International  Journal  of
Environmental Research
and Public Health
Communication
Effects of Acute Hypoxia on Lactate Thresholds and
High-Intensity Endurance Performance—A Pilot Study
Martin Faulhaber 1,2,*, Katharina Gröbner 1, Linda Rausch 1
, Hannes Gatterer 3
and Verena Menz 1


Citation: Faulhaber, M.; Gröbner, K.;
Rausch, L.; Gatterer, H.; Menz, V.
Effects of Acute Hypoxia on Lactate
Thresholds and High-Intensity
Endurance Performance—A Pilot
Study. Int. J. Environ. Res. Public
Health 2021, 18, 7573. https://
doi.org/10.3390/ijerph18147573
Academic Editors: Zbigniew
Jastrz˛ebski, Guillermo Felipe López
Sánchez, Łukasz Radzimi´nski and
Maria Skalska
Received: 8 June 2021
Accepted: 13 July 2021
Published: 16 July 2021
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1
Department of Sport Science, University Innsbruck, 6020 Innsbruck, Austria;
K.Groebner@student.uibk.ac.at (K.G.); Linda.Rausch@uibk.ac.at (L.R.); Verena.Menz@uibk.ac.at (V.M.)
2
Austrian Society of Alpine and High-Altitude Medicine, 6414 Mieming, Austria
3
Institute of Mountain Emergency Medicine, Eurac Research, 3910 Bolzano, Italy; Hannes.Gatterer@eurac.edu
*
Correspondence: Martin.Faulhaber@uibk.ac.at; Tel.: +43-512-507-45893
Abstract: The present project compared acute hypoxia-induced changes in lactate thresholds (meth-
ods according to Mader, Dickhuth and Cheng) with changes in high-intensity endurance performance.
Six healthy and well-trained volunteers conducted graded cycle ergometer tests in normoxia and in
acute normobaric hypoxia (simulated altitude 3000 m) to determine power output at three lactate
thresholds (PMader, PDickhuth, PCheng). Subsequently, participants performed two maximal 30-min cy-
cling time trials in normoxia (test 1 for habituation) and one in normobaric hypoxia to determine mean
power output (Pmean). PMader, PDickhuth and PCheng decreased signiﬁcantly from normoxia to hypoxia
by 18.9 ± 9.6%, 18.4 ± 7.3%, and 11.5 ± 6.0%, whereas Pmean decreased by only 8.3 ± 1.6%. Cor-
relation analyses revealed strong and signiﬁcant correlations between Pmean and PMader (r = 0.935),
PDickhuth (r = 0.931) and PCheng (r = 0.977) in normoxia and partly weaker signiﬁcant correlations
between Pmean and PMader (r = 0.941), PDickhuth (r = 0.869) and PCheng (r = 0.887) in hypoxia. PMader
and PCheng did not signiﬁcantly differ from Pmean (p = 0.867 and p = 0.784) in normoxia, whereas
this was only the case for PCheng (p = 0.284) in hypoxia. Although investigated in a small and
select sample, the results suggest a cautious application of lactate thresholds for exercise intensity
prescription in hypoxia.
Keywords: anaerobic threshold; high altitude; maximal lactate steady state
1. Introduction
Endurance training sessions under hypoxic conditions are part of altitude training
concepts for competitive athletes [1], as well as in preventive and therapeutic settings [2,3].
The positive effects of hypoxia application on sport performance and health outcomes
have been extensively described in literature, but there are also negative reports [4,5] that
should not be ignored, especially since negative health effects (e.g., an increased mechanic
stress against the cerebral vessel wall) are also suspected [5]. The determination of exercise
intensity zones plays a key role in regulating training adaptations and preventing under or
over strain. Anaerobic threshold concepts are very popular to prescribe intensity zones
for endurance training; however, it remains unclear whether such concepts are still valid
under hypoxic conditions. Despite its practical relevance, scientiﬁc literature dealing with
anaerobic threshold concepts in hypoxia is scarce and, for example, ventilatory thresholds
seem to be more reduced compared to lactate thresholds [6]. Thus, it remains unclear if
intensity zones based on lactate or ventilatory threshold concepts are adequate tools for
training prescription in hypoxia.
Recently, Weckbach et al. [7] reported that peak power output (Pmax) and power
output at different lactate thresholds (LT), derived from incremental exercise testing, were
signiﬁcantly reduced in acute hypoxia (2650 m) compared to low altitude. Interestingly,
the presented data revealed that the reduction in LT power output was more pronounced
compared to Pmax by 20 to 90% depending on the LT concept [7]. However, it remains
Int. J. Environ. Res. Public Health 2021, 18, 7573. https://doi.org/10.3390/ijerph18147573
https://www.mdpi.com/journal/ijerph
Int. J. Environ. Res. Public Health 2021, 18, 7573
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unclear whether the reduction in LT also reﬂects a similar decrement in high-intensity
endurance performance. If hypoxia-induced changes in LT differ markedly from changes
in maximal steady-state performance, the validity of these threshold concepts for exercise
prescription under acute hypoxic conditions would be limited. The present pilot study
should contribute to ﬁlling this knowledge gap and, therefore, compared different LTs,
derived from incremental exercise testing, with high-intensity endurance performance in
normoxic and acute hypoxic conditions. Based on a previous study evaluating endurance
performance at 3200 m [8] and data of Weckbach et al. at 2650 m [7], we hypothesised that
power output at the lactate thresholds would be more impaired by an acute exposure to
hypoxia compared to endurance performance.
2. Materials and Methods
2.1. Participants and Study Design
Six (three females, three males) students (age: 25 ± 3 years; body height: 176 ± 3 cm;
body weight: 71 ± 5 kg; altitude of residence: 677 ± 134 m) from the Department of
Sport Science (University of Innsbruck) volunteered to participate in this pilot study. All
of them were regularly active for more than 3 h per week including various disciplines
(as is common for active sport students), but none of them were competitive endurance
athletes. Participants completed a routine health screening using an adapted physical
activity readiness questionnaire (PAR-Q) before inclusion in the study. Medical clariﬁcation
by a physician was undertaken if the PAR-Q identiﬁed speciﬁc issues that required further
investigation. Exclusion criteria were pre-existing acute or chronic diseases, pregnancy or
lactation and regular smoking of more than ﬁve cigarettes per day.
Participants were informed about the experimental details and gave informed consent
before commencing the study. The study was carried out in conformity with the ethical
standards laid down in the 1975 Declaration of Helsinki. Since the study was designed as
a pilot project the identical protocol of the subsequent main study was approved by the
Board for Ethical Questions in Science of the University of Innsbruck, Austria (Certiﬁcate
of good standing, 12/2021).
The study was designed as a within-subject design (without cross-over). Participants
conducted ﬁve cycle ergometer (Cyclus 2, RBM, Leipzig, Germany) tests in a ﬁxed order
(Figure 1). Tests 1 and 2 were maximal incremental tests in normoxic (test 1) and hypoxic
conditions (test 2). Test 1 and 2 were separated by a recovery period of 7 to 10 days.
Tests 3 to 5 were maximal 30-min time trials in normoxic (tests 3 and 4) and hypoxic
conditions (test 5), and tests were separated by recovery periods of 2 to 7 days. Test 3
served for habituation and was not included into statistical analyses. Adjustments of the
cycle ergometer (e.g., saddle height) were ﬁxed before the ﬁrst test and kept constant for
the subsequent tests. All tests took place in the laboratories of the University of Innsbruck
(Department of Sport Science, 590 m). Tests under hypoxic conditions were conducted in
a normobaric hypoxic chamber (LowOxygen Systems, Berlin, Germany) adjusted at an
inspiratory fraction of oxygen of 15.4% corresponding to a simulated altitude of about
3000 m. The hypoxic system provides a high air ﬂow keeping the inspiratory fraction
of oxygen constant and to avoid an excessive increase in inspiratory fraction of carbon
dioxide as reported in previous studies [9–11].
Int. J. Environ. Res. Public Health 2021, 18, x FOR PEER REVIEW 
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Figure 1. Experimental design including the sequence of the tests and the breaks between tests. 
2.2. Tests and Measurements 
2.2.1. Maximal Incremental Tests 
Participants rested for about 5 min in a sitting position on the cycle ergometer before 
resting parameters were taken. Workload started at 80 W for female and 100 W for male 
participants and was increased by 20 W every 3 min until subjective exhaustion. Heart 
t
(M430 P l
Vi
A
t i )
it
d Bl
d l
t t
t
ti
(S
Figure 1. Experimental design including the sequence of the tests and the breaks between tests.
Int. J. Environ. Res. Public Health 2021, 18, 7573
3 of 8
2.2. Tests and Measurements
2.2.1. Maximal Incremental Tests
Participants rested for about 5 min in a sitting position on the cycle ergometer before
resting parameters were taken. Workload started at 80 W for female and 100 W for male
participants and was increased by 20 W every 3 min until subjective exhaustion. Heart
rate (M430, Polar, Vienna, Austria) was monitored. Blood lactate concentrations (Super
GL Ambulance, Dr. Müller Gerätebau, Freital, Germany) were analysed from capillary
blood samples taken from the hyperaemised earlobe at the end of the resting phase, during
the last 30 s of each stage and about 3 min after cessation of the test. Pmax was deﬁned
as the last completed work rate plus the fraction of time spent in the ﬁnal uncompleted
work rate multiplied by 20 W [12]. Maximal heart rate (HRmax) was deﬁned as the highest
5-s average, and maximal blood lactate concentration (BLAmax) was considered as the
value of the last sample about 3 min after test termination. Heart rate and blood lactate
values were transferred to an automated software (winlactat, Mesics, Münster, Germany)
to determine LTs. In accordance with the study of Weckbach et al. [7], we selected three
different methods for the detection of the LT: (a) ﬁxed 4-mmol/L blood lactate concentration
according to Mader et al. [13], (b) lactate concentration of 1.5 mmol/L above the minimal
lactate equivalent according to Dickhut et al. [14], and (c) maximal perpendicular distance
from the blood lactate concentration curve to the line drawn from start- to endpoint (also
known as Dmax method) according to Cheng et al. [15]. Outcome parameters of the maximal
incremental tests were Pmax, HRmax as well as power output and heart rate at the three LT
(PMader, PDickhuth, PCheng and HRMader, HRDickhuth, HRCheng).
2.2.2. Maximal 30-min Time Trials
Time trials were conducted as described in detail in previous studies [8,16]. In brief:
testing began with warm-up periods of 5 min at 100/150 W (females/males) followed by
5 min at 150/200 W (females/males). Then, the cycle ergometer was shifted to a ﬁxed
pedal force so that pedalling at 100 rpm produced about 70% of Pmax (determined by the
maximal incremental test in normoxia). Participants were encouraged to choose a maximal
pedalling rate that could be maintained for the respective test duration. Heart rate was
measured continuously (chest belt, Polar, Austria), and capillary blood samples were taken
from the hyperaemised earlobe after 7 and 27 min to determine blood lactate concentrations
(BLA7 and BLA27) (Super GL Ambulance, Dr. Müller Gerätebau, Germany). Outcome
parameters were mean power output (Pmean) and mean heart rate (HRmean), which were
automatically calculated by the software of the ergometer, BLA7 and BLA27.
2.3. Statistics
Statistical analyses were performed using SPSS 24.0 (IBM, Vienna, Austria). Data were
checked for normal distribution using the Shapiro–Wilk test. Since data were normally
distributed (except for BLA7 and BLA27), paired t-tests (Wilcoxon rank tests for BLA7 and
BLA27) were used to compare outcome parameters in normoxic versus hypoxic conditions.
In the next step, focusing on power output parameters separated for normoxic and hypoxic
conditions, Pearson correlation analyses between power output at the LT and Pmean were
performed, and potential differences were tested by paired t-tests. In addition, the hypoxia-
related reductions in power output at the LTs and in Pmean were compared with paired
t-tests to test whether lactate thresholds are affected differently by acute hypoxia compared
to high-intensity endurance performance. The level of signiﬁcance was set at p < 0.05. Data
are presented as means ± SD.
3. Results
The results of the maximal incremental tests revealed a signiﬁcant decrease in Pmax
by approximately 12% from normoxia to hypoxia (249 ± 25 versus 221 ± 36 W, p = 0.005).
HRmax (189 ± 10 versus 186 ± 8 bpm, p = 0.217) and BLAmax (11.9 ± 2.5 versus 13.1 ± 0.9,
p = 0.166) did not signiﬁcantly differ from normoxia to hypoxia.
Int. J. Environ. Res. Public Health 2021, 18, 7573
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Power output and heart rate at the different LT and parameters of the maximal 30-min
time trials are shown in Table 1. Power output decreased for all threshold concepts by about
12 to 19%, whereas heart rate values showed small (0 to 5%) and not signiﬁcant changes
from normoxia to hypoxia. Pmean decreased signiﬁcantly from normoxia to hypoxia by
approximately 8%, and HRmean was slightly lower in hypoxia compared to normoxia,
although not statistically signiﬁcant. Blood lactate concentrations during the time trials
did not signiﬁcantly differ between normoxia versus hypoxia (BLA7: 6.1 ± 2.2 versus
6.3 ± 2.2 mmol/L, p = 0.873; BLA27: 8.9 ± 2.5 versus 9.4 ± 2.0 mmol/L, p = 0.385).
Table 1. Power output and heart rate at different lactate thresholds and during maximal 30-min time
trials in normoxia and hypoxia. Values are means ± SD. p-Values refer to a comparison of normoxia
and hypoxia.
Normoxia
Hypoxia
Difference (%)
p-Value
Lactate thresholds based on stepwise maximal cycle ergometries
PMader (W)
194 ± 26
158 ± 33
−18.9 ± 9.6
0.004
HRMader (bpm)
167 ± 8
160 ± 12
−4.5 ± 6.8
0.154
PDickhuth (W)
179 ± 24
146 ± 22
−18.4 ± 7.3
0.001
HRDickhuth (bpm)
161 ± 8
153 ± 16
−5.1 ± 7.0
0.140
PCheng (W)
194 ± 30
172 ± 28
−11.5 ± 6.0
0.005
HRCheng (bpm)
167 ± 9
167 ± 11
+0.3 ± 8.0
0.977
Maximal 30-min time trials
Pmean (W)
195 ± 34
179 ± 32
−8.3 ± 1.6
<0.001
HRmean (bpm)
175 ± 12
170 ± 8
−2.7 ± 4.4
0.203
P, power output; HR, hear rate. Lactate thresholds were determined according to the methods of Mader et al.
(Mader), Dickhuth et al. (Dickhuth) and Cheng et al. (Cheng) [13–15]. Pmean, mean power output; HRmean, mean
heart rate.
Correlation analyses for normoxia (Figure 2a) data revealed strong and signiﬁcant
correlations for power output at the three LT and Pmean (PMader: r = 0.935, p = 0.006;
PDickhuth: r = 0.931, p = 0.007; PCheng: r = 0.977, p = 0.001). Furthermore, PMader and PCheng
did not signiﬁcantly differ from Pmean (p = 0.867 and p = 0.784 respectively), whereas
PDickhuth was signiﬁcantly lower compared to Pmean (p = 0.045). With respect to hypoxic
conditions (Figure 2b), we also found signiﬁcant correlations, but for PDickhuth and PCheng,
we found slightly weaker correlations (PMader: r = 0.941, p = 0.005; PDickhuth: r = 0.869,
p = 0.024; PCheng: r = 0.887, p = 0.019). PMader and PDickhuth were signiﬁcantly lower
compared to Pmean (p = 0.007 and p = 0.005), whereas there was no signiﬁcant difference for
PCheng (p = 0.284).
Comparing hypoxia-related impairments in power output at the three LT and in Pmean,
signiﬁcant differences were found for PMader and PDickhuth but not for PCheng (Figure 3).
Int. J. Environ. Res. Public Health 2021, 18, 7573
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Figure 2. Association between mean power output during the time trial and power output at three 
different lactate thresholds (blue = PMader, red = PDickhuth, green PCheng) [11–13]. Data are presented for 
normoxic (upper panel) und hypoxic conditions (lower panel). (a): normoxic conditions; (b): 
hypoxic conditions 
Comparing hypoxia-related impairments in power output at the three LT and in 
Pmean, significant differences were found for PMader and PDickhuth but not for PCheng (Figure 3). 
Figure 2. Association between mean power output during the time trial and power output at
three different lactate thresholds (blue = PMader, red = PDickhuth, green PCheng) [11–13]. Data are
presented for normoxic (upper panel) und hypoxic conditions (lower panel). (a): normoxic conditions;
(b): hypoxic conditions.
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Figure 3. Hypoxia-related changes in power output at the three lactate thresholds (PMader, PDickhuth, 
PCheng) and in mean power output during the maximal 30-min time trial (Pmean) [13–15]. P-values 
refer to a comparison to Pmean. Values are means ± SD. 
4. Discussion 
The presented data show that acute hypoxia impaired power output at different LT 
and Pmean as expected. In accordance with our hypothesis, the results also demonstrate 
that the reduction in Pmean was clearly lower (approximately 8%) compared to lactate 
thresholds estimations (12% to 19%). Correlations between power output at the LT and 
Pmean were found in normoxic as well as in acute hypoxic conditions. However, hypoxia-
related decreases in power output at two LT (PMader and PDickhuth) were significantly greater 
compared to the hypoxia-related decrease in Pmean resulting in significant differences to 
Pmean in hypoxia. 
Although LT are often validated for specific exercise protocols, exercise modes and 
populations, the observed strong correlations in normoxic conditions between power 
output at the LT (PMader, PDickhuth, PCheng) and Pmean were well documented [17] and in 
accordance with our findings. The method of Dickhuth et al. [14] was designed to detect 
the first rise in blood lactate concentration and can be categorised as an aerobic lactate 
threshold [17]. This observation was also reported in the review article of Faude et al. [17], 
and, therefore, the significant underestimation of Pmean in our study was not surprising. 
However, this underestimation of Pmean does not limit the application of this LT in exercise 
prescription by model-specific intensity zones. 
Regarding the hypoxia-induced changes in power output, the three LT showed more 
pronounced reductions compared to Pmean. From a practical point of view, the application 
of LT-based intensity zones, although fitting in normoxic conditions, can result in an 
underestimation of endurance capacity and therefore sub-optimal or even ineffective 
training loads when determined and applied in acute hypoxic conditions. Since the 
method according to Cheng et al. [15] only slightly underestimated Pmean and, 
furthermore, showed a strong correlation to Pmean under hypoxic conditions, it seems that 
exercise intensity prescriptions based on this method may be more robust against 
hypoxic-related underestimations. Based on the observation that resting lactate 
concentrations are not influenced by moderate hypoxia (e.g., 3000 m) but are markedly 
pronounced during exercise at the same absolute intensity level [18,19], the following 
explanations may be reasonable: LT models, defined by a fixed blood lactate concentration 
(i.e., 4 mmol/l) or adding a fixed value (i.e., 1.5 mmol/l) to an individual minimum may 
be directly affected by changes in the absolute lactate values (e.g., under acute hypoxia). 
Figure 3. Hypoxia-related changes in power output at the three lactate thresholds (PMader, PDickhuth,
PCheng) and in mean power output during the maximal 30-min time trial (Pmean) [13–15]. p-Values
refer to a comparison to Pmean. Values are means ± SD.
4. Discussion
The presented data show that acute hypoxia impaired power output at different LT
and Pmean as expected. In accordance with our hypothesis, the results also demonstrate that
the reduction in Pmean was clearly lower (approximately 8%) compared to lactate thresholds
estimations (12% to 19%). Correlations between power output at the LT and Pmean were
found in normoxic as well as in acute hypoxic conditions. However, hypoxia-related
decreases in power output at two LT (PMader and PDickhuth) were signiﬁcantly greater
compared to the hypoxia-related decrease in Pmean resulting in signiﬁcant differences to
Pmean in hypoxia.
Although LT are often validated for speciﬁc exercise protocols, exercise modes and
populations, the observed strong correlations in normoxic conditions between power
output at the LT (PMader, PDickhuth, PCheng) and Pmean were well documented [17] and in
accordance with our ﬁndings. The method of Dickhuth et al. [14] was designed to detect
the ﬁrst rise in blood lactate concentration and can be categorised as an aerobic lactate
threshold [17]. This observation was also reported in the review article of Faude et al. [17],
and, therefore, the signiﬁcant underestimation of Pmean in our study was not surprising.
However, this underestimation of Pmean does not limit the application of this LT in exercise
prescription by model-speciﬁc intensity zones.
Regarding the hypoxia-induced changes in power output, the three LT showed more
pronounced reductions compared to Pmean. From a practical point of view, the application
of LT-based intensity zones, although ﬁtting in normoxic conditions, can result in an
underestimation of endurance capacity and therefore sub-optimal or even ineffective
training loads when determined and applied in acute hypoxic conditions. Since the
method according to Cheng et al. [15] only slightly underestimated Pmean and, furthermore,
showed a strong correlation to Pmean under hypoxic conditions, it seems that exercise
intensity prescriptions based on this method may be more robust against hypoxic-related
underestimations. Based on the observation that resting lactate concentrations are not
inﬂuenced by moderate hypoxia (e.g., 3000 m) but are markedly pronounced during
exercise at the same absolute intensity level [18,19], the following explanations may be
reasonable: LT models, deﬁned by a ﬁxed blood lactate concentration (i.e., 4 mmol/L) or
adding a ﬁxed value (i.e., 1.5 mmol/L) to an individual minimum may be directly affected
by changes in the absolute lactate values (e.g., under acute hypoxia). In contrast, the LT
model by Cheng et al. [15] also considers the shape of the blood lactate curve and thus
Int. J. Environ. Res. Public Health 2021, 18, 7573
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the individual lactate kinetics, which seems to be a crucial point in evaluating exercise
capacity [20].
To the best of our best knowledge, this is the ﬁrst study comparing hypoxia-related
changes in lactate thresholds with changes in endurance performance (i.e., 30-min time-trial
performance). The inclusion of a ﬁrst time trial for familiarisation improved the validity of
the hypoxia-related changes in the second and third time trial because it was shown that
time-trial performance improves from a ﬁrst to a second test [16]. The small sample size
and the resulting susceptibility for individual outliers represent the main limitation of the
present study. For example, the correlation analysis in hypoxia revealed r = 0.887 for PCheng
versus Pmean (p = 0.019). However, the exclusion of one person (a statistical borderline
outlier) would result in r = 0.959, (p = 0.010, n = 5). In addition, this experiment was
conducted in a speciﬁc group of healthy subjects with an above-average ﬁtness level and
results cannot be directly transferred either to elite athletes or to speciﬁc patient groups.
5. Conclusions
According to the hypothesis, power output at the lactate thresholds were more im-
paired by an acute exposure to hypoxia compared to high-intensity endurance performance
reaching statistical signiﬁcance for the methods of Mader et al. and Dickhuth et al. In
conclusion, the application of LT for exercise intensity prescription in hypoxia, even when
determined under such conditions, may be prone to errors. The results of this pilot study
should provide a basis for future larger-scale investigations dealing with this topic in
different target groups.
Author Contributions: Conceptualisation, M.F. and V.M.; methodology, M.F.; formal analysis, K.G.
and M.F.; writing—original draft preparation, M.F. and L.R.; writing—review and editing, M.F., V.M.
and H.G. All authors have read and agreed to the published version of the manuscript.
Funding: This research received no external funding.
Institutional Review Board Statement: The study was conducted according to the guidelines of the
Declaration of Helsinki and approved by the Board for Ethical Questions in Science of the University
of Innsbruck, Austria (Certiﬁcate of good standing, 12/2021).
Informed Consent Statement: Informed consent was obtained from all subjects involved in the study.
Data Availability Statement: The data are not publicly available due to ethical considerations on
preserving the anonymity of study participants.
Conﬂicts of Interest: The authors declare no conﬂict of interest.
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Effects of Acute Hypoxia on Lactate Thresholds and High-Intensity Endurance Performance-A Pilot Study.
Faulhaber, Martin,Gröbner, Katharina,Rausch, Linda,Gatterer, Hannes,Menz, Verena