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Introduction
Maximal oxygen uptake (V
Ç
O
2
peak/max) and maximal power
output (P
max
) attained during ergometric testing are the most
frequently applied indicators of endurance capacity. After recog-
nizing the disadvantages arising from peak ergometric measure-
ments (necessity of maximal effort, dependency on motivation/
attitude of subject/investigator, difficulty to guarantee measure-
ment precision during high intensity exercise, or lacking sensi-
tivity for small changes in endurance capacity) several working
groups have developed alternative models utilizing submaximal
parameters. As a result, within the last two decades, perform-
ance diagnoses and training prescriptions in endurance sport
have often relied upon blood lactate curves from incremental ex-
ercise tests [68]. However, irrespective of their longer history of
application [149], submaximal indicators derived from gas ex-
change measurements have gained less attention although their
noninvasive nature renders them attractive.
Together with sports medicine, cardiology and pneumology rep-
resent medical disciplines that traditionally apply cardiopulmo-
nary exercise testing. Therefore, an ideal framework for perform-
ance diagnosis and exercise prescription should be also valid for
patients with impaired function of the heart or lungs. This is par-
ticularly important because endurance exercise has been imple-
mented as a therapeutic measure in several cardiac and pulmo-
nary disease entities, e.g. obstructive airway disease (COPD), cor-
onary artery disease (CAD), or chronic heart failure (CHF). Obvi-
Abstract
The first part of this article intends to give an applicable frame-
work for the evaluation of endurance capacity as well as for the
derivation of exercise prescription by the use of two gas ex-
change thresholds: aerobic (AerT
GE
) and anaerobic (AnT
GE
). Aer-
T
GE
corresponds to the first increase in blood lactate during incre-
mental exercise whereas AnT
GE
approximates the maximal lac-
tate steady state. With very few constraints, they are valid in
competitive athletes, sedentary subjects, and patients. In the
second part of the paper, the practical application of gas ex-
change thresholds in cross-sectional and longitudinal studies is
described, thereby further validating the 2-threshold model. It
is shown that AerT
GE
and AnT
GE
can reliably distinguish between
different states of endurance capacity and that they can well de-
tect training-induced changes. Factors influencing their relation-
ship to the maximal oxygen uptake are discussed. Finally, some
approaches of using gas exchange thresholds for exercise pre-
scription in athletes, healthy subjects, and chronically diseased
patients are addressed.
Key words
nplease add
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1
Affiliation
1
Institute of Sports and Preventive Medicine, University of Saarland, Saarbrücken, Germany
2
Department of Morphological and Physiological Sciences, Universidad Europea de Madrid, Madrid, Spain
3
Cooper Institute Center for Human Performance and Nutrition Research, Dallas, Texas, USA
Correspondence
T. Meyer, M.D., Ph.D ´ Institute of Sports and Preventive Medicine, University of Saarland, Faculty of
Clinical Medicine ´ Campus, Bldg. 39.1 ´ 66123 Saarbrücken ´ Germany ´ Phone: + 49 (0) 681302 37 50 ´
Fax: + 49(0)68130242 96 ´ E-mail: t.meyer@rz.uni-sb.de
Accepted after revision: n
Bibliography
Int J Sports Med 2005; 26: 1±11 Georg Thieme Verlag KG ´ Stuttgart ´ New York ´
DOI 10.1055/s-2004-830514 ´
ISSN 0172-4622
T. Meyer
1
A. Lucía
2
C. P. Earnest
3
W. Kindermann
1
A Conceptual Framework for Performance
Diagnosis and Training Prescription from
Submaximal Parameters ± Theory and Application
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ously, in these patients there are several other (disease-specific)
aspects to be considered prior to the commencement of training.
But in the absence of contraindications, prescription of exercise
(intensity) might be done according to the framework outlined
below which is based on submaximal ªthresholdº concepts.
It is acknowledged that the term ªthresholdº does not perfectly
reflect the physiological processes which form the basis for the
endurance indicators discussed below [17,106]. Some readers
might prefer ªtransitionº instead. However, as this article is pri-
marily intended to give outlines for practical applications, the
more common term ªthresholdº was chosen. It emphasizes that
the thresholds represent important landmarks within the spec-
trum of workloads. For purposes of endurance capacity assess-
ment and exercise prescription, this is undoubtedly the most im-
portant aspect.
Lactate Threshold Concepts
The use of blood lactate concentrations for ergometric evalua-
tions and exercise prescriptions is based on the simple and reli-
able determination of this glucose metabolite from capillary
blood and on its property to increase exponentially during incre-
mental exercise. Available lactate models almost exclusively fit
into one of two categories [62, 89], i.e., they approximate either
1. the first increase in blood lactate concentrations above resting
values during incremental exercise (termed ªanaerobicº
threshold by Wasserman [152]; but ªaerobicº threshold by
Kindermann [62])
or
2. the maximal lactate steady state (MLSS) representing the ex-
ercise intensity above which a continuous increase in blood
lactate is unavoidable (ªanaerobicº threshold according to
Kindermann and McLellan [62, 89,134]).
Within this paper the thresholds will be called aerobic lactate
threshold (AerT
LA
) and anaerobic lactate threshold (AnT
LA
), re-
spectively.
(Unfortunately, there has been a lot of confusion concerning the
terms ªaerobicº and ªanaerobicº. It was argued that there is no
complete absence of anaerobic metabolism even at rest. In addi-
tion, the rather transitional nature of changes in metabolic pro-
cesses from very low to high intensities was emphasized. How-
ever, we would like to lead the readers attention to the applica-
tion-oriented background of the models. Apart from the naming,
no real disagreement exists that at least for clinicians and
coaches the first rise in blood lactate during incremental exercise
and the maximal lactate steady state represent two clearly dis-
cernible phenomena each with a different meaning [32,57]. The
reason to adopt the Kindermann/McLellan terminology with in
this review is that it covers both ªthresholdsº ± although it does
not solve all problems. Consequently, it is acknowledged that the
terms ªaerobicº and ªanaerobicº do not precisely represent the
physiological process that underlie these thresholds.)
When the assessment of a threshold models validity is intended
with regard to performance prediction and exercise prescription,
studies have to consider the described physiological back-
grounds. Correlation analyses between one threshold and com-
petition results alone touch only one aspect [14, 56, 66,124,139].
Almost uniformly, satisfactory relationships between various
submaximal lactate indices and performance measures have
been documented [142]. But additional constant-load tests of
long duration are usually warranted to investigate the metabolic
meaning of the thresholds ± i.e. their applicability for purposes of
training categorisation [13,144]. Theoretically, such tests should
lead to blood lactate concentrations in the range of resting values
for intensities corresponding to the aerobic threshold. Small in-
creases of the workload above this intensity are expected to elicit
slightly elevated lactate levels without an exponential rise. In-
tensities corresponding to the anaerobic threshold give the high-
est possible equilibrium between lactate release and uptake.
Thus, small further increases of the workload will unavoidably
induce rising lactate concentrations. Training studies demon-
strating the sensitivity of a threshold model for changes in en-
durance capacity should ideally complete the set of validation
steps [1,34]. Surprisingly, an acceptable validation along these
lines has been done for very few models only [143].
The results from sound investigations utilizing constant-load
tests of sufficient duration substantiate the 2-threshold frame
described above. As early as 1986, Ribeiro et al. documented only
slight increases in blood lactate concentrations at an intensity
corresponding to the aerobic threshold whereas cycling at the
anaerobic threshold (ªsecond break pointº in lactate curve) elic-
ited average steady-state lactate values of 5 mmol ´l
±1
[119]. A
workload between anaerobic threshold and V
Ç
O
2max
was not sus-
tainable for the majority of 8 subjects for more than 15 minutes,
and lactate concentrations approached 10 mmol ´l
±1
. However,
the authors failed to rule out that there are intensities more
closely above the anaerobic threshold that could have been
maintained under steady lactate conditions.
Smaller differences between investigated workloads were chos-
en by another working group [145] who intended to validate the
model of the ªindividual anaerobic thresholdº (IAT; [135]). And it
was shown that even workloads only 5% above the IAT led to in-
creasing lactate concentrations and premature cessations of con-
stant exercise before the intended duration of 45 min was
reached.
These findings correspond well to the results from other investi-
gators who used similar graphical models to determine aerobic
and anaerobic threshold and applied constant-load tests of 30
[16, 90] or 45 min duration [111], respectively. In addition, these
studies indicate that the critical power [105] does not necessarily
represent the maximal lactate steady state. Although represent-
ing the earliest and most frequently cited approach [81], fixed
lactate concentrations ± usually 2 and 4 mmol ´l
±1
± do not ap-
propriately determine aerobic [111] or anaerobic thresholds
[16,134]. However, it has to be mentioned that even for the
well-validated model of Stegmann et al. [134] for unknown rea-
sons there exist some results which point out that it might over-
estimate the intensity of the individual maximal lactate steady
state in single subjects [69, 92]. The most likely explanation is
that there occur false threshold determinations due to the some-
what complicated graphical procedure.
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Aerobic Gas Exchange Threshold (AerT
GE
)
During incremental exercise, the first rise in blood lactate con-
centration leads to an overproportional increase of carbon diox-
ide output (ªexcess CO
2
º; [4]) as related to oxygen uptake due to
the bicarbonate buffering of the proton resulting from the disso-
ciation of lactic acid [152]. As a consequence of a slightly rising
carbon dioxide partial pressure, there is a compensatory in-
creased stimulus for ventilation mediated via the carotid bodies
[151]. Thus, minute ventilation (V
E
) is also increasing overpro-
portionally. And this is why the workload corresponding to these
events is sometimes termed ªventilatory thresholdº or ªventila-
tory threshold 1º although it is primarily a metabolic phenome-
non as reflected in Wassermans choice to call it ªanaerobic
thresholdº [149,152]. However, as indicated by the physiological
basis, this intensity reflects the ªaerobicº lactate threshold
[22, 35,36, 91,129,140,160] as it was described in the preceding
chapter. Consequently, we will use the term ªaerobic gas ex-
change thresholdº (AerT
GE
) for the rest of the text.
Graphical determination of AerT
GE
is usually done by the V-slope
method [9] which depicts V
Ç
CO
2
on the y-axis and V
Ç
O
2
on the x-
axis (Fig. 1). After an initial linear relationship, there appears a
sudden upward bend indicating the excess CO
2
being exhaled.
The intersection of two regression lines for the upper and the
lower part of the function indicates AerT
GE
which is, by defini-
tion, an oxygen uptake. If the corresponding workload during in-
cremental exercise is to be determined the time constant for oxy-
gen has to be considered. A modification of the V-slope method ±
detection of the workload where the slope of the relation V
Ç
CO
2
/
V
Ç
O
2
becomes larger than 1 ± has been proposed by the same
working group, thereby further eliminating investigator bias
[137]. Computerized solutions are available for a long time al-
ready [108].
There are three other criteria suggested in the literature to detect
AerT
GE
:
± the first rise in the ventilatory equivalent for O
2
(V
E
/V
Ç
O
2
)
without a concomitant rise in the ventilatory equivalent for
CO
2
(V
E
/V
Ç
CO
2
) ± not really different from plotting V
E
vs. V
Ç
O
2
because no new data are added
± the first overproportional increase in the respiratory exchange
ratio (RER = V
Ç
CO
2
/V
Ç
O
2
) ± just another expression of the origi-
nal V-slope method and often difficult to detect
± the first increase in the expiratory fraction of O
2
± it repre-
sents the consequence of hyperpnea, adds a new parameter,
but is still primarily dependent on ventilation and not on met-
abolic parameters
It can be recommended to rely mainly on the V-slope method as
the most direct approach [9] utilizing only measurements of
V
Ç
CO
2
and V
Ç
O
2
[4]. The employment of ventilation data adds a
source of variance because the individual sensitivity of chemore-
ceptors to the partial pressure of carbon dioxide together with
the central processing of their afferences becomes relevant
[106]. Therefore, it might be the best solution to use the courses
of V
E
and EqO
2
in a supportive manner only for cases of indeter-
minate AerT
GE
from the sole application of the V-slope method.
Due to technical constraints, precise measurements of V
E
were
available earlier than determinations of V
Ç
CO
2
. These circum-
stances might partly explain why there is a number of studies
which support the view that the physiological link between
AerT
LA
and AerT
GE
is absent or coincidental although the se-
quence of events from the appearance of lactate to an enhanced
ventilation seems attractive and evident. Not surprisingly, it is a
striking feature of most of these studies that they used only ven-
tilation data for the determination of AerT
GE
[40,42,51, 53,107,
114,128]. But exercise ventilation is controlled by numerous fac-
tors other than lactate appearance and its resulting increase in
the partial pressure of CO
2
which renders these procedures more
unreliable than V-slope [51,106,154,155]. Therefore, such studies
can detect incongruencies between exercise-induced hyperpnea
and the lactate increase, but hardly between AerT
GE
and AerT
LA
.
Recognizing these shortcomings an influential review arrived at
the conclusion that ª¼little doubt should exist that the (aerobic)
blood lactate and ventilatory responses are causally linkedº [68].
However, even when perfectly complying with the above de-
scribed determination schedule for AerT
GE
, the inherent varia-
tion of gas exchange measurements can lead to inaccuracies. Ob-
jectivity (= inter-observer reliability) and reproducibility (= re-
peatability) of AerT
GE
have been questioned as well as the per-
centage of indeterminate thresholds [49, 94,127,159]. Computer-
ized procedures [108] as well as data transformation enabling
easier decisions [8] have been suggested without finally solving
the methodological problems. Therefore, duplicate determina-
tions only from experienced observers, utilization of multiple
criteria, and plausibility controls for computer results have be-
come scientific standard. In 1996, a list of procedural recommen-
dations was published from a group that mainly works with
cardiac patients [94]. It can be regarded as useful for healthy in-
dividuals, too. If all these precautions are met, AerT
GE
determina-
tions can be regarded as valid [10,38,48,67,85, 95,138] even if
there seems to remain a small number of indeterminate thresh-
olds for varying and sometimes unknown reasons, particularly in
unfit subjects [38, 61,94].
When, in contrast to the above given recommendations, ventila-
tory data are mainly used for the determination there is a danger
of mixing up the AerT
GE
with the respiratory compensation
Fig.1 Determination of AerT
GE
by the V-slope method in one cardiac
patient. The arrow indicates the V
Ç
O
2
at AerT
GE
.
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threshold (see next chapter). In a knowledgeable review McLel-
lan called this ª¼the single most common methodological error
in the literatureº [89]. Unfortunately, this evaluation was pub-
lished in a journal with low impact and not widely spread. And
it failed to change the facts as evidenced by an own survey being
conducted in 2002 on 49 papers from the four most influential
sports medicine journals. They were elected from the years
1991± 2000 provided they reported values for AerT
GE
as well as
for V
Ç
O
2max
. A thorough review revealed that almost 50% of these
articles reported values which were hardly in agreement with
the physiological basis of AerT
GE
, i.e. most times too high abso-
lute values or too high percentages of V
Ç
O
2
peak. Beneath inad-
equate exercise protocols (too slow increment, too large steps,
breaks between stages, and inadequate degree of effort spent at
maximal exercise) an obvious mixing up with the respiratory
compensation threshold (= anaerobic gas exchange threshold =
AnT
GE
) ± most often on the basis of using only ventilation data ±
was the most common mistake (own unpublished data). The lat-
ter might even occur when V
Ç
CO
2
is utilized on the y-axis because
of a noticeable increase in V
Ç
CO
2
close to MLSS. Due to the steep-
ening characteristic of the lactate curve in this region, the first
increase in blood lactate might be ªoverlookedº by inexperienced
observers. Nevertheless, the best solution to obtain reliable re-
sults is the consequent application of the V-slope method [9]
and of ramp exercise protocols (also appropriate for V
Ç
O
2
peak de-
termination) although they are not optimal for the simultaneous
determination of lactate thresholds.
Anaerobic Gas Exchange Threshold (AnT
GE
)
The anaerobic gas exchange threshold (AnT
GE
) represents the on-
set of exercise-induced hyperventilation, i.e. an overproportional
increase of V
E
as related to V
Ç
CO
2
[9,117,129]. By definition, it is a
ªventilatoryº phenomenon, and this is reflected in the term ªre-
spiratory compensation pointº (RCP) which is most often used in
the literature. However, for the purposes of this review we will
consistently use AnT
GE
to maintain uniform terminology.
Graphically, AnT
GE
is determined similar to V-slope but with V
E
on the y-axis and V
Ç
CO
2
on the x-axis (Fig. 2). Two regression lines
are fitted for the upper and the lower part of the relation, and
their intersection represents AnT
GE
. The first systematic increase
in the ventilatory equivalent for CO
2
or the first decrease in the
expiratory fraction of CO
2
can be taken as alternative indicators.
However, they do not provide new information beyond a differ-
ent representation of the onset of exercise-induced hyperventila-
tion. When V
E
is plotted against V
Ç
O
2
the AnT
GE
represents a sec-
ond upward bending of the graph above AerT
GE,
which led to the
naming ªventilatory threshold 2º [2].
The physiological basis of AnT
GE
is less clear than that of AerT
GE
because there are several stimuli for ventilation during exercise.
It was hypothesized that the metabolic acidosis resulting from
insufficient buffering of lactic acid might be the main responsi-
ble factor. The workloads between AerT
GE
and AnT
GE
were conse-
quently termed the zone of ªisocapnic bufferingº [150] ± or aero-
bic-anaerobic transition by others [62]. However, experimental
correction of the pH to resting levels did not completely prevent
hyperventilation but was sufficient to delay it [96]. Additional
non-humoral stimuli have to be considered as partly responsible
for the occurrence of AnT
GE
, e.g. core temperature [155], potassi-
um [21] and local ªmetaboreceptorsº [87,133], or mechanical re-
ceptors [57] in the muscles.
There are some cross-sectional studies that describe the location
of AnT
GE
more closely by comparing it with known indicators of
endurance capacity. In 11 subjects being tested on a treadmill,
Dickhuth et al. [35] observed AnT
GE
slightly (0.8 km´h
±1
when
expressed as running speed) above their AnT
LA
(baseline lactate
concentration + 1.5 mmol ´l
±1
, [124]). This is substantiated by
findings from another working group which found AnT
GE
on
average 49 W above the maximal lactate steady state (= 239 W)
in 11 young students on a cycle ergometer [33]. And during
30-min constant power tests ªjust belowº AnT
GE
in only 3 un-
trained subjects the resulting lactate concentrations were not
compatible with a steady state whereas cycling ªjust aboveº
AnT
GE
led to exhaustion after 10 min and a lactate increase to ap-
proximately 11 mmol´ l
±1
in a single subject [129]. Only Ahmaidi
et al. reported no significant differences between AnT
LA
and
AnT
GE
in 11 subjects of fair endurance capacity [2]. But it was sur-
prising that in one of their participants the difference between
both workloads reached 100 W (AnT
LA
higher). Taken together,
published results indicate that AnT
GE
might slightly overestimate
the maximal lactate steady state and, therefore, be located
slightly above AnT
LA
. This results in a performance diagnosis
model as depicted in Fig. 3.
Unfortunately, in contrast to AerT
GE
there exist very few scientific
investigations about methodological problems of the AnT
GE
de-
termination. Two studies indicate sufficient reproducibility
[5, 35] in 33 and 11 subjects, respectively. Objectivity could not
be addressed in one of these studies [35] because a computer cal-
culated the thresholds. But the other authors reported significant
but (in absolute terms) small inter-investigator differences [5].
And nothing is known about the percentage of indeterminate
AnT
GE
s. One reason for the low number of investigations might
be the high degree of effort being necessary to reach intensities
above AnT
GE
which is a prerequisite for its determination [109].
Patients with a low endurance capacity often cannot reach these
stages because symptoms or subjective exhaustion occur earlier.
Fig. 2 Determination of AnT
GE
in an endurance athlete. The arrow in-
dicates the V
Ç
O
2
at AnT
GE
.
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Application of the Gas Exchange Thresholds in
Cardiopulmonary Exercise Testing and Training
Prescription
Athletes and other healthy populations
Several studies have reported the AerT
GE
and/or AnT
GE
in subjects
with different fitness levels using mostly ramp-like gradual tests
with short-duration (~ 1 min) workloads. Extensive research has
been conducted in professional road cyclists. In these athletes,
AerT
GE
and AnT
GE
correspond to 70 ±75% V
Ç
O
2max
and 85 ±90%
V
Ç
O
2max
, respectively [73]. In other competitive endurance ath-
letes, AnT
GE
is located at comparable or slightly lower intensities,
i.e. ~ 85% V
Ç
O
2max
in marathon/long-distance runners, canoeists,
rowers or pentathletes [19], ~ 80% V
Ç
O
2max
in middle-distance
runners, and between 80 and 85% V
Ç
O
2max
in long- and short-dis-
tance top-level triathletes during cycling exercise [103], at ~ 80%
V
Ç
O
2max
in younger triathletes on a treadmill [18], or at ~ 90%
V
Ç
O
2max
in endurance swimmers (vs. 60% in sprinters) [131]. In
trained triathletes, AerT
GE
occurs at different oxygen uptakes for
each discipline, i.e. ~ 74 % V
Ç
O
2max
in treadmill running vs. ~ 63% in
ergometer cycling [126]. In paraplegic athletes (V
Ç
O
2
peak
~ 40 ml´ kg
±1
´ min
±1
) evaluated during incremental wheelchair
exercise, AerT
GE
occurred at 56% of V
Ç
O
2
peak [148].
Both AerT
GE
and AnT
GE
as percentages of V
Ç
O
2
peak/max reflect, at
least partly, the degree of adaptation of humans to endurance ex-
ercise and their fitness level. Compared with highly endurance-
trained humans, AerT
GE
and/or AnT
GE
occur at considerably lower
intensities in subjects with inferior endurance training back-
ground (AerT
GE
in non-professional well-trained cyclists at 65%
V
Ç
O
2max
vs. 70 ±75 % V
Ç
O
2max
in professionals; [28]). In only moder-
ately trained cyclists, AerT
GE
and AnT
GE
were found to be located
at 58 and 75% V
Ç
O
2max
, respectively [7]. In rhythmic gymnasts or
dancers (AerT
GE
at ~ 60 and ~ 45% V
Ç
O
2max
, respectively; [6]),
physically fit adults (non-athletes; AnT
GE
at 79% V
Ç
O
2max
; [141])
or healthy sedentary adults (AerT
GE
at ~ 50 ±58% V
Ç
O
2
peak;
[29, 50,79]) AerT
GE
rarely reaches or surpasses 60% V
Ç
O
2
peak
[82]. Research within large population samples has elicited no
remarkable gender differences in the intensity (% V
Ç
O
2max
) corre-
sponding to AerT
GE
in sedentary adults [50,152]. The same seems
to be true in endurance-trained individuals, where no major dif-
ference is observed for AnT
GE
between males and females [58].
Older subjects
Some research has been conducted in healthy elderly people not
engaged in regular endurance training and on the possible effects
of ageing on the AerT
GE
[3, 84,112,115]. In individuals with a mean
age between 55 and 75 y (V
Ç
O
2
peak ~ 25 ml´kg
±1
´ min
±1
), AerT
GE
has often been reported to occur at ~ 60% V
Ç
O
2
peak, correspond-
ing to a V
Ç
O
2
value of 15 ±17 ml´ kg
±1
´ min
±1
[3,115], although it
has also been observed to approach 20 ml ´kg
±1
´ min
±1
in elderly
subjects under 75 y of age [112] and in physically active octoge-
narians [84]. Even 28 ml´ kg
±1
´ min
±1
at AerT
GE
have been report-
ed in physically active sexagenarians [84].
In a cross-sectional study aiming at indirectly assessing the ef-
fects of ageing on aerobic fitness, Paterson and co-workers deter-
mined the AerT
GE
by use of a ramp-like treadmill protocol in a
large sample of healthy men (n = 124) and women (n = 97) rang-
ing in age from 55 to 85 yrs [112]. As expected, the absolute
workload eliciting AerT
GE
decreased significantly with age in
both sexes. However, the rate of age-decline in V
Ç
O
2
peak was
greater than that of AerT
GE
, which resulted in AerT
GE
occuring at
a considerably higher proportion of V
Ç
O
2
peak, i.e. 77 vs. 84%
V
Ç
O
2
peak in the youngest and oldest men, and 80 vs. 90% V
Ç
O
2
peak
in the youngest and oldest women, respectively. Furthermore,
less than 11% of variance in AerT
GE
(expressed as ml ´kg
±1
´ min
±1
)
was explained by the ageing process itself.
In agreement with the aforementioned findings, the AerT
GE
of
healthy, untrained older people (mean: 68 y) occurred at consid-
erably higher relative intensities than in their younger controls
(mean: 23 y), i.e. 60 vs. 50% V
Ç
O
2
peak [115]. Malatesta and co-
workers have recently reported the AerT
GE
to occur at very high
submaximal intensities (~ 80% V
Ç
O
2
peak) in physically active sex-
agenarians and octogenarians [84]. Taken together, these find-
ings would suggest that the age-decline in (absolute) V
Ç
O
2
peak is
partly compensated for by an increase in the % V
Ç
O
2
peak at which
AerT
GE
occurs. In endurance-trained elderly men (i.e., master
marathoners with a mean age of 62 y and a mean V
Ç
O
2max
of
~ 50 ml´ kg
±1
´ min
±1
), AerT
GE
and AnT
GE
occurred at similar rela-
tive intensities than those reported in young endurance athletes,
i.e. at ~ 65 and ~ 85% V
Ç
O
2max
, respectively [71]. These findings
might indicate that habituation to high degrees of effort enables
Fig. 3 Model for the delineation of exercise
intensities (= training zones) by use of gas
exchange thresholds. Typical values for en-
durance-trained and untrained subjects as
well as for chronically diseased patients are
shown in the squares.
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higher maximal ergometric measurements and, consequently,
lower relative values for AerT
GE
and AnT
GE
.
Children and adolescents
Compared with sedentary adults, AerT
GE
occurs at slightly higher
relative workloads in healthy children from 5 to 16 yrs of age, i.e.
at a V
Ç
O
2
of 25± 40 ml´ kg
±1
´ min
±1
and 60 ±65% V
Ç
O
2max
on average
[30,46,54, 82, 83,113,117,122]. Healthy untrained adults reach
50±58% V
Ç
O
2
peak [29, 50,79] and rarely surpass 60% V
Ç
O
2
peak
[82]. Furthermore, in endurance-trained male children (11±
13 yrs), AerT
GE
was reported to occur at very high relative inten-
sities, i.e., ~ 80% V
Ç
O
2max
[147]. This might indicate a less well-de-
veloped acidosis tolerance in the young [39,157] ± particularly
marked after predominantly aerobic endurance training ± which
leads to comparably lower maximal lactate concentrations [26].
Diseased populations
Extensive research has been conducted on subjects with various
chronic diseases associated with abnormally low V
Ç
O
2
peak (usu-
ally < 15±20 ml ´kg
±1
´ min
±1
) and poor exercise tolerance (e.g.
peak power output < 100 W during cycle ergometer tests) due to
impaired cardiac output, altered gas exchange in the lung, and/or
severe muscle deconditioning, namely: patients with chronic
heart failure [47, 63, 86,130,153,156], cardiac transplant recipi-
ents [80], patients with primary pulmonary hypertension
[31,121] or coronary artery disease [45,125], cancer patients
[104] and survivors [15], and others [12,23, 65,102,120]. V
Ç
O
2
(ml´min
±1
or ml ´kg
±1
´ min
±1
) at AerT
GE
is considerably lower in
these patients than in healthy controls and tends to decrease
with the severity of the disease, which renders AerT
GE
a valid in-
dicator of functional capacity in these patients. For instance, the
AerT
GE
of patients with chronic heart failure decreases progres-
sively as New York Heart Association functional class (NYHA) ad-
vances [64, 86]: 33 ml´kg
±1
´ min
±1
in healthy controls vs. 23, 17,
and 13 ml´ kg
±1
´ min
±1
in class I, II, and III patients, respectively
[86]. Furthermore, in this population (different etiologies) the
risk of early death was shown to increase considerably if the
V
Ç
O
2
at AerT
GE
was < 11 ml ´ kg
±1
´ min
±1
[47].
It must be emphasized, however, that although in healthy sub-
jects deconditioning is associated with a lower % V
Ç
O
2
peak at the
AerT
GE
[132], in many of the aforementioned patients the % V
Ç
O
2-
peak at AerT
GE
is quite high [86,121], e.g. ~ 74% in patients with
primary pulmonary hypertension vs. 60% V
Ç
O
2
peak in healthy
controls [121] or ~ 72 % V
Ç
O
2
peak in chronic heart failure patients
[47]. In addition, patients with congestive heart failure demon-
strate increases in the relative intensity at AerT
GE
with the se-
verity of the disease reaching 75% V
Ç
O
2
peak in patients of NYHA
class IV (mean V
Ç
O
2
peak: 9.2 ml´ kg
±1
´ min
±1
). This apparently
paradoxical phenomenon is likely due to an attenuated rise of
V
Ç
O
2
above AerT
GE
and/or the fact that in many of these patients
exercise tolerance is remarkably low. This means that any in-
crease in V
Ç
O
2
above resting values (~ 3.5 ml ´kg
±1
´ min
±1
) repre-
sents a rather high percentage of the subjects V
Ç
O
2
peak [121]. In
liver transplant recipients with chemotherapy-induced severe
muscle atrophy (mean V
Ç
O
2
peak of 22 ml ´ kg
±1
´ min
±1
), AerT
GE
oc-
curred at low workloads in absolute terms (V
Ç
O
2
of 1.2 l´min
±1
)
but at high relative intensities (nearly ~ 73% actual V
Ç
O
2
peak;
[136]).
In summary, relative intensities of AerT
GE
and AnT
GE
vary with
(and are largely determined by) endurance training and subse-
quent fitness level, health status, or age. When thresholds are re-
ported relative to V
Ç
O
2max
, a sufficient degree of effort is a prereq-
uisite for appropriate interpretation. Diminished acidosis toler-
ance (children, elderly) as well as submaximal cessation of exer-
cise (lacking motivation), and symptom limitation (disease) lead
to increasing percentages. In severely ill patient populations this
can render relative values almost meaningless. The highest
workloads eliciting both thresholds have been reported in top-
level endurance athletes. In these subjects, it is not uncommon
to detect AerT
GE
and AnT
GE
at ~ 75 % and 90% V
Ç
O
2max
, respectively.
In sedentary subjects average values of 55% for AerT
GE
and 75%
for AnT
GE
are representative. It is of particular interest that abso-
lute values of AerT
GE
expressed in ml ´kg
±1
´ min
±1
have prognos-
tic power in chronically diseased humans.
Thresholds reflect differences in endurance capacity
(cross-sectional and longitudinal studies)
Both AerT
GE
and AnT
GE
reflect endurance capacity, i.e. the adapta-
tion of humans to endurance exercise. For instance, when com-
paring professional with elite amateur cyclists (~ 35000 vs.
24000 km covered during both training and competition each
year), it appears that V
Ç
O
2max
is not sensitive enough to reflect
the small differences in endurance capacity that exist between
these subjects. V
Ç
O
2max
approached a similar mean value of
~ 75 ml´ kg
±1
´ min
±1
in both groups despite obvious differences
in fitness and performance level [78]. Significant differences,
however, were found for the workload (W, W ´kg
±1
or % V
Ç
O
2max
)
eliciting both AerT
GE
and AnT
GE
. The high values of both thresh-
olds in professional riders, particularly that of AnT
GE
(~ 386 W
on average or ~ 90% V
Ç
O
2max
) was thought to reflect the ability of
these riders to tolerate very high workloads (= 350 W) during
long time intervals (= 20 min) without intolerably high lactate
concentrations in the blood.
However, it is obvious that longitudinal studies are the most ap-
propriate methodological approach to investigate if gas ex-
change thresholds reflect adaptations to endurance training. In
a meta-analysis that covered the years from 1967 to 1994 and
34 studies performed mostly with non-athletes (of which 13 re-
ported values for AerT
GE
), Londeree [70] calculated that AerT
GE
was on average less responsive to training than AerT
LA
. Obvi-
ously, no standardization of training loads was available. Also,
threshold determination methodology varied between studies.
These problems, together with the independency of the pooled
samples, made meaningful comparisons between AerT
GE
and
AerT
LA
difficult. However, similar findings were reported in two
studies from one working group that measured training effects
on both AerT
LA
and AerT
GE
(determined by use of ventilation data
alone) in one sample of subjects, suggesting that metabolic
adaptations at the muscle level occur more readily than subse-
quent changes in ventilatory control [42,114]. Their discrepant
findings for both types of thresholds might be explained by the
sole use of ventilation for the determination of AerT
GE
(see chap-
ter ªAerobic gas exchange thresholdº). This is not to say that
AerT
GE
and AnT
GE
do not show significant improvements with
endurance training. In a classic study, Davis et al. [32] reported
a marked improvement in the workload eliciting AerT
GE
(44% in-
crease when expressed as absolute V
Ç
O
2
and 15% when expressed
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relative to V
Ç
O
2
peak) after a 9-wk training program (4 d ´wk
±1
)in
previously sedentary middle-aged men. Comparable findings
were obtained by Smith and ODonnell [132] in physically active
middle-aged men.
In studies with top-class endurance athletes, both thresholds
were highly responsive to training. In world-class cyclists, the
power outputs eliciting AerT
GE
and AnT
GE
significantly increased
from the start of the season to the competition months (spring)
by ~ 8% and 6%, respectively [75]. Corresponding findings have
been obtained when analysing the AerT
GE
response to training
in another group of professional cyclists [55]. Similarly, in top-
class endurance runners the running velocity eliciting AerT
GE
sig-
nificantly increased by ~ 10% during the season [20]. In contrast,
there are indications that the V
Ç
O
2max
of world-class endurance
athletes is insensitive to training interventions over the compet-
itive season despite significant improvements in AerT
GE
/AnT
GE
[74,75].
In middle-distance runners, the improvement induced by an en-
durance training program including highly intense sessions has
been reported to be more marked for AnT
GE
than for AerT
GE
[110]. In elite 400-meter runners, Röcker et al. [123] reported a
longer isocapnic buffering phase (the distance between AerT
GE
and AnT
GE
) compared with (non-elite) endurance runners and
sedentary subjects. Taken together, both findings suggest that
very intense training sessions (such as those performed by 400-
meter runners) induce an improvement in buffering capacity
rather than in muscle oxidative capacity. As a result, the train-
ing-associated improvements in AnT
GE
are more marked than
those of AerT
GE
. In professional road cyclists, however, yearly
training (~ 30 000 km´ year
±1
) is based mostly on long sessions
of moderate intensity involving mainly aerobic pathways that in-
duce similar improvements in both thresholds [27].
Using 432 previously sedentary subjects of both sexes (aged 17 to
65 y), Gaskill et al. in 2001 evaluated the effects of 20 weeks ex-
ercise training intensity relative to the AerT
GE
on the degree of
improvements in a) the workload (V
Ç
O
2
) eliciting AerT
GE
and b)
V
Ç
O
2
peak [44]. Supervised cycle ergometer training was per-
formed 3 times per week. Exercise training progressed from the
HR corresponding to 55% V
Ç
O
2max
for 30 min to the HR associated
with 75% V
Ç
O
2max
for 50 min for the final 6 weeks. The subjects
were retrospectively divided into groups based on whether exer-
cise training was initiated below, at, or above AerT
GE
. Training in-
tensity (relative to AerT
GE
) accounted for about 26% of the im-
provement in the V
Ç
O
2
level at the AerT
GE
but had no effect on
V
Ç
O
2max
. That is, higher intensities (> AerT
GE
) resulted in larger
gains in the V
Ç
O
2
at the AerT
GE
but not in V
Ç
O
2max
. Researchers from
this multi-centre project have shown that there exists a strong
familial [43] and genetic contribution to both the workload elic-
iting the AerT
GE
and its response to training [41]. Future research
might determine specific candidate genes associated with the
trainability of AerT
GE
.
Some studies have also confirmed significant increases in the
AerT
GE
induced by training in individuals with low functional ca-
pacity. As an example, in patients with coronary artery disease,
the V
Ç
O
2
(in ml´ kg
±1
´ min
±1
) at AerT
GE
increased by as much as
~ 25% after 1 y of aerobic training combined with strength train-
ing [125]. Similar findings (26% improvement) have been report-
ed in elderly humans after a 3-month interval training program:
two weekly sessions consisting of walking/jogging bouts alter-
nating with rest periods until achieving a total exercise time of
1 h by the end of the program [3]. Even in chronic heart failure
patients AerT
GE
is responsive to training. After 12 weeks of en-
durance training on a cycle ergometer (45 min, 4 ± 5 days per
week), moderate improvements of 11% were noted [98,100,
101]. This is in accordance with other studies which used AerT
GE
as a secondary parameter only [11, 37, 53].
Application of AerT
GE
and AnT
GE
in exercise prescription
As early as 1978, the validity of the ªrelative percent conceptº, i.e.
prescribing training intensities as percentages of maximal ergo-
metric values, was substantially criticized [60] and instead the
use of AerT
GE
as reference recommended. A more recent investi-
gation concerning the metabolic meaning of given percentages
of VO
2
max and HR
max
substantiates these findings [97]. AerT
GE
and AnT
GE
can be used to delineate intensity ªzonesº for endur-
ance training (Fig. 3). These are usually prescribed by means of
ªtargetº heart rates or running velocities. However, meanwhile
in competitive cycling more sophisticated technical solutions ex-
ist. Athletes have their own bicycle equipped with a portable
powermeter. This device measures the actual power output di-
rectly at the crank which enables prescribing intensities in W.
In an attempt to quantify competition intensity, Lucía et al.
(1999) used a simple model derived from a preceding ramp test:
zone 1 or ªlow intensityº, zone 2 or ªmoderate intensityº, and
zone 3 or ªhigh intensityº ± that is, below AerT
GE
, between AerT
GE
and AnT
GE
, and above AnT
GE
, respectively [72]. This approach has
been used to quantify exercise loads in one of the most extreme
endurance exercises undertaken by humans: the Tour de France
[72,76, 77]. During the 1997 Tour de France (total duration of
~ 100 h for the 7 subjects being studied), the % time spent in
zones 1, 2, and 3 was 70, 23, and 7%, respectively [72]. This ap-
proach has also been used to quantify the training loads of elite
endurance athletes over a sports season. For example, research
with professional cyclists has shown that, from fall (pre-compe-
tition) to spring (competition period) the percentage contribu-
tion of high-intensity training (zone 3) increased from 1 to 8%
whereas that of low-intensity workloads (zone 1) decreased
from 88 to 77%, respectively [73].
In a training study within a more sedentary population (n = 432),
Gaskill et al. [44] categorized intensity similarly: below, at, or
above AerT
GE
. Another working group used different training tar-
gets: 50% and 70 or 75% of the difference between AerT
GE
and
V
Ç
O
2max
in 10 and 9 healthy individuals, respectively [25, 32].
McLellan and Skinner noted significantly larger training effects
after 8 weeks of cycle ergometry when AerT
GE
was the training
reference compared with V
Ç
O
2max
[93]. However, the number of
tested subjects (n = 6 vs. n = 8, respectively) was very low, and
V
Ç
O
2max
was chosen as criterion variable.
As endurance exercise has gained importance for rehabilitative
purposes after chronic disease, the assessment of appropriate ex-
ercise intensities becomes important. However, physicians are
often reluctant to exercise these patients to the maximum. This
is why the AerT
GE
represents an attractive reference particularly
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in this population. This has been acknowledged by some in car-
diac rehabilitation [88] but has more often been considered by
pneumologists. Guidelines for rehabilitation in pulmonary pa-
tients have adopted corresponding intensity recommendations
[158]. Not surprisingly, AnT
GE
was not used for prescription pur-
poses because too many patients do not reach sufficiently high
intensities during exercise testing to allow its determination.
The most often cited study is one from Casaburi et al. [24] which
demonstrated that 11 COPD (chronic obstructive pulmonary dis-
ease) patients who trained for 8 weeks at a workload corre-
sponding to 60% of the difference AerT
GE
±V
Ç
O
2max
had larger
training gains than 8 similar patients who trained at 90% of the
AerT
GE
only. This was interpreted in a way that AerT
GE
represents
an intensity to be surpassed for ensuring training effect. Such in-
terpretations led Puente-Maestu et al. (2000) to the choice of an
intensity of AerT
GE
plus 25% of the difference to V
Ç
O
2max
for their
8-week training program [116]. Another training study used the
heart rate at AerT
GE
as intensity prescription for 20 COPD pa-
tients [146], but other investigators questioned the justification
of this approach [60,161].
In the last decade several training studies were conducted in
chronic heart failure (CHF) patients. In this population, AerT
GE
seems to be an attractive reference, too, but has only been used
for evaluation of the functional capacity for a long time [99]. Two
very recent publications shed light on the usefulness of AerT
GE
also for CHF patients [99,101]. The authors were able to demon-
strate that AerT
GE
serves well for exercise prescription and the
evaluation of training effects without causing undue health risks.
In accordance with Katch et al. [60] intensity prescription was
given to the patients as a workload.
Conclusions
An applicable framework has been outlined for the evaluation of
endurance capacity as well as for the derivation of exercise pre-
scription by use of gas exchange thresholds. With very few con-
straints, it is valid for competitive athletes, sedentary subjects,
and recreational patients. After summarizing the relationship
between blood lactate, acid-base status, and gas exchange during
incremental exercise, the existence of two meaningful gas ex-
change thresholds (AerT
GE
and AnT
GE
) was explained and a model
for intensity prescription introduced. Then the validity of both
thresholds for the evaluation of fitness differences (cross-sec-
tional view) and changes in endurance capacity (longitudinal)
was documented. Finally, some approaches of using gas ex-
change thresholds for exercise prescription in athletes, healthy
and chronically diseased subjects were addressed.
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