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Living high-training low: Tolerance and acclimatization in elite endurance

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Article  in  European Journal of Applied Physiology · February 2006

DOI: 10.1007/s00421-005-0065-9 · Source: PubMed

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Eur J Appl Physiol (2006) 96: 66–77
DOI 10.1007/s00421-005-0065-9
O R I GI N A L A R T IC L E
Julien V. Brugniaux Æ Laurent Schmitt Æ Paul Robach
Hervé Jeanvoine Æ Hugues Zimmermann
Gérard Nicolet Æ Alain Duvallet
Jean-Pierre Fouillot Æ Jean-Paul Richalet
Living high-training low: tolerance and acclimatization
in elite endurance athletes
Accepted: 12 September 2005 / Published online: 26 October 2005

Springer-Verlag 2005
Abstract The ‘‘living high-training low’’ (LHTL) model
is frequently used to enhance aerobic performance.
However, the clinical tolerance and acclimatization
process to this intermittent exposure needs to be exam-
ined. Forty one athletes from three federations (cross-
country skiers, n=11; swimmers, n=18; runners, n=12)
separately performed a 13 to 18-day training at the
altitude of 1,200 m, by sleeping either at 1,200 m (CON)
or in hypoxic rooms (HYP), with an O2 fraction corre-
sponding to 2,500 m (5 nights for swimmers and 6 for
skiers and runners), 3,000 m (6 nights for skiers, 8 for
swimmers and 12 for runners) and 3,500 m (6 nights for
skiers). Measurements performed before, 1 or 15 days
after training were ventilatory response (HVRe) and
desaturation (DSaO2e) during hypoxic exercise, an
evaluation of cardiac function by echocardiography, and
leukocyte count. Lake Louise AMS score and arterial O2
saturation during sleep were measured daily for HYP.
Subjects did not develop symptoms of AMS. Mean
nocturnal SaO2 decreased with altitude down to 90% at
3,500 m and increased with acclimatization (except at
3,500 m). Leukocyte count was not affected except at
3,500 m. The heart function was not affected by LHTL.
Julien V. Brugniaux (&) Æ L. Schmitt Æ A. Duvallet
J.-P. Fouillot Æ Jean-Paul Richalet
Laboratoire ‘‘Réponses cellulaires et fonctionnelles à l’hypoxie’’
EA2363, ARPE, UFR SMBH, Université Paris 13, 74 rue Marcel
Cachin, 93017 Bobigny cedex, France
E-mail: jbrugniaux@free.fr
Tel.: +33-1-48387757
Fax: +33-1-48387777
G. Nicolet Æ L. Schmitt
Centre National de Ski Nordique, 39220 Premanon, France
Paul Robach
Ecole National de Ski et d’Alpinisme, 74401 Chamonix, France
H. Jeanvoine
Hopital de St Claude, 39200 St Claude, France
Hugues Zimmermann
Hôpital de Champagnole, 39300 Champagnole, France
Signs of ventilatory acclimatization were present imme-
diately after training (increased HVRe and decreased
DSaO2e) and had disappeared 15 days later. In conclu-
sion, LHTL was well tolerated and compatible with
aerobic training. Comparison of the three patterns of
training suggests that a LHTL session should not exceed
3,000 m, for at least 18 days, with a minimum of
12 h day
1 of exposure.
Keywords Intermittent hypoxia Æ Hypoxic ventilatory
response Æ Cardiac function Æ Leukocyte count Æ
Nocturnal arterial saturation
Introduction
Intermittent exposure to hypoxia has been proposed as a
new technique for altitude training. This method namely
‘‘living high-training low’’ (LHTL) consists of combin-
ing acclimatization at moderate altitude with low alti-
tude training (Levine et al. 1991). The aim of this
technique is to enhance erythrocyte volume while keep-
ing similar training load than at sea level. LHTL has
been shown to enhance aerobic performance and red cell
mass (Levine and Stray-Gundersen 1992; Levine and
Stray-Gundersen 1997). However, there is no clear
consensus, since other studies did not find any
improvement neither in performance (Hahn et al. 2001),
nor in red cell mass (Ashenden et al. 1999). Despite the
lack of evidence of a clear efficiency of LHTL, more and
more endurance athletes use it by their own means, with
personal hypoxic tents or rooms. Moreover a miscon-
ception wants that the higher the altitude, the more
efficient it is, leading some athletes to sleep in severe
hypoxia without any medical control.
Exposure to hypoxia from hours to days may lead to
several clinical conditions, which could impede the effi-
cacy of a training session. Only few studies focused on
the effects of intermittent exposure to altitude on cardiac
function, while it is well established for years that
chronic hypoxia may lead to cardiac morphological

changes such as right ventricular hypertrophy associated
with an increase in pulmonary arterial pressure (Hult-
gren and Miller 1965). Hypoxia is known to suppress the
immune status (Pyne et al. 2000), which may predispose
the athletes to infections. Acute mountain sickness
(AMS), characterized by headache, sleep disturbances,
fatigue and nausea may also interfere in the first few
days of training during altitude exposure.
On the other hand, exposure to hypoxia induces
acclimatization through an enhancement of the hypoxic
ventilatory response (HVR), as reported during chronic
(Forster et al. 1971; Sato et al. 1994) or intermittent
(Katayama et al. 1998) hypoxia. An increase in venti-
lation at altitude counterbalances oxygen desaturation
and therefore improves oxygen transport and aerobic
performance (Richalet et al. 2002). This augmentation of
HVR due to acclimatization persists for a few days after
the return to normoxia, and then fades away (Sato et al.
1994). HVR has been shown to increase with intermit-
tent hypoxia (Katayama et al. 1998; Townsend et al.
2002), but to our knowledge only Townsend et al. (2002)
focused on de-acclimatization after LHTL and found a
time-dependent increase in HVR for endurance athletes,
which persisted 2 days after the end of the session.
Several factors can influence the efficacy of a LHTL
training session. A debate is currently going on about
the optimal duration, the level of altitude, the duration
of daily exposure and the optimal delay between the
training session and the programmed competitions.
Furthermore, national and international sports institu-
tions may address ethical aspects of LHTL training and
may be interested in evidence based presence or absence
of detrimental or ergogenic effects of such training
procedures.
The main objective of this study is to determine the
influence of factors such as the degree and duration of
hypoxia on the balance between beneficial effects of
LHTL and potentially detrimental effects of hypoxia.
More specifically
1. Is LHTL tolerated by athletes to allow an important
training load (i.e. up to 3h 30 per day)?
2. How daily and/or total exposure to hypoxia do affect
ventilatory acclimatization and clinical status?
3. Does the probable increase in HVRe persist 15 days
after the end of the session, and do the possible
harmful effects disappear 15 days after the end of
LHTL?
Methods
This work is composed of three studies based on the
LHTL model described by Levine et al. (1991). Three
different populations of elite athletes were studied: cross-
country skiers, swimmers and runners. Subjects were
classified as elite by their participation to national and
international competition and were registered on a na-
tional list including all French elite athletes.
67
The first study with cross-country skiers took place
during the summer 2002. The second study with swim-
mers was realized during the winter 2002–2003. The last
study, on runners, was performed during the autumn
2003. Modifications in procedures took into account the
results of the preceding study.
This work is part of a multicenter study sponsored by
the International Olympic Committee and the French
Ministry of Sports. The Ethics Committee of Paris
Necker Hospital approved these studies, and all subjects
gave their voluntary written informed consent to par-
ticipate in the protocol.
Subjects (Table 1)
For each study, subjects were divided in two groups, a
LHTL group (HYP) and a Control group (CON). After

the determination
 of maximal oxygen uptake
V_ O2 max at the altitude of 1,200 m, the subjects were
of equivalent V_ O2 max randomly assigned to the two
fitness-matched groups.
Cross-country skiers
Eleven athletes from the ‘‘Fédération Française de Ski
Nordique’’ (seven biathletes, two nordic-combined ski-
ers and two cross country skiers) were divided in two
groups: control group (CONcs, n=5) and hypoxic
group (HYPcs, n=6). There were three female athletes
in each group. Athletes participated either in the World
Cup or in the European Cup.
Swimmers
Eighteen national level from the ‘‘Fédération Française
de Natation’’ divided in two groups of nine subjects with
one female in each group: control group (CONs, n=9)
and hypoxic group (HYPs, n=9). Swimmers partici-
pated either in International (World and European cup)
or National trials.
Runners
Twelve elite from the ‘‘Fédération Française d’Athlé-
tisme’’ were divided in two groups of six male subjects:
control group (CONr, n=6) and hypoxic group (HYPr,
n=6). They participated either in International (World
and European cup) or National trials.
Cross-country skiers and swimmers had some expe-
rience of altitude training. They used to train for short
sessions at moderate altitude but they had never used
this technique before. Runners had no experience with
altitude training. All athletes were unacclimatized to
high altitude before coming to Prémanon, they had not
been exposed to altitudes higher than 1,500 m at least in
the month preceding the study.
68

Table 1 Anthropometric characteristics and V_ O2 max of the subjects

Group Cross-country skiers Swimmers Runners

CONcs (n=5) HYPcs (n=6) CONs (n=9) HYPs (n=9) CONr (n=6) HYPr (n=6)

Age (years) 20±1.8 23±3.9 17±0.6 20±3.2** 23±1.5 25±5.2

Weight (kg) 63.6±5.8 67.2±8.7 67.6±6.4 70.8±8.8 63.5±5.8 64.9±5.0
Height (cm) 173.8±5.1 174.5±6.1 180.3±6.8 178.9±4.7 178.2±4.6 176.1±5.2
V_ O2 max (ml min
1 kg
1) 58.6±8.7 59.7±6.3 58.5±1.9 57.9±1.9 63.3±4.2 63.3±2.5

Values are means ± SD

**P<0.05 HYP vs. CON. V_ O2 max : maximal oxygen uptake

Study design (Table 2)
All the studies were led in the ‘‘Centre National de Ski
Nordique’’ (CNSN) of Prémanon, Jura, FRANCE. It
consisted in three major phases: pre-training, training
and post-training. Evaluations were conducted at
Prémanon (1,200 m), before (PRE), at the end (POST1)
of the training session and/or 15 days after the training
session (POST2).
Pre-training period
Athletes went to Prémanon (1,200 m) during the aerobic
preparation period of their competitive season, i.e. at the
beginning of a new season. This period stands at least
2 months after the end of their respective national or
international cup and/or championship. The 3–4 days of
the Pre-training period were devoted to pre tests (PRE).
Echocardiography, blood sampling and performance
tests were realized first. Then, the HVRe test was per-
formed.
Training session
It was based on the LHTL model with incremental
altitude depending on the study groups and the duration
of the session (13 days for swimmers or 18 days for
cross-country skiers and for runners). Altitudes ranged
between 2,500 and 3,500 m. At POST1 some tests were
realized as at PRE.
The training session for the cross-country skiers was
composed of three levels of altitude of six nights (and
days) each. Altitudes were 2,500, 3,000 and 3,500 m.
Athletes spent 11 h day
1 in their hypoxic rooms (Ta-
ble 2). For the swimmers, the session was composed of 5
nights of pre-acclimatization at 2,500 m and 8 nights at
3,000 m. Mean time spent in hypoxic rooms was
16 h day
1 (Table 2). Finally for the runners, we used
the same altitudes as for study 2 but pre-acclimatization
lasted 6 nights at 2,500 m followed by 12 nights at
3,000 m. Subjects spent 14 h day-1 in hypoxic rooms
(Table 2).
Post-training period
After the training session at Prémanon, subjects con-
tinued to have controlled training activities at home, i.e.
near sea level. Athletes came back to Prémanon 15 days
after the end of LHTL training for 3 days to perform the
POST2 tests, identical to those realized at PRE and/or at
POST1. Our tests were performed during the first two
days of POST2 (as in PRE and POST1). Athletes con-
tinued to have light training activities during the POST2
measurements.
Training quantification
The quantification of the training stimulus, in term of
volume and intensity, was determined in experiments
according to the method of Mujika et al. (1996). Briefly,

Table 2 Summary of procedures

Study PRE 2,500 m 3,000 m 3,500 m POST1 POST2

(before the session) (end of the session) (15 days after the end)

Cross-country Blood sampling 6 nights 6 nights 6 nights Blood sampling Blood sampling
skiers (n=11) Echocardiography 11 h day
1 11 h day
1 11 h day
1 Echocardiography
V_ O2 max test HVRe test in hypoxia in hypoxia in hypoxia HVRe test
Swimmers (n=18) Blood sampling 5 nights 8 nights Blood sampling Blood sampling
Echocardiography 16 h day-1 16 h day-1 Echocardiography
V_ O2 max test HVRe test in hypoxia in hypoxia HVRe test
Runners (n=12) Blood sampling 6 nights 12 nights Blood sampling Blood sampling
Echocardiography 14 h day
1 14 h day
1 Echocardiography
V_ O2 max test HVRe test in hypoxia in hypoxia HVRe test

PRE: 3–4 days preceding the beginning of the session. POST1: 1–2 days following the end of the session. POST2: 3 days holding 15 days
after the end of the session
AMS (CON, HYP) and nocturnal SaO2 (HYP) were measured daily for each study. V_ O2 max : maximal oxygen uptake test; HVRe
hypoxic ventilatory response at exercise

before the experiments, during a routine incremental test
to exhaustion, lactate concentrations were measured.
We determined five levels of lactate concentration (2,
4, 6, 10 and 16 mmol l
1) corresponding to five levels
training load (I, II, III, IV and V). Each level of lactate
concentration corresponded to a level of heart rate
which was used to control workload in the field during
all the duration of our experiments. This model, which
originally determined the training load by multiplying
the intensity with the number of kilometers swam, can
also be applied while running. CON and HYP group
always trained together; hence training load was quan-
titatively and qualitatively equivalent between CON and
HYP groups in each study.
Hypoxic rooms
The normobaric hypoxia was obtained by extracting
oxygen from ambient air (OBS, Husøysund, Norway).
Altitudes of 2,500, 3,000 and 3,500 m were obtained
with an O2 fraction (FIO2) corresponding to 0.174,
0.164 and 0.154 respectively. Calculation of the FIO2
corresponding to the required altitudes took into
account the altitude of Prémanon. Since the gas com-
position was continuously monitored, O2 fraction was
permanently adjusted along the session and was kept
stable. Moreover it was verified that opening the door
of the room slowly for few seconds, even many times
per day did not change FIO2. For safety reasons, O2
and CO2 compositions were monitored. Similarly
arterial O2 saturation of each subject, obtained by
transcutaneous oximetry (see Measurements), was
also monitored. Each room was connected to a central
monitoring room under the control of a medical
doctor.
Measurements
Complete results concerning performance and hemato-
logical changes (red cell mass, hematocrit, hemoglobin)
for these three studies will be presented elsewhere and
have been partly published in abstracts (Robach et al.
2002, 2005; Brugniaux et al. 2005). A brief summary of
the results will be given here.
Acute mountain sickness (AMS)
Acute mountain sickness was evaluated daily in the early
morning using the Lake Louise questionnaire (The Lake
Louise consensus 1992). Questions are divided in two
parts: AMS self-assessment (headache, gastrointestinal
symptoms, fatigue, dizziness and sleep disturbances) and
clinical assessment (ataxia and dyspnea). AMS self-
assessment symptoms were ranked from 0 to 3 for each
item. For example concerning sleep disturbances, 0
represents normal sleep while 3 corresponds to very poor
sleep.
69
Nocturnal arterial O2 saturation (SaO2)
The nocturnal SaO2 was monitored in HYP subjects
during the last night in normoxia (basal values) and
during all the nights of the training session using a finger
pulse oximeter (NPB 290 Nellcor Puritan Bennett, Ire-
land). Nocturnal SaO2 values presented were mean of
values recorded every minute while in bed after turning
the light off.
Leukocyte count
Leukocyte count of all subjects of the three studies was
determined at PRE, POST1 and POST2 in a blood sample
obtained from an antecubital vein (Pentra 120 analyzer,
ABX, Montpellier, France). Blood sampling moments
were standardized, i.e. around 8:00 in the morning.
Echocardiography
A trained cardiologist used an ultrasound imager (So-
noheart, Sonosite, Bothell, WA, USA) to evaluate the
resting cardiac morphological changes at PRE (for all
studies), POST1 (for swimmers and runners) or POST2
(for cross-country skiers). Complete two-dimensional,
TM-echography and Doppler parameters for left cardiac
function were recorded following classical procedures:
aorta, left atrium, left ventricle diastolic and systolic
diameters, mitral flow velocities and cardiac output.
Tricuspid regurgitation (TR) was detected by color-flow
Doppler on 4-chamber apical or modified parasternal
views. TR peak velocity was measured by continuous-
wave Doppler. A systolic (PAPs) pulmonary arterial
pressure was calculated by adding the right atrial pres-
sure (taken as 5 mm Hg) to the right atrium–right ven-
tricle gradient. Pressure gradients between the right
atrium and the right ventricle were then calculated by
the Bernoulli equation: DP=4V2. For technical reasons,
PAPs was not measured for swimmers and RV Sys was
not measured for cross-country skiers. This technique of
echocardiography has previously been used by our team
in field conditions (Richalet et al. 2005).
Performance and hematology
We chose a trial corresponding to the speciality of ath-
letes, using a treadmill for cross-country skiers and
runners and a test in swimming pool for swimmers.
Hemoglobin and hematocrit were assessed by blood
sampling and red cell volume was determined by a CO-
dilution method. The methods of measurements for
V_ O2 max and hematological parameters will be de-
scribed elsewhere.
Hypoxic ventilatory response at exercise (HVRe)
Hypoxic ventilatory response at exercise was determined
at PRE (for all studies), POST1 (for swimmers and
runners) and POST2 (for cross-country skiers). This test
70
is a submaximal exercise test performed at a power
output corresponding to 30% of the normoxic V_ O2 max
measured before the training session. We used a slightly
modified test previously described by Richalet et al.
(1988) which is composed of four phases of 5 min each:
rest in normoxia, rest in hypoxia (corresponding to
11.5% of oxygen in gas mixture, i.e. 4,800 m), exercise in
hypoxia (11.5% of oxygen in gas mixture), exercise in
normoxia. In our studies, oxygen fraction in gas mixture
was determined taking into account the altitude of
Prémanon (1,200 m). Three parameters were monitored:
heart

rate  (HR, bpm), pulmonary ventilation
V_E ; l min
1 and arterial O2 saturation (SaO2, %). HR
was continuously recorded with a numeric S810 Polar
Recorder (Polar, Kempele, Finland). Data were trans-
ferred by telemetry to a computer, via a RS 232 Polar
interface, for further analysis with the Polar precision
performanceTM SW4 software. SaO2 was measured by
an ear lobe pulse oximeter (Ohmeda Biox 3740, Louis-
ville, USA). Pulmonary ventilation was recorded breath
by breath and averaged every 30 seconds (CPX/D car-
diopulmonary exercise system; Medical Graphics, Min-
neapolis, MN, USA). Calculated parameters were:
Hypoxic Ventilatory Response at exercise (HVRe),
Hypoxic Cardiac Response at exercise (HCRe) and de-
saturation at exercise (DSaO2e) (Richalet et al. 1988) (see
below for the calculation formulas of DSaO2e, HVRe
and HCRe).
Statistical analysis
All data are expressed as mean ± SD. Given the small
number of subjects in each group we used non-para-
metric tests. To compare results before and 15 days after
the altitude training camp, we used the Wilcoxon test of
rank. To compare the two groups we used the U-Mann
Whitney test. The Statview version 5.0 statistical pack-
age was used for these analyses. The level of significance
was set at P £ 0.05.
Results
Summary of performance and hematological parameters
V_ O2 max at POST1 tended to increase for HYP swim-
mers (+8.1%, P=0.09) and was significantly enhanced
for HYP runners (+7.1%, n=5). Concerning skiers
V_ O2 max was not modified along the study. At POST2
V_ O2 max values were similar to basal level for swimmers
but remained higher for HYP runners compared with
PRE (+3.4%, n=5). V_ O2 max was not modified in

hDSaO2 e ð%Þ ¼ normoxic SaO2 e
hypoxic SaO
  2e
HVRe 1 min kg
1
1 _
_ _
_
¼ hypoxic exercise V E
normoxic exercise V E =DSaO2 e=body weight  100
HCRe ðbpmÞ ¼ ðhypoxic exercise HR
normoxic exercise HRÞ=DSaO2 e:
both studies for CON groups. Red cell volume was
globally not modified among HYP groups, except for
swimmers in which it increased by 8.5% at POST1 vs.
PRE. Red cell volume tended to decrease at POST2 for
CONcs. In the same time plasma volume was not
modified between groups or along with each study.
Hemoglobin and hematocrit were globally not modified
along with the sessions in all studies.
Training
In each study, training volume as well as intensity were
kept equivalent in both groups (results not shown).
Training stimulus was decreased over the 15-day period
between the end of the LHTL session and the POST2
measurements. Around two-thirds of the training con-
sisted in endurance training at relatively low heart rate
(below 75% of maximal heart rate) and without accu-
mulation of lactate (i.e. intensity I and II). The last third
of the training program was performed above the onset
of blood lactate accumulation (development of anaero-
bic endurance and speed/weight lifting exercises).
Acute mountain sickness (Lake Louise Score)
Whatever the study and/or the group of subjects con-
sidered, nobody developed acute mountain sickness.
Analysis of the responses to the AMS questionnaire
demonstrates that the subjects did not complain of
headache, gastrointestinal symptoms, dizziness or ataxia
and dyspnea. However fatigue and sleep disturbances
were frequently mentioned but without any significant
difference between hypoxic and control groups. The
maximal individual scores during the three sessions were
1.0, 2.4 and 0.8 respectively for HYPcs, HYPs and
HYPr.
Nocturnal arterial O2 saturation (SaO2) (Fig. 1)
Cross-country skiers
Nocturnal SaO2 was lower at altitude. At 1,200 m, it was
96.8±0.8% and it decreased during the first night in hy-
poxia compared with the basal value. Mean SaO2 for a
given altitude decreased from 93.6±0.5% at 2,500 m to
91.7±1.1% at 3,000 m (P<0.05) and to 89.8±0.5% at
3,500 m (P<0.05). SaO2 increased progressively during
the 2,500 m step from 92.7±0.5% during the first night to
94.2±0.8% during the last night of the step (6th night of
the session) (P<0.05). There was only a tendency during
the 3,000 m step (from 89.8±2.8 to 92.7±0.5%,
i
 71

Fig. 1 Mean nocturnal

saturation per night in hypoxia
for subjects of the three groups.
Values are means ± SD.
1,200 m Basal measure realized
at the altitude of Prémanon
(1,200 m), prior to the hypoxic
exposure. *P<0.05 vs. 3,000 m.
#P<0.05 vs. the first night at
this altitude

P=0.07) and there was no significant change during the
last step of altitude (3,500 m). While the lowest individual
SaO2 was 92% during the first night at 2,500 m, this value
fell at 87% for the first night at 3,000 m (3 subjects under
90%) ant at 86% at 3,500 m (3 subjects under 90%).
During the last night at 3,500 m there was still one subject
who presented a value of 89%. (Fig. 1a)
SaO2 increased between the first and the last night of
each step of altitude (from 91.2±0.8 to 92.4±1.5%
during the 2,500 m step, from 90.4±1.4 to 92.7±1.7%
during the 3,000 m step, P<0.05). The lowest individual
value was 90% during the first night at 2,500 m and
89% during the first night at 3,000 m (only one subject
under 90%). (Fig. 1b)

Swimmers Runners

Basal value at 1,200 m (96.1±0.8%) was significantly SaO2 at 1,200 m was 95.5±0.8% during the last night
higher than during the first night at 2,500 m. There was before the beginning of the LHTL session and was sig-
a significant decrease of mean SaO2 between the last nificantly higher than during the first night in hypoxia.
night at 2,500 m and the first night at 3,000 m (P<0.05). SaO2 did not significantly increase along with the 6-day
72
period at 2,500 m. SaO2 decreased from 93±1.3 to
91.7±1.2% between the last night at 2,500 m and the first
at 3,000 m (P<0.05). SaO2 increased from 91.7±1.2 to
92.7±1.4% between the first and the last night at 3,000 m
(P<0.05). The lowest value was 90% during the first
night at 2,500 m (for one subject) and 91% during the first
at 3,000 m (for four subjects). (Fig. 1c)
Subjects of all studies presented some episodic de-
saturations during the night (result not shown). The
lowest recorded desaturation was 83% at 2,500 m and
81% at 3,000 and 3,500 m. Surprisingly, the greatest
individual desaturations did not occur only during the
first night but all along the study at a given step of
altitude. Episode of desaturation was short (less than
30 s), with a total duration below 2 min for the whole
night. Since we did not measure ventilation during sleep,
we cannot say if these episodes of desaturation occurred
during sleep apneas.
Leukocytes count (Fig. 2)
All values remained with normal limits whatever the
group and the condition. Leukocytes count for cross-
country skiers was not modified between PRE and
POST1 for CONcs, but was not statistically decreased
for HYPcs. This decrease was maintained and became
significant at POST2 (
9% vs. PRE, P<0.05) (Fig. 2a).
Leukocytes for swimmers presented a 10% decrease
between PRE and POST1 for CONs (P<0.05), but va-
lues returned to the basal level at POST2. On the other
hand leukocyte count for HYPs was not modified along
the session (Fig. 2b). Similarly leukocyte count for
runners was not modified during the session whatever
the group of subjects (Fig. 2c).
Echocardiography (Table 3)
Cross-country skiers
Between PRE and POST2, there was no change in the
echocardiographic parameters in both groups. The 19%
Fig. 2 Leukocyte count of
athletes of the three groups
before (PRE), at the end
(POST1) and 15 days after
the end (POST2) of the
LHTL sessions. Values
are means ± SD.
*P<0.05 vs. PRE
increase in mean PAPs between PRE and POST2 was
not significant. However four out of six skiers presented
an increase in PAPs.
Swimmers
Right ventricle/left ventricle ratio slightly increased for
HYPs between PRE and POST1, so that the difference
between the two groups became significant at POST1
compared with PRE (P<0.05). RV Dia was not altered
by LHTL. Because RV Dia was 9% higher in POST1
than in PRE for HYPs, the difference between groups
was significant at POST1 (P<0.05). RV Sys was sig-
nificantly higher in HYPs than CONs at PRE and this
difference remained significant at POST1 (P<0.05). EF
significantly decreased (
14%) between PRE and
POST1 in CONs (P<0.05), whereas it stayed similar for
HYP.
Runners
There was no significant difference between PRE and
POST1 measurements or between the two groups.
However, similarly to cross-country skiers in POST2,
PAPs in HYPr was not modified at POST1, but mean
PAPs was higher by 18.7% compared with PRE.
Hypoxic ventilatory response at exercise (Table 4)
No change was found in HVRe, HCRe or DSaO2e be-
tween PRE and POST2 or between groups of cross-
country skiers. Swimmers presented a 24% decrease in
DSaO2e between PRE and POST1 for CONs (P<0.05).
In the HYPs group, HVRe increased (+30%, P<0.05)
and DSaO2e decreased (31%, P<0.05) at POST1 com-
pared with PRE. In CON runners, HCRe decreased
between PRE and POST1 (P<0.05) while there was no
alteration in HYPr. At the same time HVRe decreased
between PRE and POST1 for CONr (
24%, P<0.05).
In the HYPr group, HVRe increased by 74% (P<0.05)
Table 3 Echocardiographic parameters at rest

Group Cross-country skiers Swimmers Runners

CONcs (n=5) HYPcs (n=6) CONs (n=9) HYPs (n=9) CONr (n=6) HYPr (n=6)

PRE POST2 PRE POST2 PRE POST1 PRE POST1 PRE POST1 PRE POST1

PAPs (mm Hg) 21.00±4.18 20.00±3.54 17.50±4.18 20.83±3.76 27.20±4.55 24.00±3.39 22.33±2.94 26.50±2.65
RV/LV 0.43±0.10 0.42±0.08 0.41±0.02 0.43±0.04 0.46±0.11 0.44±0.08 0.52±0.07 0.56±0.05** 0.42±0.13 0.41±0.07 0.40±0.06 0.41±0.07
RV Dia (mm) 22.20±4.20 21.60±4.72 20.50±1.00 21.33±3.33 23.33±5.05 22.89±3.98 26.11±3.76 28.56±2.65** 21.83±6.85 21.00±3.85 22.00±2.74 22.40±3.44
RV Sys (mm) 19.22±4.60 20.22±3.31 23.22±3.03** 24.33±2.40** 18.67±6.22 18.50±4.14 18.00±2.00 18.80±3.03
EF (%) 0.62±0.02 0.63±0.02 0.68±0.08 0.69±0.08 0.70±0.06 0.60±0.05* 0.64±0.08 0.64±0.08 0.72±0.09 0.69±0.07 0.68±0.02 0.68±0.03

Values are mean ± SD; PAPs systolic pulmonary arterial pressure (mm Hg); RV/LV right ventricle/left ventricle ratio during diastole; RV Dia right ventricle diameter in end diastole
(mm); RV Sys right ventricle diameter in end systole (mm); EF left ventricular ejection fraction (%)
*P<0.05 vs. PRE, **P<0.05 HYP vs. CON

Table 4 Hypoxic cardiac and ventilatory response at exercise

Group Cross-country skiers Swimmers Runners

CONcs (n=5) HYPcs (n=6) CONs (n=9) HYPs (n=9) CONr (n=6) HYPr (n=6)

PRE POST2 PRE POST2 PRE POST1 PRE POST1 PRE POST1 PRE POST1

HCRe (bpm
1.%) 0.99±0.39 1.15±0.36 1.14±0.19 1.14±0.31 0.85±0.28 0.87±0.21 0.89±0.22 0.90±0.26 0.82±0.15 0.69±0.14* 0.64±0.21 0.86±0.31
HVRe (l.min
1.kg
1) 1.04±0.72 0.84±0.60 0.76±0.15 0.90±0.47 0.79±0.31 1.02±0.48 0.74±0.40 0.96±0.49* 0.79±0.18 0.60±0.14* 0.62±0.27 1.08±0.33*
DSaO2e (%) 22.4±6.8 23.2±6.14 22.5±4.7 23.3±6.9 25.2±4.5 19.1±4.4* 27.1±6.9 18.8±3.5* 30.7±6.2 31.3±11.2 29.7±3.8 24.2±7.7*

Values are mean ± SD; HCRe: hypoxic cardiac response at exercise; HVRe: hypoxic ventilatory response at exercise; DSaO2e: difference of arterial saturation between normoxic and
hypoxic exercise. *P<0.05 vs. PRE
73
74
and DSaO2e decreased by 19% (P<0.05) from PRE to
POST1.
Discussion
The main findings of this study were: (1) fatigue and
sleep disturbance were sometimes observed but no AMS
symptoms developed along with the sessions. (2) Noc-
turnal saturation decreased with altitude and thereafter
athletes progressively developed acclimatization leading
to increase in SaO2 (except at 3,500 m for cross-country
skiers). (3) Immune status was not affected except at
3,500 m for cross-country skiers. (4) Cardiac function
was globally not modified by LHTL except a slight in-
crease in PAPs but within normal limits. (5) HVRe was
enhanced at POST1 but signs of ventilatory acclimati-
zation had faded away at POST2.
Procedures of our studies were adapted from the
conclusions of the preceding one. For the first study we
chose a relatively short session when compared with
those classically recommended in the literature (4 weeks,
Levine 2002) but with a higher altitude, to allow athletes
to perform many sessions during different mesocycles of
training over the year. The lack of improvement in
performance and the relatively poor acclimatization at
3,500 m, lead us to use a lower level of altitude. How-
ever in the same time we kept a similar total time spent
in hypoxia (208 h for swimmers vs. 198 h for cross-
country skiers). Because of the limited modifications in
performance observed with swimmers we decided to
change the procedure for runners. We kept the same
altitude design, since it was well tolerated, but we in-
creased the time spent in altitude essentially by length-
ening the duration of the LHTL session (252 h, i.e.
14 h day
1 during 18 days).
Two main reasons may explain the relatively low
V_ O2 max measured among our elite endurance athletes.
First of all V_ O2 max test were performed at an altitude
of 1,200 m which is known to induce a decrease in
V_ O2 max of 5–6% (Robergs et al. 1998) or more (Gore
et al. 1996). Secondly, values of cross-country skiers can
be partly explained by the fact that 5 women were part
of our study. Finally it can also be due to the period of
the experiments in the season: we can reasonably
imagine that our subjects were not at their peak of
performance.
Acute mountain sickness (Lake Louise Score)
Symptoms of AMS can appear from altitudes exceeding
2,000 m (Richalet and Herry 2003) and progressively
disappear with acclimatization after a few days of resi-
dence at the same altitude. On the other hand, AMS
score increases with altitude (Richalet et al. 1999). In our
study we observed no modification of the AMS score
whatever the study or the altitude considered. The only
symptoms mentioned were fatigue and sleep
disturbances, but without any significant difference be-
tween groups, so that they cannot be related to inter-
mittent altitude exposure, but rather to training and
other environmental factors.
Nocturnal arterial O2 saturation (SaO2)
The values of nocturnal saturation were in agreement
with those commonly found at these altitudes (lowest
mean SaO2 for HYPs during the first night at 3,500 m:
89±1.8%). A marked desaturation is known to repre-
sent hypoventilation during sleep, which leads to hyp-
oxemia and may trigger pathological manifestations. In
patients with heart failure, the presence of sleep apneas
is related to left ventricular systolic dysfunction (Java-
heri 2000). In the present study, no change in ventricular
ejection fraction was observed in the HYP group sug-
gesting that the limited degree of desaturation observed
had no consequence on the contractility of the left
ventricle
As expected, nocturnal SaO2 decreased with increas-
ing altitude. We also observed that nocturnal SaO2 in-
creased with time, at a given level of altitude. This result
can be related to the lower hypoxic exercise-induced
desaturation observed at POST1. An increase in SaO2 or
lesser desaturation is a well-known sign of acclimatiza-
tion (Richalet et al. 2005). Thus, at least 6 nights at
2,500 m followed by six nights at 3,000 m are sufficient
to induce a progressive acclimatization. However at
3,500 m, this duration seems to be too short to obtain a
complete acclimatization, since SaO2 did not increase
significantly with time.
Leukocytes count
Immune status is known to be impaired after an expo-
sure to continuous hypoxia. Actually Pyne et al. (2000)
showed a decrease in immune status for elite swimmers
after a 21-day training camp at 2,102 m. To our
knowledge no other team previously studied immune
status during a LHTL session. Our results showed a
trend to decrease in leukocytes for HYPcs whereas val-
ues stayed similar for CONcs. Contrary to cross-country
skiers, HYPs and HYPr did not present any significant
modification of leukocytes count. The decrease observed
only for the study in which the altitude reached 3,500 m
supports the idea that this altitude was excessive. This
observation is in agreement with others from our team
(Tiollier et al. 2005) who found a depletion of secretory
immunoglobulin A (sIgA) consecutively to the same
session. However contrary to Pyne et al. (2000), who
concluded that training-induced changes may be sec-
ondary to those induced by altitude, we were not able to
determine if altitude or training was the main determi-
nant of observed changes in leukocytes. Hence, these
results suggest that LHTL is well tolerated by athletes
up to a maximal altitude of 3,000 m. Although a slight
 75

decrease in leukocyte count was shown in the control method developed by Weil et al. (1970), which is an iso-
group of swimmers, values remained within normal capnic test at rest. We preferred to use a method simu-
limits. As already mentioned, values for all groups re- lating exercise conditions closer to real altitude exposure,
mained within normal limits and, moreover, these rela- i.e. hypoxia and hypocapnia (poikilocapnic), derived
tive alterations were not coupled with major added from Richalet et al. (1988). Therefore, CO2 was not
infections. controlled and ventilatory response to CO2 was not as-
sessed. However, HVR has been shown to be similar be-
tween isocapnic and poikilocapnic at rest for an exposure
Echocardiography
up to 48 h (Tansley et al. 1998). In our study, we focused
on the response at exercise (HVRe), more appropriate to
We did not observe any LHTL-induced change in the
evaluate athletes. Townsend et al. (2002) found an in-
left systolic function at rest. Hence, contrarly to Liu
crease in resting HVR two days after a 20-day LHTL
et al. (1998), we did not find an improvement in the
session (8–10 h day-1 at 2,650 m) in well-trained runners
systolic cardiac function with LHTL. Left diastolic
despite previous findings that sea level endurance training
function (assessed by the E wave/A wave ratio, results
depressed HVR (Katayama et al. 1999). In our case,
not shown) was not modified, as found by Liu et al.
training was controlled and equivalent for CON and
(1998), suggesting the absence of change in the pre- or
HYP in each study. Thus a possible lower volume or
afterload. At exercise, some cardiac modifications could
intensity of training cannot explain the increase in HVRe
occur with chronic hypoxia. Sawka et al. (2000) evi-
for the HYPs and HYPr groups at the end of the session.
denced that cardiac work at exercise, quantified as the
On the other side the depression of HVR due to endur-
product of heart rate by mean arterial pressure, can be
ance training (Katayama et al. 1999) can explain that
enhanced after acclimatization. Similarly the authors
HVRe for HYPcs at POST2 was not significantly differ-
suggested a decrease in cardiac output during sub-
ent from basal measurement. Townsend et al. (2002) also
maximal exercise consecutively to acclimatization.
found that the magnitude of HVR was less important two
Exposure to chronic hypoxia is well known to induce
days after the end of the session than after fifteen days of
pulmonary hypertension and right ventricular hyper-
LHTL, even if it was still higher than before the session,
trophy (Hultgren and Miller 1965). Right ventricular
while in our study, HVRe returned to basal values
hypertrophy is proportional to the severity of pulmo-
15 days after the end of the session.
nary hypertension (Hultgren and Miller 1965). PAPs for
Evidence of diminished resting HVR at the fourth
cross-country skiers and runners presented a slight but
day after the return to sea level consecutive to 12 days of
insignificant increase of around 19%. However a type-II
continuous hypoxia at 3,810 m had already been ob-
error cannot be discarded. Furthermore it was not
served (Sato et al. 1994). However Forster et al (1971)
coupled with modifications in RV Dia or RV/LV ratio,
observed that HVR remained elevated 45 days after the
for which an increase is classically admitted as an indi-
return to normoxia from a 45-day sojourn at 3,100 m. In
rect indicator of pulmonary hypertension.
our study 15 days after the altitude sojourn, we did not
To the best of our knowledge, the only studies that
find any difference in HVRe or DSaO2e compared with
dealt with pulmonary hemodynamics by using an
PRE. During this period of 15 days, skiers were no more
intermittent model of hypoxia concerned miners that
subjected to hypoxia and continued their endurance
stayed for a few days or weeks at altitude and the same
training, which would have blunted their chemoreceptor
time at lowland, this shift pattern being repeated for
sensitivity (Katayama et al. 1999).
months (Sarybaev et al. 2003; Richalet et al. 2002). This
CONs presented a decrease in DSaO2e at POST1,
model of exposure, defined as ‘‘chronic intermittent
which could be surprising when we look at the two other
hypoxia’’, is different from our model where the inter-
control groups who did not show any change in DSaO2e.
mittence was performed during the same 24-h period.
In fact, two control subjects presented an increase in
However even in that chronic model, intermittent hy-
total hemoglobin mass (Robach et al. 2005), which could
poxia did not increase PAPs measured in normoxia after
have contributed to a better O2 transport during exercise
a maximum of 31 months (Richalet et al. 2002) or
and thus a smaller exercise-induced decrease in SaO2 in
3 years (Sarybaev et al. 2003) of intermittent exposure.
hypoxia.

Hypoxic ventilatory response at exercise

In the present study HVRe increased at the end of the
session, which supports the general consensus that hyp-
oxic exposure increases the hypoxic ventilatory response,
as reported during continuous (Forster et al. 1971; Sato
et al. 1994) or intermittent (Katayama et al. 1998;
Townsend et al. 2002) exposure, whatever the technique
of HVR measurement (Richalet et al. 1999; Sato et al.
1994). In fact, most studies use a modification of the
Methodological considerations
This study had suffered from some methodological
limitations. First, some interpretations may be specula-
tive because of the small number of subjects (possible
type-II error). Actually studies with elite athletes are
hard to lead mainly because of there tight schedules.
Moreover, the choice of the time of experiments in the
season may not have been optimal, since the fitness level
76
of all athletes was not fully stabilized at the beginning of
the session. It could explain some modifications ob-
served in CON groups (especially during the HVR test).
The differences in the profile of exposure of each
group made comparison relatively difficult to do. First
the protocols were determined in order to test various
profiles of LHTL sessions (regarding acclimatization
and tolerance on one hand, and performance and
hematology on the other hand), as asked by the Inter-
national Olympic Committee (IOC). Secondly, as men-
tioned above, we tried to optimize each study from the
results of the preceding one. The wish of the IOC was to
have an overview of the LHTL method in order to
implement regulations of the use of LHTL with simu-
lated altitude.
Finally we could not exclude a possible placebo ef-
fect. However studies were not performed in a double
blind manner, which limited the placebo effect.
Conclusion
We can conclude from the present study, that the
training protocol used did not induce any significant
clinical disorder. A minimum of six nights at a maximal
altitude of 3,000 m, preceded by a few days at a lower
altitude seems to be necessary and sufficient to trigger
the acclimatization process. On the other hand, six
nights at 3,500 m seem to be too short to develop
acclimatization. Limited cardiac changes may occur, but
all parameters stayed within the normal physiological
range. Similarly a slight alteration of the leukocyte count
may occur consecutively to an exposure to 3,500 m.
Athletes can thus use this type of training without major
risks for health. However because of possible nocturnal
SaO2 desaturation, a medical survey could be required,
or at least athletes have to be instructed to the use of
oximeters (how to adjust alarms for example).
Although the number of subjects was limited and not
all the possible combinations of characteristics of LHTL
sessions were explored, this study allows to suggest opti-
mal conditions for this type of training session. A maximal
altitude of 3,000 m (with few days of pre-acclimatization
at a lower altitude), during at least 18 days and with a
minimum of 12 h day
1 in hypoxia seem to be required. A
time period of 15 days after the end of the session is too
long to maintain the signs of acclimatization.
Acknowledgements This study was supported by grants from the
International Olympic Committee and the French Ministry of
Sports. The skillful assistance of Patrick Bouchet for software
development is gratefully acknowledged.
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