The Influence of Acute Oral Lactate Supplementation on Responses to Cycle Ergometer Exercise: A Randomized, Crossover Pilot Clinical Trial

Abstract

The purpose of this study was to investigate the potential ergogenic effects of an oral lactate supplement. For this double-blind, randomized, placebo-controlled crossover design, fifteen recreational exercisers (nine males, six females) ingested a placebo or a commercially available lactate supplement prior to cycle ergometer exercise. Primary outcomes included peak oxygen uptake (VO2peak; via indirect calorimetry), VO2 at the ventilatory threshold, and work rate at the lactate threshold (arterialized venous blood from a heated hand) determined during incremental exercise to fatigue, and power output during a 20-min cycling time trial. Compared with placebo, the oral lactate supplement (19 ± 1 mg/kg body mass) did not influence VO2peak (placebo: 44.3 ± 7.8 vs. oral lactate: 44.3 ± 7.1 mL/kg/min (mean ± SD); p = 0.87), VO2 at the ventilatory threshold (placebo: 1.63 ± 0.25 vs. oral lactate: 1.65 ± 0.23 L/min; p = 0.82), or work rate at the lactate threshold (placebo: 179 ± 69 vs. oral lactate: 179 ± 59 W; p = 0.41). Throughout the 20-min time trial, the work rate was slightly greater (4%) with oral lactate (204 ± 41 W) compared with placebo (197 ± 41 W; main effect of treatment p = 0.02). Collectively, these data suggest that this commercially available lactate supplement did not acutely influence the physiological responses to incremental cycle ergometer exercise but elicited a modest ergogenic effect during the short-duration time trial.

Full text

Citation: Ewell, T.R.; Bomar, M.C.;
Brown, D.M.; Brown, R.L.; Kwarteng,
B.S.; Thomson, D.P.; Bell, C. The
Influence of Acute Oral Lactate
Supplementation on Responses to
Cycle Ergometer Exercise: A
Randomized, Crossover Pilot Clinical
Trial. Nutrients 2024,16, 2624.
https://doi.org/10.3390/nu16162624
Academic Editor: David Varillas-
Delgado
Received: 11 July 2024
Revised: 5 August 2024
Accepted: 7 August 2024
Published: 9 August 2024
Copyright: © 2024 by the authors.
Licensee MDPI, Basel, Switzerland.
This article is an open access article
distributed under the terms and
conditions of the Creative Commons
Attribution (CC BY) license (https://
creativecommons.org/licenses/by/
4.0/).
nutrients
Article
The Influence of Acute Oral Lactate Supplementation on
Responses to Cycle Ergometer Exercise: A Randomized,
Crossover Pilot Clinical Trial
Taylor R. Ewell, Matthew C. Bomar, David M. Brown, Reagan L. Brown, Beatrice S. Kwarteng, David P. Thomson
and Christopher Bell *
Department of Health and Exercise Science, Colorado State University, Fort Collins, CO 80523-1582, USA;
taylor.ewell@colostate.edu (T.R.E.)
*Correspondence: christopher.bell@colostate.edu
Abstract: The purpose of this study was to investigate the potential ergogenic effects of an oral
lactate supplement. For this double-blind, randomized, placebo-controlled crossover design, fifteen
recreational exercisers (nine males, six females) ingested a placebo or a commercially available lactate
supplement prior to cycle ergometer exercise. Primary outcomes included peak oxygen uptake
(VO
2peak
; via indirect calorimetry), VO
2
at the ventilatory threshold, and work rate at the lactate
threshold (arterialized venous blood from a heated hand) determined during incremental exercise
to fatigue, and power output during a 20-min cycling time trial. Compared with placebo, the oral
lactate supplement (19
±
1 mg/kg body mass) did not influence VO
2peak
(placebo: 44.3
±
7.8 vs. oral
lactate: 44.3
±
7.1 mL/kg/min (mean
±
SD); p= 0.87), VO
2
at the ventilatory threshold (placebo:
1.63
±
0.25 vs. oral lactate: 1.65
±
0.23 L/min; p= 0.82), or work rate at the lactate threshold (placebo:
179
±
69 vs. oral lactate: 179
±
59 W; p= 0.41). Throughout the 20-min time trial, the work rate
was slightly greater (4%) with oral lactate (204
±
41 W) compared with placebo (197
±
41 W; main
effect of treatment p= 0.02). Collectively, these data suggest that this commercially available lactate
supplement did not acutely influence the physiological responses to incremental cycle ergometer
exercise but elicited a modest ergogenic effect during the short-duration time trial.
Keywords: supplement; ergogenic; ergolytic; VO2peak; performance; FTP20
1. Introduction
Lactate has been incorrectly characterized as a facilitator of fatigue and harbinger
of muscle soreness. In contemporary physiology, the appreciation of lactate has evolved,
and it is now recognized, amongst other things, as a versatile fuel source, a signaling
molecule [
1
], a potential regulator of clinically relevant myokines such as interleukin-6 [
2
,
3
]
and fibroblast growth factor-21 [
4
], and a promoter of buffering capacity [
5
,
6
]. Considering
these favorable and physiologically relevant properties, lactate supplementation has been
proposed as a potential ergogenic aid [
5
,
7
–
9
] and, based on observations in rodents, as an
intervention to promote adaptation to exercise training [
10
,
11
]. To date, the human exercise
data are somewhat limited. Several studies have explored physiological responses to lactate
infusions, but these have typically focused on clinical and/or metabolic outcomes rather
than exercise performance [
12
–
16
]. While a moderate number of studies have explored
oral lactate administration [
5
,
6
,
8
,
9
,
17
–
19
], the results have been inconclusive. Further, none
have examined the influence of oral lactate on the cardiometabolic responses to incremental
exercise, such as peak oxygen uptake (VO2peak) or lactate and ventilatory thresholds.
The purpose of this study was to investigate the potential ergogenic effects of a
commercially available oral lactate supplement in healthy young adults who were regular
exercisers. The primary outcomes were conventional parameters that have been established
as predictors of endurance performance and markers of training status: VO
2peak
, VO
2
at
Nutrients 2024,16, 2624. https://doi.org/10.3390/nu16162624 https://www.mdpi.com/journal/nutrients

Nutrients 2024,16, 2624 2 of 14
ventilatory threshold, work rate at lactate threshold, and the maximal mean power that
could be sustained during a 20-min stationary cycle ergometer time trial. We hypothesized
that acute oral lactate supplementation would favorably modify each of these outcomes
relative to a placebo.
2. Materials and Methods
2.1. Participants
This project was approved by the Institutional Review Board of Colorado State Uni-
versity (Protocol #4933H), conducted according to the guidelines of the Declaration of
Helsinki, and registered as a clinical trial (NCT06371521). Written informed consent was
provided by all participants prior to the initiation of any research activities. Healthy young
adults were prospectively recruited by T.R.E., M.C.B., D.M.B., R.L.B., and B.S.K. Inclusion
criteria consisted of age between 18 and 30 years old, and participation in a minimum
of 150 min/week of moderate-intensity endurance exercise during the previous twelve
months. Exclusion criteria included pregnancy, breastfeeding, use of an oral lactate supple-
ment within the previous 4 weeks, use of magnesium supplements within the previous
4 weeks, unwillingness to abstain from the use of other potentially ergogenic supplements
throughout participation in the study, and inability or unwillingness to perform vigorous
cycle ergometer exercise.
2.2. Brief Summary of Protocol and Experimental Design
A randomized, double-blind, placebo-controlled, crossover design was used to min-
imize the influence of between-participant variation typically associated with a parallel
design [
20
]. Further, although crossover designs are often associated with a relatively
larger participant dropout [
20
], this was not anticipated in the current study on account
of the brief nature of the intervention. All data were collected in the laboratories of the
Department of Health and Exercise Science at Colorado State University, Fort Collins, CO,
USA. Following screening, study participants were habituated to two stationary cycle
ergometer exercise protocols: a ramp test and a 20-min time trial. Over four separate visits,
participants then completed two incremental exercise tests for voluntary fatigue and two
endurance performance tests requiring a maximal sustained effort over 20 min (similar to
a 20-min functional threshold power test (FTP
20
)). Thirty minutes prior to each test, par-
ticipants ingested capsules containing either a placebo or a commercially available lactate
supplement (Sportlegs, Sport Specifics Inc., Longmont, CO, USA). To avoid the potential
confounding influence of diurnal fluctuations, the scheduling of the incremental exercise
tests and time trials was kept constant (within ~2 h) for each individual participant. The
washout period (i.e., the time between trials) was a minimum of 48 h; across participants, it
ranged from 48 h to 7 days. The methods were not changed after trial commencement.
2.3. Randomization
The assignment order of placebo and oral lactate was randomized by T.R.E., using an
online randomizer (Research Randomizer Version 4.0, Social Psychology Network, Wes-
leyan University, Middletown, CT, USA, https://www.randomizer.org/, accessed on 11
October 2023) in a 1:1 allocation. The order of the specific exercise tests was “pseudoran-
dom” in that it was dictated through a combination of research participants’ availability for
testing and the availability of appropriately skilled/qualified research personnel. consider-
ations included the duration of the specific tests (i.e., the laboratory visits for vo
2peak
and
lactate threshold tests were of longer duration than the visits for time trials) and the need
for a phlebotomist (i.e., only required for lactate threshold tests).
2.4. Screening
Potential research participants reported to the laboratory for an initial screening visit
that consisted of a medical history/screening questionnaire, assessment of body mass and
height, and measurement of VO
2peak
. Height was measured using a stadiometer, and body

Nutrients 2024,16, 2624 3 of 14
mass was measured using a physician’s scale. These data were used to calculate body mass
index. VO
2peak
was assessed during incremental cycle ergometer exercise (20–35 W/min)
to voluntary fatigue using an electromagnetically braked ergometer (Corvial Cpet, Lode
BV, Groningen, The Netherlands) and indirect calorimetry (ParvoMedics TrueOne 2400;
Salt Lake City, UT, USA), as previously described [2,21,22].
2.5. Habituation
To habituate participants to the exercise protocols and avoid the confounding influence
of a potential learning effect, two familiarization sessions were completed. These sessions
were almost identical to the data collection visits described below; blood collection and
placebo/lactate ingestion were not included in the habituation sessions.
2.6. VO2peak and Ventilatory and Lactate Thresholds
VO
2peak
was assessed during incremental cycle ergometer exercise (20–35 W/min) to
voluntary fatigue using an electromagnetically braked ergometer and indirect calorimetry.
Exhaled gases were analyzed for volume and concentration of oxygen and carbon dioxide.
VO
2peak
was recorded as the greatest value for VO
2
averaged over 30 s. Based on previous
studies in our lab [
23
], the coefficient of variation for the measurement of VO
2peak
is 3.1%.
The ventilatory threshold was determined using established procedures [
24
]. Every 60 s,
arterialized venous blood (~2–3 mL) was sampled from a venous catheter placed in a
dorsal hand vein; the hand and forearm were wrapped in a heated blanket [
25
]. Blood was
immediately transferred to pre chilled tubes coated with sodium fluoride and potassium
oxalate that were then returned to an ice slurry. Within 30 min of blood collection, lactate
concentration was determined using an automated analyzer (YSI 2900, Xylem Inc.; White
Plains, NY, USA). The work rate at the lactate threshold was identified as previously
described [
26
]. In addition to gas exchange variables and blood lactate, heart rate (via
short-range telemetry; Polar T31, Bethpage, New York, NY, USA) and ratings of perceived
exertion (RPE; Borg scale) [
27
] were determined throughout the test. Once the participants
had reached volitional fatigue, participants completed a verification phase [
28
]. The work
rate was decreased (to ~0–50 watts at the request of the participants) to provide temporary
(2 to 4 min) reprieve from strenuous exercise. The work rate was then rapidly increased
(i.e., within seconds) to a value that would have been attained had the participant cycled
for an additional 120 s beyond VO
2peak
(e.g., if the ramp function was 25 W/min and a
participant reached fatigue at 325 W, the verification work rate was increased to 375 W).
Participants exercised at this higher work rate until volitional fatigue, at which point VO
2
and blood lactate concentration were determined.
2.7. Twenty-Minute Exercise Trial
Participants completed a test very similar to an FTP
20
[
29
], using an air-braked cycle
ergometer (Concept2 BikeErg, Concept2 Inc., Morristown, VT, USA), as previously de-
scribed [
30
]. This test involved the determination of the maximal mean power that could be
sustained over 20 min. The FTP
20
is able to predict cycling performance and is commonly
used in laboratories and by cyclists of varied abilities (recreational to professional) to assess
performance and training status [
29
]. RPE and heart rate were recorded at 5, 10, 15, and
20 min. To facilitate a maximal effort and to remove any potential ventilatory burden,
expired gases were not collected during this test. Based on previous studies in our lab [
30
],
the coefficient of variation for the FTP20 is 3.0%.
2.8. Lactate Supplement
Both the placebo and the commercially available lactate supplement (Sportlegs, Sport
Specifics, Inc., Longmont, CO, USA) were provided in capsules by the study sponsor (Sport
Specifics, Inc., Loveland, CO, USA). To facilitate double blinding of all researchers and
participants, capsules were delivered in containers labeled “A” and “B”, and the key was
provided in a sealed envelope that was stored in a secure location by a colleague not

Nutrients 2024,16, 2624 4 of 14
affiliated with the project. Certificates of analysis were provided by a third party (New
Generation Wellness, Inc., Colorado Springs, CO, USA). The ingredients of the lactate
supplement were calcium lactate, magnesium lactate, and vitamin D3 (cholecalciferol);
the total lactate per capsule was 372 mg. Within the USA, these ingredients are generally
regarded as safe (i.e., satisfy the criteria for GRAS status) by the USA Food and Drug
Administration. The placebo was organic rice starch. Visually, the placebo and lactate
supplement were indistinguishable. To maintain ecological validity, individual dosing was
as per the manufacturers’ guidelines: one capsule per 50 lbs (22.7 kg) body mass, rounded
up. For example, a participant with a body mass of 120 lbs received three capsules; a
participant with a body mass of 185 lbs received four capsules, etc.
2.9. Statistics
This was a pilot study thus sample size was not predetermined. Sequence and period
effects specific to our crossover design were calculated following published guidelines [
31
].
R Studio (version 2023.03.0 + 386) was used to run linear mixed models to compare variables
of interest with the lme4 and lmerTest packages [
32
,
33
]. “Subjects” was always considered
a random effect, to account for repeated measures. The effect size metric used for the linear
mixed models was conditional R
2
. For single-factor tests (e.g., VO
2peak
), Yuen’s test was
used. For two-factor tests (e.g., heart rate through the 20-min exercise trial), both condition
and time were considered fixed effects. Significant main effects were further investigated
via Tukey’s Honestly Significant Difference tests using the emmeans package. Following
an estimation statistics approach [
34
], the effect size as Hedges’ g and the corresponding
95% confidence intervals (CI) were calculated. Relations of interest were explored using
Pearson correlation. All data are presented as mean
±
standard deviation unless otherwise
specified. Data were considered statistically significant when p< 0.05. Estimation plots
were created using GraphPad Prism 10 (GraphPad Software, Inc., Boston, MA, USA). All
other figures were created using SigmaPlot (Grafiti LLC., Palo Alto, CA, USA).
3. Results
Participant recruitment and data collection and analysis took place between October
2023 and June 2024. The participant flow through the protocol is presented in Figure 1
(Incremental Exercise test) and Figure 2(Time Trial). Two flow diagrams are necessary as
the placebo and oral lactate assignments were different between tests. Nineteen healthy
young regular exercisers were enrolled, of which four ended their participation prema-
turely: two participants were unable to tolerate blood sampling, and two participants were
lost to follow-up (unresponsive to scheduling emails and texts). The remaining fifteen
completed the study without incident or adverse event. Study participants comprised
nine males and six females (age: 24
±
3 years; body mass: 75.5
±
12.7 kg (~166
±
28 lbs);
body mass index: 24.8
±
2.3 kg/m
2
(mean
±
standard deviation)). The ingested dose
of lactate supplement was 19
±
1 mg/kg. Based on published guidelines recommended
for classifying research participants [
35
,
36
], the study cohort comprised four males and
one female considered untrained (Performance Level 1), three males and four females
considered recreationally trained or active (Performance Level 2), and two males and one
female considered trained (Performance Level 3). None of the participants were considered
well-trained or professional (Performance Levels 4 and 5, respectively).

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Figure 1. Consolidated standards of reporting trials (CONSORT) flow diagram for incremental
exercise test.

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Figure 2. Consolidated standards of reporting trials (CONSORT) flow diagram for FTP20.
3.1. Incremental Exercise Test
Individual and group data from the incremental exercise test are presented in
Figure 3A–F.
One participant was unable to complete the verification phase in the oral
lactate condition due to nausea during/after the VO
2peak
assessment; it was unclear if
this nausea was due to exercise, oral lactate, or some combination of both. Data from this
participant were included in all formal statistical comparisons except those pertaining to
the verification phase. There were no sequence or period effects for any of the presented
variables (all p> 0.12). Compared with placebo, the oral lactate supplement did not influ-
ence VO
2peak
(Panel A: placebo 44.3
±
7.8 vs. oral lactate 44.3
±
7.1 mL/kg/min; p= 0.87,

Nutrients 2024,16, 2624 7 of 14
Hedges’ g: 0.00 (95% CI
−
0.21, 0.18)), work rate at VO
2peak
(Panel B: placebo 300
±
64 vs.
oral lactate 304
±
62 W; p= 0.86, Hedges’ g: 0.06 (95% CI
−
0.08, 0.19)), heart rate at VO
2peak
(Panel C: placebo 176
±
10 vs. oral lactate 176
±
11 beats/min; p= 0.94, Hedges’ g:
−
0.15
(95% CI
−
0.65, 0.24)), respiratory exchange ratio at VO
2peak
(Panel D: placebo 1.14
±
0.06 vs.
oral lactate 1.15
±
0.08; p= 0.47, Hedges’ g: 0.14 (95% CI
−
0.36, 0.61)), VO
2
at ventilatory
threshold (Panel E: placebo 1.63
±
0.25 vs. oral lactate 1.65
±
0.23 L/min; p= 0.82, Hedges’
g: 0.08 (95% CI
−
0.37, 0.45)), or the blood lactate response during exercise (Panel F). Further
inspection of blood lactate data revealed no difference between placebo and the oral lactate
supplement on pre-exercise (post capsule ingestion) blood lactate concentration (placebo
0.99
±
0.33 vs. oral lactate 0.95
±
0.24 mmol/L; p= 0.98, Hedges’ g:
−
0.12 (95% CI
−
0.85,
0.70)), blood lactate concentration at the end of the verification phase (placebo 8.22
±
2.90
vs. oral lactate 7.46
±
2.11 mmol/L; p= 0.40, Hedges’ g:
−
0.21 (95% CI
−
0.70, 0.29)), and
work rate at the lactate threshold (placebo 179
±
69 vs. oral lactate 179
±
59 Watts; p= 0.41,
Hedges’ g: 0.04 (95% CI
−
0.461, 0.744)). In addition, oral lactate supplementation had no
effect on time to fatigue during the ramp test (placebo 624
±
59 vs. oral lactate 635
±
60 s;
p= 0.85, Hedges’ g: 0.19 (95% CI
−
0.148, 0.444)), or during the verification phase (placebo
40
±
20 vs. oral lactate 47
±
32 s; p= 0.75, Hedges’ g: 0.24 (95% CI
−
0.197, 0.871)). VO
2
at the end of the verification phase was slightly lower than VO
2peak
for both treatments
(placebo: 44.3
±
7.8 vs. 39.6
±
6.3 and oral lactate 44.3
±
7.1 vs. 39.0
±
7.7 mL/kg/min;
p< 0.001); oral lactate supplementation did not influence this response (p= 0.69). Visual
inspection of Panels C and D (heart rate and RER at VO
2peak
) suggested one participant had
an unusual/exaggerated response to oral lactate (i.e., appreciably lower heart rate and RER).
This participant’s data were not considered as outliers, nor were there any reported or observed
peculiarities that would cause us to consider excluding this participant. However, for sake of
clarity, we repeated the statistical analyses with these data excluded. While this resulted in
minor changes in overall p-values, none of the conclusions were modified (i.e., comparisons
that were previously interpreted as statistically significant/non-significant did not change).
3.2. Twenty-Minute Exercise Time Trial (FTP20)
Group and individual data from the 20-min exercise time trial are presented in
Figure 4A–D. There were no sequence or period effects for any of the presented vari-
ables (all p> 0.073). Compared with placebo, oral lactate supplementation improved mean
work rate sustained through the 20-min exercise trial (placebo 197
±
41 vs. oral lactate
204
±
41 Watts; main effect of treatment p= 0.02, Conditional R
2
: 0.87; Panel A shows
group data and Panel B individual data). Inspection of the individual data revealed that
time trial performance was improved in eleven participants and decreased in the remaining
four (3 males and one female). The mean change in performance with oral lactate was
7
±
13 Watts (range:
−
18 to +26 Watts) corresponding to an overall 4% improvement. The
magnitude of improvement in performance was not related to VO
2peak
, mean work rate,
work rate at lactate threshold, or dose (mg/kg) of oral lactate (all p> 0.06). During the
time trial, heart rate (Panel C-group data) increased over time (p< 0.001, Conditional R
2
:
0.86) and was not different between placebo and oral lactate supplementation (p= 0.74).
Similarly, RPE (Panel D-group data) increased over time (p< 0.001, Conditional R
2
: 0.85)
and was also not different between placebo and oral lactate supplementation (p= 0.24).

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Figure 3. Oral lactate had no influence on the physiological responses to ramp exercise. Panels
(A–E): The paired mean difference between placebo and oral lactate as illustrated using estimation
plots. Both conditions are plotted on the left axes as a slopegraph: each paired set of observations is
connected by a line. The paired mean difference is plotted on a floating axis on the right. Symbols
represent individual mean differences, the horizontal line at zero provides reference, the other
shows the actual mean difference. The error bars around the heavy solid horizontal line are the 95%
confidence intervals. Panel (A): Oral lactate had no influence on peak oxygen uptake (VO
2peak
). Panel
(B): Oral lactate had no influence on work rate at VO
2peak
. Panel (C): Oral lactate had no influence on
heart rate at VO
2peak
. Panel (D): Oral lactate had no influence on respiratory exchange ratio (RER) at
VO
2peak
. Panel (E): Oral lactate had no influence on the VO
2
at ventilatory threshold. Panel (F): Oral
lactate had no influence on blood lactate concentration during incremental exercise. Panels (A–E)
show individual data, discriminated by sex. Panel (F) shows mean and standard deviation of group
data. Exercise time was normalized to % of time to exhaustion to promote visual clarity.

Nutrients 2024,16, 2624 9 of 14
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the actual mean difference. The error bars around the heavy solid horizontal line are the 95% confi-
dence intervals. Panel (A): Oral lactate had no influence on peak oxygen uptake (VO
2peak
). Panel (B):
Oral lactate had no influence on work rate at VO
2peak
. Panel (C): Oral lactate had no influence on
heart rate at VO
2peak
. Panel (D): Oral lactate had no influence on respiratory exchange ratio (RER) at
VO
2peak
. Panel (E): Oral lactate had no influence on the VO
2
at ventilatory threshold. Panel (F): Oral
lactate had no influence on blood lactate concentration during incremental exercise. Panels (A–E)
show individual data, discriminated by sex. Panel (F) shows mean and standard deviation of group
data. Exercise time was normalized to % of time to exhaustion to promote visual clarity.
3.2. Twenty-Minute Exercise Time Trial (FTP
20
)
Group and individual data from the 20-min exercise time trial are presented in Figure
4A–D. There were no sequence or period effects for any of the presented variables (all p >
0.073). Compared with placebo, oral lactate supplementation improved mean work rate
sustained through the 20-min exercise trial (placebo 197 ± 41 vs. oral lactate 204 ± 41 Was;
main effect of treatment p = 0.02, Conditional R
2
: 0.87; Panel A shows group data and Panel
B individual data). Inspection of the individual data revealed that time trial performance
was improved in eleven participants and decreased in the remaining four (3 males and
one female). The mean change in performance with oral lactate was 7 ± 13 Was (range:
−18 to +26 Was) corresponding to an overall 4% improvement. The magnitude of im-
provement in performance was not related to VO
2peak
, mean work rate, work rate at lactate
threshold, or dose (mg/kg) of oral lactate (all p > 0.06). During the time trial, heart rate
(Panel C-group data) increased over time (p < 0.001, Conditional R
2
: 0.86) and was not
different between placebo and oral lactate supplementation (p = 0.74). Similarly, RPE
(Panel D-group data) increased over time (p < 0.001, Conditional R
2
: 0.85) and was also not
different between placebo and oral lactate supplementation (p = 0.24).
Figure 4. Oral lactate evoked a modest improvement in 20-min cycle ergometer time trial perfor-
mance without influencing heart rate or ratings of perceived exertion (RPE). Panels (A,B) show
group (A) and individual (B) data for work rates over the 20-min trial. Panel (C): Oral lactate had
no influence on heart rate during the time trial. Panel (D): Oral lactate had no influence on RPE
Figure 4. Oral lactate evoked a modest improvement in 20-min cycle ergometer time trial performance
without influencing heart rate or ratings of perceived exertion (RPE). Panels (A,B) show group (A)
and individual (B) data for work rates over the 20-min trial. Panel (C): Oral lactate had no influence
on heart rate during the time trial. Panel (D): Oral lactate had no influence on RPE during the time
trial. Panels (A,C,D) show mean and standard deviation of group data. Panel (B) shows individual
responses; data have been offset from 5-min markers to promote visual clarity.
4. Discussion
The major findings of the current study were, compared with placebo, oral lactate
supplementation did not influence any of the physiological responses during incremental
exercise to fatigue, including VO
2peak
, VO
2
at ventilatory threshold, work rate at lactate
threshold, and work rate at VO
2peak
. However, during the 20-min time trial (FTP
20
),
the sustained work rate was modestly (4%) increased with the oral lactate supplement,
suggestive of a potential ergogenic effect.
Previous studies of oral lactate supplements in human exercise trials have yielded
mixed results. Direct comparisons with the current data are problematic as dosing, the
nature of the exercise, and the primary outcomes appear inconsistent across studies. For
example, time to exhaustion during constant load (low-to-moderate intensity) exercise was
unaffected by the addition of lactate to a carbohydrate sports drink [
17
,
18
]. Bicarbonate and
pH were greater during three hours of constant load cycling following ingestion of a poly-
lactate solution [
19
]. Time to exhaustion during short-duration, high-intensity treadmill
exercise was barely extended (<2%) by high doses of lactate ingestion [
6
]. Neither 20- nor
40-km time trial performance was influenced by lactate ingestion [
8
,
9
]. Time to exhaustion
during high-intensity cycle ergometer exercise was appreciably extended (17%) by high
doses of oral lactate [
5
]. More recently, other commercially available supplements contain-
ing lactate have been shown to have unappreciable effects on skeletal muscle endurance
during resistance exercise [
37
,
38
] but interpretation pertaining to lactate supplementation
per se was complicated by the addition of other potentially active ingredients.
Major differences between the current and previous study [
5
] reporting a 17% exten-
sion of time to exhaustion pertain to dosing and exercise. In the previous study, 120 mg/kg

Nutrients 2024,16, 2624 10 of 14
of lactate was ingested; this dose was approximately six-fold greater than the dose used
in the current study (19
±
1 mg/kg). The rationale for our dose was based on a desire to
maintain ecological validity by providing the dose recommended by the manufacturer and
presumably used by the product consumers. In contrast, the dose used in the previous
study was based on pilot dose-response investigations comparing circulating bicarbonate
concentrations following ingestion of 20, 120, and 220 mg/kg of lactate. Thus, it appears
plausible the differences between the magnitudes of relative improvements (4 vs. 17%)
between the two studies could be attributed to vastly different dosing regimens. In support
of this notion, two other studies using similar doses of the same commercially available
lactate supplement used in the current study, showed no ergogenic benefit to 20- and 40-km
time trial performance [
8
,
9
]. However, dosing may not be the most critical explanation as
in a separate study, large doses of lactate (400 mg/kg sodium lactate) evoked only small
improvements (~3 s) in time to exhaustion during treadmill sprinting [
6
]. An alternate
explanation pertains to the selection of exercise testing protocols. The previous studies
appear to be focused on the buffering abilities of lactate together with its properties as a
versatile fuel source. To best exploit these characteristics, one might consider an exercise
protocol that provided a challenge to acid-base balance regulation while also stressing
the relatively limited stores of muscle glycogen. Our rationale for incorporating a 20-min,
FTP
20
style time trial was exercise of similar type and duration decreases skeletal muscle
glycogen [
39
–
41
] and lowers pH [
42
,
43
]. The 20-min time trial is also a popular test fre-
quently used by cyclists [
29
]. The study that has shown the greatest ergogenic effect of
oral lactate used an exercise protocol comprising time to exhaustion during high-intensity
exercise, preceded by multiple 60-s intervals of cycling at 100% of maximal power out-
put [
5
]. We felt that the 20-min time trial was more reflective of the demands of competition
than time to exhaustion, and evokes physiological challenges that, in theory, could be
alleviated with lactate supplementation. Based on the current and previous studies of
oral lactate supplementation [
5
,
8
,
9
], future investigators may wish to use shorter-duration,
higher-intensity protocols.
To the best of our knowledge, we are the first to demonstrate that low-dose lactate
ingestion has no influence on the physiological responses to incremental exercise to vol-
untary fatigue. The absence of an effect on VO
2peak
is not necessarily unsurprising as
lactate per se is not usually considered a determinant of peak metabolic rate; rather, the
delivery and utilization of oxygen drive this parameter. In contrast, and almost implied by
definition, lactate availability should have a direct influence on the lactate threshold and yet
our data revealed a negligible effect. There are several potential explanations that are not
necessarily mutually exclusive. These include unchanged lactate availability on account of
metabolism of the ingested lactate within the gut, and/or insignificant transport of ingested
lactate into the circulation. Other studies have also reported no change in circulating lactate
following lactate ingestion [
5
,
6
,
8
,
9
]. Additional proposed explanations pertained to the
pharmacokinetics of ingested lactate (i.e., time to peak lactate following ingestion) or the
possibility that the dose of ingested lactate relative to endogenous lactate production was
trivial. Isotopic tracer studies would be required to definitively address these questions.
Careful consideration of the study population is important for ergogenic aid studies.
Interventions that benefit elite athletes may not always provide similar benefits to recre-
ational exercisers, and vice versa. In the current study, although a history of regular exercise
was the primary inclusion criteria, our study population comprised people considered
to be untrained, recreationally trained or active, and trained [
35
,
36
]. We considered the
influence of endurance training status on the ergogenic effect of oral lactate by exploring
statistical relations between the magnitude of improvement in time trial performance, and
VO
2peak
, lactate threshold, and baseline time trial performance; none of these relations
were significant (all p> 0.06). These statistics might imply that training status and baseline
athletic ability may not be determinants of the response to oral lactate supplementation.
Work rates during the 20-min time trial were increased by 4% (7 Watts). While this
magnitude of improvement is small, it is worth considering that the difference between

Nutrients 2024,16, 2624 11 of 14
athletes who do and do not finish competitive events on the winners’ podium are often
also very small, sometimes only seconds apart. Alternatively, the participants in the current
study were mostly recreational exercisers, and therefore these small improvements with the
oral lactate supplement may not be as relevant. Irrespective, the observation that work rate
was slightly increased in the absence of any change in perceived exertion or heart rate may
have greater direct implications for training than for competition. That is, if moderately
greater training stimulation can be provided to skeletal muscle without the need for greater
effort, this may eventually favorably modify performance during competition. Recent
training studies in rodents coupled with long-term lactate administration provide support
for this notion [10,11].
Limitations
There are several limitations in the current study that warrant further consideration.
The primary limitation pertains to lactate dosing. As previously stated, we wished to
use the dose recommended by the manufacturer to promote ecological validity and the
overall applicability of our findings. Similar approaches in studies of the same lactate
supplement have been followed [
8
,
9
]. Unfortunately, the guidelines provided by the
manufacturer appear somewhat crude and potentially too small. The recommendation
by the manufacturer to ingest one capsule per 50 lbs of body mass, rounded up to the
next 50 lbs increment, likely contributed to variability between participants. That is,
participants with body mass close to, but either side of 50 lbs thresholds may have received
appreciably different doses. To illustrate, one participant weighed 149 lbs (67.7 kg) and
received three capsules, but another participant weighed 153 lbs (69.5 kg) and received
four capsules. When considered relative to body mass, these guidelines produced different
doses (16.5 vs. 21.4 mg/kg). It is plausible that variability between participants with
respect to lactate dosing contributed to the overall variability in the time-trial performance.
However, this appears unlikely as there was no relation between lactate dose and the
magnitude of improvement in time trial work rate with oral lactate. Instead, considering
the larger doses used in other studies [
5
], it appears more likely that the dose delivered in
the current study was insufficient to evoke a stronger ergogenic effect. Somewhat related,
during participant recruitment, we did not consider recent changes in body mass as part
of the exclusion criteria. This oversight could have contributed to increased inter-/intra-
participant variability in dosage, especially in participants whose change in mass resulted
in crossing a 50-pound threshold. Fortunately, no participants changed body mass during
the period spanning data collection, thus intra-participant dosing was constant across trials.
Other potential limitations include an absence of consideration for menstrual phase
in the female participants, and standardization of pre-exercise nutrition in the total study
population. Both menstrual phase [
44
] and pre-exercise nutrition [
45
] can influence athletic
performance. While we acknowledge these limitations, we believe their influence on our
data to be minimal on account of the randomization of treatments, thereby removing any
systematic bias, and our surmise that inconsistencies in circulating sex hormones in the
females collectively had less of an influence on the data than oral lactate ingestion.
Although the magnitude of improvement in time-trial performance with oral lactate
was not related to VO
2peak
, mean work rate, work rate at lactate threshold, or dose (mg/kg)
of oral lactate (all p> 0.06), given that p-values of bivariate correlations are influenced by
sample size, it appears possible that in a larger cohort some of these variables may have been
significantly associated with the magnitude of improvement. Thus, significant associations,
if present, may be revealed in future studies employing larger population cohorts.
The collection of blood for quantification of parameters other than lactate, such as pH
and bicarbonate, may have provided useful insight into potential mechanisms contributing
to the observed moderate ergogenic effect. Unfortunately, these analyses were not feasible
on account of the available funds supporting the project.
Finally, additional considerations that may be relevant for future work but were
beyond the scope of the current study include characterization of the gut microbiota and the

Nutrients 2024,16, 2624 12 of 14
potential influence of genetic polymorphisms encoding for monocarboxylate transporters
(MCTs). With respect to the former, the gut microbiota is likely to play an important role in
the metabolism of ingested lactate [
46
], and exercise training status is a known modifier
of the gut microbiota [
47
,
48
]. It is plausible that differences may exist in the responses to
oral lactate between adults who are recreationally trained compared with well-trained and
professional athletes. As for the latter, MCTs are critical to the regulation of lactate and its
transport between anatomical compartments. The function of MCTs is in part determined
by genetics. Polymorphisms of MCTs influence athletic performance and responses to
exercise, including lactate and ventilatory thresholds and substrate utilization [
49
–
51
]. In
the context of the current study, responses to oral lactate may also be partially determined
by specific gene variants of MCTs. This may be a useful consideration when contemplating
variability between participants in future studies.
5. Conclusions
Low dose oral lactate ingestion appears to have neither ergolytic nor ergogenic effects
on the physiological responses to incremental exercise in healthy young adult habitual
exercisers. However, the same oral lactate dose was able to evoke a modest ergogenic
effect during a 20-min time trial. In the context of athletic performance and competition,
sometimes a small advantage can be sufficient to achieve success. Given the heterogeneity
and size of the study cohort, the relevance of this final statement should be interpreted
with caution.
Author Contributions: Conceptualization, C.B.; methodology, C.B.; formal analysis, T.R.E. and C.B.;
investigation, T.R.E., M.C.B., D.M.B., R.L.B. and B.S.K.; resources, C.B. and D.P.T.; data curation, T.R.E.
and C.B.; writing—original draft preparation, T.R.E., M.C.B. and C.B.; writing—review and editing,
T.R.E., M.C.B., D.M.B., R.L.B., B.S.K., D.P.T. and C.B.; visualization, C.B.; supervision, D.P.T. and
C.B.; project administration, C.B.; funding acquisition, C.B. All authors have read and agreed to the
published version of the manuscript.
Funding: This research was funded by Sport Specifics, Inc., Longmont, CO, USA.
Institutional Review Board Statement: The study was conducted in accordance with the Declaration
of Helsinki and approved by the Institutional Review Board of Colorado State University (Protocol
Code #4933H; 10 October 2023).
Informed Consent Statement: Informed consent was obtained from all subjects involved in the study.
Data Availability Statement: The data presented in this study are available on request from the
corresponding author.
Acknowledgments: Vector used in the Graphical Abstract downloaded from: https://shmector.com/
free-vector/people/cyclist_vector/4-0-1198, accessed on 7 July 2024.
Conflicts of Interest: The authors declare no conflicts of interest. The funders had no role in the design
of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or
in the decision to publish the results.
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