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O R I G I N A L A R T I C L E
Je re my Cornolo Jean-Pierre Fouillot Laurent SchmittCamillo
Povea Paul Robach Jean-Paul Richalet
Interactions between exposure to hypoxia and the
training-inducedautonomic adaptations in a live hightrain low
session
Accepted: 22 September 2005 Springer-Verlag 2005
Abstract The autonomic and cardiovascular adaptationsto hypoxia
are opposite to those resulting from aerobictraining. We
investigated (1) whether exposure to hy-poxia in a live hightrain
low (LHTL) session limits the
autonomic and cardiovascular adaptations to training,and (2)
whether such interactions remain 15 days afterthe end of the LHTL.
Eighteen national swimmerstrained for 13 days at 1,200 m, living
(16 h day1) eitherat 1,200 m (live lowtrain low, LLTL) or at a
simulatedheight of 2,5003,000 m (LHTL). Subjects were inves-tigated
at 1,200 m before and at the end of the trainingsession, and after
the following 15 days of sea-leveltraining. Cardiovascular
parameters and the autonomiccontrol assessed by spectral analysis
of RR and dia-stolic blood pressure (DBP) variability were obtained
inthe resting supine position and in response to anorthostatic
test. At the end of the 13-day training, rest-
ing heart rate (HR) and sympathetic modulation onheart decreased
in LLTL (10.1% and 25.4%,P
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the discontinuous hypoxic exposure would not modifythe
training-induced cardiovascular and autonomicadaptations in elite
athletes. Moreover we evaluatedwhether possible changes remained
after a following 15-day training at sea level. A passive head-up
tilt (HUT)test assessed the cardiovascular and autonomic
adapta-tions to LHTL and the following training (Beitzke et
al.2002; Fu et al. 2004; Gratze et al. 1998).
Methods
The study was conducted on healthy, sea-level, nativecompetitive
swimmers (males, n=16; females, n=2):400 m front crawl (n=16) or
long-distance (n=2)specialists, recruited for their participation
in a nationalchampionship. After having given their written
in-formed consent to participate in the study, a medicalexamination
and echocardiography were performed.Then, the subjects were matched
by gender and maxi-mal oxygen uptake _VO2max
to either a live low
train low group (LLTL, n=9, aged 17.00.1 years,
height 180.32.3 cm, body weight 67.52.1 kg,_VO2max=58.51.9 ml
min
1 kg1; mean SEM) oran LHTL group (n=9, aged 19.91.0 years,
height178.91.6 cm, body weight 70.82.9 kg,_VO2max=57.91.8 ml
min
1 kg1). The procedures,training sessions and residence were at
1,200 m abovesea level (Ecole Nationale de Ski Nordique, Pre
manon,France, barometric pressure, Pb = 674 mmHg). TheLLTL lived
and slept at ambient Pb (1,200 m asl),while the LHTL lived and
slept (16 h/day) at a simu-lated altitude obtained through an
oxygen extractionsystem (OBS, Husysund, Norway): 5 days at2,500 m
(inspired O2 fraction, FiO2=17.4%) fol-
lowed by 8 days at 3,000 m (FiO2=16.4%). All thesubjects trained
for 13 days at 1,200 m in a 25-m pool.Subjects gave their informed
written consent and theprotocol was approved by the ethics
committee of theNecker Hospital, Paris.
Protocol
The present study is part of an evaluation of the effectsof an
LHTL session. Results concerning performanceand haematology have
been presented (Brugniaux et al.2005; Robach et al. 2005). The
subjects were investigated
before (PRE), at the end of the training camp (POST1),and after
2 weeks of training following the trainingcamp (POST2).
A HUT test was performed in the morning (08:3013:00) after a
light breakfast without coffee, before thedaily workouts in the
training camp. Subjects per-formed the HUT in the same order. At
POST1, theinterval between the last continuous nocturnal
hypoxicexposure and recordings was 14.5 h. To avoid short-term
effects of exercise on HR variability (HRV)(Furlan et al. 1993),
the last training session was on the
previous day or earlier. Subjects sat quietly for 30 min.Then,
they were instrumented in the upright positionand strapped on a
manually operated tilt bed with footsupport and tilted supine.
After 10 min, values werecollected for 3 min. When these
measurements werecompleted, the subjects were exposed to 60
HUT.After 6 min of standing, values were collected for4 min.
Finally, the subjects were returned to the supineposition. The HUT
was terminated in case of presyn-cope (Task Force on Syncope,
European Society ofCardiology 2001).
Since respiration modulates autonomic activity,breathing
patterns affects the spectral power of the HRV(Akselrod 1995).
Subjects with a spontaneous breathingfrequency below 9 b min1 in
the supine position wereinstructed to breath at 12 b min1 for 2 min
beforebeing exposed to HUT. If HRV parameters of the12 b min1
period were different from those of thespontaneous breathing
frequency period, the subjectswere excluded from the study.
However, audio instruc-tion could have influenced the HRV
recordings (Ber-nardi et al. 2000).
The study started in December during the prepara-tion period for
competitive swimming, after a period ofrelative detraining. In the
training camp 2 daily work-outs of 2 h each, 7 days per week, were
supervised by anational coach. According to Avalos et al.
(2003)improvement of the swimming aerobic capacity requiresa large
amount of aerobic training. For that purpose, thepredominant
training intensity was close to the bloodlactate accumulation
threshold (OBLA), while two tothree high load workouts were
performed to maximisethe impact of the LHTL. The training regimen
wasreduced between POST1 and POST2, similar to the2-week training
period preceding a major competition
(Avalos et al. 2003; Mujika et al. 1996). Trainingintensity and
volume were quantified according toMujika et al. (1996).
Progressive swimming untilexhaustion was performed before the
training camp, andthe blood lactate concentration was determined.
Thenthe training load was ranked into five intensities
(IV),corresponding to five lactate concentrations, andweighted. The
training stimulus was quantified by mul-tiplying the workout with
the training duration. BetweenPOST1 and POST2, the subjects
reported their trainingprogram in a book.
Parameters
Cardiovascular system
Beat-by-beat time series of RR intervals were recordedfrom a
standard 2-canal ECG using four ECG chestelectrodes. The RR
intervals were instantaneously ob-tained as the difference between
successive RR peaks.
Continuous beat-to-beat arterial BP was recorded
byphotoplethysmography using the vascular unloading
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technique (Parati et al. 2003). The Task Force Monitor
system (TFM) (CNSystems, Graz, Austria) providesnon-invasive
estimations of changes in the cardiovas-cular system and its
autonomic control (Beitzke et al.2002; Eckert et al. 2003; Parati
et al. 2003). The sensorwas placed on the volar surface of the
right middle fin-ger, while the right arm was maintained
horizontal.Continuous BP was corrected to oscillometric BPobtained
every minute at the brachial artery on thecontralateral arm.
Continuous and oscillometric BPsignals were transmitted to a device
monitor detectingfluctuations in a range of 50250 mmHg (5
mmHg).
Recordings of RR intervals and systolic BP (SBP)were analysed
using the sequence method to estimatethe spontaneous baroreflex
sensitivity (SBS) (Tanket al. 2000). From beat-to-beat time series
of intervalsthe TFM system identified spontaneous sequences ofthree
consecutive beats in which RR intervals andSBP either increased
(+RR/+SBP) or decreased(RR/SBP) over four cardiac beats. The
minimumchange for a rise or fall in SBP was 1 mmHg and forRR it was
4 ms beat1 (Eckert et al. 2003; Gratze
et al. 1998). The slope of the regression line was cal-culated
for each sequence of RR/SBP relationship andepisodes with
correlation coefficients r>0.95 wereevaluated. The mean of the
individual slopes was takenas a measure of the SBS.
Stroke volume (SV) was determined by transthoracicimpedance
cardiography (Beitzke et al. 2002; Gratzeet al. 1998). A circular
band electrode was placed aroundthe neck while two other electrodes
were placed on themedial line under the xyphoid at a distance of at
least3 cm from the outer electrode. A current of 400 lA and40 kHz
passed through the thorax from the electrodeplaced around the neck
to the two others. The voltage
u(t) is proportional to the thorax impedance Z (Z(t) =u(t)I0).
The first derivative (dZ/dt) of the impedancesignal Z(t) is
supplied by the cardiograph. Algorithmscalculate SV using the
Kubiceks formula, eliminatingthe influence of breathing and
detecting the maxima ofthe dZ/dt signal (C-point), the aortic
opening (B-point)and the aortic closing points (X-point). The
monitor hasa high reproducibility for consecutive SV
measures(Gratze et al. 1998) and a good correlation with
athermodilution method. Stroke index (SI), HR (1/RR),cardiac index
CI = (SV HR)/body surface area andtotal peripheral resistance index
TPRI = (mean BP/CO)/body surface area) were calculated.
Power spectral analysis of the beat-by-beat vari-ability of HR
and diastolic BP (DBP) was obtained bythe autoregressive method.
Specific characteristics ofthe power spectrum of HR and DBP
variabilityquantify sympathetic and parasympathetic control ofthe
cardiovascular system (Akselrod 1995; Pagani et al.1997; Zhang et
al. 2002; Task Force 1996). Two fre-quencies were considered: the
low (LF, 0.040.17 Hz)and the high frequency (HF, 0.170.40 Hz) band.
TheRR-LF and DBP-LF were considered as markers ofsympathetic
activity respectively on heart and
vasculature (Akselrod 1995; Pagani et al. 1997; Zhanget al.
2002). Because the RR-HF is a result of respi-ratory sinus
arrhythmia mediated by the vagus, itsamplitude reflects the
respiratory modulation of cardiacvagal outflow. The RR-LF/HF ratio
is an index of thesympatho-vagal balance (Akselrod 1995; Task
Force1996). Both LF and HF influences were expressed inabsolute
(au, ms2) and in normalised units (nu): HF nu= (HF ms2)/((LF ms2+HF
ms2)100). Normalisedunits minimise the effect of the changes in TP
on LFand HF components.
Data analysis
After being converted from analog to digital with a12-bit
resolution and sampled at 1 KHz per channel,data were transmitted
to the TFM system connectedto a PC and stored for further analysis.
After visualinspection, values were corrected by omitting
artefacts.Finally 512 RR and 256 DBP intervals and corre-sponding
variables were kept and averaged for each
condition.
Statistical analysis
Results were expressed as mean SEM. A ShapiroWilk test was
performed to ensure that the data satisfiedassumptions consistent
with a normal distribution.Then, a two-way analysis of variance was
performed toassess the effects of both time (PRE, POST1 andPOST2)
and group (LLTL and LHTL). When maineffects or interactions reached
a statistically significantlevel, the Tukey post hoc test was
applied to locate the
difference. Adaptations to the standing position wereexpressed
as a percentage of the baseline resting supinevalues. Linear
regression analyses were used to evaluateinteractions between
parameters in response to tilt. Datawere analysed using STATISTICA
(5.1) statisticalpackage. A P value
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LHTL and LLTL training session
Supine rest
At the end of the training camp HR decreased in theLLTL (6.9
bpm) but not in the LHTL (3.7 bpm)group (Fig. 1a). The RR-LF nu
decreased in the LLTLbut not in the LHTL group (Fig. 1b), while the
RR-HFnu and also the RRLF/HF remained constant (Ta-ble 2). Mean and
systolic BP and TPR did not changewhile the diastolic BP tended to
increase in the LHTLgroup (P=0.06) (Fig. 1c, Table 2). The
diastolic BP andTPR were higher in the LHTL than in the LLTL
groupand tended to be higher for mean and systolic BP(P=0.06).
Sympathetic tone on the vasculature (DBP-LF nu) fell in both groups
during the training camp(Table 2).
Head-up tilt
Responses were similar in the LLTL and LHTL groupsbefore and
after the training camp. Stroke index de-creased during HUT at PRE
and POST1, inducing anincrease in HR secondary to a rise in cardiac
sympa-thetic modulation (RR-LF nu, RR-LF/HF) and a de-crease in
vagal activity (RR-HF au, RR-HF nu)(Table 3). In both groups the
increase in sympatheticmodulation of the heart was negatively
correlated withits resting supine level (LLTL, r = 0.75,
P=0.01;
LHTL, r =
0.83, P=0.01). The decrease in SI in re-sponse to the HUT was
enhanced between PRE andPOST1 in the LLTL group concomitantly to a
rise in theincrease in HR. The TPR did not significantly changewith
HUT while DBP-LF nu increased, except in theLHTL group at PRE. The
TPR response was negativelycorrelated with the increase in HR (PRE,
r = 0.60,P=0.01; POST1, r = 0.64, P=0.006). Cardiac index,mean,
systolic and diastolic BP were maintained withHUT. SBS decreased in
both groups during the tilt,except in the LHTL group at POST1.
Post-LHTL and post-LLTL 15-day normoxic training
Supine rest
The HR was lower after the 15-day post-hypoxic train-ing period
than at the beginning of the training session(LLTL, 5.6 bpm; LHTL,
7.8 bpm) (Fig. 1a). TheRR-LF nu was lower than at the beginning of
thetraining session in both groups (Fig. 1b). Mean BP de-creased in
both groups during the training (Fig. 1c),while the systolic and
diastolic BP decreased only in theLHTL group (Table 2). The DBP-LF
nu was lowerthan before the training session in the LHTL
group(Table 2).
Head-up tilt
The decrease in SI was reduced at POST2 compared toPOST1 in the
LLTL group, and CI was lower than inthe LHTL group (Table 3). The
increase in RR-LF auand RR-LF nu with the tilt was higher at POST2
thanat PRE in the LLTL group, while the rise in HRremained in both
groups (Table 3). The decrease inRR-HF au and RR-HF nu and the
increase in RR-LF/HF in response to the tilt remained in both
groups. TheTPRI did not change with the tilt to standing
whileDBP-LF nu increased. The decrease in SBS remainedconstant in
both groups.
Discussion
The main finding from this study is that during anLHTL session,
discontinuous hypoxia (13 days,16 h day1 at a simulated height of
2,5003,000 m)interacts with the autonomic and cardiovascular
adap-tations to endurance training in highly trained athletes.The
physiological consequences of this interaction dis-appeared after a
15-day training performed at sea levelafter LHTL.
Table 1 Quantification of training
LLTL LHTL
Training camp TW1 Time (h wk1) 24.41.0 25.31.3TU wk1 833.3
772.6
TW2 Time (h wk1) 21.21.2 21.11.0TU wk1 724.0 755.0
Routine training RTW1 Time (h wk1) 15.30.6* 11.40.8*TU wk1
435.0* 373.0*
RTW2 Time (h wk1) 15.90.6* 17.11.0*TU wk1 453.0* 444.6*
Training units per week (TU wk1) calculated from the method of
Mujika et al. (1996) and time of training in hours per week (h
wk1);during the first (TW1) and the second (TW2) week of the
training camp; during the first (RTW1) and the second (RTW2) week
of trainingfollowing the training camp; for both living lowtraining
low (LLTL) and living hightraining low (LHTL) groups. Values
aremean SEM for LLTL (n=9) and LHTL (n=7)*Training camp versus
routine training: P
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LHTL and LLTL training session
Supine rest
The training session took place at the beginning of
thecompetitive season. The resting HR was decreased bytraining
(Bonaduce et al. 1998; Iellamo et al. 2002;Yamamoto et al. 2001)
and this fall paralleled the one
observed in cardiac sympathetic modulation assessedby RR-LF nu.
This fall in HR was not associatedwith an increase in vagal
activity (RR-HF nu), asobserved in high-level athletes training at
75% of theirmaximum load (Iellamo et al. 2002). The training
loadwas higher and close to a strenuous endurance trainingprogram
(Avalos et al. 2003; Mujika et al. 1996),which may modify the vagal
adaptations (Iellamoet al. 2002). A decrease in the intrinsic HR
could alsohave occurred (Bonaduce et al. 1998). The decrease inHR
and sympathetic modulation on the heartobserved in LLTL was not
significant in the LHTLgroup. These results could represent an
effect ofhypoxia, reducing the autonomic and
cardiovascularadaptations to training. Moreover, exercise
andhypoxia have similar autonomic and cardiovasculareffects
opposite to those resulting from the endurancetraining (Nakamura et
al. 1993; Bernardi et al. 1998;Cornolo et al. 2004). It is unlikely
that residual post-exercise effects occurred during the LHTL
sessionbecause: (1) post-exercise residual sympathetic tone
ismainly observed in hypertensive men (Cleroux et al.
1992) or after maximal exercise (Mourot et al. 2004;Terziotti et
al. 2001), while 85% of our training was ator below the OBLA; (2)
residual post-exercise effectsdecrease with the increase in
training status while oursubjects were national swimmers (Yamamoto
et al.2001); (3) subjects returned to their hypoxic rooms 1 hafter
their workouts while residual effects of exercisewere evidenced for
up to 2 h (Mourot et al. 2004;Terziotti et al. 2001; Howard et al.
2000). In fact,residual post-hypoxia effects may have occurred
duringthe LHTL session since the altitude used (2,5003,000 m)
corresponded to the upper limit recom-mended by Levine and
Stray-Gundersen (1992) for an
LHTL session. Residual effects of hypoxia could havepersisted
until the beginning of the training workouts,limiting the training
adaptations. Finally, these inter-actions between hypoxia and
training were small: thedecrease in HR (5.8%) and RR-LF nu (15.5%)
in theLHTL group was not significant.
Sympathetic control of the vasculature decreased inboth groups
at the end of the training session whilemean and diastolic BP and
TPR remained stable. Thisdiscrepancy could have been due to the
training- andhypoxia-induced vascular remodelling (Iwasaki et
al.2003). The higher BP and TPR after LHTL than afterLLTL may have
represented hypoxic after-effects
(Arabi et al. 1999; Bernardi et al. 1998; Xie et al. 2001).The
increase in diastolic BP observed in the LHTLgroup (9 mmHg or
14.6%) was higher than after anacute (Xie et al. 2001) or 2-night
(Arabi et al. 1999)hypoxic exposure and was mainly mediated by
TPR.Although BP and TPR did not change significantlyafter training,
the difference between the two groupsbecame significant after
training. The interactions be-tween exposure to hypoxia and
training adaptationswere limited.
Fig. 1 Mean heart rate (HR) (a), normalised low-frequency
power(LF nu) of beat-by-beat variability of RR intervals as a
marker ofthe cardiac sympathetic activity (b) and mean blood
pressure(MBP) (c) in the basal resting supine position in LLTL and
LHTLgroups before (PRE) and at the end of the 13-day training
camp(POST1), after 15 days of training following the training
camp(POST2). Bars and lines show mean SEM for LLTL (n=9) andLHTL
(n=7) *P
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Head-up tilt
Passive HUT was used to strengthen the assessment ofthe
cardiovascular and autonomic function (Beitzkeet al. 2002; Fu et
al. 2004; Gratze et al. 1998). Responsesof both groups of subjects
appeared normal (Beitzke
et al. 2002; Fu et al. 2004; Task Force 2001): tilt tostanding
decreased SI and increased HR in parallel witha rise in sympathetic
modulation and a fall in vagalactivity, maintaining a constant CI
and BP. The meanslope of SBS decreased due to activation of the
sympa-thetic nervous system: for the same shift of systolic BP,
Table 3 Percentage of changes of heart rate and blood pressure
variability and of the cardiovascular parameters during the tilt
test
LLTL LHTL
PRE POST1 POST2 PRE POST1 POST2
Heart rate and blood pressure variabilityHR 29.64.5***
41.44.5***; # 38.46.4*** 36.74.3*** 43.94.9*** 39.86.2***TP
43.018.8 * 28.013.5 16.922.3 10.532.8 38.473.4 82.9107.5RR-LF ms2
10.324.0 28.437.4 165.5104.4## 47.278.3 85.984.5 324.5285.7RR-LF nu
22.711.5 81.819.2*** 116.428.6***; # 79.625.4** 77.132.9**
95.824.1**RR-HF ms2 76.86.8* 76.76.8* 72.37.8* 80.74.9* 35.9109.9
68.114.5*RR-HF nu 51.014.8** 54.112.6** 65.67.7** 71.85.3**
59.010.9* 67.810.8**RR-LF/HF 446.0188.2* 610.8146.4** 992.3265.8*
1292.1681.4** 1256.3861.7* 1336.9494.1**DBP-LF nu 60.913.0***
80.816.7** 182.3107.9*** 38.919.2 109.353.4*** 90.821.4**
Cardiovascular parametersStroke index 23.44.1*** 33.33.5***; #
19.34.0**; $$$ 23.24.7* 25.55.8** 29.53.7**; Cardiac index 0.76.5
4.65.8 11.77.8$ 5.37.1 8.011.1 2.56.7Mean BP 3.22.0 0.21.9 5.42.4
0.421.9 0.72.0 3.72.6Systolic BP 2.21.0* 2.01.4# 1.81.3**; $ 0.71.1
0.31.0 0.11.5*Diastolic BP 5.22.3 5.32.7 10.12.8 3.02.5
1.73.6 6.52.7
TPRI 6.85.8 7.96.1 1.67.2 0.59.5 1.29.0 9.68.5SBS 60.88.4*
40.322.1* 59.52.8** 73.14.4*** 42.521.8 60.28.5*
Living lowtraining low (LLTL) and living hightraining low (LHTL)
groups before (PRE) and at the end of the 13-day training
camp(POST1), after the 15 days of training following the training
camp (POST2) in both supine and standing positions. Heart rate
(HR); Totalpower (TP); low (RR-LF) and high (RR-HF) frequency power
of RR intervals; RR-LF/HF ratio; low frequency power of
diastolicblood pressure (DBP-LF). Total peripheral resistance index
(TPRI), spontaneous baroreflex sensitivity (SBS). Values are mean
SEMfor LLTL (n=9) and LHTL (n=7)*Different between supine and
standing (%) (*P
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the increase in RR interval was reduced (Beitzke et
al.2002).
For both groups, the lower the resting supine level
ofsympathetic modulation to the heart, the higher was theincrease
in response to tilt. Thus, the training-induceddecrease in
sympathetic modulation may have facilitatedthe cardiovascular
response to the orthostatic stress.Whether the test was performed
before or after LLTLand LHTL, the tilt from supine to standing did
not in-duce an increase in TPR. This lack of response in TPRwas
compensated by a stronger increase in HR and wasneither due to
exposure to discontinuous hypoxia nor totraining. This dissociation
between the increase in sym-pathetic tone on vasculature and the
lack of increase inTPR (Fu et al. 2004) may be due to the
long-termtraining and is independent of the specific modalities
ofswimming (exercise in supine position) (Franke et al.2003).
Finally the hypoxia-induced increase and domi-nant sympathetic tone
on heart and vasculature did notlimit the further adaptations to a
tilt test performed14.5 h after the last nocturnal hypoxic
exposure(Bernardi et al. 1998; Cornolo et al. 2004).
In order to obtain the higher training-induced bene-fits, the
training load was similar to a strenuous endur-ance program of
elite swimmers (Avalos et al. 2003;Mujika et al. 1996). Since
training was conducted beforethe competitive period, we did not
increase the trainingintensity to avoid the risk of overreaching.
However, thetotal power of RR intervals tended to decrease in
theLHTL group which could have represented the initiationof a
fatigue process (Pichot et al. 2002). The hypoxicstimulus could
have been too intense or additive withtraining, perturbing the
recovery process of the athletes.The present study was associated
with autonomic car-diovascular adaptations to training in both
groups and
increase in red cell volume after LHTL, adding to theslight
improvement of swimming performance afterLHTL while it remained
constant after LLTL (Robachet al. 2005). Our results concerning
performance,haematology and acclimatisation (Brugniaux et al.
2005;Robach et al. 2005) are in agreement with previousreports
(Levine and Stray-Gundersen 1992; Rusko et al.1999).
The post-LHTL and post-LLTL 15-day normoxictraining
Supine rest
A 2-week delay is often used between an LHTL sessionand a major
competition. Thus, we conducted the2 weeks of sea-level training,
performed after the LHTLsession, according to the period of
training preceding aswimming competition, characterised by its
decreasedload (Mujika et al. 1996). Cardiovascular and auto-nomic
benefits of either LLTL or LHTL were main-tained during the
training: the decrease in resting supine
HR and sympathetic modulation persisted while theincrease in
vagal modulation on heart was reinforced.Similar benefits of this
training on HR and the auto-nomic control to the heart, and
disappearance of thedifference in BP and TPR between groups, argue
for aninteraction between discontinuous hypoxia and trainingduring
the LHTL session. Responses to head-up tiltwere similar to those
observed at the end of the LHTLtraining session. Interindividual
variability in responseto standing tended to be lower compared to
the post-training session recordings.
Conclusions
In order to investigate whether the exposure to discon-tinuous
hypoxia interacts with training-induced auto-nomic and
cardiovascular adaptations during an LHTLsession performed by
highly trained subjects, nationalelite swimmers were exposed 16 h
day1 to a 2,5003,000 m simulated altitude during a 13-day
aerobictraining camp. In the supine resting position, but not
in
response to an orthostatic test, exposure to discontinu-ous
hypoxia interacted with the autonomic and cardio-vascular
adaptations to training. This interactiondisappeared after a
following training session and didnot limit the autonomic and
cardiovascular adaptations.
Acknowledgements The author thanks the Fe de ration Francaise
deNatation and all the volunteers for their participation in this
studyat the Centre National de Ski Nordique (Pre manon, Jura).
Thisproject was supported by the International Olympic Committeeand
the French Ministry of Sports.
References
Akselrod S (1995) Components of heart rate variability:
basicstudies. In: Malik M, Camm AJ (eds) Heart rate
variability.Futura Publishing Company, Armonk, pp 147163
Arabi Y, Morgan BJ, Goodman B, Puleo DS, Xie A, Skatrud JB(1999)
Daytime blood pressure elevation after nocturnalhypoxia. J Appl
Physiol 87:689698
Avalos M, Hellard P, Chatard JC (2003) Modeling the
training-performance relationship using a mixed model in elite
swim-mers. Med Sci Sports Exerc 35:838846
Beitzke M, Pfister P, Fortin J, Skrabal F (2002)
Autonomicdysfunction and hemodynamics in vitamin B12 deficiency.
Au-ton Neurosci 97:4554
Bernardi L, Passino C, Spadacini G, Calciati A, Robergs R,
GreeneR, Martignoni E, Anand I, Appenzeller O (1998)
Cardiovas-cular autonomic modulation and activity of carotid
barore-ceptors at altitude. Clin Sci (Lond) 95:565573
Bernardi L, Wdowczyk-Szulc J, Valenti C, Castoldi S, Passino
C,Spadacini G, Sleight P (2000) Effects of controlled
breathing,mental activity and mental stress with or without
verbalisationon heart rate variability. J Am Coll Cardiol
35:14621469
Bonaduce D, Petretta M, Cavallaro V, Apicella C, Ianniciello
A,Romano M, Breglio R, Marciano F (1998) Intensive trainingand
cardiac autonomic control in high level athletes. Med SciSports
Exerc 30:691696
Brugniaux JV, Schmitt L, Robach P, Jeanvoine H, Zimmermann
H,Nicolet G, Duvallet A, Fouillot JP, Richalet JP (2005)
Livinghightraining low: tolerance and acclimatization in
eliteendurance athletes. Eur J Appl Physiol (in press)
-
7/31/2019 Corn Olo
8/8
Cleroux J, Kouame N, Nadeau A, Coulombe D, Lacourciere Y(1992)
Aftereffects of exercise on regional and systemic hemo-dynamics in
hypertension. Hypertension 19:18391
Cornolo J, Mollard P, Brugniaux JV, Robach P, Richalet JP
(2004)Autonomic control of the cardiovascular system during
accli-matization to high altitude: effects of sildenafil. J Appl
Physiol97:935940
Eckert S, Lotz N, Bergemann C, Kemper B, Petzoldt R, Tscho peD,
Horstkotte D (2003) Autonomic dysfunction indicated byreduced
baroflex sensitivity in patients with diabetes mellitus.In:
Thirteenth European Meeting on Hypertension. Milan, Italy
Franke WD, Mills KK, Lee K, Hernandez JP (2003) Trainingmode
does not affect orthostatic tolerance in chronically exer-cising
subjects. Eur J Appl Physiol 89:263270
Fu Q, Witkowski S, Levine BD (2004) Vasoconstrictor reserve
andsympathetic neural control of orthostasis.
Circulation110:29312937
Furlan R, Piazza S, DellOrto S, Gentile E, Cerutti S, Pagani
M,Malliani A (1993) Early and late effects of exercise and
athletictraining on neural mechanisms controlling heart rate.
Cardio-vasc Res 27:482488
Gratze G, Fortin J, Holler A, Grasenick K, Pfurtscheller G, Wach
P,Scho negger J, Kotanko P, Skrabal F (1998) A software packagefor
non-invasive, real-time beat-to-beat monitoring of strokevolume,
blood pressure, total peripheral resistance and forassessment of
autonomic function. Comput Biol Med 28:121142
Howard MG, Collins HL, Dicarlo SE (2000) Post-exercise
eleva-
tions in sympathetic nerve activity and baroreflex function
innormotensive rabbits. Clin Exp Hypertens 22:431444
Iellamo F, Legramante JM, Pigozzi F, Spataro A, Norbiato
G,Lucini D, Pagani M (2002) Conversion from vagal to sympa-thetic
predominance with strenuous training in high-perfor-mance world
class athletes. Circulation 105:27192724
Iwasaki KI, Zhang R, Zuckerman JH, Levine BD (2003)
Dose-response relationship of the cardiovascular adaptation
toendurance training in healthy adults: how much training forwhat
benefit? J Appl Physiol 95:15751583
Levine BD, Stray-Gundersen J (1992) A practical approach
toaltitude training: where to leave and train for optimal
perfor-mance enhancement. Int J Sports Med 13:S209S212
Mourot L, Bouhaddi M, Tordi N, Rouillon JD, Regnard J
(2004)Short- and long-term effects of a single bout of exercise on
heartrate variability: comparison between constant and interval
training exercises. Eur J Appl Physiol 92:508517Mujika I, Busso
T, Lacoste L, Barale F, Geyssant A, Chatard JC
(1996) Modeled responses to training and taper in
competitiveswimmers. Med Sci Sports Exerc 28:251258
Nakamura Y, Yamamoto Y, Muraoka I (1993) Autonomic controlof
heart rate during physical exercise and fractal dimension ofheart
rate variability. J Appl Physiol 74:875881
Pagani M, Montano N, Porta A, Malliani A, Abboud F, Birkett
C,Somers VK (1997) Relationship between spectral componentsof
cardiovascular variabilities and direct measures of
musclesympathetic nerve activity in humans. Circulation
95:14411448
Parati G, Ongaro G, Bilot G, Glavina F, Castiglioni P, Di
RienzoM, Mancia G (2003) Non-invasive beat-to-beat blood
pressuremonitoring: new developments. Blood Press Monit 8:3136
Pichot V, Busso T, Roche F, Garet M, Costes F, Duverney D,
Lacour JR, Barthe le my JC. (2002) Autonomic adaptations
tointensive and overload training periods: a laboratory study.Med
Sci Sports Exerc 34:16601666
Robach P, Schmitt L, Brugniaux JV, Roels B, Millet G, Hellard
P,Nicolet G, Duvallet A, Fouillot JP, Moutereau S, Lasne F,Pialoux
V, Olsen NV, Richalet JP (2005) Living hightraininglow: effect on
erythropoiesis and aerobic performance in highly-trained swimmers.
Eur J Appl Physiol (in press)
Rusko HK, Tikkanen H, Paavolainen L, Hamalainen I, Kal-liokoski
K, Puranen A (1999) Effect of living in hypoxia andtraining in
normoxia on sea-level _VO2max and red cell mass.Med Sci Sports
Exerc 31:S86
Tank J, Baevski RM, Fender A, Baevski AR, Graves KF, PloewkaK,
Weck M (2000) Reference values of indices of
spontaneousbaroreceptor reflex sensitivity. Am J Hypertens
13:268275
Task Force of the European Society of Cardiology, the North
American Society of pacing and Electrophysiology (1996)
Heartrate variability. Standards of measurement,
physiologicalinterpretation, and clinical use. Circulation
93:10431065
Task Force on Syncope, European Society of Cardiology
(2001)Guidelines on management (diagnosis and treatment) of
syn-cope. Eur Heart J 22:12561306
Terziotti P, Schena F, Gulli G, Cevese A (2001)
Post-exerciserecovery of autonomic cardiovascular control: a study
byspectrum and cross-spectrum analysis in humans. Eur J ApplPhysiol
84:187194
Xie A, Skatrud JB, Puleo DS, Morgan BJ (2001) Exposure tohypoxia
produces long-lasting sympathetic activation in hu-mans. J Appl
Physiol 91:15551562
Yamamoto K, Miyachi M, Saitoh T, Yoshioka A, Onodera S(2001)
Effects of endurance training on resting and post-exercisecardiac
autonomic control. Med Sci Sports Exerc 33:14961502
Zhang R, Iwasaki K, Zuckerman JH, Behbehani K, Crandall
CG,Levine BD (2002) Mechanism of blood pressure and RRvariability:
insights from ganglion blockade in humans.J Physiol (Lond)
543:337348
