would have on maximal exercise performance of a
60-second duration.
Decrement in Absolute Training Level at Altitude
One must lower the absolute workload to perform aerobic exercise at the same relative intensity at altitude as at sea level.
Otherwise, anaerobic metabolism provides a larger portion of
the energy for exercise at altitude (see Fig. 24.3), and fatigue
develops.109 Exposure to 2300 m and higher makes it nearly
impossible to train at the same absolute exercise intensity as
at sea level. Table 24.3 shows the reduction in training intensity relative to sea-level standards for six college athletes. At
4000 m, for example, the runners could train only at the in•
tensity equivalent to 39% of the sea-level VO2max, compared
to an intensity of 78% when training at sea level. The absolute
exercise training level at altitude may become so reduced that
an athlete cannot maintain peak condition for sea-level competition. In this regard, elite athletes benefit from periodically
returning from altitude to sea level for intense training to offset any “detraining” during a prolonged altitude stay (see next
section). Intermittent returns to a lower altitude would not interfere with acclimatization and might even benefit altitude
performance.8,20 Regardless of the training model, athletes
who train at altitude should include high-intensity speed work
to maintain muscle power.
COMBINE ALTITUDE STAY
WITH LOW-ALTITUDE TRAINING
Research has focused on the optimal combination of highaltitude stay plus low-altitude training in competitive runners.
Athletes who lived at 2500 m but returned regularly to 1250
m to train at near–sea-level intensity (i.e., live high–train
low) showed greater average increases in VO2max and 5000-m
run performance than athletes who lived and trained only at
2500 m or those who lived and trained only at sea level.57 This
indicates that strategies that combine (1) altitude acclimatization and (2) maintenance of sea-level training intensity provide synergistic benefits to endurance performance at sea
level. Regular training exposure to a near–sea-level environment appears to prevent the impaired systolic function (i.e.,
reduced maximum stroke volume and cardiac output) typically observed during training at altitude. Debate exists concerning whether intermittent altitude exposure increases red
blood cell mass and hemoglobin concentration.4,58
Not all individuals benefit to the same degree from a
living-high, training-low strategy. Within the group showing
physiologic and performance increases with this protocol,
certain individuals classified as “responders,” while others
showed little positive adjustment.17 These “nonresponders”
displayed a significantly smaller increase in plasma concentration of the erythrocyte-producing hormone EPO after 30
hours at altitude than the responders. Such individuals would
experience a blunted increase in hematocrit during acclimatization to altitude exposure. These findings suggest that three
prerequisites exist for benefit from the combination of altitude
living and lower-altitude training:
1. The altitude stay must take place at an elevation
high enough to raise EPO concentrations to in•
crease total red blood cell volume and VO2max.
2. The athlete must respond to the altitude stress with
increased EPO output.
3. Training must take place at an elevation low
enough to maintain training intensity and exercise
oxygen consumption at near sea-level values.
INTEGRATIVE QUESTION
Respond to a person who suggests that periodic
breath holding while exercising at sea level should
bring about similar physiologic adaptations as
training at altitude.
At-Home Acclimatization
Inability to maintain sea-level training intensity represents a
significant negative aspect of a sojourn to altitude to improve
subsequent sea-level performance from hematologic changes
with acclimatization. Failure to maintain the muscular power
outputs of sea-level training at altitude may actually initiate a
detraining effect. Application of the live high–train low training model poses significant practical and financial hurdles.
For these reasons, some endurance athletes use the banned
(and dangerous) practices of blood doping and EPO injections
to increase hematocrit and hemoglobin concentration, without
the bother and potential negative effects of an altitude stay.
A more prudent approach makes use of the observation
that altitude’s beneficial effects on erythropoiesis and aerobic
capacity require relatively short-term exposures to hypoxia.
CHAPTER 24
• Exercise at Medium and High Altitude
619
For example, daily intermittent exposures of 3 to 5 hours for
9 days to simulated altitudes of 4000 to 5500 m in a hypobaric
chamber significantly increased endurance performance, red
blood cell count, and hemoglobin concentration in elite
mountain climbers.15,83 Intermittent hypoxic training under
normobaric conditions provides an added bonus with clinical
and cardioprotective implications because such exercise augments training’s effect on selected metabolic and cardiovascular risk factors.5
In the absence of a hypobaric chamber, three approaches
create an “altitude” environment where an athlete, mountaineer, or hot-air balloonist living at sea level spends a large
enough portion of the day to stimulate an altitude acclimatization response.
22
20
Oxygen (%)
• In the Gamow Hypobaric Chamber, a person rests
and sleeps for about 10 hours each day. The chamber’s total air pressure can decrease to simulate the
barometric pressure of a preselected altitude. Reductions in barometric pressure bring about proportionate reductions in the inspired air’s PO2 to simulate altitude exposure and induce physiologic
adaptations.
• To eliminate the necessity of constructing an enclosure
to withstand differentials between sea-level ambient
air pressure and the reduced pressure in the hypobaric
chamber, one can simulate altitude at sea level by increasing the nitrogen percentage of the air within an
enclosure. Increased nitrogen percentage correspondingly reduces the air’s oxygen percentage, thus decreasing the PO2 of inspired air. Nordic skiers have applied this technique by living for 3 to 4 weeks in a
specially constructed house that provides “air” with
only 15.3% oxygen, compared with its normal concentration of 20.9%. The system requires mixing nitrogen
gas and carefully monitoring the breathing mixture.
• The Wallace Altitude Tent (Fig. 24.10), a suitcasesized unit developed by British Olympic cyclist
Shaun Wallace, continuously supplies air with an
oxygen content of approximately 15% to simulate an
altitude of 2500 m. The 70-pound unit consists of a
portable tent that fits over a normal bed; a “hypoxic
generator” (housed in an airline suitcase) continually
feeds altitude-simulating hypoxic air into the tent.
The porosity of the tent’s material limits the rate of
diffusion of outside oxygen into the tent and maintains the 15% oxygen concentration. Equilibration of
the tent’s environment at the 15% oxygen level requires about 90 minutes. The manufacturer proclaims: “Easily set up at home, or in a hotel whilst
on-the-road, the system provides the beneficial physiological adaptations associated with living at 9000′
altitude, without any compromise in training quality—the ultimate in high–low training.” Future research must verify the effectiveness of this unique
approach to endurance training.
18
16
14
12
0
60
120
180
240
Time (min)
FIGURE 24.10 • The Wallace Altitude Tent fits over a double or
queen-size bed or can be constructed for in-home use as a semipermanent cubicle. Patches of “breathable” nylon permit diffusion of
ambient oxygen (at higher PO2) into the tent (at lower PO2) to maintain
the percentage of oxygen within the tent at about 15%. A hypoxic
generator (left of tent) continuously supplies air with oxygen content
that equilibrates within the tent at near 15%. The inset shows the
time course for equilibration of air within the tent to reach the 15%
oxygen level. (Photo courtesy of Hypoxico Inc, Shaun Wallace,
Cardiff, CA.)
Summary
1. The progressive reduction in ambient PO2 as one ascends in altitude eventually causes inadequate hemoglobin oxygenation in arterial blood. Arterial desaturation produces noticeable performance
decrements in aerobic physical activities at altitudes of 2000 m and higher. Altitude does not adversely affect short-term (anaerobic) sprint and
power performances that depend on energy from
intramuscular high-energy phosphates and glycolytic reactions.
2. Reduced PO2 and accompanying hypoxia at altitude
stimulate physiologic responses and adjustments
that improve altitude tolerance during rest and exercise. Hyperventilation and increased submaximal
cardiac output via elevated heart rate are the primary immediate responses to altitude exposure.
3. Medical problems ranging from mild to lifethreatening often emerge during altitude exposure.
AMS, HAPE, and HACE are the most prominent
maladies. The potentially lethal conditions of
620
SECTION 5
4.
5.
6.
7.
8.
9.
10.
11.
• Exercise Performance and Environmental Stress
HAPE and HACE require the patient’s immediate
removal to a lower altitude.
Acclimatization entails physiologic and metabolic
adjustments that greatly improve tolerance to altitude hypoxia. The main adjustments involve
(1) reestablishment of acid–base balance of the
bodily fluids, (2) increased synthesis of hemoglobin
and red blood cells, and (3) improved local circulation and cellular metabolism. Adaptations 2 and 3
significantly facilitate oxygen transport and use.
The rate of altitude acclimatization depends on the
terrestrial elevation. Noticeable improvements occur within several days. The major adjustments require about 2 weeks, although acclimatization to
relatively high altitudes may require 4 to
6 weeks.
The alveolar PO2 averages 25 mm Hg at the summit of Mt. Everest. For acclimatized men, this re•
duces VO2max by 70%, to about 15 mL O2 ⭈ kg⫺1 ⭈
min⫺1. An unacclimatized individual loses consciousness within 30 seconds at this altitude.
Acclimatization does not fully compensate for the
•
stress of altitude. Despite acclimatization, VO2max decreases about 2% for every 300 m above 1500 m. A
significant decrement in endurance-related exercise
performance parallels the reduced aerobic capacity.
Altitude-related decrements in physiologic function
(e.g., reduction in maximum heart rate and stroke
volume) offset any beneficial effects of acclimatization. This partly explains the inability to achieve
•
sea-level VO2max values at altitude, even after acclimatization.
Despite certain altitude acclimatization adaptations
that should increase aerobic capacity and endurance
performance on return to sea level, research results
do not support such an effect. This probably results
from the altitude-related decrease in maximum heart
rate and maximum stroke volume.
Training at altitude provides no more benefit to
sea-level performance than equivalent training at
sea level.
Athletes benefit from periodically returning from
altitude to sea level for intense training to offset
any “detraining” from lower levels of exercise during a prolonged altitude stay.
References
1. Adams WC, et al. Effects of equivalent sea-level and altitude training
•
on VO2 max and running performance. J Appl Physiol 1975;39:262.
2. Agostoni P, et al. Effects of simulated altitude-induced hypoxia on exercise capacity in patients with chronic heart failure. Am J Med
2000;109:450.
3. Anholmm JD, et al. Radiographic evidence of interstitial pulmonary
edema after exercise at altitude. J Appl Physiol 1999;86:503.
4. Ashenden MJ, et al. “Live high, train low” does not change the total
haemoglobin mass of male endurance athletes sleeping at a simulated
altitude of 3000 m for 23 nights. Eur J Appl Physiol 1999;80:479.
5. Baily DM, et al. Training hypoxia: modulation of metabolic and cardiovascular risk factors in men. Med Sci Sports Exerc 2000;32:1058.
6. Bärtsh P. High altitude pulmonary edema. Med Sci Sports Exerc
1999;31(Suppl 1):S23.
7. Basnyat B, et al. Myocardial infarction or high-altitude pulmonary
edema. Wilderness Environ Med 2000; 11:196.
8. Beidleman BA, et al. Exercise responses after altitude acclimatization
are retained during reintroduction to altitude. Med Sci Sports Exerc
1997;29:1588.
9. Beidleman BA, et al. Exercise VE and physical performance at altitude
are not affected by menstrual cycle phases. J Appl Physiol
1999;86:1519.
10. Bender PR, et al. Decreased exercise muscle lactate release after high
altitude acclimatization. J Appl Physiol 1989;67:1456.
11. Boero JA, et al. Increased brain capillaries in chronic hypoxia. J Appl
Physiol 1999;86:2111.
12. Brosnan MJ, et al. Impaired interval exercise responses in elite female
cyclists at moderate simulated altitude. J Appl Physiol 2000;11:196.
13. Butterfield GE. Nutrient requirements at high altitude. Clin Sports Med
1999;18:607.
14. Butterfield GE, et al. Increased energy intake minimizes weight loss in
men at altitude. J Appl Physiol 1992;72:1741.
15. Casas M, et al. Effect of intermittent exposure to hypobaric hypoxia
and exercise on human physical performance. J Physiol Biochem (Rev
Esp Fisiol) 1997;53:160.
16. Cerretelli P. Limiting factors to oxygen transport on Mount Everest.
J Appl Physiol 1976;40:658.
17. Chapman RF, et al. Individual variation in responses to altitude training. J Appl Physiol 1998;85:1448.
18. Craig AB Jr. Olympics 1968: a post-mortem. Med Sci Sports 1969;1:177.
19. Cymerman A, et al. Operation Everest II: maximal oxygen uptake at
extreme altitude. J Appl Physiol 1989;66:2446.
20. Daniels J, Oldridge N. The effects of alternate exposure to altitude and
sea level on world-class middle-distance runners. Med Sci Sports
1970;2:107.
21. Dempsey JA. Effects of acute through life-long hypoxic exposure on
exercise pulmonary gas exchange. Respir Physiol 1971;13:62.
22. Dickinson ER, et al. Project Olympics. Schweiz Z Sportsmed
1966;14:305.
23. Dinmore AJ, et al. Intestinal carbohydrate absorption and permeability
at high altitude (5,730 m). J Appl Physiol 1994;76:1903.
•
24. Emonson DL, et al. Training-induced increases in sea level VO2max and
endurance training are not enhanced by acute hypobaric exposure. Eur
J Appl Physiol 1997;76:8.
25. Faulkner JA, et al. Maximum aerobic capacity and running performance at altitude. J Appl Physiol 1968;24:685.
26. Ferretti G, et al. Oxygen transport system before and after exposure to
chronic hypoxia. Int J Sports Med 1990;11:S15.
27. Fulco CS, et al. Maximal and submaximal exercise performance at altitude. Aviat Space Environ Med 1998;69:793.
•
28. Gavin TP, et al. Ventilation’s role in the decline in VO2max and SaO2 in
acute hypoxic exercise. Med Sci Sports Exerc 1998;30:195.
29. Gonzalez NC, et al. Increasing maximal heart rate increases maximal
O2 uptake in rats acclimatized to simulated altitude. J Appl Physiol
1998;84:164.
30. Green HJ, et al. Operation Everest II: adaptations in human skeletal
muscle. J Appl Physiol 1989;66:2454.
31. Green HJ, et al. Human skeletal muscle exercise metabolism following
an expedition to Mount Denali. Am J Physiol Regul Integr Comp Physiol. 2000;279:R1872.
32. Green HJ, et al. Increase in submaximal cycling efficiency mediated by
altitude acclimatization. J Appl Physiol 2000;89:1189.
33. Grover RF, Reeves JT. Exercise performance of athletes at sea level
and 3,100 meters altitude. In: Goddard RF, ed. The effects of altitude
on physical performance. Chicago, IL: Athletic Institute, 1967.
34. Groves BM, et al. Operation Everest II: elevated high-altitude pulmonary resistance unresponsive to oxygen. J Appl Physiol 1987;63:521.
35. Hackett PH, Roach RC. High altitude medicine. In: Auerbach PA, ed.
Wilderness medicine, management of wilderness and environmental
emergencies. St Louis, MO: Mosby-Year Book, 1995.
36. Hackett PH, et al. High-altitude cerebral edema evaluated with magnetic resonance imaging. Clinical correlation and pathophysiology.
JAMA 1998;280:1920.
37. Hannon JP, et al. Effects of altitude acclimatization on blood composition of women. J Appl Physiol 1969;26:540.
38. Harris CW, Hansen JE. Electrocardiographic changes during exposure
to high altitude. Am J Cardiol 1966;18:183.
CHAPTER 24
39. Honigman B, et al. Acute mountain sickness in a general tourist population at moderate altitude. Ann Intern Med 1993;118:587.
40. Hoppeler H, Desplanches D. Muscle structural modifications in hypoxia. Int J Sports Med 1992;13:S166.
41. Hoppeler H, et al. II. Morphologic adaptations of human skeletal muscle to chronic hypoxia. Int J Sports Med 1990;11:53.
42. Hunt J, Hillary E. The conquest of Everest. New York: EP Dutton,
1954.
43. Hurtado A. Animals in high altitudes: resident man. In: Dill DB, et al.,
eds. Handbook of physiology. Baltimore: Williams & Wilkins, 1964.
44. Insalaco G, et al. Cardiovascular and ventilatory response to isocapnic
hypoxia at sea level and at 5,050 m. J Appl Physiol 1996;80:1724.
45. Jansen GF, et al. Cerebral vasomotor reactivity at high altitude in humans. J Appl Physiol 1999;86:681.
46. Jensen K, et al. High-altitude training does not increase maximal oxygen uptake or work capacity at sea level in rowers. Scand J Sci Med
Sports 1993;3:256.
47. Kayser B, et al. Maximal lactate capacity at altitude: effect of bicarbonate loading. J Appl Physiol 1993;75:1070.
48. Kayser B, et al. Fatigue and exhaustion in chronic hypobaric hypoxia:
influence of exercising muscle mass. J Appl Physiol 1994;76:634.
49. Klausen K. Cardiac output in man in rest and work during and after acclimatization to 3800 m. J Appl Physiol 1969;21:609.
50. Klausen K. Exercise under hypoxic conditions. Med Sci Sports 1969;1:43.
51. Klausen K, et al. Effect of high altitude on maximal working capacity.
J Appl Physiol 1966;21:1191.
52. Klausen K, et al. Exercise at ambient and high oxygen pressure at high
altitude and at sea level. J Appl Physiol 1970;29:456.
53. Kollias J, Buskirk ER. Exercise at altitude. In: Johnson WR, Buskirk
ER, eds. Science and medicine of exercise and sports. New York:
Harper and Row, 1974.
54. Krasney JA. Brief review: a neurogenic basis for acute altitude sickness. Med Sci Sports Exerc 1994;26:195.
55. Lenfant CP, et al. Effect of chronic hypoxic hypoxia on the O2-Hb dissociation curve and respiratory gas transport in man. Respir Physiol
1969;7:7.
56. Levine BD, et al. Altitude training does not improve running performance more than equivalent training near sea level in trained runners.
Med Sci Sports Exerc 1992;24:769.
57. Levine BD, Stray-Gunderson J. “Living high–training low”: effect of
moderate-altitude acclimatization with low-altitude training on performance. J Appl Physiol 1997;83:102.
58. Liu Y, et al. Effect of “living high–training low” on the cardiac functions at sea level. Int J Sports Med 1998;19:380.
59. MacDougall JD, et al. Operation Everest II: structural adaptations in
skeletal muscle in response to extreme simulated altitude. Acta Physiol
Scand 1991;142:421.
60. Mairbaurl H. Red blood cell function in hypoxia at altitude and exercise. Int J Sports Med 1994;15:51.
61. Malconian MK, Rock PB. Medical problems related to altitude. In:
Pandolf K, et al., eds. Human performance physiology and environmental medicine at terrestrial extremes. Carmel, IN: Cooper Publishing
Group, 1994.
62. Manier G, et al. Pulmonary gas exchange in Andean natives with excessive polycythemia—effect of hemodilution. J Appl Physiol
1988;65:2107.
63. Maresch CM, et al. Maximal exercise during hypobaric hypoxia (447
torr) in moderate-altitude natives. Med Sci Sports Exerc 1983;15:360.
64. Mazzeo R, et al. ␤-Adrenergic blockade does not prevent the lactate response to exercise after acclimatization to high altitude. J Appl Physiol
1994;76:610.
65. Mazzeo RS, et al. Acclimatization to high altitude increases muscle
sympathetic activity both at rest and during exercise. Am J Physiol
1995;269(Renal Fluid Electrolyte Physiol. 38):R201.
66. Mazzeo RS, et al. Catecholamine response during 12 days of high-altitude exposure (4,300 m) in women. J Appl Physiol 1998;84:1151.
67. Mazzeo RS, et al. Sympathoadrenal responses to submaximal exercise
in women after acclimatization to 4,300 meters. Metabolism
2000;49:1036.
68. Mazzeo RS, et al. Catecholamine responses to alpha-adenergic blockade during exercise in women acutely exposed to altitude. J Appl Physiol 2001;90:121.
69. Melissa L, et al. Skeletal muscle adaptations to training under normobaric hypoxic versus normoxic conditions. Med Sci Sports Exerc
1997;29:238.
• Exercise at Medium and High Altitude
621
70. Mizuno M, et al. Limb skeletal muscle adaptation in athletes after
training at altitude. J Appl Physiol 1990;68:496.
71. Mizuno M, et al. Limb skeletal muscle adaptation in athletes after
training at altitude. J Appl Physiol 1990;68:496.
72. Ou LC, et al. Polycythemic responses to hypoxia: molecular and genetic
mechanisms of chronic mountain sickness. J Appl Physiol 1998;1242.
73. Pugh LCGE. Muscular exercise on Mount Everest. J. Physiol (London) 1958;141:233.
74. Pugh LCGE. Physiological and medical aspects of the Himalayan Scientific and Mountaineering Expedition, 1960–61. Br Med J 1962;2:621.
75. Pugh LCGE. Animals in high altitudes: an above 5000 meters-mountain exploration. In: Dill DB, et al., eds. Handbook of physiology.
Baltimore: Williams & Wilkins, 1964.
76. Pugh LCGE. Athletes at altitude. J Physiol (London) 1967;192:619.
77. Reeves JT. Operation Everest II; preservation of cardiac function at
extreme altitude. J Appl Physiol 1987;63:531.
78. Reynafarje C. Myoglobin content and enzymatic activity of muscle
and altitude adaptation. J Appl Physiol 1962;17:301.
79. Richalet JP. High altitude pulmonary oedema: still a place for controversy? Thorax 1995;50:923.
80. Roach RC, et al. Exercise exacerbates acute mountain sickness at
stimulated high altitude. J Appl Physiol 2000;88:581.
81. Robergs RA, et• al. Multiple variables explain the variability in the
decrement in VO2max during acute hypobaric hypoxia. Med Sci Sports
Exerc 1998;30:869.
82. Rock PB, et al. Operation Everest II. Electrocardiography during maximal exercise at extreme altitude. Med Sci Sports Exerc 1986;18:S74.
83. Rodríguez FA, et al. Intermittent hypobaric hypoxia stimulates erythropoiesis and improves aerobic capacity. Med Sci Sports Exerc
1999;31:264.
84. Rose MS, et al. Operation Everest II: nutrition and body composition.
J Appl Physiol 1988;65:2545.
85. Saito S, et al. Exercise-induced cerebral deoxygenation among untrained trekkers at moderate altitudes. Arch Environ Health
1999;54:271.
86. Saltin B, et al. Maximal oxygen uptake and cardiac output after 2
weeks at 4300 m. J Appl Physiol 1968;25:400.
87. Saltin B. Exercise and the environment: focus on altitude. Res Q Exerc Sport 1996;67:1.
88. Saltin B, et al. Morphology, enzyme activities and buffer capacity in
leg muscles of Kenyan and Scandinavian runners. Scand J Med Sci
Sports 1995;5:209.
89. Savard GK, et al. Cardiovascular response to exercise in humans following acclimatization to extreme altitude. Acta Physiol Scand
1995;154:199.
90. Sawka MN, et al. Blood volume: importance and adaptations to exercise training, environmental stresses, and trauma/sickness. Med Sci
Sports Exerc 2000;32:332.
91. Schoene RB, et al. Relationship of hypoxic ventilatory response to exercise performance on Mount Everest. J Appl Physiol 1984;56:1478.
92. Schoene RB, et al. Operation Everest II: ventilatory adaptations during gradual decompression to extreme altitude. Med Sci Sports Exerc
1990;22:804.
93. Sharp C. Exercise at altitude. BR J Sports Med 2000;34:404.
94. Stenberg, J, et al. Hemodynamic response to work at simulated altitude, 4,000 m. J Appl Physiol 1966;21:1589.
95. Suarez JM, et al. Operation Everest II. Left ventricular systolic function in man at high altitude assessed by two dimensional echocardiography. Am J Cardiol 1987;60:137.
96. Surks MJ, et al. Changes in plasma thyroxine concentration and metabolism, catecholamine excretion and basal oxygen uptake during
acute exposure to high altitude (14,100 ft). J Clin Invest
1966;45:1442.
97. Sutton JR. High altitude retinal hemorrhage. Semin Respir Med
1983;5:159.
98. Terrados N, et al. Effects of training at simulated altitude on performance and muscle metabolic capacity in competitive road cyclists.
Eur J Appl Physiol 1988;57:203.
99. Terrados N, et al. Is hypoxia a stimulus for synthesis of oxidative enzymes and myoglobin? J Appl Physiol 1990;68:2369.
100. Valdivia E. Total capillary bed in striated muscle of guinea pigs native
to Peruvian mountains. Am J Physiol 1958;194:585.
101. Westerterp-Plantenga MS, et al. Appetite at “high altitude” [Operate
Everest III (Comex-’97)]: a simulated ascent on Mount Everest.
J Appl Physiol 1999;87:391.
622
SECTION 5
• Exercise Performance and Environmental Stress
102. West JB. Do climbs to extreme altitudes cause brain damage? Lancet
1986;2:387.
103. West JB. High life: a history of high altitude physiology and medicine. New York: Oxford University Press, 1998.
104. West JB. Barometric pressure on Mt. Everest: new data and physiological significance. J Appl Physiol 1999;86:1062.
105. West JB. Invited review; pulmonary capillary stress failure. J Appl
Physiol 2000;89:2483.
106. West JB, et al. Pulmonary gas exchange on the summit of Mount
Everest. J Appl Physiol 1983;55:678.
107. Wolfel EE, et al. Systemic hypertension at 4,300 m is related to sympathoadrenal activity. J Appl Physiol 1994;76:1643.
108. Xu F, Severinghaus JW. Rat brain VEGF expression in alveolar hypoxia: a possible role in high-altitude cerebral edema. J Appl Physiol
1998;85:53.
109. Young AJ. Energy substrate utilization during exercise in extreme environments. Exerc Sport Sci Rev 1990;18:65.
110. Young AJ, Young PM. Human acclimatization to high terrestrial altitude. In: Pandolf KB, et al., eds. Human performance physiology and
environmental medicine at terrestrial extremes. Indianapolis: Benchmark Press, 1988.