Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming

Abstract

Purpose : Repeated-sprint training in hypoxia (RSH) has been shown as an efficient method for improving repeated sprint ability (RSA) in team-sport players but has not been investigated in swimming. We assessed whether RSH with arterial desaturation induced by voluntary hypoventilation at low lung volume (VHL) could improve RSA to a greater extent than the same training performed under normal breathing (NB) conditions. Methods : 16 competitive swimmers completed six sessions of repeated sprints (two sets of 16×15 m with 30 s send-off) either with VHL (RSH-VHL, n=8) or with NB (RSN, n=8). Before (pre-) and after (post-) training, performance was evaluated through an RSA test (25m all-out sprints with 35 s send-off) until exhaustion. Results : From pre- to post-, the number of sprints was significantly increased in RSH-VHL (7.1 ± 2.1 vs 9.6 ± 2.5; p<0.01) but not in RSN (8.0 ± 3.1 vs 8.7 ± 3.7; p=0.38). Maximal blood lactate concentration ([La]max) was higher at post compared to pre- in RSH-VHL (11.5 ± 3.9 vs 7.9 ± 3.7 mmol.l-137 ; p=0.04) but was unchanged in RSN (10.2 ± 2.0 vs 9.0 ± 3.5 mmol.l-138 ; p=0.34). There was a strong correlation between the increases in the number of sprints and in [La]max in RSH-VHL only (R=0.93; p<0.01).
Conclusion : Repeated sprint training in hypoxia induced by voluntary hypoventilation at low lung volume improved repeated sprint ability in swimming, probably through enhanced anaerobic glycolysis. This innovative method allows inducing benefits normally associated with hypoxia during swim training in normoxia.

Full text

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
Repeated sprint training in hypoxia induced by voluntary hypoventilation in swimming
Submission type: Original Investigation
Laurent Trincat,1 Xavier Woorons,2,3 Grégoire P. Millet1
1 ISSUL, Institute of Sport Sciences, University of Lausanne, Switzerland.
2 URePSSS, Multidisciplinary Research Unit "Sport Health & Society" – EA 7369 –
Department "Physical Activity, Muscle & Health", Lille University, France.
3 ARPEH, Association pour la Recherche et la Promotion de l'Entraînement en
Hypoventilation, Lille, France.
Contact details for the corresponding author:
Prof. Grégoire Millet
Institute of Sport Sciences (ISSUL)
Geopolis – Campus Dorigny
1015, Lausanne, Switzerland
 gregoire.millet@unil.ch
 +41 21 692 32 94
Preferred Running Head : Hypoventilation RSH in swimming
Abstract word count : 250
Main document word count : 3854
Number of figures and tables : 3 figures and 4 tables

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
ABSTRACT
Purpose: Repeated-sprint training in hypoxia (RSH) has been shown as an efficient method
for improving repeated sprint ability (RSA) in team-sport players but has not been
investigated in swimming. We assessed whether RSH with arterial desaturation induced by
voluntary hypoventilation at low lung volume (VHL) could improve RSA to a greater extent
than the same training performed under normal breathing (NB) conditions. Methods: 16
competitive swimmers completed six sessions of repeated sprints (two sets of 1615 m with
30 s send-off) either with VHL (RSH-VHL, n=8) or with NB (RSN, n=8). Before (pre-) and
after (post-) training, performance was evaluated through an RSA test (25m all-out sprints
with 35 s send-off) until exhaustion. Results: From pre- to post-, the number of sprints was
significantly increased in RSH-VHL (7.1 ± 2.1 vs 9.6 ± 2.5; p<0.01) but not in RSN (8.0 ±
3.1 vs 8.7 ± 3.7; p=0.38). Maximal blood lactate concentration ([La]max) was higher at post-
compared to pre- in RSH-VHL (11.5 ± 3.9 vs 7.9 ± 3.7 mmol.l-1; p=0.04) but was unchanged
in RSN (10.2 ± 2.0 vs 9.0 ± 3.5 mmol.l-1; p=0.34). There was a strong correlation between the
increases in the number of sprints and in [La]max in RSH-VHL only (R=0.93; p<0.01).
Conclusion: Repeated sprint training in hypoxia induced by voluntary hypoventilation at low
lung volume improved repeated sprint ability in swimming, probably through enhanced
anaerobic glycolysis. This innovative method allows inducing benefits normally associated
with hypoxia during swim training in normoxia.
Key words: RSH, swim, low pulmonary volume, saturation

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
INTRODUCTION
Over the last few years, a novel approach of hypoxic training has been investigated by
several studies.1-3 This method, the so-called repeated-sprint training in hypoxia (RSH),
consists of the repetition of short ‘all-out’ exercise bouts (<30 s) interspersed with incomplete
recoveries under hypoxic conditions. Even though experimental confirmation is needed, RSH
efficiency has been suggested to rely on the increased muscle perfusion induced by the
vasodilatory compensation associated to the hypoxia-induced reduced oxygen content. It is
now considered a different method than hypoxic training (IHT).4,5 RSH also differs from IHT
in the sense that the training intensity is maximal and therefore enables to maintain high fast-
twitch fibres (FT) recruitment. Thus, although it has recently been reported that the RSH
model may not improve sea-level performance more than the same training performed in
normoxia,6,7 it could anyway lead to a greater improvement when carried out under certain
conditions.1,2 In particular, this method has been shown to be effective for improving the
repeated-sprint ability (RSA). The number of sprints completed during an RSA test to
exhaustion was greater in cycling1 (38%) and in double poling skiing2 (58%) after as few as
six2 or eight1 training sessions of RSH. On the other hand, no improvement in RSA was
found in rugby players after RSH.3Ref_1Ref_2ref_3ref_4ref_1ref_4ref_2
One of the main difficulties inherent to hypoxic training is the access to normobaric
hypoxic facilities or devices, either for practical and financial reasons or due to the
characteristics of the sport. Some equipment8 allow training in running, cycling or even in
team-sports while in swimming, exercising in normobaric hypoxia is quite problematic.
Within the last ten years, several studies have reported that it was possible, thanks to a
technique of voluntary hypoventilation at low lung volume (VHL), to train under hypoxic
conditions without leaving sea-level or using devices that mimic altitude conditions.9-14
During biking or running exercises carried out with VHL, it has been shown that pulse

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
oxygen saturation (SpO2) could drop under 88%,11,13 a level considered as severe
hypoxaemia15 and equivalent to an altitude above 2000-m.9 Furthermore, very recently, a
study demonstrated that even in swimming, using VHL, or the so called "exhale-hold"
technique", could lead to a strong arterial desaturation and therefore could enable every
swimmer to train under hypoxic conditions14.ref_5ref_6ref_7ref_8ref_9ref_10
Implementing RSH through the VHL technique (RSH-VHL) in order to improve RSA
could be interesting for some aquatics sports. In swimming for instance, performance has
been shown to be closely related to the capacity to maintain high exercise intensities during
training.16 Moreover, in water polo, like in all terrestrial team sports, the ability to repeat
intense exercise bouts for sustained periods is essential for overall performance.17 However, it
is important to note that when exercising with VHL, the time spent at large arterial
desaturation is shorter than during the same exercise performed under real hypoxic
conditions.18 This is due to the fact that periods with normal breathing, which make SpO2
raise up again, must be interspersed with the hypoventilation periods. Consequently, during
VHL exercise, the "hypoxic dose" is lower than when exercising in an environment
impoverished in O2. However, in previous RSH studies, the overall hypoxic dose was also
very low. It is therefore unclear how the intermittent desaturation pattern occurring with VHL
would have an impact on the extent of the physiological adaptations linked to the oxidative
pathway after RSH-VHL. On the other hand, it is also noteworthy that VHL exercise elevates
the partial pressures of carbon dioxide (CO2) within the body which in turn increases blood
bicarbonate concentrations.10,12 This may have consequences on buffering capacity and could
be beneficial for pH regulation and the anaerobic metabolism capacity, as previously
reported.11 Such adaptations could be interesting for RSA since the limitation of the energy
available from the anaerobic glycolysis and the intramuscular accumulation of hydrogen ions,

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
as well as the increase in extracellular potassium, are amongst the key factors responsible for
fatigue during repeated-sprint exercise.19
So far, no study has ever investigated the effects of RSH in swimming. Also, VHL
training has never been performed at maximal velocity. The goal of the present study was
therefore to determine whether six sessions of RSH-VHL carried out in swimming could
have positive effects on repeated-sprint (RS) performance. We hypothesized that such
training would increase RSA to a greater extent than the same training carried out under
normal breathing conditions.
METHODS
Subjects
Sixteen highly-trained swimmers (9 men, 7 women) were selected to participate in
this study. Their main characteristics are presented in Table 1. Eleven of the swimmers had a
regional level whereas the other five competed at a national level. At the time of the
experiment, all swimmers had at least 9 hours per week of training in the pool plus 3 hours of
strength and conditioning training. The subjects were all non-smokers, lowlanders and not
acclimatized or recently exposed to altitude. None of them had ever used VHL training
before the study. During the protocol, the subjects were asked to avoid any exposure to an
altitude of more than 1500-m. Prior to the experiment, all swimmers carried out a medical
test and none of them had any sign of respiratory, pulmonary or cardiovascular disease.
Written voluntary informed consent was obtained from the subjects (or their parents it they
were minors) before participation and the study was approved by the institutional ethics
committee.

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
Study design
The experimental protocol consisted in performing one testing session before (pre-)
and after (post-) a specific RS training period of two weeks (six specific sessions). The
subjects were matched into pairs for gender and performance level and then randomly
assigned to the group with RS training in normoxia (RSN, n=8) or in hypoxia induced by
VHL (RSH-VHL, n=8) (Table 1). Before the experiment, a lead-in period was carried out
over four sessions in order to standardize the swimmers’ training and familiarize them with
VHL technique as well as the equipment used for the measurements. All testing and training
sessions were conducted in the same 25-m swimming pool (altitude: 417-m; water
temperature: 27°C).
Training protocol
Within six specific swimming sessions, and over a 2-week period, swimmers had to
complete, after a 1500-m standardized warm-up, two sets of 1615 m all-out front crawl
sprints, each 15-m repetition starting every 30 s. Both sets were separated by 20 min of active
recovery at low intensity. The RSN group performed the two sets with normal breathing (NB)
while the RSH-VHL group completed the sets with VHL. To perform the VHL technique,
which was well described in a previous study,14 swimmers were asked to exhale down to
functional residual capacity or a little below just before starting each 15-m sprint. Then they
had to push off the wall, glide and swim by trying to hold their breath up to the end of the 15
m. If they were not capable to do so, they were allowed to take an inhalation after exhaling
the remaining air from the lungs and reproduce the same exhale-hold procedure to finish the
sprint. At the end of each 15-m sprint, the swimmers of both groups completed the remaining
10 m at low pace while breathing normally and then recovered passively along the wall till
the next sprint. The specific swimming sessions including the RS were separated by 48-72 h.

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
The other training sessions of the week were generally performed at low intensity, near the
first ventilatory threshold.
Testing protocol
Two days before and two days after the two-week training period, swimmers of both
groups participated in one testing session including an RSA test. For the 48 h prior to each
testing session, subjects refrained from high-intensity training and exhaustive activity and
were requested to sleep at least 8 h the night before. Furthermore, they were asked to
maintain their usual diet during the intervention period, to avoid caffeine and alcohol in the
24 h preceding the measurements and to arrive at the testing sessions in a rested and hydrated
state, at least 3 h postprandial. Each subject performed the two testing sessions at the same
time and day of the week. After the same 1500-m standardized warm-up as during the RS
training sessions, they performed a single 25-m all-out sprint followed, after 3 min of
recovery at low intensity, by a second 25-m sprint. Reference velocity (RV) was calculated
from the best time recorded over the two sprints. The RSA test started after a 10-min swim
period at low intensity. It consisted of the repetition of 25-m all-out front crawl sprints with
NB. Each 25-m repetition started every 35 s so that the (passive) recovery period was about
20 s. To avoid any protective pacing strategy, subjects were requested to reach at least 98%
of the RV over the first sprint, which was the case in all of them. Then, over the following
sprints, task failure was declared when swimmers did not reach, for the second time, at least
94% of RV. Subjects were given very strong verbal encouragement over the whole test to
complete as many sprints as possible. They were never told about the criterion for task failure
and were never given any indication on the number of sprints performed.

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
Measurements
Testing data
Performance
During the RSA test, time performance of each sprint was simultaneously measured
by two experienced timekeepers. It is important to mention that in multiple experienced
timers, the error in hand timing has been shown to be very low (e.g., mean error
corresponding to -0.04 - 0.05 s) and intraclass correlation values between hand and electronic
timing is high (~0.98-0.99).20 The mean value of both measurements was recorded and sprint
velocity (SV) was calculated a posteriori. Maximal SV (SVmax) and the total number of
sprints test were assessed at pre- and post- in both groups.
Fatigue score
To assess fatigue during the RSA test, we used the percentage decrement score (Sdec)
which has been shown to be the most valid and reliable measure for quantifying fatigue in
this kind of test.19 The following formula was used:
 Sdec (%) = (100(total sprint time/ideal sprint time))-100
o Where :
 Total sprint time = sum of sprint times from all sprints.
 Ideal sprint time = number of sprintsfastest sprint time.
Blood lactate concentration ([La]) and rating of perceived exertion (RPE)
Just after the end of the RSA test, we asked the swimmers to evaluate RPE using the
Borg scale (0-10).21 Then at the first and third minute following the test, blood sample (5 µl)
was collected at the earlobe to measure [La] (Lactate Pro, Akray, Japan). The highest values
of the two samples was recorded as the maximal [La] ([La]max).

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
Training data
To assess and compare the physiological effects of the two RS modalities (i.e. with
VHL vs NB), we performed several measurements during one set of 1615 m all-out sprint in
each subject. SpO2 and heart rate (HR) were continuously measured via a pulse oximeter
(Nellcor N-595, Pleasanton, CA, USA). We used the adhesive forehead sensor Max-Fast
(Nellcor, Pleasanton, CA, USA) which was waterproofed to allow its utilization in the pool as
validated and fully described previously.14 Time performance of each sprint was also
measured during the same set to obtain SVmax and Sdec. Finally, we assessed [La] and RPE at
the end of the set.
Statistics
Data are presented as mean ± SD. The effect of treatment (RSH-VHL vs RSN) and
time (pre- vs. post-) was assessed for each of the variables using a two-way ANOVA for
repeated measures. When a significant effect was found, the Bonferroni post hoc procedure
was performed to localize the difference. Pearson linear regression analysis was performed to
find any potential linear relationship between the change in the number of sprints and the
change in [La]max during the RSA test. ANOVA for repeated measures and Student t-tests
were also used to compare the variables measured during the training sessions in both groups.
All analyses were made with Sigmastat 3.5 software (Systat Software, CA, USA). Null
hypothesis was rejected at p<0.05.
RESULTS
All subjects of both groups completed the six specific training sessions within the
two-week period. The total amount of swim training performed between the two testing
sessions was not different between RSN and RSH (number of training sessions: 11.4±0.5 vs

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
11.4±0.5; total duration: 18.5±1.7 h vs 18.6±1.8 h; total distance: 41.5±4.0 km vs 42.9±5.4
km).
Testing data
Performance and fatigue score
The results are presented in Table 2 and Figure 1. There was no difference in RV
between groups both at pre- and post-. Likewise, during the RSA test, the total number of
sprints, SVmax and Sdec were not different between RSN and RSH-VHL at the two testing
sessions. The two-way Anova showed a significant time effect for the number of sprints (p =
0.015). The post-hoc test revealed a significant increase in RSH-VHL (p < 0.01) but not in
RSN (p = 0.38). On the other hand, despite a significant time effect for SVmax (p=0.04), the
post-hoc test showed no difference in this variable at post- compared to pre- in the two
groups. Finally RV increased in both groups (p=0.03) after the training period whereas there
was no change in Sdec.
Blood lactate concentration and RPE
Due to technical problems, [La] could not be measured in two subjects (one in each
group). The two-way ANOVA showed no group effect for [La]max and RPE at the end of the
RSA test. On the other hand, there was a time effect for [La]max which was higher at post-
compared to pre- in RSH-VHL (p=0.04) and unchanged in RSN (p=0.34) (Figure 2). There
was a significant correlation between the change in the number of sprints and the change in
[La]max over the RSA test in RSH-VHL (R=0.93; p<0.01; n=7) but not in RSN (R=0.53;
p=0.23; n=7). From pre- to post-, there was no difference in RPE in either group.
Training data
Of interest is the large decrease in SpO2 observable from the start of the set for each
sprint in RSH-VHL (Figure 3). There was no difference between both groups in any of the

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
variables measured during one set of 1615 m except for Sdec (Table 3) which was lower in
RSH-VHL than in RSN (p=0.03) and time at various level of SpO2 (Table 4).
DISCUSSION
This study was the first to investigate the effects of a particular form of RSH in
swimming, in which hypoxia was induced by hypoventilation. It was also the first to use
VHL during repeated-sprint exercise. The main finding was that six sessions of RSH-VHL
could significantly improve RSA performance in swimming (i.e. number of sprints) while the
same training carried out in normoxia and under normal breathing conditions did not modify
RSA. A second original result was that RSH-VHL, unlike RSN, led to a higher [La]max and
therefore probably to a greater energy supply from the anaerobic glycolysis.
The 35% increase in the number of sprints after RSH-VHL in swimming is in line
with the results reported very recently after RSH in cyclists (38%).1 On the other hand,
competitive cross country skiers were capable of performing 58% more sprints during an
RSA test after only six sessions of RS under normobaric hypoxia.2 The authors explained the
greater efficiency of RSH in skiers than in cyclists by the fact that the upper arm muscles
contain a high proportion of FT.22,23 Yet the physiological adaptations induced by RSH that
are determinant for performance have been shown to take place in FT.5 In swimming,
propulsion is generated mainly from the upper-body muscle groups24 known for their high FT
proportion.25 However, the mean power related in front crawl26 could be lower than in double
poling.2 This may partly explain why, in the present study, the increase in the number of
sprints to exhaustion was less than in skiers2 and closer to the results reported in cyclists.1
In addition, the work-to-rest ratio is known for being paramount for the effectiveness
of RS, especially in hypoxia,27 since it determines to a large extent28 the oxidative vs
glycolytic contribution and the type of muscle fibre that are recruited. In previous studies

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
where RSH was efficient,1,2 the ratio was 1:2. In the present study, sprint and recovery
durations were ~9 s and ~21 s respectively during training sessions and ~13 s and ~22 s
during the RSA tests. Therefore the ratio was close to 1:2 and similar to the above-mentioned
studies.1,2 However, one cannot rule out that the benefits induced by RSH-VHL might have
been different with another ratio. Since the RSH studies that used a 1:5 ratio did not report
any RSA improvement,3,6,7 it is doubtful that such low ratio could lead to a more effective
RSH intervention. On the other hand, slightly increasing the recovery during RSH-VHL
(ratio ~1:3) might have helped maintain a maximal intensity during the all set. It is indeed
noticeable that swimmers who performed the set with VHL had a lower Sdec, and therefore a
reduced fatigue than the RSN group. This was probably the consequence of a conservative
pacing in order to finish the set that was perceived as challenging.
The data recorded during training demonstrate that it is possible to create an
intermittent hypoxic condition when using VHL during a swimming RS session. On average,
over the whole set, SpO2 dropped below 84% in most of the sprints (Figure 3). Such an
arterial desaturation had never been reported so far by studies dealing with VHL exercise.
The minimum level of SpO2 was even slightly lower than what was reported in a recent RSH
study.2 However, it is important to note that swimmers reached their minimum saturation
level for only a few seconds during each sprint. Furthermore, unlike in RSH (i.e. in
normobaric hypoxia), the subjects were not in hypoxic conditions during the recovery periods
since they had to breathe normally. Thus, over the whole set (including the periods of
recovery with NB), the mean SpO2 was 94.5%. Therefore, although high levels of
desaturation were reached, the overall duration sustained at SpO2 < 88% was very low (Table
4) which might have impacted on the physiological adaptations.
In particular, it is questionable whether RSH-VHL could lead to a large improvement
in muscle perfusion, as suggested after RSH.1,2 This adaptation has been proposed as a

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
determinant factor of RSA on the indirect basis (near infrared spectroscopy; NIRS) of
increased variation of muscle deoxygenation/reoxygenation during sprint/recovery. Indeed,
an enhanced O2 availability speeds up the rate of Pcr resynthesis,29 which has been shown to
be paramount in the maintenance of power production during RS.30 Unfortunately, because
there is no near infrared spectroscopy method suitable for aquatic movements, it was not
possible to verify whether the hypoxic effect of RSH-VHL may have increased muscle
oxygenation as much as after RSH. However, on the basis of recent findings, the higher the
severity of the hypoxic stress may not be the better for improving RS performance as
simulated altitudes of 4000m or above may negatively impact on the quality of training.31,32
Anyway, according to the fact that the performance gain obtained after both approaches was
rather similar, if the extent of the physiological adaptations aforementioned had been lower
after RSH-VHL than after RSH, this should have been compensated by other factors.
Interestingly, a physiological change that occurred only after RSH-VHL and that has
not been reported so far in any of the RSH studies is an increase in [La]max. This finding is
noteworthy because it suggests that using VHL instead of normobaric hypoxia to create
hypoxic conditions could enhance the anaerobic glycolysis. Recently it was shown that high-
intensity swimming exercise with VHL induced a higher [La] than the same exercise carried
out with NB.14 This phenomenon was probably the result of the fall in tissue oxygenation that
occurs during this kind of exercise and that consequently leads to a greater reliance upon non-
oxidative metabolism.12 This is certainly the reason why repeatedly performing exercises
with VHL has positive effects on the anaerobic glycolysis, as suggested before.11,14 In the
present study, based on the significant relationship between the change in [La]max and in the
number of sprints, it is likely that enhanced maximal glycogenolytic and glycolytic rates
played a role in the RSA improvement. This assumption is reinforced by a latest published
study which has found that VHL training at supramaximal intensity could significantly

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
improve performance in swimming,33 partly through an increased anaerobic glycolysis
activity. However, in the context of repeated-sprint exercise, the contribution of anaerobic
glycolysis has to be tempered since it is dependent upon exercise mode, muscle
group/composition, sprint duration and work-to-rest-interval.30
One may argue that the outcome of this study was limited by the fact that swimmers
were not blinded. It could for instance be assumed that the increase in both RS performance
and [La]max were the result of a placebo effect instead of physiological modifications. This
problem is recurrent when dealing with voluntary hypoventilation since the studies cannot be
conducted single-or double-blind. However, while a psychological effect cannot be ruled out
in the present study, it is important to note that swimmers were not aware or given any
information about the effects of VHL training. Another limitation of the present study was
that few physiological variables were measured, mainly because of the constraints of the
aquatic environment and the maximal velocity of the swimmers. Consequently, it was
difficult to fully determine the factors that led to an improvement in RS performance after
RSH-VHL. Since VHL, unlike RSH, also leads to hypercapnia and elevated blood
bicarbonate concentration,10,12 it is possible that other physiological adaptations, such as
better buffering capacity, have been involved in the increased performance. In particular, it
would have been interesting to assess whether RSH-VHL could increase the capacity for pH
regulation, a physiological adaptation that has already been reported after RSH1 or VHL
training11 and that was shown to be an important factor of RSA.34
Practical applications
A greater capacity to repeat short bouts of exercise at maximal velocity could be
valuable in most aquatics sports, such as swimming or water polo. In the former, training
intensity has been shown to be the key factor for improving performance in elite swimmers16

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
and it is well established that RSA constitutes an important factor of performance in team
sports.17 Using VHL to implement an RSH could thus be useful also in these sports.
However, few criteria seem to be useful for performing RSH-VHL. First, the effectiveness of
RS, especially in hypoxia, seems to depend on a work-to-rest ratio close to 1:2. Second, it is
probable that shorter bouts and sets would be more efficient and less psychologically
demanding. Finally, an adequate dosage and combination with the other forms of training is
required.18
In summary, this study showed for the first time that RSH-VHL could be an effective
method for improving RSA in swimming. The increase in performance occurred after only
six sessions over a two-week period. RSH-VHL also led to a greater anaerobic glycolysis
activity, which seems to have played a role in the improved RSA. Further studies are needed
to assess whether similar results could be obtained in non-aquatic sports and to determine the
physiological modifications induced by this novel approach of hypoxic training.
ACKNOWLEDGEMENTS
The authors would like to thank Nicolas Tcheng, swimming coach, for his technical
assistance. The authors declare no conflict of interest.

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
REFERENCES
1. Faiss R, Léger B, Vesin J-M, et al. Significant molecular and systemic adaptations
after repeated sprint training in hypoxia. PLoS ONE. 2013;8(2):e56522.
2. Faiss R, Willis S, Born D-P, et al. Repeated double-poling sprint training in hypoxia
by competitive cross-country skiers. Med Sci Sports Exerc. 2015;47(4):809-817.
3. Galvin HM, Cooke K, Sumners DP, Mileva KN, Bowtell JL. Repeated sprint training
in normobaric hypoxia. Br J Sports Med. 2013;47 Suppl 1(Suppl_1):i74-i79.
4. Millet GP, Faiss R, Brocherie F, Girard O. Hypoxic training and team sports: a
challenge to traditional methods? Br J Sports Med. 2013;47(Suppl_1):i6-i7.
5. Faiss R, Girard O, Millet GP. Advancing hypoxic training in team sports: from
intermittent hypoxic training to repeated sprint training in hypoxia. Br J Sports Med.
2013;47(Suppl_1):i45-i50.
6. Goods PSR, Dawson B, Landers GJ, Gore CJ, Peeling P. No Additional Benefit of
Repeat-Sprint Training in Hypoxia than in Normoxia on Sea-Level Repeat-Sprint
Ability. J Sports Sci Med. 2015;14(3):681-688.
7. Brocherie F, Girard O, Faiss R, Millet GP. High-intensity intermittent training in
hypoxia: a double-blinded, placebo-controlled field study in youth football players. J
Strength Cond Res. 2015;29(1):226-237.
8. Girard O, Brocherie F, Millet GP. On the use of mobile inflatable hypoxic marquees
for sport-specific altitude training in team sports. Br J Sports Med. 2013;47 Suppl
1(Suppl_1):i121-i123.
9. Woorons X, Mollard P, Pichon A, Lamberto C, Duvallet A, Richalet J-P. Moderate
exercise in hypoxia induces a greater arterial desaturation in trained than untrained
men. Scand J Med Sci Sports. 2007;17(4):431-436.
10. Woorons X, Mollard P, Pichon A, Duvallet A, Richalet JP, Lamberto C. Prolonged
expiration down to residual volume leads to severe arterial hypoxemia in athletes
during submaximal exercise. Respir Physiol Neurobiol. 2007;158(1):75-82.
11. Woorons X, Mollard P, Pichon A, Duvallet A, Richalet JP, Lamberto C. Effects of a 4-
week training with voluntary hypoventilation carried out at low pulmonary volumes.
Respir Physiol Neurobiol. 2008;160(2):123-130.
12. Woorons X, Bourdillon N, Vandewalle H, et al. Exercise with hypoventilation induces
lower muscle oxygenation and higher blood lactate concentration: role of hypoxia and
hypercapnia. Eur J Appl Physiol. 2010;110(2):367-377.
13. Woorons X, Bourdillon N, Lamberto C, et al. Cardiovascular responses during
hypoventilation at exercise. Int J Sports Med. 2011;32(6):438-445.

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
14. Woorons X, Gamelin F-X, Lamberto C, Pichon A, Richalet JP. Swimmers can train in
hypoxia at sea level through voluntary hypoventilation. Respir Physiol Neurobiol.
2014;190:33-39.
15. Dempsey JA, Wagner PD. Exercise-induced arterial hypoxemia. J Appl Physiol.
1999;87:1997-2006.
16. Mujika I, Chatard J-C, Busso T, Geyssant A, Barale F, Lacoste L. Effects of Training
on Performance in Competitive Swimming. Can J Appl Physiol. 1995;20(4):395-406.
17. Bishop D, Girard O, Mendez-Villanueva A. Repeated-sprint ability - part II:
recommendations for training. Sports Med. 2011;41(9):741-756.
18. Woorons X. Hypoventilation Training, Push Your Limits! (Arpeh, ed.). 2014.
19. Glaister M, Howatson G, Pattison JR, McInnes G. The reliability and validity of
fatigue measures during multiple-sprint work: an issue revisited. J Strength Cond Res.
2008;22(5):1597-1601.
20. Hetzler RK, Stickley CD, Lundquist KM, Kimura IF. Reliability and accuracy of
handheld stopwatches compared with electronic timing in measuring sprint
performance. J Strength Cond Res. 2008;22(6):1969-1976.
21. Borg G. Borg's Perceived Exertion and Pain Scales. Human Kinetics 1; 1998.
22. Mygind E. Fibre characteristics and enzyme levels of arm and leg muscles in elite
cross-country skiers. Scand J Med Sci Sports. 1995;5(2):76-80.
23. Sanchís-Moysi J, Idoate F, Olmedillas H, et al. The upper extremity of the professional
tennis player: muscle volumes, fiber-type distribution and muscle strength. Scand J
Med Sci Sports. 2010;20(3):524-534.
24. Deschodt VJ, Arsac LM, Rouard AH. Relative contribution of arms and legs in
humans to propulsion in 25-m sprint front-crawl swimming. Eur J Appl Physiol Occup
Phys. 1999;80(3):192-199.
25. Johnson MA, Polgar J, Weightman D, Appleton D. Data on the distribution of fibre
types in thirty-six human muscles. An autopsy study. J Neuro Sci. 1973;18(1):111-
129.
26. Dominguez-Castells R, Izquierdo M, Arellano R. An updated protocol to assess arm
swimming power in front crawl. Int J Sports Med. 2013;34(4):324-329.
27. Millet GP, Faiss R. Hypoxic conditions and exercise-to-rest ratio are likely paramount.
Sports Med. 2012;42(12):1081–3–authorreply1083–5.
28. Balsom PD, Seger JY, Sjödin B, Ekblom B. Physiological responses to maximal
intensity intermittent exercise. Eur J Appl Physiol Occup Phys. 1992;65(2):144-149.
29. Haseler LJ, Hogan MC. Skeletal muscle phosphocreatine recovery in exercise-trained
humans is dependent on O2availability. J Appl Physiol. 1999.

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
30. Girard O, Mendez-Villanueva A, Bishop D. Repeated-sprint ability - part I: factors
contributing to fatigue. Sports Med. 2011;41(8):673-694.
31. Goods P SR, Dawson BT, Landers GJ, Gore CJ, Peeling P. Effect of different
simulated altitudes on repeat-sprint performance in team-sport athletes. Int J Sports
Physiol Perform. 2014;9(5):857-862.
32. Bowtell JL, Cooke K, Turner R, Mileva KN, Sumners DP. Acute physiological and
performance responses to repeated sprints in varying degrees of hypoxia. J Sci Med
Sport. 2014;17(4):399-403.
33. Woorons X, Mucci P, Richalet JP, Pichon A. Hypoventilation Training at
Supramaximal Intensity Improves Swimming Performance. Med Sci Sports Exerc.
January 2016:1.
34. Bishop D, Edge J, Goodman C. Muscle buffer capacity and aerobic fitness are
associated with repeated-sprint ability in women. Eur J Appl Physiol. 2004;92(4-
5):540-547.

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
Figure 1: Average velocity in successive sprints during the repeated-sprint test before (pre-)
and after (post-) repeated-sprint training in hypoxia induced by voluntary hypoventilation at
low lung volume (RSH-VHL) or in normoxia with normal breathing (RSN). ** p < 0.01 for
difference with pre-; # p < 0.05 for difference with pre- sprint 7.

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
Figure 2: Maximal blood lactate concentration ([La]max) measured after the repeated-sprint
test before (pre-) and after (post-) repeated-sprint training in hypoxia induced by voluntary
hypoventilation at low lung volume (RSH-VHL) or in normoxia with normal breathing
(RSN). * p < 0.05 for difference with pre-.

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
Figure 3: Curves : kinetics of arterial oxygen saturation (SpO2) (A) and heart rate (HR) (B)
during one set of 16 x 15-m swimming sprints performed in hypoxia induced by voluntary
hypoventilation at low lung volume (RSH-VHL, straight line) or in normoxia with normal
breathing (RSN, dotted line). Bars : mean SpO2 (A) and HR (B) over the whole set in RSN
and RSH-VHL. ** p < 0.01 for difference with RSN.

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
Table 1 – Subjects characteristics
RSH-VHL
RSN
Number of subjects
8
8
Age (year)
15.6 ± 1.8
15.5 ± 1.9
Gender
4 female / 4 male
3 female / 5 male
Height (cm)
168 ± 6
174 ± 11
Weight (kg)
55 ± 8
64 ± 10
Level (FINA points 2014)
481 ± 106
442 ± 86
Values are mean ± SD.
Table 2 – Data of the repeated-sprint test before (pre-) and after (post-) repeated sprint
training in hypoxia induced by voluntary hypoventilation at low lung volume (RSH-VHL)
and in normoxia (RSN).
RSH-VHL
RSN
pre-
post-
pre-
post-
RV (m.s-1)
1.77  0.09
1.80  0.08*
1.77  0.11
1.80  0.12*
Total number of sprints
7.1  2.1
9.6  2.5**
8.0  3.1
8.7  3.7
SVmax (m.s-1)
1.75  0.09
1.77  0.08
1.76  0.10
1.79  0.11
Sdec
4.7  0.8
4.9  1.4
4.9  1.5
4.4  1.0
RPE (0–10)
8.3  1.3
8.6  1.1
8.6  0.8
9.2  0.7
Values are mean ± SD. RV, reference velocity; SVmax, maximal sprint velocity; Sdec,
percentage decrement score; RPE, rate of perceived exertion (Borg 0-10 scale). *p<0.05,
**p<0.01 for difference with pre-.

“Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming”
by Trincat L, Woorons X, Millet GP
International Journal of Sports Physiology and Performance
© 2016 Human Kinetics, Inc.
Table 3 – Training data recorded during one set of 16 x 15-m sprints performed in hypoxia
induced by voluntary hypoventilation at low lung volume (RSH-VHL) and in normoxia
(RSN).
RSH-VHL
RSN
First sprint velocity (m.s-1)
1.76  0.09
1.89  0.15
SVmax (m.s-1)
1.82  0.09
1.90  0.15
Sdec
1.0  3.7*
4.6  1.8
Lamax (mmol.l-1)
5.7  2.2
4.4  1.9
RPE (0–10)
8.5  1.0
8.2  1.3
HR (bpm)
157  21
162  23
Values are mean ± SD. SVmax, maximal sprint velocity ; Sdec, percentage decrement score ;
[La]max, maximal blood lactate concentration after repeated sprint set; RPE, rate of perceived
exertion (Borg 0-10 scale) ; HR, heart rate. *p<0.05 for difference with RSN.
Table 4 – Arterial oxygen saturation (SpO2) values recorded during one set of 16 x 15-m
sprints performed in hypoxia induced by voluntary hypoventilation at low lung volume
(RSH-VHL) and in normoxia (RSN).
Time (s)
Training (%)
RSH-VHL
RSN
RSH-VHL
RSN
SpO2 > 88%
Time at SpO2 > 98%
102  0.4**
216  0.3
88%
100%
95% < Time at SpO2  98%
324  0.9**
402  0.8
92.5% < Time at SpO2  95%
56  0.8**
6  0.6
90% < Time at SpO2  92.5%
24  0.7**
2  0.0
88% < Time at SpO2  90%
40  0.6**
0
SpO2 
88%
85% < Time at SpO2  88%
38  0.9**
0
12%
(80 s)
0%
82.5% < Time at SpO2  85%
34  0.7**
0
80% < Time at SpO2  82.5%
8  0.4**
0
Time at SpO2  80%
0
0
Values are mean ± SD. *p<0.05, **p<0.01 for difference with RSN.