ArticlePDF Available

Repeated Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming

Authors:
  • University of Lille, Pluridisciplinary Research Unit Sport Health & Society (URePSSS)

Abstract and Figures

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.
No caption available
… 
Content may be subject to copyright.
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 1615 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 1615 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 sprintsfastest 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 1615 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 1615 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):10813authorreply10835.
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
8
8
15.6 ± 1.8
15.5 ± 1.9
4 female / 4 male
3 female / 5 male
168 ± 6
174 ± 11
55 ± 8
64 ± 10
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 (010)
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
Lamax (mmol.l-1)
5.7 2.2
4.4 1.9
RPE (010)
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.
... Few studies have investigated the effects of such LLTH methods on swimmers performance. To the best of the authors knowledge, dryland-based intermittent hypoxic training (IHT) (Czuba et al., 2017;Park et al., 2018) and in-water swimming-specific training using voluntary hypoventilation at low-lung volume (VHL) (Woorons et al., 2016;Trincat et al., 2017) or prolonged expiration and reducedfrequency breathing (Toubekis et al., 2017) have been reported. Research on IHT effects on swimmers' performance is not conclusive. ...
... Using in-water swimming-specific exercise, Woorons et al. (2016) reported that 10 sessions of 12-20 × 25 m freestyle sprint with 15 s of recovery at a pace of 200 m freestyle permitted to improve 100, 200, and 400 m freestyle performance, mainly due to an in increase in the anaerobic glycolysis. Similarly, by making the VHL method more specific to swimming, with 2 sets of 16 × 15 m "all-out, " Trincat et al. (2017) demonstrated that the number of repeated sprints performed improved but without providing information about swimming performance. Although VHL led to strong desaturation (∼88%), the "hypoxic dose" remain lower than when using systemic hypoxia (Woorons et al., 2016). ...
... Using lower hypoxic stress with RSH-VHL method, Trincat et al. (2017) showed that SpO 2 could decrease below 84% but TABLE 1 | Exercise testing maximal parameters before (pre), 7 days (post-1), and 2-weeks (post-2) after intervention. Mean ± standard deviation; VO 2max (maximal oxygen uptake), TtE (time to exhaustion), HRmax (maximal heart rate), RER (respiratory exchange ratio). ...
Article
Full-text available
The aim of this study was to investigate the effect of a 4 weeks in-water swimming-specific repeated-sprint training in hypoxia (RSH) compared to similar training in normoxia (RSN). Following a repeated-measures, counterbalanced cross-over design, 10 swimmers were requested to perform two trials consisting of in-water repeated sprints in hypoxic (RSH, simulated 4,040 m; FiO2 = 13.7%) or normoxic (RSN, 459 m, FiO2 calibrated = 20.9%) conditions. In both conditions, 8 additional exercise including 3 sets of 5 × 15 m “all-out” sprints (corresponding to a total of 625 m), with 20 s of passive recovery between efforts and 200 m of easy swimming between sets were included at the end of their swimming program over a 4 weeks period. Hypoxic condition was generated using a simulator pumping air with lowered oxygen concentration into a facial mask. An incremental maximal test on an ergocycle, as well as 100 m and 400 m freestyle swimming performance (real competition format) were assessed before (pre), 7 days (post-1), and 2 weeks (post-2) after intervention. During training, heart rate (HR) and oxygen saturation (SpO2) were monitored. RSH showed significantly lower SpO2 (70.1 ± 4.8% vs. 96.1 ± 2.7%, P < 0.01), concomitant with higher mean HR (159 ± 11 bmp vs. 141 ± 6 bmp, P < 0.01) than RSN. No significant changes in maximal oxygen uptake, other submaximal physiological parameters, 100 or 400 m swimming performances were found. Although providing additional physiological stress, performing in-water RSH does not provide evidence for higher benefits than RSN to improve swimmers performance.
... 16,17 Although the hypoxic stimulus is not continuous when using this method, so that the physiological adaptations may not be similar to those of training in systemic hypoxia, exercise with VHL provides an additional physiological stress to produce greater or more rapid adaptations and consecutive performance enhancement compared to similar training in normoxia (i.e. with unrestricted breathing). When combined with repeated sprints, the RSH-VHL approach has proved putative benefits in swimming, 18 cycling, 19 rugby 20 and basket-ball. 21 The mechanisms induced by RSH-VHL include higher anaerobic tolerance 18,19 and oxygen uptake, 19 two major determinants of RSA performance. ...
... When combined with repeated sprints, the RSH-VHL approach has proved putative benefits in swimming, 18 cycling, 19 rugby 20 and basket-ball. 21 The mechanisms induced by RSH-VHL include higher anaerobic tolerance 18,19 and oxygen uptake, 19 two major determinants of RSA performance. 6 While it has been shown that holding breath at high lung volume during exercise could also induce severe arterial desaturation 22 and may help reduce blood acidosis and oxidative stress, 23 only the VHL technique can provoke a sufficiently fast drop in SpO 2 to perform a RSH effort. ...
... 6 While it has been shown that holding breath at high lung volume during exercise could also induce severe arterial desaturation 22 and may help reduce blood acidosis and oxidative stress, 23 only the VHL technique can provoke a sufficiently fast drop in SpO 2 to perform a RSH effort. [18][19][20][21] Due to the specific features of ice hockey (e.g. frequent shifts inducing short high-intensity sprints, partial occlusion in lower limbs occurring while skating, large neuromuscular fatigue), one may hypothesize that RSH-VHL would be particularly appropriate in ice hockey. ...
Article
This study aimed to assess the effects of an off-season period of repeated-sprint training in hypoxia induced by voluntary hypoventilation at low lung volume (RSH-VHL) on off-ice re-peated-sprint ability (RSA) in ice hockey players. Thirty-five high-level youth ice hockey players completed 10 sessions of running repeated sprints over a 5-week period, either with RSH-VHL (n =16) or with unrestricted breathing (RSN, n = 19). Before (Pre) and after (Post) the training period, subjects performed two 40-m single sprints (to obtain the reference velocity (Vref)) followed by a running RSA test (12 × 40 m all-out sprints with departure every 30 s). From Pre to Post, there was no change in Vref or in the maximal velocity reached in the RSA test in both groups. In RSH-VHL, the mean velocity of the RSA test was higher (88.9 ± 5.4 vs. 92.9 ± 3.2 % of Vref; p < 0.01) and the percentage decrement score lower (11.1 ± 5.2 vs. 7.1 ± 3.3; p < 0.01) at Post than at Pre whereas no significant change occurred in the RSN group (89.6 ± 3.3 vs. 91.3 ± 1.9 % of Vref, p =0.11; 10.4 ± 3.2 vs. 8.7 ± 2.3 %; p = 0.13). In conclusion, five weeks of off-ice RSH-VHL intervention led to a significant 4% improve-ment in off-ice RSA performance. Based on previous findings showing larger effects after shorter intervention time, the dose-response dependent effect of this innovative approach remains to be investigated.
... In turn, increased partial pressure of carbon dioxide (pCO 2 ) in the body increases the concentration of bicarbonate in the blood (Woorons et al., 2007(Woorons et al., , 2010. This may affect buffering capacity and may be beneficial for pH regulation and stimulating anaerobic metabolic efficiency, especially during intense exercise, e.g., repeated sprints (Trincat et al., 2017). ...
Article
Full-text available
Special breathing exercises performed during warm-up lead to hypercapnia and stimulation of mechanisms leading to increased exercise performance, but the effect of a device that increases the respiratory dead space volume (ARDSv) during warm-up has not been studied. The purpose of this study was to investigate the effect of 10 min warm-up with ARDSv on performance, physiological and biochemical responses during sprint interval cycling exercise (SIE). During four laboratory visits at least 72 h apart, they completed: (1) an incremental exercise test (IET) on a cycloergometer, (2) a familiarization session, and cross-over SIE sessions conducted in random order on visits (3) and (4). During one of them, 1200 mL of ARDSv was used for breathing over a 10-min warm-up. SIE consisted of 6 × 10-s all-out bouts with 4-min active recovery. Work capacity, cardiopulmonary parameters, body temperature, respiratory muscle strength, blood acid-base balance, lactate concentration, and rating of perceived exertion (RPE) were analyzed. After warm-up with ARDSv, PETCO2 was 45.0 ± 3.7 vs. 41.6 ± 2.5 (mm Hg) (p < 0.001). Body temperature was 0.6 (°C) higher after this form of warm-up (p < 0.05), bicarbonate concentration increased by 1.8 (mmol⋅L–1) (p < 0.01). As a result, work performed was 2.9% greater (p < 0.01) compared to the control condition. Respiratory muscle strength did not decreased. Warming up with added respiratory dead space volume mask prior to cycling SIE produces an ergogenic effect by increasing body temperature and buffering capacity.
... In particular, the hypoxic "dose" (i.e., degree and duration of hypoxia) under this condition is greater than what has been reported in studies using non maximal EEBH (Kume et al. 2016;Woorons et al. 2010Woorons et al. , 2017Woorons et al. , 2019a. Thus, in addition to an improved anaerobic glycolysis (Trincat et al. 2017;Woorons et al. 2016Woorons et al. , 2019b and unlike what has been reported so far (Lapointe et al. 2020;Woorons et al. 2019b), physiological adaptations favourable to muscle O 2 utilisation (e.g., improved capillarisation) may actually occur after a period of training with VHL including EEBH held up to the breaking point. ...
Article
Full-text available
Purpose: The goal of this study was to assess the effects of repeated running bouts with end-expiratory breath holding (EEBH) up to the breaking point on muscle oxygenation. Methods: Eight male runners participated in three randomized sessions each including two exercises on a motorized treadmill. The first exercise consisted in performing 10-12 running bouts with EEBH of maximum duration either (separate sessions) at 60% (active recovery), 80% (passive recovery) or 100% (passive recovery) of the maximal aerobic velocity (MAV). Each repetition started at the onset of EEBH and ended at its release. In the second exercise of the session, subjects replicated the same procedure but with normal breathing (NB). Arterial oxygen saturation (SpO2), heart rate (HR) and the change in vastus lateralis muscle deoxy-haemoglobin/myoglobin (Δ[HHb/Mb]) and total haemoglobin/myoglobin (Δ[THb/Mb]) were continuously monitored throughout exercises. Results: On average, the EEBHs were maintained for 10.1 ± 1.1 s, 13.2 ± 1.8 s and 12.2 ± 1.7 s during exercise at 60%, 80% and 100% of MAV, respectively. In the three exercise intensities, SpO2 (mean nadir values: 76.3 ± 2.5 vs 94.5 ± 2.5 %) and HR were lower with EEBH than with NB at the end of the repetitions whereas the mean Δ[HHb/Mb] (12.6 ± 5.2 vs 7.7 ± 4.4 µm) and Δ[THb/Mb] (- 0.6 ± 2.3 vs 3.8 ± 2.6 µm) were respectively higher and lower with EEBH (p < 0.05). Conclusion: This study showed that performing repeated bouts of running exercises with EEBH up to the breaking point induced a large and early drop in muscle oxygenation compared with the same exercise with NB. This phenomenon was probably the consequence of the strong arterial oxygen desaturation induced by the maximal EEBHs.
... Repeated-sprint training in hypoxia has been shown to induce greater improvement of repeated-sprint performance than in normoxia (Brocherie et al., 2017). Also, repeated sprintinduced arterial desaturation through voluntary hypoventilation at low lung volume induced greater enhancement in competitive swimmers than in normoxia (Trincat et al., 2017), and the magnitude of the improvement (+35%) was comparable to that obtained with repeated sprinting in hypoxia in cycling (+38%) (Faiss et al., 2013) and in double poling cross-country skiing (+58%) (Faiss et al., 2015). Similar or even greater improvements might be expected with a regular use of the WHBM. ...
Article
Full-text available
The Wim Hof breathing method (WHBM) combines periods of hyperventilation (HV) followed by voluntary breath-holds (BH) at low lung volume. It has been increasingly adopted by coaches and their athletes to improve performance, but there was no published research on its effects. We determined the feasibility of implementing a single WHBM session before repeated sprinting performance and evaluated any acute ergogenic effects. Fifteen amateur runners performed a single WHBM session prior to a Repeated Ability Sprint Test (RAST) in comparison to voluntary HV or spontaneous breathing (SB) (control) in a randomized cross-over design. Gas exchange, heart rate, and finger pulse oxygen saturation (SpO 2) were monitored. Despite large physiological effects in the SpO 2 and expired carbon dioxide (VCO 2) levels of both HV and WHBM, no significant positive or negative condition effects were found on RAST peak power, average power, or fatigue index. Finger SpO 2 dropped to 60 ± 12% at the end of the BHs. Upon the last HV in the WHBM and HV conditions, end-tidal CO 2 partial pressure (PETCO 2) values were 19 ± 3 and 17 ± 3 mmHg, indicative of respiratory alkalosis with estimated arterial pH increases of +0.171 and of +0.181, respectively. Upon completion of RAST, 8 min cumulated expired carbon dioxide volumes in the WHBM and HV were greater than in SB, suggesting lingering carbon dioxide stores depletion. These findings indicate that despite large physiological effects, a single WHBM session does not improve anaerobic performance in repeated sprinting exercise.
... Moreover, a possible contributing factor to the increased likelihood of upper respiratory tract infections may be through breathing in cold air and cooling the body surface, which may lead to bronchoconstriction and increased vasoconstriction in the nasal passages [13]. This is particularly relevant given that swimming training largely involves intermittent breathing rhythms, contributing to transient states of hypoxia [73]. Furthermore, it has been shown that exercise training above 80% of VO 2max contributes to lymphocyte apoptosis and a decrease in circulating white blood cells [74]. ...
Article
Full-text available
Cold water swimming (winter or ice swimming) has a long tradition in northern countries. Until a few years ago, ice swimming was practiced by very few extreme athletes. For some years now, ice swimming has been held as competitions in ice-cold water (colder than 5 °C). The aim of this overview is to present the current status of benefits and risks for swimming in cold water. When cold water swimming is practiced by experienced people with good health in a regular, graded and adjusted mode, it appears to bring health benefits. However, there is a risk of death in unfamiliar people, either due to the initial neurogenic cold shock response or due to a progressive decrease in swimming efficiency or hypothermia.
... Other systemic or local LLTH methods based on the repetition of "all-out" efforts can be used to induce a potent physiological stimulus, up-regulate signaling pathways and eventually maximize performance outcomes. For instance, when hypoxia is induced by voluntary hypoventilation at low lung volume (VHL) (Trincat et al., 2017), RSH can also ameliorate performance compared to training with unrestricted breathing, as demonstrated by Lapointe et al. in basketball players. These authors reported that, after 8 RSH-VHL sessions including changes of direction, gains may be attributed to greater muscle reoxygenation, enhanced muscle recruitment strategies, and improved K + regulation to attenuate the development of muscle fatigue, especially in type-II muscle fibers. ...
... Arterial oxygen saturation (SpO 2 ) was continuously measured during S1 and S2 with Nellcor N-595 the pulse oximeter (Nellcor Inc., Pleasanton, CA, USA) and with the Max-Fast adhesive forehead sensor (Nellcor), which was applied above the right orbital area. This sensor has already been used during intense cycle exercise in hypoxia [18] and during repeated-sprint exercise with VHL [6,8,19]. An adjustable headband was placed over the forehead sensor to ensure gentle, consistent pressure on the sensor device. ...
Article
Eight well-trained male cyclists participated in two testing sessions each including two sets of 10 cycle exercise bouts at 150% of maximal aerobic power. In the first session, subjects performed the exercise bouts with end-expiratory breath holding (EEBH) of maximal duration. Each exercise bout started at the onset of EEBH and ended at its release (mean duration: 9.6±0.9 s; range: 8.6–11.1 s). At the second testing session, subjects performed the exercise bouts (same duration as in the first session) with normal breathing. Heart rate, left ventricular stroke volume (LVSV), and cardiac output were continuously measured through bio-impedancemetry. Data were analysed for the 4 s preceding and following the end of each exercise bout. LVSV (peak values: 163±33 vs. 124±17 mL, p<0.01) was higher and heart rate lower both in the end phase and in the early recovery of the exercise bouts with EEBH as compared with exercise with normal breathing. Cardiac output was generally not different between exercise conditions. This study showed that performing maximal EEBH during high-intensity exercise led to a large increase in LVSV. This phenomenon is likely explained by greater left ventricular filling as a result of an augmented filling time and decreased right ventricular volume at peak EEBH.
Thesis
La capacité à répéter des efforts de courte durée et d’intensité maximale est considérées comme un indicateur de la performance dans de nombreux sports intermittents (sports collectifs, sports d’opposition). Ce travail de thèse s’est focalisé sur l’étude de la fatigue neuromusculaire induite par une répétition de sprints et de l’impact que peut avoir l’hypoxie sur le développement de celle-ci. Il est établi qu’en condition normale l’origine de cette fatigue est d’avantage musculaire (périphérique) dès les premiers sprints alors qu’une fatigue dites centrale, correspondant à une incapacité du système nerveux centrale à recruter le muscle de manière optimale, apparait lors des derniers sprints. La réalisation de ce type d’effort en hypoxie a pour effet d’exacerber l’apparition de la fatigue, notamment centrale, de deux manières potentielles. Soit via une diminution de la quantité d’oxygène fournit au cerveau, ce qui aurait un effet direct diminuant l’activité cérébrale et donc la commande motrice nécessaire à l’exercice. Soit via la réduction de l’arrivée de l’oxygène au niveau musculaire, qui engendrerait une diminution de la part d’énergie produite par le métabolisme aérobie, qui serait redirigé vers le métabolisme anaérobie, connu pour produire davantage de déchets métaboliques. Ces derniers sont liés à des voies afférentes qui inhibe de manière indirect la commande motrice. L’un des objectifs était de pouvoir isoler ces deux mécanismes grâce à la mise en place d’une hypoxie musculaire localisée afin de voir si cela suffirait à induire une augmentation de la fatigue centrale. Les résultats présentés suggèrent que les deux types d’hypoxies diminuent la performance en sprint de manière similaire mais via des mécanismes distincts. L’hypoxie générale impact d’avantage le développement de la fatigue centrale via un effet direct sur le cerveau alors que l’hypoxie localisée augmente surtout la fatigue périphérique via l’accumulation de métabolites. Cependant la méthode utilisée dans cette étude et classiquement dans la littérature induit un délai entre la fin du sprint et la mesure de fatigue, ce qui peut induire une sous-estimation et une mauvaise interprétation de l’étiologie de celle-ci et ne permet pas d’établir une cinétique précise du développement de la fatigue. C’est pourquoi suite à cette première étude, l’objectif était de développer une méthode permettant des mesures régulières et sans délai de la fatigue neuromusculaire. Ce travail présente le développement et la validation d’un nouvel ergomètre permettant des mesures de la fonction neuromusculaire intégrées pendant un exercice de sprint répétés sur vélo.
Article
Full-text available
Purpose: This study aimed to determine whether hypoventilation training at supramaximal intensity could improve swimming performance more than the same training carried out under normal breathing conditions. Methods: Over a 5-week period, sixteen triathletes (12 men, 4 women) were asked to include twice a week into their usual swimming session one supramaximal set of 12 to 20 x 25m, performed either with hypoventilation at low lung volume (VHL group) or with normal breathing (CONT group). Before (Pre-) and after (Post-) training, all triathletes performed all-out front crawl trials over 100, 200 and 400m. Results: Time performance was significantly improved in VHL in all trials [100m: - 3.7 ± 3.7s (- 4.4 ± 4.0%); 200m: - 6.9 ± 5.0s (- 3.6 ± 2.3%); 400m: - 13.6 ± 6.1s (-3.5 ± 1.5%)] but did not change in CONT. In VHL, maximal lactate concentration (+ 2.35 ± 1.3 mmol.L-1 on average) and the rate of lactate accumulation in blood (+ 41.7 ± 39.4%) were higher at Post- than at Pre- in the three trials whereas they remained unchanged in CONT. Arterial oxygen saturation, heart rate, breathing frequency and stroke length were not altered in both groups at the end of the training period. On the other hand, stroke rate was higher at Post- compared to Pre- in VHL but was not different in CONT. The measurements of gas exchange over the 400-m trial revealed no change in peak oxygen consumption as well as in any pulmonary variable in both groups. Conclusion: This study demonstrated that VHL training, when performed at supramaximal intensity, represents an effective method for improving swimming performance, partly through an increase in the anaerobic glycolysis activity.
Book
Full-text available
This book is the result of several years of scientific research regarding an original and innovative sporting training method: hypoventilation training. Empirically applied in the 1950's by runners from Eastern Europe, among which the famous Czech athlete Emil Zatopek, hypoventilation training has been extensively utilized in swimming since the early 1970's, instigated by American trainer James Counsilman. The scientific studies undertaken over the last decade have enabled the development of a training or physical preparation method, that can be of benefit for a great number of sports requiring intense exertion: athletics, swimming, cycling, combat sports, team sports, racket sports… Athletes, trainiers, physical coaches, teachers and students of sport and physical education, as well as those involved or interested in human physical performance can find in this book how it is possible, theoretically and practically, to push one’s limit without breaking the law relating to sporting ethics, nor the need of expensive and heavy devices.
Article
Full-text available
Background/aim With the evolving boundaries of sports science and greater understanding of the driving factors in the human performance physiology, one of the limiting factors has now become the technology. The growing scientific interest on the practical application of hypoxic training for intermittent activities such as team and racket sports legitimises the development of innovative technologies serving athletes in a sport-specific setting. Methods Description of a new mobile inflatable simulated hypoxic equipment. Results The system comprises two inflatable units—that is, a tunnel and a rectangular design, each with a 215 m3 volume and a hypoxic trailer generating over 3000 Lpm of hypoxic air with FiO2 between 0.21 and 0.10 (a simulated altitude up to 5100 m). The inflatable units offer a 45 m running lane (width=1.8 m and height=2.5 m) as well as a 8 m×10 m dome tent. FiO2 is stable within a range of 0.1% in normal conditions inside the tunnel. The air supplied is very dry—typically 10–15% relative humidity. Conclusions This mobile inflatable simulated hypoxic equipment is a promising technological advance within sport sciences. It offers an opportunity for team-sport players to train under hypoxic conditions, both for repeating sprints (tunnel configuration) or small-side games (rectangular configuration).
Article
Full-text available
In 2007, Wilber1 presented the main altitude/hypoxic training methods used by elite athletes: ‘live high—train high’ (LHTH) and ‘live high—train low’ (LHTL); sleeping at altitude to gain the haematological adaptations (increased erythrocyte volume) but training at sea level to maximise performance (maintenance of sea-level training intensity and oxygen flux). The LHTL method can be accomplished through a number of methods and devices: natural/terrestrial altitude, nitrogen dilution, oxygen filtration and supplemental oxygen. Another method is the ‘live low—train high’ (LLTH) method including intermittent hypoxic exposure at rest (IHE) or during intermittent hypoxic training sessions (IHT). Noteworthy, all supporting references were conducted with endurance elite athletes (ie, cyclists, triathletes, cross-country skiers, runners, swimmers, kayakers and rowers) and there is an extensive literature relative to LHTH as well as LHTL. However, there is a lack of evidence for the applicability of these methods in team-sport athletes. In recent times, media reports have provided us with coverage of some high-profile clubs or national squads in various team-sport disciplines undertaking fitness programmes at altitude during the early preseason or in preparation of a major competition. Despite the evident observation that athletes from different team sports and from all around the world are using altitude training more than ever before, it is …
Article
Full-text available
Repeated sprint ability (RSA) is a critical success factor for intermittent sport performance. Repeated sprint training has been shown to improve RSA, we hypothesised that hypoxia would augment these training adaptations. Thirty male well-trained academy rugby union and rugby league players (18.4±1.5 years, 1.83±0.07 m, 88.1±8.9 kg) participated in this single-blind repeated sprint training study. Participants completed 12 sessions of repeated sprint training (10×6 s, 30 s recovery) over 4 weeks in either hypoxia (13% FiO2) or normoxia (21% FiO2). Pretraining and post-training, participants completed sports specific endurance and sprint field tests and a 10×6 s RSA test on a non-motorised treadmill while measuring speed, heart rate, capillary blood lactate, muscle and cerebral deoxygenation and respiratory measures. Yo-Yo Intermittent Recovery Level 1 test performance improved after RS training in both groups, but gains were significantly greater in the hypoxic (33±12%) than the normoxic group (14±10%, p<0.05). During the 10×6 s RS test there was a tendency for greater increases in oxygen consumption in the hypoxic group (hypoxic 6.9±9%, normoxic (−0.3±8.8%, p=0.06) and reductions in cerebral deoxygenation (% changes for both groups, p=0.09) after hypoxic than normoxic training. Twelve RS training sessions in hypoxia resulted in twofold greater improvements in capacity to perform repeated aerobic high intensity workout than an equivalent normoxic training. Performance gains are evident in the short term (4 weeks), a period similar to a preseason training block.
Article
To assess the impact of ‘top-up’ normoxic or hypoxic repeat-sprint training on sea-level repeat-sprint ability, thirty team sport athletes were randomly split into three groups, which were matched in running repeat-sprint ability (RSA), cycling RSA and 20 m shuttle run performance. Two groups then performed 15 maximal cycling repeat-sprint training sessions over 5 weeks, in either normoxia (NORM) or hypoxia (HYP), while a third group acted as a control (CON). In the post-training cycling RSA test, both NORM (13.6%; p = 0.0001, and 8.6%; p = 0.001) and HYP (10.3%; p = 0.007, and 4.7%; p = 0.046) significantly improved overall mean and peak power output, respectively, whereas CON did not change (1.4%; p = 0.528, and -1.1%; p = 0.571, respectively); with only NORM demonstrating a moderate effect for improved mean and peak power output compared to CON. Running RSA demonstrated no significant between group differences; however, the mean sprint times improved significantly from pre- to post-training for CON (1.1%), NORM (1.8%), and HYP (2.3%). Finally, there were no group differences in 20 m shuttle run performance. In conclusion, ‘top-up’ training improved performance in a task-specific activity (i.e. cycling); however, there was no additional benefit of conducting this ‘top-up’ training in hypoxia, since cycle RSA improved similarly in both HYP and NORM conditions. Regardless, the ‘top-up’ training had no significant impact on running RSA, therefore the use of cycle repeat-sprint training should be discouraged for team sport athletes due to limitations in specificity.
Article
Purpose: Repeated-sprint training in hypoxia (RSH) was recently shown to improve repeated-sprint ability (RSA) in cycling. This phenomenon is likely to reflect fiber type-dependent, compensatory vasodilation, and therefore, our hypothesis was that RSH is even more beneficial for activities involving upper body muscles, such as double poling during cross-country skiing. Methods: In a double-blinded fashion, 17 competitive cross-country skiers performed six sessions of repeated sprints (each consisting of four sets of five 10-s sprints, with 20-s intervals of recovery) either in normoxia (RSN, 300 m; FiO2, 20.9%; n = 8) or normobaric hypoxia (RSH, 3000 m; FiO2, 13.8 %; n = 9). Before (pre) and after (post) training, performance was evaluated with an RSA test (10-s all-out sprints-20-s recovery, until peak power output declined by 30%) and a simulated team sprint (team sprint, 3 × 3-min all-out with 3-min rest) on a double-poling ergometer. Triceps brachii oxygenation was measured by near-infrared spectroscopy. Results: From pretraining to posttraining, peak power output in the RSA was increased (P < 0.01) to the same extent (29% ± 13% vs 26% ± 18%, nonsignificant) in RSH and in RSN whereas the number of sprints performed was enhanced in RSH (10.9 ± 5.2 vs 17.1 ± 6.8, P < 0.01) but not in RSN (11.6 ± 5.3 vs 11.7 ± 4.3, nonsignificant). In addition, the amplitude in total hemoglobin variations during sprints throughout RSA rose more in RSH (P < 0.01). Similarly, the average power output during all team sprints improved by 11% ± 9% in RSH and 15% ± 7% in RSN. Conclusions: Our findings reveal greater improvement in the performance of repeated double-poling sprints, together with larger variations in the perfusion of upper body muscles in RSH compared with those in RSN.
Article
This study examined the effects of 5 weeks (∼60 min/training, 2 days/week) of run-based high-intensity, repeated-sprint ability and explosive strength / agility / sprint training in either normobaric hypoxia (RSH; FIO2 14.3%) or in normoxia (RSN; FIO2 21.0%) on physical performance in 16 highly-trained, under-18 male footballers. For both RSH (n = 8) and RSN (n = 8) groups, lower limb explosive power, sprinting (10 to 40 m) times, maximal aerobic speed, repeated-sprint (10 x 30 m, 30-s rest) and repeated-agility (6 x 20 m, 30-s rest) abilities were evaluated in normoxia before and after supervised training. Lower limb explosive power (+6.5±1.9% vs. +5.0±7.6% for RSH and RSN, respectively; both P<0.001) and performance during maximal sprinting increased (from -6.6±2.2% vs. -4.3±2.6% at 10 m to -1.7±1.7% vs. -1.3±2.3% at 40m for RSH and RSN, respectively; P values ranging from <0.05 to <0.01) to a similar extent in RSH and RSN. Both groups improved best (-3.0±1.7% vs. -2.3±1.8%; both P<0.05) and mean (-3.2±1.7%, P<0.01 vs. -1.9±2.6%, P<0.05 for RSH and RSN, respectively) repeated-sprint times, while sprint decrement did not change. Significant interactions effects (P<0.05) between condition and time were found for repeated-agility ability related-parameters with very likely greater gains (P<0.05) for RSH than RSN (initial sprint: 4.4±1.9% vs. 2.0±1.7% and cumulated times: 4.3±0.6% vs. 2.4±1.7%). Maximal aerobic speed remained unchanged throughout the protocol. In youth highly-trained football players, the addition of ten repeated-sprint training sessions performed in hypoxia vs. normoxia to their regular football practice over a 5-week in-season period was more efficient at enhancing repeated-agility ability (including direction changes), while it had no additional effect on improvements in lower limb explosive power, maximal sprinting and repeated-sprint ability performance.
Article
This study aimed to assess the impact of three simulated altitude exposure heights on repeat sprint performance in team sport athletes. Ten trained male team sport athletes completed three sets of repeated sprints (9 x 4 s) on a non-motorised treadmill at sea-level or at simulated altitudes of 2000, 3000 and 4000 m. Participants completed four trials in a random order over 4 weeks, with mean power output (MPO), peak power output (PPO), blood lactate concentration (BLa) and oxygen saturation (SaO2) recorded after each set. Each increase in simulated altitude corresponded with a significant decrease in SaO2. Total work across all sets was highest at sea-level and correspondingly lower at each successive altitude (p<0.05; sea level < 2000 m < 3000 m < 4000 m). In the first set, MPO was reduced only at 4000 m, but for subsequent sets, decreases in MPO were observed at all altitudes (p<0.05; 2000 m < 3000 m < 4000 m). PPO was maintained in all sets except for set 3 at 4000 m (p<0.05, vs sea level and 2000 m). BLa levels were highest at 4000 m and significantly greater (p<0.05) than at sea-level after all sets. These results suggest that 'higher may not be better', as a simulated altitude of 4000 m may potentially blunt absolute training quality. Therefore, it is recommended that a moderate simulated altitude (2000-3000 m) be employed when implementing intermittent hypoxic repeat sprint training for team sport athletes.