Sports Medicine

https://doi.org/10.1007/s40279-021-01581-z

REVIEW ARTICLE

Identification of Non‑Invasive Exercise Thresholds: Methods,

Strategies, and an Online App
Daniel A. Keir1,2 · Danilo Iannetta3 · Felipe Mattioni Maturana4 · John M. Kowalchuk1,5 · Juan M. Murias3

Accepted: 3 October 2021

© The Author(s), under exclusive licence to Springer Nature Switzerland AG 2021

Abstract
During incremental exercise, two thresholds may be identified from standard gas exchange and ventilatory measurements.
The first signifies the onset of blood lactate accumulation (the lactate threshold, LT) and the second the onset of metabolic
acidosis (the respiratory compensation point, RCP). The ability to explain why these thresholds occur and how they are
identified, non-invasively, from pulmonary gas exchange and ventilatory variables is fundamental to the field of exercise
physiology and requisite to the understanding of core concepts including exercise intensity, assessment, prescription, and
performance. This review is intended as a unique and comprehensive theoretical and practical resource for instructors, clini-
cians, researchers, lab technicians, and students at both undergraduate and graduate levels to facilitate the teaching, compre-
hension, and proper non-invasive identification of exercise thresholds. Specific objectives are to: (1) explain the underlying
physiology that produces the LT and RCP; (2) introduce the classic non-invasive measurements by which these thresholds
are identified by connecting variable profiles to underlying physiological behaviour; (3) discuss common issues that can
obscure threshold detection and strategies to identify and mitigate these challenges; and (4) introduce an online resource
to facilitate learning and standard practices. Specific examples of exercise gas exchange and ventilatory data are provided
throughout to illustrate these concepts and a novel online application tool designed specifically to identify the estimated LT
(θLT) and RCP is introduced. This application is a unique platform for learners to practice skills on real exercise data and for
anyone to analyze incremental exercise data for the purpose of identifying θLT and RCP.

1 Introduction clinical exercise laboratories across the world, facilitate the

The measurement of respired volumes of oxygen (­ O2) and
carbon dioxide (­ CO2) during exercise provides non-inva-
sive insight into the ability of the cardiorespiratory system
to adjust O
­ 2 transport and C ­ O2 removal to the demands
imposed by increases in muscle metabolism. These meas-
urements, which are routinely used in teaching, research, and
* Daniel A. Keir
dkeir@uwo.ca
1
School of Kinesiology, The University of Western Ontario,
AHB 3G18, 1151 Richmond Street, London, ON N6A 3K7,
Canada
2
Toronto General Research Institute, Toronto General
Hospital, Toronto, ON, Canada
3
Faculty of Kinesiology, University of Calgary, Calgary, AB,
Canada
4
Department of Sports Medicine, University of Tübingen,
Baden‑Württemberg, Germany
5
Department of Physiology and Pharmacology, The University
of Western Ontario, London, ON, Canada
indirect quantification of the rates of O­ 2 uptake (V̇ O2), ­CO2
removal (V̇ CO2), and minute ventilation (V̇ E). Decades ago,
it was recognized that the profiles of these variables dur-
ing incremental exercise provide a window into changes in
muscle metabolism and their systemic effects [1–3]. These
changes are traditionally defined as exercise “thresholds”.
During incremental exercise, two thresholds may be iden-
tified from pulmonary gas exchange and ventilatory meas-
ures. These are commonly (but not universally) referred
to as the “estimated lactate threshold (θLT)” (although gas
exchange threshold is frequently used) and the respiratory
compensation point (RCP). From a mechanistic perspec-
tive, the θLT reflects the highest metabolic rate not associ-
ated with elevated blood lactate concentrations [4] and the
RCP reflects the metabolic rate at which the body can no
longer prevent accumulation of hydrogen ions (­ [H+]) associ-
ated with increased lactate and C ­ O2 production [2]. In young
healthy individuals, the V̇ O2 at which the θLT and RCP occur
relative to maximal rate of ­O2 uptake (V̇ O2max) varies widely
about a mean of 63% (range: 49–74%) and 83% (range:
73–94%) of V̇ O2max in women and 58% (range: 45–73%) and

Vol.:(0123456789)

Key Points
During incremental exercise, two thresholds may be
identified from standard gas exchange and ventilatory
measurements. The first signifies the onset of lactate
elevation (estimate lactate threshold, θLT) and the second
the onset of metabolic acidosis (the respiratory compen-
sation point, RCP).
The θLT and RCP are fundamental to the field of exer-
cise science and requisite to the understanding of key
concepts in sports medicine including exercise intensity,
assessment, prescription, and performance. This review
summarizes the physiology underlying the θLT and RCP,
and discusses strategies to approach their non-invasive
identification during incremental exercise.
Gas exchange and ventilatory profiles do not always
follow a “textbook” template and can be influenced by
behaviours (e.g., abnormal breathing responses) that
complicate θLT and RCP detection. With the objective
of standardizing approaches to θLT and RCP identifica-
tion, this review provides specific examples of both
“textbook” and “abnormal” templates, outlines detailed
approaches to avoid potential misclassifications, and
introduces a state-of-the-art open-source online applica-
tion for the knowledge user to practice their skills and
analyze data (https://​exerc​iseth​resho​lds.​com/.)
82% (range: 69–96%) of V̇ O2max in men, for θLT and RCP,
respectively [5, 6]. In addition to V̇ O2max, the θLT and RCP
of incremental exercise represent key parameters of aerobic
function that are used to stratify exercise intensity [7–11],
assess aerobic fitness [12], and predict exercise perfor-
mance [13] and even health outcomes in clinical populations
[14]. The ability to explain why these exercise thresholds
occur and how they may be identified from pulmonary gas
exchange and ventilatory measures is important for exercise
science professionals and key learning outcomes in exercise
physiology courses. Competency in this area is required to
fully understand the concepts of exercise intensity and pre-
scription and a key component for a commercial, clinical, or
research career in exercise physiology.
With the aim of facilitating the teaching, comprehen-
sion, standardization, and skills required to identify these
exercise thresholds, this review will: (1) explain the under-
lying physiological mechanisms that produce the θLT and
RCP; (2) introduce the classic non-invasive measurements
by which these thresholds (i.e., θLT and RCP) are identified
by connecting variable profiles to underlying physiologi-
cal behaviour; (3) discuss common issues that can obscure
D. A. Keir et al.
threshold detection and strategies to identify and mitigate
these challenges; and (4) introduce an online resource to
facilitate learning and standard practices. Specific exam-
ples of exercise gas-exchange and ventilatory data during
incremental cycling exercise will be provided throughout to
illustrate these concepts. The accompanying online appli-
cation introduced in this paper will provide a standardized
platform by which to upload and analyze incremental exer-
cise data and an opportunity for novice users to practice their
skills on real incremental exercise data. This paper assumes
a basic understanding of exercise metabolism and control
of breathing. For comprehensive reviews on these topics,
the interested reader is referred to [15–17]. In addition, to
obtain a richer appreciation for the seminal work that led
to the development of these concepts (all of which cannot
be adequately acknowledged here), the interested reader
is referred to the historical summary in Poole et al. [18].
Finally, methodological considerations are limited to sam-
pling of expired gases and flows during incremental exercise
and do not detail thresholds derived from blood lactate data.
2 Exercise Thresholds and Exercise Intensity
The exercise physiology and sports medicine literatures
contain countless terms and descriptions of different
exercise thresholds. Common to each is that they iden-
tify a metabolic “boundary” at which muscle metabolism
changes in a way that alters cellular and physiological
homeostasis and prompts a compensatory adjustment of
the cardiorespiratory support system. Decades ago, Brian
Whipp and colleagues demonstrated that V̇ O2 and blood-
lactate responses to constant work rate exercise change in
relation to two metabolic boundaries [19, 20]. Exercise
below, between, and above these two boundaries reproduc-
ibly yields common physiological strain in the muscle met-
abolic, gas-exchange and ventilation, and blood acid–base
responses [21–23] to exercise with direct implications for
muscle fatigue [24, 25], perception of effort [26, 27], and
exercise tolerability [28, 29]. These metabolic bounda-
ries provide the framework for Whipp’s exercise inten-
sity domain schema that partitions exercise intensity into
moderate, heavy, and very heavy (or severe [30]) intensity
domains. The physiological basis of this framework and
its implications for exercise research and performance are
integral to the understanding of exercise thresholds and
have been reviewed extensively by Poole and Jones [30]
and Rossiter [16].
For simplicity, the two metabolic boundaries can be
framed in relation to the concepts of metabolic acido-
sis (an increase in cellular hydrogen ion concentration
­( [H +]) (reduction in cellular pH) consequent to mus-
cle metabolism) and physiological homeostasis (a set of
Identification of the Estimated Lactate Threshold and Respiratory Compensation Point
self-regulating processes that maintain stability while
adjusting to exercise conditions). The moderate-heavy-
intensity boundary marks the highest metabolic rate not
associated with metabolic acidosis or disruption to physi-
ological homeostasis. The heavy-severe-intensity boundary
denotes the highest metabolic rate at which physiological
homeostasis can be maintained despite a slight but sta-
ble metabolic acidosis. Above this boundary, metabolic
acidosis worsens progressively with respect to exercise
intensity and duration at a given intensity, and physiologi-
cal homeostasis fails. Importantly, these two boundaries
occur at widely variable fractions of V̇ O2max [5, 31]. Thus,
adequate classification and prescription of exercise requires
that the metabolic rates at which these boundaries occur
are identified, and neither should be assumed to occur at
a fixed %V̇ O2max.
Within the incremental exercise paradigm, these meta-
bolic boundaries are surpassed on route to a maximal effort
and may be estimated by identifying alterations in lactate
measurements from blood draws, or gas-exchange and ven-
tilatory responses from measures of respired gas exchange
and flow at the mouth. Numerous different terminologies
and methods for identification of these changes exist, each
with their own strengths and limitations [11], and it is
beyond the scope of this review to summarize each. In the
context of this review, methodological considerations will
focus on the sampling of expired gases and flows during
incremental exercise with some reference to thresholds
derived from blood lactate data. With respect to blood-
lactate thresholds, we consider the lactate threshold (LT)
and lactate turn point (LTP) to reflect the moderate-heavy-
and heavy-severe-intensity boundaries, respectively. When
referring to non-invasive methods for identification of these
boundaries, we describe an approach that incorporates
simultaneous inspection of a multitude of gas-exchange
and ventilatory profiles [32] and, thus, refer to the esti-
mated lactate threshold (θLT) and respiratory compensa-
tion point (RCP). Importantly, the identification of θLT
includes (and, thus, is synonymous with) the popular gas
exchange threshold (GET) and first ventilatory threshold
­(VT1) (described in Sect. 4.3) and the identification of RCP
includes the second ventilatory threshold ­(VT2) (described
in Sect. 5.2). One caveat is that the former is accepted as
the moderate-heavy-intensity boundary without question
whereas there is debate about the latter [33, 34].
3 Exercise Protocols and Maximal Rate
of ­O2 Uptake (VO
̇ 2max)
For non-invasive identification of exercise thresholds, par-
ticipants are required to perform a graded (i.e., step) or
progressive (i.e., ramp) incremental exercise test endured
to the limit of tolerance while respiratory gases and flows
are recorded continuously from the mouth. Measuring the
rate of ­O2 uptake (i.e., V̇ O2) during an exercise protocol
designed to increase metabolic demand through muscle
work (i.e., power output) provides valuable insight into
the body’s ability to take up, deliver, and utilize O
­ 2 for the
resynthesis of adenosine triphosphate (ATP). Most exercise
protocols use cycle ergometers or treadmills, and involve
incrementally increasing metabolic demand by increasing
power output or treadmill speed and/or grade. In every
individual, there is a metabolic rate at which measured V̇
O2 cannot increase further despite increases in exercise
power output. This V̇ O2, which may or may not exhibit a
“plateau”, gives an estimation of V̇ O2max [35–37].
For the evaluation of θLT, RCP, and V̇ O2max, protocols
involving application of work rate (i.e., power output or
speed) in a ramp- or step-incremental pattern with frequent
incrementation (~ 2 min per increment or less) are opti-
mal. With these protocols, V̇ O2 increases smoothly with
time, making it easier to detect alterations in the slope of
gas-exchange and ventilatory response profiles and their
associated metabolic rates (i.e., corresponding V̇ O2 val-
ues). The rate of incrementation (e.g., W/min or W/step)
should be chosen judiciously to ensure that total exercise
time is sufficiently long to discern changes in gas exchange
and ventilatory profiles (e.g., a minimum of ~ 10 min). For
example, in average healthy young adults who perform
ramp-incremental cycling exercise from a baseline of 20 W,
incrementation slopes of 20–30 W/min lead to exhaustion
in ~ 8–12 min. However, in those whose exercise capacity is
severely limited (e.g., chronic heart disease), a lower ramp
slope (e.g., 5–10 W/min) and baseline work rate may be
needed to ensure enough data for threshold detection (see,
e.g., [38]).
The rate of incrementation (e.g., W/min or W/step)
does not impact the metabolic rate at which θLT or RCP
are detected [39, 40] but does affect the work rate at which
they occur [39–41]. In other words, the metabolic rate at
θLT and RCP are constant and independent of the incre-
mental protocol, but the work rates at which the V̇ O2 at
θLT or RCP occurs will vary dependent on the incremental
protocol [39, 41]. Such findings: (1) appear to support that
both θLT and RCP represent robust metabolic boundaries;
(2) highlight why both θLT and RCP should always be iden-
tified in terms of ̇V̇ O2; and (3) have critical implications
for selecting a power output or speed associated with θLT
and RCP (see [7, 33, 42] for details). For these reasons, the
procedures and examples provided throughout this paper
focus on incrementation rates of 20–30 W per min achieved
in either ramp- or step-incremental protocols and with V̇ O2
displayed on the abscissa.

4 Estimated Lactate Threshold (θLT)
4.1 Physiological Bases of the Lactate Threshold
Figure 1 displays a schematic representation of muscle metabo-
lism and its effects on blood lactate, acid–base status, and pul-
monary gas exchange at exercise intensities below (Fig. 1a) and
above (Fig. 1b) the lactate threshold. To maintain adequate ATP
for the increasing metabolic demand imposed by incremental
exercise, the ATP resynthesis pathways in skeletal muscle must
upregulate. Activation of muscle glycolysis (and glycogenoly-
sis) is associated with increased production of pyruvate (­ Pyr−)
(and lactate ­(La−)), the end-product of glycolysis. At intensi-
ties approaching the lactate threshold, ­Pyr− production within
the muscle cytosol and ­Pyr− uptake and oxidation within the
mitochondria are approximately equal, and thus P ­ yr− conver-
−
sion to ­La (catalyzed by lactate dehydrogenase (LDH)) and
­La− accumulation and concentration remain low (Fig. 1a). With
increasing metabolic demand above the lactate threshold, how-
ever, the rate of ­Pyr− production exceeds that of its uptake and
oxidation within mitochondria such that the cytosolic accumula-
tion of ­Pyr− (and nicotinamide adenine dinucleotide [NADH]
and protons ­[H+]) is directed increasingly towards ­La− produc-
tion resulting in progressively greater cytosolic accumulations
of ­La− and ­H+ and a rise in [­ La−] (Fig. 1b). Importantly, given
the cytosolic location of LDH, a high LDH activity (relative to
the activity of regulatory enzymes for glycolysis and Pyr- oxi-
dation), and an equilibrium constant for LDH directed towards
­La− formation, the reduction of P ­ yr− to ­La− is favoured and
rapid [43].
As ­La− and H ­ + accumulate within the cytosol, co-transport
of both metabolites from muscle to blood increases, facilitated
by membrane-bound monocarboxylate transporters (MCT)
[44]. The enhanced efflux of these metabolites from muscle
somewhat attenuates the cytosolic accumulation of both and
thus delays the development of a metabolic (lactic) acidosis,
while coincidently raising the extracellular (including blood)
­La− ­([La−]) [45]. Therefore, the intramuscular build-up of L­ a− is
reflected in the blood with a relatively similar time course such
that active muscle ­[La−] displays a similar pattern to that of
blood ­[La−] [46, 47]. At progressively higher exercise intensities
above the lactate threshold, blood (and muscle) [­ La−] continue
to rise owing, in part, to the progressively greater activation of
muscle glycolysis (and glycogenolysis) and a disproportionately
higher rate of ­La− efflux from muscle (rate of appearance in
blood) compared to its uptake and metabolism in muscle and
other tissues (rate of disappearance from blood) [48]. The met-
abolic rate associated with increased concentration of blood
­La− is defined as the “lactate threshold”.
The increase in [­ La−] is accompanied by higher intra- and
extracellular ­[H+] (i.e., reduced pH (= -log [­ H+])), although
increases in [­ La−] (mM changes) far exceed those of [­ H+]
D. A. Keir et al.
(nM changes), in part because protons are highly reactive
and interact with negative charges on, for example, amino
acids and proteins, and hydroxide (­ OH−) and bicarbonate
­(HCO3−) molecules (see [49–51] for excellent reviews on
acid–base balance). From a gas-exchange and acid–base
perspective, there are systems in place to “defend” the
acid–base status within muscle and blood and, thus, avoid
acidosis. An important mechanism for controlling both
arterial blood ­[H+] and ­PCO2 involves the bicarbonate-CO2
system and the reversible hydration-dehydration of ­CO2,
catalyzed by carbonic anhydrase (CA):
CA
H+ + HCO−3 ↔ H2 CO3 ↔ H2 O + CO2 (1)
In this reaction, the blood ­[H+] is controlled through the com-
bination of H ­ + with ­HCO3− to produce C ­ O2, which along with
the ­CO2 produced during mitochondrial substrate oxidation (i.e.,
pyruvate dehydrogenase-catalyzed decarboxylation of P ­ yr− and
reactions of the tricarboxylic acid cycle), is delivered to and
eliminated at the lung (i.e., as pulmonary V̇ CO2; see differences
in ­CO2 delivery to the lung and V̇ CO2 between Fig. 1a and b).
4.2 Direct Identification of LT
To directly identify LT, blood [­ La−] is collected during step-
incremental exercise in which work rate is increased at regu-
lar intervals (usually 2–4 min) until the participant reaches
exhaustion. Blood ­[La−] is sampled at the end of each work-
rate interval and plotted in relation to V̇ O2 or work rate. The
resultant curvilinear blood [­ La−] versus V̇ O2 profile (see,
e.g., Figs. 2h and 3h) is then scrutinized to identify the V̇ O2
at which blood [­ La−] begins to rise above its resting concen-
tration. This V̇ O2 defines the LT. Because blood ­[La−] and
V̇ O2 take time to stabilize during exercise, their relationship
within an individual can be influenced by the step duration
and number of steps [52]. Longer steps (e.g., 10 min) are
likely to provide a more accurate representation of the blood
­[La−] associated with a given V̇ O2, but to maintain reason-
able test durations, fewer steps are performed (typically with
greater work rate amplitudes), which reduces the precision
of LT identification. In addition, numerous strategies exist to
identify the initial rise in blood ­[La−] (summarized in [52]).
Together, these factors influence the accuracy, precision, and
confidence of identifying the V̇ O2 at which LT occurs [52].
4.3 Non‑Invasive Identification of LT (θLT)
It is possible to estimate the LT without collecting blood
samples (i.e., non-invasively). By displaying and carefully
examining gas-exchange and ventilatory data, one can esti-
mate with a high degree of accuracy the V̇ O2 at which the
arterial blood ­La− becomes elevated above resting concen-
trations, i.e., the “estimated LT” (θLT). Below the lactate
Identification of the Estimated Lactate Threshold and Respiratory Compensation Point

Fig. 1  Illustration of the (a) Myocyte 1

muscle-blood and blood-lung
interfaces and their connection
via the circulation (from bottom
right to top left of each figure:
arterial-venous-pulmonary- Left heart
Pi + ADP ATP Pi + ADP ATP Pi + ADP ATP
arterial) to highlight muscle
PCr Cr PCr Cr
metabolism below (a) versus VO2
•

above (b) the metabolic rate at Alveoli

the lactate threshold (LT) and •
its influence on blood chemistry VE
PCr Cr
and pulmonary gas exchange Glycogen H+ H+ H+ ADP ATP
and ventilation. Font sizes are • ADP
VCO2
modified to emphasize differ- ATP
e–
ences in “concentration” or NAD+ NAD+ FAD+ Pi + ADP
Right heart
“production” of key substrates NADH NADH FADH2
(e.g., oxygen ­(O2), phospho- ATP
O2
creatine (PCr)) and metabolic CO2
Pyruvate Acetyl- TCA
by-products (e.g., carbon CoA
Venous LDH
dioxide ­(CO2), lactate ­(La−), Mitochondria
bicarbonate ­(HCO3−), hydrogen
+ –
H & La CO2
ions ­(H+), inorganic phosphate
(Pi), adenosine diphosphate Myocyte 2
(ADP) and to highlight differ- HbO2 Arterial
ences in “rate” of pulmonary Pyruvate La–
variables ­(O2 uptake (V̇ O2);
­CO2 excretion rate (V̇ CO2); and
(b) Myocyte 1
ventilation (V̇ E)). Arrow thick-
[H+]
ness indicates the relative “flux”
of metabolic pathways (e.g., La–
glycogenolysis, lactate dehydro-
genase (LDH), pyruvate dehy- Left heart Pi + ADP ATP Pi + ADP ATP Pi + ADP ATP
drogenase, and tricarboxylic
PCr Cr PCr Cr
acid (TCA) cycle) and transport •
VO2
pathways for key substrates and Alveoli
metabolic by-products (e.g., •
creatine (Cr) kinase shuttle, VE PCr Cr
electron ­(e−) transport). ATP Glycogen H+ H+ H+ ADP ATP
adenosine triphosphate, FADH2 • ADP
reduced flavin adenine dinu- VCO2 ATP
e–
cleotide, FAD+ oxidized flavin NAD+ NAD+ FAD+
Right heart Pi + ADP
adenine dinucleotide, HbO2 NADH NADH FADH2
oxyhemoglobin, NADH reduced ATP
nicotinamide adenine dinucleo- CO2 O2
Pyruvate Acetyl- TCA
tide, NAD+ oxidized nicotina- HCO3– CoA
Venous LDH
mide adenine dinucleotide + Mitochondria
–
H+ & La– CO2
HCO3
+
Myocyte 2 H+ & La–

HbO2 Arterial
Pyruvate La–

threshold, oxidative phosphorylation provides nearly all of
the energy required for exercise: O­ 2 is consumed and C
­ O2 is
produced at approximately the same rate depending on the
substrate being oxidized and V̇ CO2 increases linearly with
V̇ O2. Above the LT, the L ­ a−-associated increases in blood
+ −
­H combine with ­HCO3 to produce an additional source
of ­CO2 (Eq. 1 is shifted towards production of C­ O2), which
causes an increase in V̇ CO2 relative to V̇ O2. When plotted,
the V̇ CO2–V̇ O2 relationship (also termed the “V-slope”)
exhibits a transition in slope (or “breakpoint”), referred to
as the gas exchange threshold (GET), which is coincident
with the onset of blood L­ a− accumulation (i.e., an increase
−
in ­[La ] above resting values). The GET relies exclusively
on the V̇ CO2 versus V̇ O2 relationship and serves as a non-
invasive method for identifying the metabolic rate associated
with the LT (compare Fig. 2a and h).
Because ventilation (V̇ E) is regulated by ­CO2 delivery to
the lungs to minimize excessive C ­ O2 accumulation, V̇ E also
begins to increase disproportionately to V̇ O2. As a result, a
“breakpoint” is observed in the V̇ E versus V̇ O2 relationship
 D. A. Keir et al.

(a) (b)

(c) (d)

(e) (f)

(g) (h)

Fig. 2  Schematic representation of blood-lactate and common gas-
exchange and ventilatory variables that are collected during incre-
mental exercise and used to identify the estimated lactate threshold
(θLT) and respiratory compensation point (RCP). Rate of ­CO2 excre-
tion (V̇ CO2), respiratory exchange ratio (RER), minute ventilation (V̇
E), ventilatory equivalent of oxygen uptake (V E/V O2), end-tidal pres-
̇ ̇
sure of ­CO2 ­(PETCO2), ventilatory equivalent of V̇ CO2 (V̇ E/V̇ CO2),
end-tidal pressure of O­ 2, ­(PETO2) and blood-lactate concentration are
plotted in relation to rate of oxygen uptake (V̇ O2). The vertical lines
intersecting the abscissa of each figure indicate the V̇ O2 associated
with θLT and RCP
Identification of the Estimated Lactate Threshold and Respiratory Compensation Point
(a)
(c)
(e)
(g)
Fig. 3  Breath-by-breath gas exchange and ventilatory variables of a
representative participant collected during a 30 W/min ramp-incre-
mental cycling test to exhaustion. Blood lactate values (h) are from
the same participant collected on a different day. Data points corre-
spond to the sixth minute of constant-work rate exercise at 50, 80,
110, 140, and 170 W and eighth minute of constant-work rate exer-
cise at 200, 230, 260, and 290 W, and have been presented elsewhere
[77]. The solid vertical line intersecting the abscissa of each figure
(b)
(d)
(f)
(h)
indicates the oxygen uptake (V̇ O2) associated with the estimated lac-
tate threshold (θLT). V̇ CO2 rate of ­CO2 excretion, V̇ E minute ventila-
tion, V̇ E/V̇ CO2 and V̇ E/V̇ O2 ventilatory equivalent for the rate of ­CO2
excretion and oxygen uptake, respectively, RER respiratory exchange
ratio, PETCO2 and P ­ ETO2 end-tidal partial pressure for ­CO2 and ­O2,
respectively, VT1 first ventilatory threshold, GET gas exchange
threshold, LT blood lactate threshold

(commonly referred to as the first ventilatory threshold or
­VT1, Fig. 2c), which is coincident with the GET. Therefore,
the θLT may be identified by finding either GET or V ­ T1, but
for greater accuracy and confidence, both should be com-
bined along with the other measures described below.
Other helpful indices that should be used to corroborate
estimations of the θLT when plotted against V̇ O2 are: the
respiratory exchange ratio (RER, V̇ CO2/V̇ O2 ratio), ventila-
tory equivalents for V̇ O2 (V̇ E/V̇ O2) and V̇ CO2 (V̇ E/V̇ CO2),
and, with breath-by-breath systems (as opposed to mixing-
chamber based systems), the partial pressures of end-tidal
­O2 and C ­ O2 ­(PETO2 and P­ ETCO2, respectively). The textbook
response profiles for each of these variables are displayed
in Fig. 2 along with the V̇ CO2 versus V̇ O2 (and GET), V̇ E
versus V̇ O2 (and ­VT1) and blood ­[La−] versus V̇ O2 (and LT)
relationships.
In a relaxed, non-anxious participant, below θLT the RER
versus V̇ O2 relationship remains stable or rises slightly
(Fig. 2b), but above the θLT, the upward trajectory of RER
steepens. In normal situations, this change-point coincides
with the increase in V̇ CO2 relative to V̇ O2 (Fig. 2a); how-
ever, V̇ CO2 (and thus, RER) may also increase abruptly if
the participant spontaneously begins to breathe more vig-
orously than needed. To confirm whether “hyperpnea” (a
rise in ventilation that is proportional to metabolic need
and return of ­CO2 to the lung) and not “hyperventilation”
(a rise in ventilation that exceeds metabolic need and return
of ­CO2 to the lung) is the cause of the θLT, it is necessary
to examine ventilatory equivalent and end-tidal pressure
(or fractional expired concentration) relationships. Ventila-
tory equivalents are simply the ratios of V̇ E to V̇ O2 (V̇ E/V̇
O2) and to V̇ CO2 (V̇ E/V̇ CO2) associated with a single breath
or the average of multiple breaths, whereas end-tidal pres-
sures are the partial pressures of O ­ 2 and C
­ O2 detected at
the end of exhalation. After descending exponentially to a
plateau, the V̇ E/V̇ O2 versus V̇ O2 becomes relatively stable
below θLT but exhibits a systematic rise that commences at
θLT (Fig. 2d). The ­PETO2 and P ­ ETCO2 reflect alveolar ­PO2
and arterial ­PCO2, which are regulated by V̇ E in a manner
dependent on requirements for ­O2 uptake (i.e., V̇ O2) and ­CO2
removal (i.e., V̇ CO2). Because V̇ E rises in proportion to V̇ O2
and V̇ CO2 below θLT, alveolar P ­ O2 and arterial P
­ CO2 remain
relatively stable. During this sub-θLT region, tidal volume
and expiratory time increase, which brings P ­ ETO2 closer to
alveolar ­PO2 and ­PETCO2 closer to arterial ­PCO2 [2]. As
a result, P ­ ETO2 and ­PETCO2 decline and rise, respectively
(Fig. 2e and g), below θLT. When transitioning above θLT,
increases in V̇ E closely track V̇ CO2 rather than V̇ O2, and so
the ­PETCO2 and V̇ E/V̇ CO2 versus V̇ O2 relationships remain
stable or plateau (onset of “isocapnic buffering” period;
Fig. 2e and f) whereas the P ­ ETO2 versus V̇ O2 relationship
exhibits a systematic rise (Fig. 2g). In mixing-chamber
D. A. Keir et al.
systems, gas-exchange and ventilation are computed from
the mixing of several breaths collected in a chamber and,
therefore, end-tidal breath measurements are not possible.
In such instances, mean F ­ EO2 and ­FECO2 (reflective of mean
alveolar ­PO2 and ­PCO2) can be substituted to aid in the esti-
mation of θLT. Although the profiles of F ­ EO2 and F
­ ECO2 will
track those of P­ ETO2 and P­ ETCO2, their absolute values are
influenced by mixing-chamber volume and V̇ E, and there-
fore should not be considered to reflect those of ­PETO2 and
­PETCO2.
When estimating θLT, each of these profiles and their
associated variables (i.e., GET and ­VT1) should be examined
and considered together. In addition to mastering the correct
non-invasive identification of θLT, this recommendation also
helps to develop a deeper understanding of gas-exchange and
ventilatory signals, and what their profiles can tell us about
metabolism and the integrated cardiopulmonary responses
to incremental exercise. Finally, good understanding of
what these signals represent can also help prevent common
mistakes when interpreting gas-exchange and ventilatory
response to incremental exercise. “Textbook” gas-exchange
and ventilatory responses to incremental exercise and their
relation to the blood ­La− profile are presented as a schematic
in Fig. 2 and with real breath-by-breath data in Fig. 3. Note
that in such “normal” situations, the V̇ O2 at θLT equals that
of LT.
4.4 Practical Tips for Identifying the θLT
4.4.1 Ignoring Exercise Onset
The data displayed in Figs. 2 and 3 exclude data collected
at baseline and the first minute after exercise onset. Gas
exchange and ventilatory profiles during the early portion
of incremental exercise are dependent on how quickly gas
exchange and the cardiovascular and respiratory systems
respond following the onset of exercise (i.e., their kinetics)
and do not reflect changes in blood ­La− [16]. Between and
within individuals, the kinetics of V̇ O2, V̇ CO2, and V̇ E are
not identical and can be altered independently by many fac-
tors [53]. At the onset of ramp-incremental exercise, V̇ O2
increases linearly with work rate after an initial time interval
that is determined by both the transit delay of deoxygenated
blood from the working muscles to be expressed at the lung
and the kinetics component of muscle V̇ O2 as it adjusts to the
energetic demands imposed by the ramp [54, 55]. In healthy
individuals, this “mean response time” is ~ 30 s (typically
between 20 and 60 s) [56], but can be longer in those with
slower V̇ O2 kinetics (e.g., [57]). In addition, compared to V̇
O2 kinetics, V̇ CO2 and V̇ E kinetics are slower [53] and, thus,
any of the profiles that contain V̇ CO2 or V̇ E will deviate from
the template in Fig. 2 and impair the identification of θLT.
For these reasons, data within the first minute of exercise
Identification of the Estimated Lactate Threshold and Respiratory Compensation Point
and at baseline should always be excluded before attempting
to identify θLT. Those seeking greater detail on the concept
of mean response time, its calculation, and importance for
exercise prescription are referred to the reviews by Boone
and Bourgois [55] and Keir et al. [42].
4.4.2 Avoiding a Pseudo‑θLT
Unlike the examples provided in Figs. 2 and 3, sometimes
participants may spontaneously hyperventilate in the base-
line period and throughout the early portion of progressive
exercise. Breathing at a rate that exceeds the gas exchange
requirements set by tissue metabolism unloads C ­ O2 stores
within the body (predominantly in the form of ­HCO3−;
Eq. (1) is shifted to the right) and arterial P ­ CO2 falls. In
most individuals, the hyperventilation typically subsides as
work rate rises, but this might affect our ability to accurately
estimate θLT using the criteria listed in the previous section.
Any period of excessive ­CO2 unloading at the onset of
incremental exercise will reduce the rate at which V̇ CO2
rises because a portion of the ­CO2 produced by increased
metabolism will be used to replenish ­CO2 stores (i.e., the
rate at which Eq. (1) proceeds towards the production of
­CO2 will not be as rapid). After ­CO2 stores are refilled—
which depends on the magnitude and duration of prior C ­ O2
unloading, the time taken to restore normal ventilation, and
the rapidity of ­CO2 reloading—V̇ CO2 will reassume a trajec-
tory reflective of the metabolic response to exercise. Con-
sequently, a breakpoint or “pseudo-threshold” in the V̇ CO2
versus V̇ O2 relationship will be observed in the absence of
elevation in blood [­ La−] concentration (Fig. 4a) [58, 59]
and, thus, the identified θLT may not reflect LT. Because V̇
E is coupled more closely to a ­CO2-linked mechanism and
not V̇ O2 [15, 60], the V̇ E versus V̇ O2 relationship also will
display a pseudo-threshold (Fig. 4c).
In most cases of prior spontaneous hyperventilation,
a pseudo-threshold will occur at a V̇ O2 below the θLT. In
such instances, it remains possible to identify θLT. How-
ever, to avoid selection of a pseudo-threshold, examination
of the RER versus V̇ O2 relationship is necessary. In normal
situations, RER remains relatively stable (or only slightly
increases) until the θLT (Figs. 2b and 3b). If instead reloading
of ­CO2 is occurring during this period, an early descent in
RER relative to V̇ O2 and upward turn point will be observed
(Fig. 4b). This turn point will coincide with the pseudo-
thresholds observed in the V̇ CO2 and V̇ E versus V̇ O2 relation-
ships, and is entirely unrelated to blood ­La− concentrations
(Fig. 4h). Prior to identification of θLT, it is first necessary
to rule out the potential confounding effects of ­CO2 stor-
age by confirming the absence of an early turn point in the
RER versus V̇ O2 relationship. Thereafter, all data up to the
pseudo-threshold should be ignored and standard criteria
for θLT detection are applied to all subsequent data. Figure 4
exhibits the profile of an individual who spontaneously
hyperventilated in the early portion of the ramp-incremental
protocol. Note that the θLT can be identified correctly if data
prior to the pseudo-θLT are ignored.
The best practice to eliminate or prevent the occurrence
of a pseudo-threshold is to ensure that the incremental test
does not commence from a state of hyperventilation-induced
hypocapnia. Most incremental protocols are preceded by a
period of low-intensity baseline work. In situations where
gas exchange measures can be obtained during this period,
the RER should be monitored throughout. With hyperven-
tilation at these low intensities, the RER may approach or
exceed 1.0 but may be as low as 0.9 depending on substrate
utilization. The test should not be initiated if the RER is
above 1.0 or if the RER-time profile is declining. In such
cases, it is best to restart the test or, where permitted, extend
the baseline period until the RER reaches a stable value
below 1.0 (usually 0.75–0.9).
4.5 Summary of Strategy to Identify θLT
1. Do not begin the test until RER reaches a stable value
that is below 1.0;
2. Plot all variables against V̇ O2 (rather than work rate or
time);
3. Do not include data from baseline or from the early tran-
sition to the exercise;
4. Confirm the absence of a turn point in RER;
5. Find the GET and ­VT1, then use other plots to corrobo-
rate the estimation of θLT;
6. When identifying V ­ T1, ignore data within the final 1/3
of the test. As discussed in the next section, there is a
second ventilatory threshold; however, this strategy may
not be helpful in those with limited exercise capacity
or situations in which a submaximal V̇ O2 is achieved at
“peak” exercise (see Sect. 6.3).
The interested reader seeking more detailed guidance on
non-invasive estimation of θLT from incremental exercise
test data is invited to consult the flow chart depicted in Fig.
S1 of the Online Supplementary Material.
5 Respiratory Compensation Point
5.1 Physiological Bases
As the metabolic demand is increased above LT (e.g., by
progressing to higher power outputs in an incremental
test), the muscle [­ La−] increases and so too does its trans-
port out of the muscle, leading to a progressive increase in
blood ­[La−]. Despite a rising metabolic demand and blood
­[La−], increases in blood ­[H+], initially, are minimized
 D. A. Keir et al.

(a) (b)

(c) (d)

(e) (f)

(g) (h)

owing primarily (~ 65%) to interactions between H ­ + and the
bicarbonate-CO2 buffering system (Eq. 1) and also to hemo-
globin in red blood cells (~ 30%) and proteins and phos-
phates in blood plasma (~ 5%) [61]. The combination of H ­ +
−
and ­HCO3 leads to additional C ­ O2 formation and increases
­CO2 flux to the lung, resulting in increased V̇ E and exhaled
­ O2, thereby minimizing increases in intra- and extracellular
C
­[H+] [62]. However, at a metabolic rate well above the LT,
the bicarbonate-CO2 buffering system is unable to meet the
on-going challenges of increasing ­H+ and ­CO2 production,
which, along with a continuing rise in blood ­[La−], results
also in a progressive rise in blood ­[H+] (i.e., a developing
 Identification of the Estimated Lactate Threshold and Respiratory Compensation Point
◂Fig. 4  Breath-by-breath gas-exchange and ventilatory variables and
blood-lactate profile of a representative participant. These data were
collected using the same instruments and protocols as those that were
depicted in Fig. 3; however, a different participant was being tested.
The turn point in the RER versus V̇ O2 relationship (b) is indicative
of altered ­CO2 dynamics (due in this case to prior hyperventilation).
This increases the likelihood of a “pseudo-threshold” (PT) appearing
in the V̇ CO2 (a) and V̇ E versus V̇ O2 (c) relationships that are unrelated
to blood lactate. The dashed vertical line intersecting the abscissa of
each figure indicates the V̇ O2 at which the PT occurs. Note from h
that beyond this V̇ O2, blood lactate remains at resting concentrations.
If all data up to the turn point in RER are ignored, then the true gas
exchange threshold (GET) and first ventilatory threshold (­VT1) may
be identified and corroborated by the profiles of V̇ E–V̇ O2, V̇ E/V̇ CO2,
­PETO2, and P ­ ETCO2. The solid vertical line identifies the V̇ O2 asso-
ciated with estimated lactate threshold (θLT). Above this V̇ O2, blood
lactate becomes elevated, confirming the non-invasive identification
of LT. V̇ CO2 rate of C ­ O2 excretion, V̇ E minute ventilation, V̇ E/V̇ CO2
and V̇ E/V̇ O2 ventilatory equivalent for the rate of ­CO2 excretion and
oxygen uptake, respectively, RER respiratory exchange ratio, PETCO2
and PETO2 end-tidal partial pressure for ­CO2 and ­O2, respectively, LT
blood lactate threshold
metabolic acidosis) [63]. Coincident with the developing
acidosis, the rise in V̇ E increases relative to the on-going
rise in both V̇ CO2 and V̇ O2 (i.e., a hyperventilation relative
to both V̇ CO2 and V̇ O2). The resultant pulmonary elimina-
tion of additional ­CO2 (relative to ­CO2 accumulation) and
lowering of arterial ­PCO2 helps to maintain the flux of the
carbon anhydrase equilibrium reaction (Eq. 1) towards the
consumption of protons and, thus, attenuates the rise in
blood ­[H+]. The metabolic rate associated with the transi-
tion to a higher rate of increase of V̇ E (relative to V̇ CO2 and
V̇ O2) is referred to as the respiratory compensation point (or
RCP). Figure 5 displays a schematic representation of mus-
cle metabolism, its impact on blood-lactate and acid–base-
status, and their relation to pulmonary gas exchange and
ventilatory responses at exercise intensities below (Fig. 5a)
and above (Fig. 5b) the metabolic rate at RCP.
Although not without controversy [33, 34], the RCP has
consistently been shown to reflect the highest metabolic
rate (or exercise intensity) that may be sustained in steady-
state conditions with little disruption to the body’s internal
environment (or the maximal metabolic steady-state) and
its surrogate thresholds: the critical power, maximal lactate
steady state (MLSS), and the lactate turn point (sometimes
referred to as L ­ T2) [7, 64, 65]. For an opposing viewpoint
see Broxterman et al. [34]. The critical power is the asymp-
tote of the power-time relationship [66], MLSS is the highest
constant-work rate associated with elevated but stable blood
­[La−] [45], and lactate turn point is the V̇ O2 at which blood
­[La−] accelerates upwards from a prior period of ascent [67].
The V̇ O2 at RCP has been shown to coincide with each of
the critical power [65, 68], MLSS [6, 39], and the lactate
turn point [64], but the work rate at which RCP is identified
does not [41, 65, 68, 69]. Importantly, dissociations between
the work rate at the maximal metabolic steady state and the
work rate at the RCP simply reflect the (hidden) non-linear
nature of increase in V̇ O2 in relation to work rate during
typical incremental tests to exhaustion [33, 42]. Our research
supports the view that the RCP of incremental exercise is a
ventilatory manifestation of the transition across the meta-
bolic boundary associated with maximal metabolic steady
state. Therefore, in the context of this review, the metabolic
rate of RCP is considered equivalent to the surrogates of
this critical intensity including critical power, MLSS, and
lactate turn point.
5.2 Identification of the Respiratory Compensation
Point (RCP)
Figures 2 and 6 illustrate the theoretical and actual pro-
files, respectively, of gas-exchange, ventilatory and blood-
lactate responses that typically occur below versus above
the RCP. Up to the RCP, V̇ E rises in proportion with the
metabolic rate and the need to eliminate C ­ O2 (i.e., hyper-
pnea) (Fig. 2a). Consequently, ­PETCO2 remains remark-
ably constant in the range of V̇ O2 between LT and RCP,
termed the phase of “isocapnic buffering” [2] (Fig. 1e).
The RCP, therefore, represents the end of the isocap-
nic buffering phase, the onset of hyperventilation (rela-
tive to both V̇ O2 and V̇ CO2), the intensity at which blood
­La− accumulation accelerates (Fig. 2h) [63], and for con-
stant work rate exercise, the highest V̇ O2 associated with
steady-state lactate concentrations in the blood [7]. This
hyperventilatory RCP response can also be observed as
a second inflection (or “breakpoint”) in the V̇ E versus V̇
O2 relationship (i.e., ­VT2; see Fig. 1c). This behaviour is
confirmed by a deviation from stability in the V̇ E/V̇ CO2
versus V̇ O2 relationship (Fig. 2f), along with a more rapid
rise in the V̇ ̇E/V̇ O2 versus V̇ O2 relationship (Fig. 2d).
Examination of end-tidal pressures is particularly useful
when identifying the RCP. Above RCP, as V̇ E exceeds the
requirement to match V̇ O2 and V̇ CO2, a rise in ­PETO2 and
fall in ­PETCO2 will occur. Coincident with onset of hyper-
ventilation (i.e., the RCP) and end of the isocapnic buffering
period, ­PETCO2 begins to decline from a position of relative
stability (Fig. 1e). The fall in ­PETCO2 often occurs gradually
rather than as a steep decline. Similarly, after RCP, ­PETO2
will rise with a slope that mirrors the decline in ­PETCO2
(Fig. 1g). As discussed above, ­FEO2 and ­FECO2 may be sub-
stituted for P ­ ETO2 and P ­ ETCO2 when using gas-exchange
collection systems that utilize mixing-chamber as opposed
to breath-by-breath technology.
Like the θLT, for accurate RCP detection, it is important
to examine these profiles (and their associated variables, i.e.,
­VT2) in combination to prevent overestimating the V̇ O2 at
which the true RCP occurs (see below).
 D. A. Keir et al.

Fig. 5  Illustration of the Myocyte 1

muscle-blood and blood-lung (a) [H+]
interfaces and their connection
via the circulation (from bottom La–
right to top left of each figure:
arterial-venous-pulmonary- Left heart Pi + ADP ATP Pi + ADP ATP Pi + ADP ATP
arterial) to highlight muscle
• PCr Cr PCr Cr
metabolism below (a) versus VO2
above (b) the metabolic rate at Alveoli
the respiratory compensation •
point (RCP) and its influence on VE PCr Cr
blood chemistry and pulmonary Glycogen H+ H+ H+ ADP ATP
gas exchange and ventila- • ADP
tion. Font sizes are modified VCO2 ATP
e–
to emphasize differences in NAD+ NAD+ FAD+ Pi + ADP
Right heart
“concentration” or “production” NADH NADH FADH2
of key substrates (e.g., oxygen ATP

­(O2), phosphocreatine (PCr))

CO2 O2
Pyruvate Acetyl- TCA
and metabolic by-products (e.g., HCO3– CoA
Venous LDH
carbon dioxide (­ CO2), lactate + Mitochondria
­(La−), bicarbonate ­(HCO3−), H+ & La– CO2
HCO3–
hydrogen ions (­ H+), inorganic +
phosphate (Pi), adenosine Myocyte 2 H+ & La–
diphosphate (ADP) and to high- HbO2 Arterial
light differences in the “rate” Pyruvate La–
of pulmonary variables (­ O2
uptake (V̇ O2); ­CO2 excretion Myocyte 1
(b)
rate (V̇ CO2); and ventilation (V̇ [H+]
E)). Arrow thickness indicates
the relative “flux” of metabolic La–
pathways (e.g., glycogenolysis, Arterial
lactate dehydrogenase (LDH), chemoreflex Pi + ADP ATP Pi + ADP ATP Pi + ADP ATP
Left heart
pyruvate dehydrogenase, and
• PCr Cr PCr Cr
tricarboxylic acid (TCA) cycle) VO2
and transport pathways for Alveoli
key substrates and metabolic •
by-products (e.g., creatine
(Cr) kinase shuttle, electron
VE PCr Cr
Glycogen H+ H+ H+ ADP ATP
­(e−) transport). ATP adenosine • ADP
triphosphate, FADH2 reduced VCO2 ATP
e–
flavin adenine dinucleotide, NAD+ NAD+ FAD+
Right heart Pi + ADP
FAD+ oxidized flavin adenine NADH NADH FADH2
dinucleotide, HbO2 oxyhemo-
CO2
ATP
globin, NADH reduced nicoti- O2
Pyruvate Acetyl- TCA
namide adenine dinucleotide, HCO3
– CoA
Venous LDH
NAD+ oxidized nicotinamide + Mitochondria
H+ & La–
adenine dinucleotide HCO3
– CO2
+
Myocyte 2 H+ & La–

Pyruvate La–
HbO2 Arterial

5.3 Practical Tips for Identifying RCP
5.3.1 Identification of the Isocapnic Buffering Phase
As first described by Whipp et al. [2], the classic P­ ETCO2
response to incremental exercise is characterised by a pro-
gressive rise at intensities below the θLT, a plateau in the
region between θLT and RCP (i.e., isocapnic buffering), and a
decline in the supra-RCP phase (Fig. 2e). However, in some
cases, this profile is not observed, or the timing related to
the profile is offset. If prior hyperventilation occurs, the iso-
capnic buffering region may be difficult to discern because
of the effects of ­CO2 storage on ­CO2 return to the lung,
and, thus, on V̇ E. If V̇ CO2 dynamics are slowed, the rate
of rise in V̇ E is reduced (compare Fig. 6c to Fig. 7c). In
some individuals, this reduction is facilitated by a reduction
in breathing frequency (Fig. 7h), which causes ­PETCO2 to
continue to rise beyond θLT (Fig. 7e). This phenomenon has
two consequences that impact θLT and RCP detection. First,
the onset of the isocapnic buffering region may be difficult
Identification of the Estimated Lactate Threshold and Respiratory Compensation Point
(a)
(c)
(e)
(g)
Fig. 6  Breath-by-breath gas-exchange and ventilatory variables and
blood-lactate profile of a representative participant different from
those depicted in Figs. 3 and 4. The solid vertical line intersecting the
abscissa of each figure indicates the oxygen uptake (V̇ O2) at which
the respiratory compensation point (RCP) occurs. Note from c the
change-point in V̇ E versus V̇ O2 ­(VT2). This rise in V̇ E is confirmed to
be hyperventilation (and not hyperpnea) because it is coincident with
a fall in ­PETCO2 from a period of stability (i.e., “isocapnic buffering”
(b)
(d)
(f)
(h)
period; e and by a rise in V̇ E/V̇ CO2 (f). V̇ CO2 rate of ­CO2 excretion,
V̇ E minute ventilation, V̇ E/V̇ CO2 and V̇ E/V̇ O2ventilatory equivalent
for the rate of C
­ O2 excretion and oxygen uptake, respectively, RER
respiratory exchange ratio, PETCO2 and PETO2 end-tidal partial pres-
sure for C
­ O2 and O­ 2, respectively, VT1 first ventilatory threshold, VT2
second ventilatory threshold, GET gas exchange threshold, LT blood
lactate threshold, θLT estimated lactate threshold

to identify, and second, the P
­ ETCO2 between θLT and RCP
will exhibit a slight downward slope that either continues to
RCP or plateaus at a supra-θLT V̇ O2 (see Fig. 7e).
5.3.2 Ensuring RCP is not Overestimated
When progressing to V̇ O2 values in excess of RCP and close
to V̇ O2max, it is not uncommon, particularly in fitter individu-
als, to maintain a robust hyperventilatory response (Fig. 7
displays such a profile) [70]. Given the significant increase
in ­O2 cost and work of breathing that would be required to
expand tidal volume at these higher, severe intensities, the
progressive increase in V̇ E (and the “extra” hyperventila-
tory response) is achieved mainly by an increase in breath-
ing frequency (Fig. 7h). When this occurs V̇ E accelerates
upward relative to V̇ O2 (compare Fig. 7c to Figs. 3c or 4c
Figs. 3c or 4c). This acceleration typically occurs after RCP
making it difficult to discern RCP from the V̇ E or V̇ E/V̇ CO2
versus V̇ O2 relationships. In such instances, the profiles of
V̇ E/V̇ CO2 and ­PETCO2 are helpful. Recall that after the RCP,
the V̇ E/V̇ CO2 and ­PETCO2 versus V̇ O2 relationships exhibit
a systematic rise and fall, respectively; both from preced-
ing periods of stability (Figs. 2, 3, and 4e, f). To ensure the
RCP is not overestimated, it is important to confirm that the
profile of V̇ E/V̇ CO2 rises from a period of stability (Figs. 2f
and 3f) rather than from a period of ascent (Fig. 7f) and that
­PETCO2 falls from a period of stability (Figs. 2e and 3e)
rather than decline (Fig. 7e). When identifying RCP, these
profiles should be examined together to ensure that V̇ O2 at
RCP is not overestimated.
5.3.3 Using the V̇ E versus V̇ CO2 Relationship
Plotting V̇ E versus V̇ CO2 rather than V̇ O2 also helps to visu-
alize the RCP. During incremental exercise, V̇ E rises in uni-
son with V̇ CO2 until the RCP. Thereafter a disproportionate
rise in V̇ E relative to V̇ CO2 is observed. While useful for
visualization purposes, this approach yields a V̇ CO2 and
not the V̇ O2 at which the RCP appears. For this reason, one
must then estimate the V̇ O2 associated with that V̇ CO2 value.
This may be done by examination of the V̇ CO2 versus V̇
O2 relationship either subjectively by visual inspection or
objectively by non-linear modelling and interpolation—a
feature that is fully automated and available in the “Exercise
Thresholds” application described in Sect. 7.
5.3.4 Sometimes a RCP is Absent
Because RCP typically occurs at a high fraction of V̇ O2max,
to ensure an accurate identification of RCP, it is imperative
that participants be motivated and encouraged to continue
exercise for as long as possible such that the limit of exercise
tolerance is reached and the exercise protocol terminated at
D. A. Keir et al.
or near the participant’s V̇ O2max. Participants unfamiliar with
physical exertion or in pathological states in which exercise
intolerance is a major symptom may not be capable of pro-
ducing a truly maximal effort. For example, in a group of
1995 individuals with reduced ejection fraction heart fail-
ure, only 783 (39%) exhibited a RCP [14]. In most cases,
the absence of a RCP confirms a submaximal incremental
exercise performance. However, some populations that are
uniquely characterized with a mechanical ventilatory con-
straint (e.g., chronic obstructive pulmonary disorder) may
be unable to mount a hyperventilatory response despite a
“maximal” effort and its associated metabolic acidosis [71,
72].
5.4 Summary of Strategy to Identify the RCP
1. Plot all variables against V̇ O2 (rather than work rate or
time);
2. Do not include data from baseline or from the early tran-
sition to the exercise;
3. Confirm the absence of a turn point in RER;
4. Find the ­VT2, then use other plots (particularly V̇ E/V̇
CO2 and ­PETCO2 vs. V̇ O2 relationships) to corroborate
estimation of RCP;
5. When identifying ­VT2, focus on V̇ O2 data range above
θLT;
6. If a turn point in RER is present, the isocapnic buffering
period may not be evident and the ­PETCO2 versus V̇ O2
relationship may mislead proper identification.
The flow chart depicted in Fig. S2 of Online Supplemen-
tary Material provides further guidance for the identification
of RCP.
6 Other Considerations
6.1 Accuracy
The θLT and RCP are used as a non-invasive means to iden-
tify the V̇ O2 associated with the LT and maximal metabolic
steady state, respectively. Although the exact metabolic
rates at which these occur are not known, when the crite-
ria described above are applied correctly, the identified θLT
and RCP should validly denote these metabolic boundaries.
Thereafter, the accuracy and precision of the measurement
are largely determined by the signal-to-noise ratios of the
gas exchange and ventilatory variables. Inherent to breath-
ing are irregularities that cause point-to-point fluctuations
in the pulmonary gas exchange and ventilatory data [73].
The magnitude of this “noise” varies between individuals
and within individuals on different days [73, 74], and the
resulting variability around the mean V̇ O2 response impacts
Identification of the Estimated Lactate Threshold and Respiratory Compensation Point
(a)
(c)
(e)
(g)
Fig. 7  Breath-by-breath gas-exchange and ventilatory variables of
a representative participant different from those in Figs. 3, 4, and 5.
Note from b the presence of a change-point in RER versus V̇ O2 (due
in this case to prior-hyperventilation) and the pseudo-threshold (PT)
that appears at that V̇ O2. As a consequence of prior-hyperventilation,
­CO2 dynamics are altered and an “isocapnic buffering” period for
­PETCO2 is harder to discern (e). Note that ­PETCO2 stabilizes before
(b)
(d)
(f)
(h)
the LT and gradually declines thereafter. V̇ CO2 rate of C ­ O2 excretion,
V̇ E minute ventilation, V̇ E/V̇ CO2 and V̇ E/V̇ O2 ventilatory equivalent
for the rate of C
­ O2 excretion and oxygen uptake, respectively, RER
respiratory exchange ratio, PETCO2and PETO2 end-tidal partial pres-
sure for C
­ O2 and O­ 2, respectively, VT1 first ventilatory threshold, VT2
second ventilatory threshold, GET gas exchange threshold, LT blood
lactate threshold, θLT estimated lactate threshold

the precision with which these data can be used to identify
θLT and RCP. For steady-state exercise below LT, V̇ O2 (and
V̇ CO2) fluctuates about its mean by an average of ~ 100 mL/
min (range: 70–200 mL/min) [73, 74]. Anecdotally, this
value of ± 100 mL/min has been adopted as the minimal
acceptable error for θLT and RCP, and is often used as a
cut-off of inter-rater agreement in research investigations.
6.2 Inconclusive Tests
As mentioned, sometimes θLT and RCP are not clearly iden-
tifiable. This may occur because of prior hyperventilation
(e.g., a “pseudo-threshold” may appear in close proximity
to LT), unnatural breathing patterns (e.g., frequent coughs,
swallows, volitional breathing), low signal-to-noise ratio
data, or because the participant did not produce a truly
exhaustive effort. In situations in which the θLT and RCP
are not discernible and the purpose of the incremental exer-
cise test was to identify these thresholds, the test should be
repeated on another occasion. Often, participants without
prior experience with exhaustive incremental exercise and
pulmonary gas exchange measurements will, on their second
attempt, produce an effort that is closer to maximum and
data with less noise. When a repeat test is not possible, θLT
and RCP should be reported as inconclusive. In clinical situ-
ations such as chronic heart failure, the absence of θLT, pres-
ence of θLT and not RCP, and presence of both θLT and RCP,
are associated with improvements in prognosis compared to
patients who exhibit neither θLT nor RCP [14].
6.3 Patient Populations
Incremental exercise paired with respiratory gas exchange
and ventilatory measurement provides a means by which to
evaluate the coordinated function of the physiological sys-
tems that support the exchange of gases (i.e., O­ 2 and ­CO2)
between air and tissue. The ability of the cardiorespiratory
and vascular systems to support muscle metabolism deter-
mines exercise performance. Various clinical conditions are
characterized by defects along this gas-exchange pathway
that impair the ability to sustain or produce higher exercise
efforts. Because θLT and RCP represent the upper limits of
comfortably sustainable (metabolic steady-state without
disruption to physiological homeostasis) and uncomfortably
sustainable (metabolic steady-state with disruption to physi-
ological homeostasis) exercise, or the moderate- and heavy-
intensity domains, respectively, identification of both can
help characterize the overall function of the cardiorespira-
tory system and the severity of exercise limitation in patient
populations. Thus, both should be identified and reported
following cardiopulmonary exercise tests [75].
The pathophysiology of various chronic conditions
will contribute to defects at different locations along the
D. A. Keir et al.
gas-exchange pathway that may contribute to deviations in
the “templates” described above and influence the expres-
sion of θLT and RCP. For example, those with McArdle
syndrome, who are unable to use glycogen, do not produce
lactate; whereas those with chronic obstructive pulmonary
disease (COPD), who have high airway resistance, may be
incapable of compensatory hyperventilation. Although the
unique gas-exchange and ventilatory patterns exhibited by
such conditions are beyond the scope of this review, the
strategies provided above should help to optimize condi-
tions for θLT and RCP detection. As outlined in Sect. 2, in
those with low exercise capacity, it is imperative that the
rate of incrementation of the protocol is sufficiently low to
allow for ~ 10 min (or more) of data for confident exercise
threshold identification [38, 76].
7 Introduction to the “Exercise Thresholds”
Application
Appropriate identification of θLT and RCP require the collec-
tion of high-quality gas exchange and ventilatory data and
the ability to interpret the response profiles for the variables
of interest with the underlying physiology. Of importance
for the identification of the exercise intensity thresholds (or
boundaries) is that the ventilatory and gas exchange plots
are examined in combination rather than simply focussing
on a single variable. This task can be made easier by opti-
mal organization and assembly of variable profiles. Note
that in each figure, the profiles are displayed together, in
perfect alignment, each with V̇ O2 on the abscissa, and with
the identical x-axis ranges. Organization of data in this way
allows one to corroborate estimations of θLT or RCP from
one variable with others and is a helpful means by which to
ensure consistency and rigor. With the objective of facilitat-
ing standardization of the methods and strategic approaches
outlined in this review, the interested reader is encouraged
to explore and utilize an online tool available at https://e​ xerc​
iseth​resho​lds.​com/. The application was designed specifi-
cally as a platform to analyze incremental exercise test data
for the purpose of θLT and RCP detection. The “practice”
section provides access to 40 individual ramp-incremental
datasets. Using the unique analysis interface, the user can
apply the approaches outlined in this review to guide their
identification of the θLT and RCP. Submitted estimates can
be compared to the θLT and RCP identified by the authors of
this paper. In addition, the “analyze” tab provides a means
by which the user can upload their own data. Datasets from
most commercially available metabolic testing unit are com-
patible and allow anyone to make use of the novel analysis
platform to assist with θLT and RCP identification.
Identification of the Estimated Lactate Threshold and Respiratory Compensation Point
8 Conclusion
The gas-exchange and ventilatory profiles measured during
incremental exercise provide a non-invasive window into
changes in muscle metabolism accompanying greater levels
of muscle work and their systemic effects. The physiologi-
cal adjustments that occur at LT and RCP reflect impor-
tant intensity-specific events that can be used to establish
exercise intensity, interpret fitness and training effective-
ness, predict performance, and classify disease severity.
To appropriately interpret the non-invasive measurements
used to identify θLT or RCP, it is imperative to establish
an understanding of the underlying physiological mecha-
nisms that produce these thresholds and common behav-
iours that can complicate threshold detection. In addition
to reviewing fundamental concepts and with the objective
of standardizing approaches for θLT and RCP identification,
this paper highlights common issues that complicate θLT and
RCP detection, and strategies to identify and mitigate these
challenges. In addition, an online resource is introduced to
facilitate learning and standard practices. It is our hope that
this review is adopted as a resource to facilitate the teach-
ing, comprehension, and proper identification of exercise
thresholds in the classroom, laboratory, and clinic.
Supplementary Information The online version contains supplemen-
tary material available at https://​doi.​org/​10.​1007/​s40279-​021-​01581-z.
Declarations
Authors’ contributions D.A.K. and J.M.M. contributed to conception
and design of the article. D.A.K prepared the figures and drafted and
revised the manuscript. Exemplary data were collected and analysed
by D.A.K. and D.I. The online application was designed by F.M.M.
with input from D.A.K., J.M.M., and D.I. All authors contributed to
the drafting and revising of the manuscript. All authors approved the
final manuscript and agree to be accountable for all aspects of the work.
Funding The representative data assembled in the figures are the prod-
uct of a research and equipment grant awarded to J.M.K by the Natural
Science and Engineering Research Council of Canada (NSERC; RGP-
2015-00084) and to J.M.M by the NSERC (RGPIN-2016-03698) and
the Heart and Stroke Foundation of Canada (1047725).
Conflict of interest Daniel A. Keir, Danilo Iannetta, Felipe Mattioni
Maturana, John M. Kowalchuk, and Juan M. Murias declare that they
have no conflicts of interest relevant to the content of this review.
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