Effect of Acute Exposure to Moderate Altitude on Muscle Power: Hypobaric Hypoxia vs. Normobaric Hypoxia
Effect of Acute Exposure to Moderate Altitude on Muscle Power: Hypobaric Hypoxia vs. Normobaric Hypoxia
Bele n Feriche 0 3 4
Amador Garca-Ramos 0 3 4
Carmen Caldero n-Soto 1 3 4
Franchek 3 4
Drobnic 2 3 4
Juan G. Bonitch- Go ngora 0 3 4
Pedro A. Galilea 2 3 4
Joan Riera 2 3 4
Paulino 3 4
0 Department of Physical Education and Sport, University of Granada , Granada , Spain,
1 High Performance Centre of Sierra Nevada, High Sport Council , Granada , Spain,
2 Department of Sport Physiology, Grup d'Investigacio en el Rendiment i la Salut de l'Esportista d'Alt Nivell Esportiu del Centre D'Alt Rendiment, High Sport Council , Barcelona , Spain
3 Funding: This study has been supported by a Grant from the Ministry of education, culture and Sport of Spain, Reference 14/UPB10/07. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
4 Editor: John Calvert, Emory University , United States of America
When ascending to a higher altitude, changes in air density and oxygen levels affect the way in which explosive actions are executed. This study was designed to compare the effects of acute exposure to real or simulated moderate hypoxia on the dynamics of the force-velocity relationship observed in bench press exercise. Twenty-eight combat sports athletes were assigned to two groups and assessed on two separate occasions: G1 (n517) in conditions of normoxia (N1) and hypobaric hypoxia (HH) and G2 (n511) in conditions of normoxia (N2) and normobaric hypoxia (NH). Individual and complete force-velocity relationships in bench press were determined on each assessment day. For each exercise repetition, we obtained the mean and peak velocity and power shown by the athletes. Maximum power (Pmax) was recorded as the highest Pmean obtained across the complete force-velocity curve. Our findings indicate a significantly higher absolute load linked to Pmax (,3%) and maximal strength (1RM) (,6%) in G1 attributable to the climb to altitude (P,0.05). We also observed a stimulating effect of natural hypoxia on Pmean and Ppeak in the middle-high part of the curve (>60 kg; P,0.01) and a 7.8% mean increase in barbell displacement velocity (P,0.001). No changes in any of the variables examined were observed in G2. According to these data, we can state that acute exposure to natural moderate altitude as opposed to simulated normobaric hypoxia leads to gains in 1RM, movement velocity and power during the execution of a force-velocity curve in bench press.
During ascent to higher altitude, the partial pressure of oxygen (O2) in the air
gradually diminishes and this reduces the arterial partial pressure of O2 leading to
tissue hypoxia . It is known that endurance performance is compromised at
hypoxic enviroments and mean reductions in VO2max of 6% per 1000 m of ascent
have been described . For short-duration high-intensity activities lasting less
than 1 min, the predominant energy source is phosphorylation and non-oxidative
production of ATP . Given that explosive performance is not aerobic
dependent, short-explosive actions should not be impaired by altitude. In fact, it
was observed during the Mexico City Olympics Games in 1968 (at 2240 m) in
sprint events .
Peronnet et al.  proposed that air density decrement at altitude (,3%
reduction for each 305 m rise ) diminish the energy cost of running at high
velocities without impairing energy availability. The reduction in external
resistance to movement  and/or the modified muscle recruitment pattern due
to increased anaerobic metabolism [7, 8], could be related to this reduced energy
cost and thus improve performance in rapid actions such as throws, jumps or
blows [5, 6]. However, strength and resistance training at altitude have been
scarcely addressed in the scientific literature. Some studies have related the severe
hypoxia of high altitude (.5500 m) to muscle deterioration and reduced
muscular function [9, 10] and power , including a loss of up to 15% lean mass
, along with a reduced strength gain (26.4%) compared to that produced in
conditions of normoxia for the same training exercise .
In contrast, the effect of exposure to a real moderate altitude (20003000 m asl)
on muscle power has not yet been adequately addressed, despite this being the
altitude most athletes select for training. Recently, Scott et al. did not find an effect
of moderate and high acute simulated hypoxic stimulus (fraction of inspired
oxygen [FiO2] of 0.16 and 0.13) during a resistance high intensity in back squat
and dead lift exercises on force and power measurements . Conversely,
Chirosa et al.  reported an improvement in the force-velocity curve for half
back squat in 5 recreational athletes after rapidly ascending to an altitude of
2320 m. Using the load at which maximum power was achieved in normoxia, in
acute moderate hypoxia, 4% gains in velocity and 7% gains in power were
produced (P,0.05). Likewise, performance of 27 elite swimmers was assessed in
normoxia and at acute moderate altitude, and a small yet non-significant
improvement was recorded in 50 m front crawl time, attributed to an increase
(+3.2%; P,0.05) in velocity during the first 15 m . Also in swimming, for a
given velocity in 400 m (freestyle), Mercade et al.  noted changes in
swimming technique (ie, a 2.4% increase in cycle frequency) induced by acute
exposure to real moderate altitude, although these changes could not be correlated
with the physiological alterations that accompanied the ascent.
In general, this effect of altitude on the mechanical components of an athletes
movement has not been dealt with in detail. The available literature has mainly
addressed the hypothesis of the reduced energy cost improving isolated high speed
running times  through a reduction in aerodynamic resistance in direct
proportion to rapid displacement velocities in individuals (eg, running) or objects
(eg, hurling) [5, 6]. In contrast, we focused our study on the relationship
hypoxiamovement (eg, leg displacement) rather than on its consequence (eg, the starting
velocity of a kicked ball), opening up a new line of investigation that considers the
effects of both air composition and its resistance. Given that athletes attend
training camps at real altitude, this study aims to compare the effect of a reduction
in barometric pressure and/or changes in air composition on the capacity to
develop explosive efforts in bench press following real versus simulated acute
exposure to moderate hypoxia.
Materials and Methods
Written informed consent to participate in this study was obtained from each
subject. For individuals younger than 18 years, authorization was obtained from
their parents or legal guardian. The study protocol was consistent with the
principles outlined in the Declaration of Helsinki and was approved by the Ethics
Committee of the University of Granada.
A repeated measures design was employed with two independent groups (G1 and
G2). Subjects in both groups were tested on two occasions separated by a rest
period of 48 h. Subjects in G1 were tested first in conditions of normoxia (N1)
and then following their ascent to the High Performance Centre of Sierra Nevada
(Spain) at 2320 m asl to determine the effect of conditions of hypobaric hypoxia
(HH). Subjects in G2 were first tested in conditions of normoxia (N2) and then
after exposure to simulated normobaric hypoxia (NH) at the High Performance
Center of Sant Cugat (NE Spain). Simulated NH was achieved by breathing a
mixture of air impoverished in oxygen (15.7% FiO2) corresponding to an altitude
of 2300 m. Complete forcevelocity relationships for only-concentric bench press
(BP) were obtained on each assessment day in each subject. For each test, the
variables power and velocity using each load, maximal strength (1RM) and the
load linked to maximum power were calculated and subjected to intra- and
Twenty-eight male Olympic combat sports athletes (wrestling n516, judo n57
and taekwondo n55) voluntarily participated in the study. All subjects were in
their competition period and had participated in national and international
competitions at least since the year prior to the study outset. Sports experience
was .8 years and the athletes trained for a mean of 1018 h per week. None of the
subjects were taking drugs, medication, or dietary supplements known to
influence physical performance. Descriptive characteristics of the subjects are
provided in Table 1. A test for unpaired data detected no significant differences
between the two groups.
Subjects visited the laboratory after refraining from intense physical activity for at
least 48 h. Before the tests they undertook a standard warm up protocol consisting
of 15 min of activation, joint mobility and stretching exercises and a further warm
up in which they performed two sets of 5 repetitions at maximum velocity in BP
using a 20 kg weight (,2030% 1RM). The rest interval between sets was 3 min.
Individual forcevelocity relationships were determined via a progressive load
test in only-concentric phase BP. The starting load was 20 kg and this was
increased by 10 kg per set until the individuals 1RM. One set of 2 to 4 repetitions
was performed per load. The recovery period between sets was 3 min for velocities
>1 mNs21 or 5 min for velocities ,1 mNs21. All the tests were performed in a
Smiths machine in which the barbell was attached to both ends, with linear
bearings on two vertical bars allowing only vertical movements.
Subjects commenced the test by supporting the barbell with arms extended
above the chest. From this position, the barbell was lowered in a continuous
movement until it was around 5 cm from the chest and this position maintained
for 3 s. Next, the subjects were instructed to perform a purely concentric action as
fast as possible to return to the starting position. No bouncing, arching of the back
or launching of the barbell was allowed. Trained spotters were present when high
loads were lifted to ensure safety. Subjects were verbally encouraged to successfully
complete each exercise.
Mechanical variables were recorded using a linear position transducer (Real
Power Pro Globus, Codgne, Italy linked to a Tesys 400) and Ergo System 8.5
software. The system was fixed to the barbell such that the cable was vertically
displaced and informed of the barbell trajectory at a frequency of 1000 Hz. For
each repetition, we obtained a mean and maximum value of the velocity (V) and
power (P). Only the best repetition for each load in terms of the greatest mean
power generated (Pmean) was entered in the subsequent analysis. We established as
maximum power (Pmax), the highest Pmean recorded across the full curve. The
load corresponding to Pmax for each subject was obtained from the load-Pmean
polynomic equation constructed using data for the exercise sets comprising the
Subjects assigned to the NH test wore a silicon mask connected to an
oxygendepleting respiratory system (HYP100, Hypoxic Inc System, Shekou Shenzhen,
China) from 5 min before warm up to test completion.
Data are presented as mean standard deviation (SD). The normality of data
distribution was checked using the Shapiro-Wilk test. The influence of hypoxia
exposure for each group (pre vs. post) on each dependent variable was assessed
with paired t-tests. Performance absolute differences on each group (HH-N1 vs.
NH-N2) were used to compare hypobaric vs. normobaric hypoxia effects.
Wilcoxon and Mann-Whitney U tests were used when data was not normally
distributed. In that case, confidence intervals were estimated following
HodgesLehmans procedure. Furthermore, mean power values were extrapolated from
the force-velocity curve at fixed loads (20, 40, 60, 80 and 100% 1RM) relative to
the corresponding 1RM in each condition (N1, N2, HH and NH). The magnitude
of the main differences between comparisons was also expressed as standardized
mean difference (Cohens d effect size; ES). The criteria to interpret the magnitude
of the ES were as follows: ,0.25trivial, 0.20.65small, 0.61.25moderate, 1.2
2.05large, 24.0) very large and .45extra large . Significance was set at
P#0.05. All statistical tests were performed using SPSS version 20.0 (SPSS,
Intragroup comparisons revealed a moderate increment in 1RM (+5.73%;
ES50.3) and a small increase in the overall load corresponding to Pmax (+3.29%;
ES50.2) compared to normoxia values in G1 attributable to the subjects ascent to
a moderate altitude, whereas no differences were detected in G2 (Table 2). When
the effect of two hypoxia conditions were compared (effect of G1 vs effect of G2),
natural hypoxia only was linked to a higher RM (P50.01; ES51.1) together a
moderate increase to the load corresponding to Pmax near to signification
Tables 3 and 4 provide the values of Pmean, Ppeak and Vmean for the different
loads in G1 and G2 respectively. Comparisons of HH vs. N1 revealed significant
increases at HH in Pmean, Ppeak and Vmean from 60 kg, except in the Ppeak at 80 kg
in which the significance was border liner (P,0.08). In contrast, the same
comparison in G2 indicated no significant differences for any of the loads
Table 5 display a second analysis in which means for Pmean, Ppeak, Vmean and
Vpeak recorded for light loads (20 to 50 kg) and heavy loads (60 to 100 kg) were
compared within groups. This comparison revealed a small effect (ES50.20) from
of natural hypoxia (G1) on all the variables recorded using heavy weights
(P,0.01) and only a trivial (ES,0.20) but significant on the Vpeak generated using
1RM51 repetition maximum; Pmax5maximum power; LoadPmax5absolute load linked to maximum power; %RMPmax5percentage of 1RM linked to
maximum power; N5conditions of normoxia; H5conditions of hypoxia; G15group 1; G25group 2; P5p-value.
light weights. In contrast, under conditions of simulated hypoxia (G2) no gains
were produced in any of the variables examined.
Finally, Figure 1 shows the Pmean values recorded in the two groups for different
1RM percentages (20, 40, 60, 80 and 100% 1RM), adjusted in each case to the
normoxia 1RM or hypoxia 1RM. We observed no differences in the Pmean
values recorded in G1 (N1 vs. HH) or G2 (N2 vs. NH) at any % 1RM (i.e. hypoxia
power curve for 1RM of hypoxia vs normoxia power curve for 1RM of normoxia).
However, when the two curves were expressed relative to the normoxia 1RM,
powers in G1 were overestimated for HH vs. N1 at 80 to 100% 1RM (P,0.01). No
appreciable changes in lower % 1RM values in G1 were detected nor were any
(Data display truncated with n,5). Load (kg); Pmean5mean power; Ppeak5peak power; Vmean5mean velocity; n5number of values included in the analysis;
Cond5test conditions. N5normoxia; HH5hypobaric hypoxia. P5p-value.
(Data display truncated with n#5). Load (kg); Pmean5mean power; Ppeak5peak power; Vmean5mean velocity; n5number of values included in the analysis;
Cond5test conditions. N5normoxia; NH5normobaric hypoxia. P5p-value.
differences detected for any of the loads examined in G2. Accordingly, the % 1RM
corresponding to the Pmax recorded in conditions of HH was higher (P50.005;
ES50.8) when the load was adjusted to the 1RM recorded in conditions of
normoxia or N1 (60.053.88% 1RM), and differed from the value obtained when
the load was adjusted to the 1RM observed in conditions of hypobaric hypoxia
HH (56.944.35% 1RM). In contrast no such shift was produced in G2
Pmean5mean power; Ppeak5peak power; Vmean5mean velocity; Vpeak5peak velocity; n5number of values included in the test; Cond5test conditions.
N5normoxia; NH5normobaric hypoxia. P5p-value.
As the main finding of our study, we observed an effect on the behavior of the
force-velocity curve of acute exposure to a moderate altitude compared to
negligible effects of simulated conditions of hypoxia. Contrary to conditions of
normoxia or simulated hypoxia, real hypoxia resulted in a faster displacement
velocity of the barbell and a higher Pmean for a given workload in BP, which led to
a higher load corresponding to Pmax (+3.29%) and a gain in 1RM (+5.73%)
(P,0.05). Thus, real altitude effect improves the velocity of a loaded movement
and it seems that this effect is more linked to the reduced density of air than to
diminished availability of O2. However, the interaction effect between air pressure
decrements and O2 availability was not studied and could potentially be
responsible for the results. One of the novelties of this study was that these
changes were detected in a basic training exercise rather than in complete
competition activities or through the analysis of the trajectory of a thrown or hit
object. According to the results of our study, the loads used for training at normal
altitude cannot be translated to training programs performed at higher altitude.
This is especially true, given the relevance of locating and assessing the behavior of
maximum power for rapid force training prescription.
The aim of this study was to discriminate the influence of oxygen availability
and/or barometric pressure reduction on power and velocity performance during
a whole force-velocity curve. Although previous research has investigated whether
a period of resistance training performed while breathing normobaric hypoxic air
can induce muscle hypertrophy [19, 20], power and velocity of the movement
have not been frequently examined or controlled. Only Scott et al. ,
monitored power and force trends over 5 sets of 5 repetitions at 80% of 1RM
under acute moderate and high normobaric hypoxia, showing no differences from
normoxic conditions. However, the exposition to a real altitude improves
performance in short-duration actions such as throws, jumps, or launching
objects [5, 6]. A recent study performed with 18 young male swimmers, from the
Junior Spanish National team, revealed an average improvement of muscular
Ppeak and Vpeak of 12.071.81% and 6.561.22% respectively in overloaded
squat jump after ascent to a moderate altitude . In agreement with this
finding, the data observed for BP exercise in conditions of HH (G1) indicate a
higher Vpeak than that produced in normoxia lifting both light (2050 kg;
P,0.01) and heavy weights (60100 kg; P,0.001) (see Table 5). However,
according to mean power and velocity values attained with light weights, the
magnitude of the effect reached ,60 kg in Vpeak was trivial, which compromises
the practical value of this result. We consider that lack of changes in power and
velocity with low weights may be inherent to the nature of the exercise used in the
study. A traditional BP executed at maximum velocity comprises a breaking phase
at the end of the movement, likely due to the increased activity of the antagonist
musculature and reduced actions of agonist muscles, which avoids losing the grip
on the barbell and the stopping of movement . This deceleration diminishes
as the load lifted increases [23, 24], such that when deceleration constitutes a high
% in the repetition (,52% for light loads), large changes in Vpeak and Vmean are
needed for differences to be detected in the repetition. In contrast, the lower %
deceleration produced with heavy loads (,23%) means that small changes in
these velocities can lead to significant changes in the whole repetition . This
could justify the Pmean and Vmean increments only at loads >60 kg in real altitude
and the lack of changes when reporting mean velocity and power values attained
with light loads (Tables 35; Fig. 1). In agreement with the results of G2, Scott et
al. did not find a moderate simulated hypoxia effect (FiO2516%) on mean and
peak force and power variables during a period of high intensity resistance
Despite of limited evidence, there is increasing research examining the
physiological effects of hypoxia on resistance training. A recent review of
resistance training adaptation mechanisms described a relationship between
metabolic stress induced by the build-up of H+ or by low O2 saturation (SaO2)
and the recruitment of additional fast twitch muscle fibers . Then, one
possibility is that ascent in altitude induce an anaerobic morpho-functional
profile that improves the recruitment of high threshold motor units leading to
perform the movement faster. But in an opposite way, the lack of changes in peak
and mean power in G2 breathing air impoverished in O2 (FiO2 15.7%) questions
this idea. It is known that hypoxia and insufficient brain oxygenation reduce the
electrical activity of neurons [25, 26]. In this sense, some studies have linked
diminished oxygenation of the prefrontal cortex in conditions of acute hypoxia
(FiO2 13%, ,3500 m) to electromyographic abnormalities in the muscles
involved in 10-s sprints . However, for isolated short-burst brief actions such
as those assessed in this study (,5 s plus 35 min rest), this effect is not observed
in moderate or high normobaric hypoxia (1613% FiO2) , been needed SaO2
levels ,82% (which happened above altitudes of 3500 m asl) . In contrast,
real altitude, combining hypoxia and air density reductions, seems to improve the
force-velocity relationship in G1. An additional benefit of the natural vs.
simulated hypoxia has been also concluded in other studies after chronic
exposure. Millet et al, showed mean improvement in power output of 4.1% at real
altitude vs. 1% with artificial hypoxia. However, the main physiological
mechanisms remain unclear [28, 29], and in any case, they were not related with
the changes of the motor skill that could be associated with altitude.
No differences in Pmax under normoxic conditions were obtained between the
experimental groups. However, we observed a moderate increase in the effect of
real altitude respect the simulated in the overall load linked to Pmax (effect of G1
vs. effect of G2; ES50.7). Thus, the Pmax in normoxia and/or simulated hypoxia
was recorded for around 3% less load than when the exercise was executed under
real hypoxia. Other authors have also described that acute natural hypoxia
increases the load corresponding to Pmax by 5.6% in half squat . However, the
increased 1RM at real altitude in comparison to the simulated hypoxic conditions
(5.58%; ES51.1), determines that this effect disappears when the Pmax load is
expressed as a % of the corresponding 1RM. Figure 1 in the results shows plots of
Pmean vs. % 1RM in the different study conditions. The Pmean values obtained
differ according to the 1RM considered in each case when comparing N, HH or
NH. Under real hypoxia, 1RM underwent an increase close to 6% with respect to
the value recorded in conditions of N (P,0.01), which was not observed for NH.
By adjusting the Pmean curve using as reference the 1RM recorded for N, the
power curve is shifted upwards and to the right such that Pmean is overestimated
for loads .60% 1RM compared to the curve obtained using the 1RM observed for
HH. This finding has several practical applications that coaches need to consider
when prescribing power training at altitude. For example, if we use the same loads
for training under conditions of normoxia as we use for HH, we will be
developing more power at loads above the load linked to Pmax, and less
power using loads below that linked to Pmax, assuming the exercise is always
executed at maximum velocity.
One of the limitations of this study is that the design does not allow us to
determine whether or not there are interaction effects between the change in air
density and the low O2 pressure of the air breathed by the subject on the power
recorded. On that purpose, a third experimental condition at real altitude
breathing a 21% FiO2 should have been included. Also, this study has been
conducted after an acute exposure to hypoxia and the differences between real and
normobaric simulated hypoxic conditions might be greater after a period of
muscular power training (altitude camps normally are three weeks long). From
our results, we can conclude that breathing air with reduced O2 pressure (by
15.7%) or being naturally exposed to moderate altitude had different effects on
the variables examined. It would seem that as for conditions of normoxia,
movement velocity and load adjustment should both be considered when
planning an altitude strength training protocol since these are the real indicators
of the true load of the work undertaken. Since improved power has been linked to
better neuromuscular characteristics [30, 31], our results indicate the change in air
resistance produced when moving to a higher altitude could promote these
adaptations, allowing for the development of greater power, unlike the situation
for NH. The increasing tendency of change shown by 1RM and the load linked to
Pmax in the G1 group suggests a need to adjust the training load during weight
training sessions at altitude to avoid reducing the muscle stimulus. Thus, by
adjusting strength training loads we could help avoid the loss of muscle mass and/
or inter- and intra-muscle coordination that are common after periods of altitude
training . There is a need for longitudinal studies that will provide information
on muscle behavior following training in real conditions of hypoxia. This will
enable athletes to add to the benefits of altitude those arising from training
focused on the exercise technique and its rapid execution in sports modalities
other than endurance.
Our findings indicate that acute exposure to moderate hypoxia leads to gains in
velocity and power when executing a force-velocity curve in BP. Unlike the case
for simulated conditions of altitude, at real altitude, the load at which Pmax was
recorded was 3.3% higher, and means power values above those of normoxia for
the rest of the middle-high zone of the curve were observed for a similar absolute
load. We therefore recommend not transferring loads calculated for strength
training in conditions of normoxia to real altitude. A displacement of some 6% of
1RM in conditions of HH will reduce the training stimulus in greater proportion
as loads approach that corresponding to the maximum (1RM), movement
velocity being the best indicator of workload. The stimulating effect of hypoxia on
the speed of loaded movement in this study happened at real altitude and seems
more related to reduced air density than to reduced inspired O2, although the
main mechanism remain unclear.
The authors thank the staff of the High Performance Centre of Sierra Nevada and
the High Performance Centre of Sant Cugat for their collaboration and
commitment to this study. We also thank all athletes and coaches who selflessly
participated in this study.
Conceived and designed the experiments: BF PP CC-S FD. Performed the
experiments: BF AG-R PP CC-S JB-G FD JR PG. Analyzed the data: BF AG-R PP
CC-S JB-G FD JR PG. Contributed reagents/materials/analysis tools: BF CC-S JR
PG FD JB-G. Contributed to the writing of the manuscript: BF PP. Testing
schedule: BF JB-G FD. Data base conformation: BF PP AG-R. Statistical analysis:
BF PP AG-R FD. Discussion of the results: BF AG-R PP CC-S JB-G FD JR PG.
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