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The V·O₂ slow component, a slowly developing increase in V·O₂ during constant-work-rate exercise performed above the lactate threshold, represents a progressive loss of skeletal muscle contractile efficiency and is associated with the fatigue process. This brief review outlines the current state of knowledge concerning the mechanistic bases of the V·O₂ slow component and describes practical interventions that can attenuate the slow component and thus enhance exercise tolerance. There is strong evidence that, during constant-work-rate exercise, the development of the V·O₂ slow component is associated with the progressive recruitment of additional (type II) muscle fibers that are presumed to have lower efficiency. Recent studies, however, indicate that muscle efficiency is also lowered (resulting in a "mirror-image" V·O₂ slow component) during fatiguing, high-intensity exercise in which additional fiber recruitment is unlikely or impossible. Therefore, it seems that muscle fatigue underpins the V·O₂ slow component, although the greater fatigue sensitivity of recruited type II fibers might still play a crucial role in the loss of muscle efficiency in both situations. Several interventions can reduce the magnitude of the V·O₂ slow component, and these are typically associated with an enhanced exercise tolerance. These include endurance training, inspiratory muscle training, priming exercise, dietary nitrate supplementation, and the inspiration of hyperoxic gas. All of these interventions reduce muscle fatigue development either by improving muscle oxidative capacity and thus metabolic stability or by enhancing bulk muscle O2 delivery or local Q·O₂-to-V·O₂ matching. Future honing of these interventions to maximize their impact on the V·O₂ slow component might improve sports performance in athletes and exercise tolerance in the elderly or in patient populations.
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Slow Component of V
˙O
2
Kinetics: Mechanistic
Bases and Practical Applications
ANDREW M. JONES
1
, BRUNO GRASSI
2
, PETER M. CHRISTENSEN
3
, PETER KRUSTRUP
3
,
JENS BANGSBO
3
, and DAVID C. POOLE
4
1
Sport and Health Sciences, College of Life and Environmental Sciences, St. Luke’s Campus, University of Exeter,
Exeter, UNITED KINGDOM;
2
Department of Medical and Biological Sciences, School of Medicine, University of
Udine, Udine, ITALY;
3
Department of Exercise and Sport Sciences, University of Copenhagen, The August Krogh
Building, Universitetsparken, Copenhagen, DENMARK; and
4
Departments of Kinesiology, Anatomy and Physiology,
Kansas State University, Manhattan, KS
ABSTRACT
JONES, A. M., B. GRASSI, P. M. CHRISTENSEN, P. KRUSTRUP, J. BANGSBO, and D. C. POOLE. Slow Component of V
˙O
2
Kinetics: Mechanistic Bases and Practical Applications. Med. Sci. Sports Exerc., Vol. 43, No. 11, pp. 00–00, 2011. The V
˙O
2
slow
component, a slowly developing increase in V
˙O
2
during constant-work-rate exercise performed above the lactate threshold, represents
a progressive loss of skeletal muscle contractile efficiency and is associated with the fatigue process. This brief review outlines the
current state of knowledge concerning the mechanistic bases of the V
˙O
2
slow component and describes practical interventions that
can attenuate the slow component and thus enhance exercise tolerance. There is strong evidence that, during constant-work-rate
exercise, the development of the V
˙O
2
slow component is associated with the progressive recruitment of additional (type II) muscle
fibers that are presumed to have lower efficiency. Recent studies, however, indicate that muscle efficiency is also lowered (resulting
in a ‘‘mirror-image’’ V
˙O
2
slow component) during a fatiguing, high-intensity exercise in which additional fiber recruitment is
unlikely or impossible. Therefore, it seems that muscle fatigue underpins the V
˙O
2
slow component, although the greater fatigue
sensitivity of recruited type II fibers might still play a crucial role in the loss of muscle efficiency in both situations. Several
interventions can reduce the magnitude of the V
˙O
2
slow component, and these are typically associated with an enhanced exercise
tolerance. These include endurance training, inspiratory muscle training, priming exercise, dietary nitrate supplementation, and the
inspiration of hyperoxic gas. All of these interventions reduce muscle fatigue development either by improving muscle oxidative
capacity and thus metabolic stability or by enhancing bulk muscle O
2
delivery or local Q
˙O
2
-to-V
˙O
2
matching. Future honing of these
interventions to maximize their impact on the V
˙O
2
slow component might improve sports performance in athletes and exercise toler-
ance in the elderly or in patient populations. Key Words: SKELETAL MUSCLE, METABOLISM, ENERGETICS, EFFICIENCY,
FATIGUE, EXERCISE TOLERANCE
After the commencement of constant-work-rate (CWR)
exercise situated below the so-called lactate threshold
(LT) or gas exchange threshold (GET), pulmonary O
2
uptake (V
˙O
2
) rises relatively rapidly to attain a new steady
state within a few minutes of exercise onset (90,128). If the
work rate is above the LT, however, the attainment of a steady
state is at least delayed (102,128,132) owing to the emergence
of a supplementary, slowly developing component of the V
˙O
2
response (14,95). When the work rate is below the ‘‘critical
power’(CP)(68),theeventualV
˙O
2
steady state is greater
than the value that would be predicted from the sub-LT V
˙O
2
work rate relationship; when the work rate is above the CP,
no steady state is achievable but, rather, V
˙O
2
continues to rise
with time until the V
˙O
2max
is reached, heralding the imminent
termination of exercise (102,126,128) ( F1Fig. 1). These charac-
teristic V
˙O
2
profiles have been used to classify the various
exercise intensity domains, namely, ‘‘moderate’’ (GLT),
‘‘he a vy’’ ( 9LT but GCP), and ‘‘severe’ (9CP) (100,102,132).
Whereas the V
˙O
2
response to GLT exercise is well described,
after the exclusion of phase 1, by a monoexponential function,
the V
˙O
2
response to 9LT exercise has been shown to be better
described by biexponential processes with the second term
being delayed onset (14). This suggests a time-dependent, as
well as intensity-dependent, loss of muscle efficiency as 9LT
exercise proceeds.
This ‘‘slow component’’ of V
˙O
2
is not trivial: in the severe
domain, its magnitude can exceed 1 LImin
j1
and represent
Q25% of the total increase in V
˙O
2
above the preexercise
baseline (98). The V
˙O
2
slow component is therefore dis-
tinct from the relatively modest ‘‘O
2
drift’’ (G200 mL of O
2
)
that may attend moderate exercise of a prolonged duration
(i.e., Q60 min). On a purely academic level, the V
˙O
2
slow
component phenomenon is of interest because its study is
likely to enhance our basic understanding of muscle ener-
getics, metabolic control, and the determinants of the effi-
ciency of skeletal muscle contraction. From a more functional
Address for correspondence: Andrew M. Jones, Ph.D., Sport and Health
Sciences, College of Life and Environmental Sciences, St. Luke’s Campus,
University of Exeter, Heavitree Road, Exeter, EX1 2LU, United Kingdom;
E-mail: a.m.jones@exeter.ac.uk.
Submitted for publication January 2011.
Accepted for publication April 2011.
0195-9131/11/4311-0000/0
MEDICINE & SCIENCE IN SPORTS & EXERCISE
Ò
Copyright Ó2011 by the American College of Sports Medicine
DOI: 10.1249/MSS.0b013e31821fcfc1
1
Copyeditor: Jamaica Polintan
Copyright @ 2011 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
perspective, the V
˙O
2
slow component is of importance be-
cause it seems to be closely related to the progressive loss
of muscle homeostasis and the development of fatigue that
is evident during 9LT exercise (23,68,111). Study of the V
˙O
2
slow component may therefore provide insights into the
determinants of exercise (in)tolerance in both healthy and
patient populations; this, in turn, might aid the develop-
ment of pharmacological, nutritional or exercise-related in-
terventions with the potential to enhance human performance,
health and well-being.
This invited review reflects the proceedings of a sympo-
sium of the same title that was presented at the 2010 Amer-
ican College of Sports Medicine meeting in Baltimore.
Surprisingly, the last American College of Sports Medicine
symposium that focused specifically on the V
˙O
2
slow com-
ponent was presented in 1993 (98). More than 250 scientific
articles on this topic have been published since that date,
and hence, the purpose of this review was to provide a con-
temporary overview of what is known, and what is still not
known, about the V
˙O
2
slow component. The review consists
of four interrelated parts. First, Dr. David C. Poole provides
the historical background to the discovery of the V
˙O
2
slow
component and its eventual recognition as an essential fea-
ture of the physiological response to high-intensity exercise.
Second, Dr. Bruno Grassi outlines key findings concerning
the mechanistic bases of the V
˙O
2
slow component emanat-
ing from experiments using the isolated in situ dog gas-
trocnemius preparation. Third, Peter M. Christensen, M.Sc.,
and Drs. Peter Krustrup and Jens Bangsbo review evidence
from invasive studies in human volunteers, which provide
insight into the role of muscle fiber type and fiber recruit-
ment on the V
˙O
2
slow component. Finally, Dr. Andrew M.
Jones discusses the practical interventions that can attenu-
ate the V
˙O
2
slow component and thus predispose to en-
hanced exercise tolerance and considers the implications
of these effects for understanding the physiological under-
pinnings of the V
˙O
2
slow component.
V
˙O
2
SLOW COMPONENT: HISTORY
AND SIGNIFICANCE
When one reads research papers and standard texts from
much of the 20th century, the control of pulmonary V
˙O
2
(and, by inference, muscle V
˙O
2
) kinetics is assumed to be
a linear first-order system. This characterization implies that
ATP–V
˙O
2
coupling is rate-limited by a single first-order re-
action (i.e., the mitochondrial creatine kinase reaction) (126)
such that V
˙O
2
kinetics is not rate-limited by O
2
transport
per se. Several ‘‘fundamental’’ tenets of exercise physiology
are founded on this notion. Specifically: 1) V
˙O
2
increases
as a unitary function of work rate (i.e., the gain = 9–11 mL
of O
2
Imin
j1
IW
j1
for cycle exercise) across the range of
achievable V
˙O
2
values. 2) Irrespective of work intensity, the
V
˙O
2
profile ascribes to a single exponential process. 3) The
FIGURE 1—Schematic framework illustrating the approximate location of key parameters of aerobic function (LT/GET, CP, and V
˙O
2max
) on the
incremental/ramp exercise test (upper left panel) and demonstrating the profiles of V
˙O
2
(upper middle panel) and blood lactate concentration (upper
right panel) to CWR exercise in the moderate (GLT/GET), heavy (9LT/GETGCP), and severe (9CP to V
˙O
2max
) exercise intensity domains. Arrows
depict point of exhaustion during severe-intensity exercise. Hatched areas denote V
˙O
2
slow component that increases V
˙O
2
above that predicted for the
work rate from the V
˙O
2
–work rate relation in the upper left panel (i.e., unloaded cycling V
˙O
2
+È10 mL of O
2
Imin
j1
IW
j1
). Note that, for heavy
exercise (9LT/GETGCP), the V
˙O
2
slow component can be stabilized at a submaximal V
˙O
2
; however, for severe exercise (9CP), the slow component
drives V
˙O
2
to V
˙O
2max
.Lower panel illustrates the intensity domain dependency of the V
˙O
2
slow component with its maximum value being achieved
just above CP. For higher work rates, the V
˙O
2
slow component decreases because the V
˙O
2max
represents the upper limit for its expression.
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time constant (T, time-to-reach 63% of the response as well
as the mean response time, MRT) is invariant with work
rate. 4) The O
2
deficit can simply be calculated as $V
˙O
2
T.
An important consequence of the acceptance of item 1) is
the almost-ubiquitous tradition of characterizing exercise
‘intensity’’ as percent V
˙O
2max
.
There is much support for the first-order linearity of V
˙O
2
from muscles contracting in vitro (frog sartorius) (60,92)
and in situ (dog gastrocnemius) (97). Furthermore, Riggs’s
(108) concept of ‘‘superposition’’ provides a rigorous test
for the first-order linearity of V
˙O
2
. Considering the pulse/
impulse as the input function, for which the first integral
is the step and the second is the ramp, across these differ-
ent work-forcing functions (i.e., pulse, step, ramp), the pa-
rameters of the V
˙O
2
(output) (i.e., T, MRT, gain) should be
identical. However, empirical evidence has only supported
the first-order linearity of V
˙O
2
for exercise within the
moderate-intensity domain (i.e., below the LT or GET).
Crucially, for higher work rates in the heavy (9LT/GET)
and severe (9CP) domains, a slow component of the V
˙O
2
kinetics emerges, which becomes superimposed on the un-
derlying and faster primary or fundamental response (Fig. 1).
Thus, the V
˙O
2
slow component, which may amount to as
much as 1000–1500 mL of O
2
Imin
j1
, challenges our under-
standing of muscle energetics and the foundational tenets
of exercise physiology listed above. First, for CWR exercise
in the heavy or severe domains, the end-exercise gain may
increase considerably above 9–11 mL of O
2
Imin
j1
IW
j1
(57,112). Second, the V
˙O
2
kinetics are no longer well fit by
a single exponential response. Third, the MRT increases.
Fourth, confidence in the calculation of the O
2
deficit is
eroded, in part, by lack of formal characterization (i.e., linear,
exponential, or other) (14,95,129) of the V
˙O
2
slow compo-
nent and the presumption that the end-exercise or steady-state
V
˙O
2
is the appropriate frame of reference (15,127). Finally,
as V
˙O
2
increases as a function of time during CWR exercise,
the practice of describing a given exercise intensity relative
to V
˙O
2max
is fatuous (see also Jones et al. [68]).
It is extraordinary that the technology to measure V
˙O
2
and thus identify the V
˙O
2
slow component has been in ex-
istence for more than a century. However, because the V
˙O
2
slow component has been inexplicable based on our con-
ventional understanding of muscle energetics, its presence
has been either systematically ignored or explained away.
Perhaps the first evidence for the existence of the V
˙O
2
slow
component emerged in 1913 in the data of Krogh and
Lindhard (79); however, it escaped detailed scientific scru-
tiny at that time. A decade later, in 1923, Hill and Lupton
(61) reported that, for one subject, V
˙O
2
increased by more
than 0.5 LImin
j1
between the 4th and 27th minute of tread-
mill running. Possibly because this diverged from contem-
porary models of energetics, it was explained away as the
result of ‘‘a painful blister on the foot causing inefficient
movement’’ (61). Moreover, published in 1961, Astrand and
Saltin’s (4) profiles of V
˙O
2
during fatiguing high-intensity
exercise demonstrate clearly V
˙O
2
slow components that
drive V
˙O
2
to V
˙O
2max
and portend exhaustion. Unfortu-
nately, in the Textbook of Work Physiology (3), just two
pages before reproduction of those actual V
˙O
2
profiles,
V
˙O
2
is depicted fictitiously as rising in a strictly linear fa-
shion with work rate to V
˙O
2max
(3, p. 300–302). While this
profile may be observed with the rapidly incremented or
ramp test (Fig. 1, upper left panel), it is certainly not evi-
dent in any situation where the V
˙O
2
slow component has
time to emerge (Fig. 1, middle upper and lower panels).
Another important consequence of the V
˙O
2
slow compo-
nent evident from Astrand and Saltin’s (4) and subsequent
publications (e.g., Åstrand and Rodahl (3) and Poole et al.
[102]) is that its capacity to drive V
˙O
2
to V
˙O
2max
extends
the range of work rates at which V
˙O
2max
may be achieved,
provided that exercise is continued either to exhaustion or
at least for a sufficient duration for the V
˙O
2
slow component
to develop fully. This property of 9CP exercise has defined
the extremities of the severe exercise intensity domain.
Specifically, CP is the highest power output (or, more cor-
rectly, metabolic rate) (12) for which V
˙O
2
can be stabilized
below V
˙O
2max
(68). By definition, all severe-intensity work
rates (i.e., 9CP) drive V
˙O
2
to V
˙O
2max
. Beyond the upper
limit of the severe domain, what has been termed extreme
(62,132) is characterized as exercise that is so intense that
exhaustion intervenes before the kinetics of V
˙O
2
allows
V
˙O
2max
to be achieved (this domain is omitted from Fig. 1
for clarity).
Despite some scientists’ contention that the V
˙O
2
response
could and should be described by a single exponential pro-
cess that is invariant with exercise intensity (33,93), by
the mid 1970s, the compelling weight of evidence demon-
strated that, for heavy and severe exercise, V
˙O
2
kinetics (on-
and off-transient) become more complex, and the overall
response is slowed in comparison with moderate exercise
(Fig. 1) (58,90,128). Recognition that the V
˙O
2
slow com-
ponent was a reproducible event and of sufficient magni-
tude to contribute importantly to overall exercise energetics
and possibly exercise tolerance led Hagberg et al. (51) to
investigate its mechanistic bases. Using presumptive esti-
mates of the O
2
cost of the respiratory muscles and eleva-
tions in body temperature (the so-called ‘‘Q
10
effect’’), they
concluded that these two mechanisms could account for
essentially all of the V
˙O
2
slow component (review Poole
et al. [98,102]). Irrespective of this conclusion, recognition
that the V
˙O
2
slow component occurs only above LT/GET
(57,112,129) and that many other potentially calorigenic
processes are manifested simultaneously justified consider-
ation of multiple additional putative mediators. These in-
cluded lactate itself (via its stimulation of gluconeogenesis
and other mechanisms); exercising muscle temperature (the
principal site of any Q
10
effect) (129); catecholamines; res-
piratory, cardiac, and auxiliary muscle work (e.g., arms for
stabilization during cycle ergometry); and reduced contrac-
tile efficiency of higher-order fibers (fast twitch, type IIa/b/
d/x) (review Poole et al. [98]). Further correlative studies
supported that the profile of blood lactate accumulation
V
˙O
2
SLOW COMPONENT: MECHANISMS AND APPLICATIONS Medicine & Science in Sports & Exercise
d
3
Copyright @ 2011 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
was more closely related to that of the V
˙O
2
slow component
than were ventilation, HR, body temperature or catechol-
amines (28,102).
A crucial advance in resolving the mechanistic bases for
the V
˙O
2
slow component was use of the constant-infusion
thermodilution technique, pioneered by Andersen and Saltin
(2), to make high-fidelity leg (and contracting muscle) blood
flow and V
˙O
2
measurements (101). Using that technique to
compartmentalize the V
˙O
2
slow component, Poole et al.
(101) determined that the dominant portion (980%) arose
from within the contracting muscles, thereby truncating the
list of candidate mechanisms to those extant at that site
(
F2 Fig. 2). As a result, focused subsequent experiments dis-
qualified muscle temperature (75), catecholamines (42), and
increased muscle or blood lactate concentration (99) as vi-
able mediators of the V
˙O
2
slow component and emplaced
muscle fiber energetics and recruitment patterns center stage
(Fig. 2). Subsequent studies have confirmed that the domi-
nant portion of the V
˙O
2
slow component derives from
within the contracting muscles (74,83). Using
31
P magnetic
resonance spectroscopy, Rossiter et al. (111) established that
the V
˙O
2
slow component was associated with a slow com-
ponent of muscle phosphocreatine concentration ([PCr]),
indicating that the slow component is linked to a greater
ATP cost of force production rather than an elevated V
˙O
2
cost of ATP production (i.e., $P/O ratio) per se.
There is substantial evidence in the animal (rat [44,106,
125] and mouse [32]) and human (30,52,118) literature
that fast-twitch fibers (type II), compared with slow-twitch
(type I) fibers, have a greater ATP cost for contractile activ-
ity owing to different chemical-to-mechanical coupling effi-
ciencies, more rapid actomyosin turnover, far faster calcium
pump activity (120), and less efficient FAD versus NAD-
linked >-glycerolphosphate shuttle activity (135). Thus, while
extrapolations from in vitro to in vivo energetics should be
made with caution (55), there is a solid foundation for the
hypothesis that exercise, which recruits a greater proportion
of type II fibers, will require a greater ATP (and thus V
˙O
2
)
cost. Empirical testing of this hypothesis has been hampered
by limitations including poor signal-to-noise fidelity and
spatial resolution issues with existing technologies (e.g.,
EMG, magnetic resonance imaging (MRI)). Notwithstanding
these considerations, beginning with the observation of a
weak correlation between increased iEMG activity and V
˙O
2
slow component amplitude by Shinohara and Moritani (117),
there is support, using experimental perturbations such as
priming exercise (21,35), manipulations of pedal frequency
(104), glycogen depletion (27,86), preferential blockade of
slow-twitch fiber recruitment (84), and exercise training
(114), for greater (presumably type II) fiber recruitment
occurring in synchrony with the V
˙O
2
slow component. Other
EMG (19,94,96) and MRI-based studies (37,115) support
this thesis. It is also pertinent that the V
˙O
2
slow compo-
nent is greater in individuals with a higher proportion of
type II versus type I fibers in the musculus vastus lateralis
(13,67,103). Moreover, in the rat, the V
˙O
2
slow component
is associated with a preferential increase in blood flow
and presumably greater recruitment of low oxidative fast-
twitch muscle fibers (type IIb/d/x) (29). It is becoming in-
creasingly evident, however, that the V
˙O
2
slow component
need not be dependent on recruitment of more fibers per se
but, rather, may be driven by metabolic processes occurring
within fibers that are already recruited (124,138).
V
˙O
2
SLOW COMPONENT: LESSONS FROM
ANIMAL MODELS
As discussed above, the ‘‘slow component’’ of V
˙O
2
ki-
netics is often considered to be mainly caused by a pro-
gressive recruitment of fibers as exercise proceeds and those
FIGURE 2—An array of putative mediators of the V
˙O
2
slow component. Note that, at least in healthy individuals during cycle ergometry, the bulk of
the V
˙O
2
slow component derives from intramuscular sites within the exercising limbs. However, insofar as remote events (e.g., increased work of
breathing, altered arterial O
2
pressures) may affect exercising muscle blood flow and therefore O
2
delivery distribution, they may affect the V
˙O
2
slow component to a surprising degree. See text for further details.
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fibers initially recruited become fatigued. The main experi-
mental evidence in favor of this concept derives from EMG
(19) and MRI (37) studies, as well as from experiments in
which glycogen depletion (86), and selective neural block-
ade of type I fibers (84) was obtained. As discussed in
Jones et al. (67), an alternative (or concurrent) explanation
for the V
˙O
2
slow component could involve an increase in
metabolic demands within the already recruited fibers that
are fatiguing (see, e.g., Pringle et al. [104] and Scheuermann
et al. [116]).
An excellent experimental model to discriminate between
these hypotheses is presented by the isolated dog gastroc-
nemius preparation in situ, originally used by Piiper et al.
(97) to study skeletal muscle V
˙O
2
kinetics. Using this mo-
del, Grassi et al. have investigated the roles of convective
(45,48) and diffusive (46) O
2
delivery as limiting factors for
the V
˙O
2
kinetics, as well as the putative roles of pyruvate
dehydrogenase activation (47), nitric oxide synthase (NOS)
inhibition (49), and CK inhibition (50) in the regulation of
V
˙O
2
kinetics. In this preparation, all muscle fibers are
maximally activated (tetanic contractions) from the begin-
ning of the contraction period, by direct electrical stimula-
tion of the motor nerve. Thus, a sequential activation of
motor units (the mechanism supposedly responsible for the
V
˙O
2
slow component, see above) is, by definition, impos-
sible. In this preparation, a ‘‘modulation’’ of the metabolic in-
tensity of contractions (in terms of percentages of V
˙O
2
peak)
can be accomplished by modulating the frequency of the
contractions: with one contraction every 2 s (45,46), V
˙O
2
should correspond at ‘‘steady state’’ to È60% of V
˙O
2
peak,
whereas with one contraction every 1 s (48), V
˙O
2
peak was
reached.
Was a V
˙O
2
slow component observed in these experi-
ments? The answer is not straightforward. If we consider
the ‘‘classic’’ slow component (that is a further increase in
V
˙O
2
with time above the expected steady state), there was
no slow component in the experiments at a relatively low
metabolic intensity (45,46), there was a slow component in
a minority of the experiments at an intermediate meta-
bolic intensity (47,49), and there was a slow component in
the majority of the experiments at peak V
˙O
2
(48). Interest-
ingly, a V
˙O
2
slow component was not observed in the
experiments carried out at an intermediate metabolic inten-
sity, but in which the muscle was pump-perfused with a
markedly elevated constant blood flow (50). This may rep-
resent indirect evidence that the V
˙O
2
slow component is
related to O
2
availability. It is possible that, under these
experimental conditions, increased bulk muscle blood flow
and/or a better local matching of blood flow to metabolic
rate increased ‘‘metabolic stability’’ (139) and reduced fa-
tigue development and the associated loss of muscle effi-
ciency. In contrast, in conditions of spontaneous blood flow
adjustment, such as during exercise in humans, blood flow
distribution to active fibers may be suboptimal and may
contribute to fatigue development and the loss of muscle
efficiency, which is reflected in the V
˙O
2
slow component.
In the previously mentioned studies, the fact that the
muscles significantly fatigued during the 3-min (or 4-min)
contraction period was neglected. The values of the fatigue
index (the ratio between force at the end of the contraction
period and the initial force) ranged between 0.84 (45) and
0.64 (48). In other words, there was no V
˙O
2
slow compo-
nent or only a small V
˙O
2
slow component, but in the pres-
ence of a significant fall (by È15%–35%) in force output.
When the V
˙O
2
data from one of these studies (49) were
taken and ‘‘normalized’’ per unit of force, there was a clear
V
˙O
2
slow component, the amplitude of which corresponded
on average to È20% of the total amplitude of the V
˙O
2
in-
crease (138). Thus, in the ‘‘classic’’ V
˙O
2
slow component,
described in exercising humans during CWR exercise, the
latter is maintained (possibly by recruiting additional fibers)
at the expense of an increasing V
˙O
2
. In the isolated muscle
in situ model, on the other hand, the muscle cannot recruit
additional fibers, force decreases as a consequence of fa-
tigue, and V
˙O
2
remains essentially constant ( F3Fig. 3). This
phenomenon was termed a mirror image of the slow com-
ponent (138). The two scenarios have a common denomi-
nator, namely, a reduced efficiency of muscle contractions:
constant mechanical power output, with an increasing V
˙O
2
;
or, conversely, a substantially constant V
˙O
2
, but with a de-
creasing force. The study of Zoladz et al. (138) therefore
demonstrated that the reduced efficiency of muscle con-
traction, and thus the putative mechanism responsible for
the V
˙O
2
slow component, is not necessarily related (or due)
to a progressive recruitment of muscle fibers.
A reduced efficiency of muscle contractions is, in fact,
typically associated with fatigue (11,136). The two phenom-
ena have several common denominators, such as a decrease
FIGURE 3—In the ‘‘classic’’ slow component of V
˙O
2
kinetics (upper
panels), CWR exercise is maintained (possibly by recruiting addi-
tional fibers) at the expense of an increasing V
˙O
2
. In the isolated muscle
in situ model (138), the muscle cannot recruit additional fibers, force
decreases as a consequence of fatigue and V
˙O
2
is essentially constant
(lower panels). The two scenarios have a common denominator, that is,
a fatigue-induced reduced efficiency of muscle contractions.
V
˙O
2
SLOW COMPONENT: MECHANISMS AND APPLICATIONS Medicine & Science in Sports & Exercise
d
5
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in the Gibbs free energy of ATP hydrolysis, a decrease in PCr
and glycogen concentrations, as well as increases in [H
+
],
[ADP], [P
i
], [IMP], [NH
3
], etc. (1,40). The V
˙O
2
slow com-
ponent, or its mirror image, would then be associated with
(or be a consequence of) a lower level of ‘‘metabolic stabil-
ity’’ (139). Good metabolic stability in skeletal muscles dur-
ing rest-to-work transitions is associated with good exercise
tolerance, and results, for a given increase in V
˙O
2
, in a less
pronounced decrease in PCr and the cytosolic phosphoryla-
tion potential, as well as in a less pronounced increase in [Pi],
[ADP
free
], [AMP
free
], and [IMP
free
](139).
The slow component of V
˙O
2
kinetics is associated with
a slow component of PCr kinetics (111), that is with an in-
creased ‘‘phosphate cost’’ of force production, which would
explain the reduced contractile efficiency. Thus, the V
˙O
2
slow component would be associated with (or caused by)
a decreased efficiency of the contractile machinery (increase
of the ATP/power output ratio) rather than by a decreased
efficiency of the ATP production system (increase in the
V
˙O
2
/ATP ratio). This means that a ‘‘CWR’’ exercise, that is,
an exercise characterized by a constant external mechan-
ical power output, would be associated, in the presence of
progressive fatigue, with a progressively higher ATP turn-
over rate.
Is anything like the ‘‘mirror image’’ of the V
˙O
2
slow com-
ponent, which was observed in the isolated muscle prepa-
ration in situ, observed in exercising humans as well? The
answer is yes. In the study by Ribeiro et al. (107), for ex-
ample, the subjects had to keep their pulmonary V
˙O
2
constant
during cycling exercise carried out for 40 min at È55%,
È65%, and È75% of the previously determined V
˙O
2max
.To
do so, the subjects had to decrease their mechanical power
output. The decrease was linearly related to exercise intensity,
ranging from È5% at a V
˙O
2
corresponding to È55% of
V
˙O
2max
,toÈ15% at a V
˙O
2
corresponding to È75% of
V
˙O
2max
. In another study by Stoudemire et al. (119), the
FIGURE 4—Mean TSEM power output, iEMG, and V
˙O
2
profiles during 3 min of all-out exercise (open symbols) and work-matched severe-intensity
CWR exercise performed to the limit of tolerance (closed symbols) on a cycle ergometer. A. Mean power profile during 3 min of all-out cycle exercise
evidences an early peak before falling to attain a value that is not different from the CP (dashed horizontal line); the mean power profile for the CWR
test is shown as a solid horizontal line. The corresponding V
˙O
2
profiles are shown in B. Note that the V
˙O
2max
(dashed horizontal line) is attained in both
tests but is reached rapidly in the all-out test but only after the development of the V
˙O
2
slow component during CWR exercise. When transformed into
a ‘‘gain’’ (i.e., V
˙O
2
/power) (C), a V
˙O
2
slow component phenomenon is observed for both modes of exercise and the gain is higher for all-out exercise.
This V
˙O
2
slow component-like response during all-out exercise occurs despite a substantial fall in iEMG over time, in contrast to the progressive
increase in iEMG during CWR exercise (D). Data from Vanhatalo et al. (124).
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subjects had to maintain, during 30 min of running on a
treadmill, pulmonary V
˙O
2
at a constant level correspond-
ing to that associated (during an incremental test) with a
blood lactate concentration of È4 mM. To do so, the sub-
jects had to progressively reduce (by È15% at the end of the
30-min period) their running speed. Most recently and per-
haps most convincingly, Vanhatalo et al. (124) reported that
the V
˙O
2
slow component was greater in a 3-min all-out cycle
test, in which peak power is attained within the first 10 s
before progressively falling with time to attain the CP, com-
pared with a 3-min maximal CWR test (124) (
F4 Fig. 4). The
iEMG declined by 26 % during the all-out test and increased
by 60 % during the CWR test from the first 30 s to the last
30 s of exercise (Fig. 4). The considerable reduction in mus-
cle efficiency in the all-out test in the face of a progressively
falling iEMG indicates that increased muscle activation in-
cluding progressive fiber recruitment is not requisite for
the V
˙O
2
slow component to develop during voluntary exer-
cise in humans. These effects are essentially identical to the
‘mirror image’’ of the V
˙O
2
slow component, which was ob-
served in the canine skeletal muscle preparation in situ (138).
The strategy of maintaining the highest work rate asso-
ciated with steady-state levels of relevant variables, such
as pulmonary V
˙O
2
, HR, muscle and blood pH, and blood
lactate concentration, is based on the ‘‘maximal lactate
steady-state’’ (16) or ‘‘critical power’’ (68) concepts. In this
scenario, the strategy of maintaining the highest work rate
associated with reasonably good metabolic stability and ef-
ficiency of muscle contractions seems to represent a key
factor for successful endurance performance. High-class
marathon runners, for example, perform their marathon race
at the highest possible running velocity at which they can
maintain, throughout the race, unchanged blood pH (140)
and presumably the lowest energy cost of running. It seems
to represent ‘‘common sense,’’ in biological terms, that a
system tries to maintain, as far as is possible, conditions of
metabolic steady states to prevent (or minimize) the occur-
rence of fatigue. In this respect, the slow component of V
˙O
2
kinetics (but also of other variables) represents a deviation
from a steady state. The more pronounced this deviation,
the more marked the consequences on fatigue and exercise
(in)tolerance would likely be (23). As an example, Salvadego
et al. (113) recently observed that, in obese adolescents ex-
ercising at 80% V
˙O
2max
, the amplitude of the V
˙O
2
slow
component was linearly and inversely related to the time to
exhaustion during the test.
V
˙O
2
SLOW COMPONENT: ADDRESSING THE
MECHANISTIC BASES IN HUMANS
Multiple studies have demonstrated that the contracting
muscles are contributing to the pulmonary V
˙O
2
slow com-
ponent (74,83,101). It is also evident that the muscle V
˙O
2
slow component represents a decline in muscular efficiency,
which is ameliorated with training (80) (
F5 Fig. 5). It is, how-
ever, unclear what is causing the muscle V
˙O
2
slow compo-
nent and thus the lowering of muscle work efficiency. As
illustrated in F6Figure 6, it has been suggested to be caused
by a progressive increase in muscle temperature, acidosis, or
changes in fiber-type recruitment and/or mitochondrial P/O
ratio. These possibilities will be discussed in this section.
As mentioned previously, an increase in muscle tem-
perature does not seem to influence the muscle V
˙O
2
slow
component to a significant extent (39,85). In one study,
submaximal knee extensor exercise (43 W) was performed
for 10 min with and without prior passive heating, and no
differences were observed in muscle V
˙O
2
or total energy
turnover despite a 1.5-C higher mean temperature in the
heated trial compared with control (37.9-C vs 36.4-C) (39).
In another study, subjects cycled for 20 min at moderate and
heavy exercise intensities on separate days eliciting 50%
and 80% V
˙O
2max
, respectively (85). A V
˙O
2
slow compo-
nent was only observed during the intense work with an
increase in V
˙O
2
from 2.62 LImin
j1
after 3 min of exercise
to 2.76 LImin
j1
after 6 min of exercise with a further in-
crease to 2.87 LImin
j1
after 20 min of cycling. However,
there was no difference in the change of muscle temperature
between the moderate and heavy exercise, being 1.0-C
versus 1.1-C, respectively, between 3 and 6 min and 1.1-C
versus 1.3-C from 6 to 20 min.
Muscle pH was only lowered during the intense cycling
in which the V
˙O
2
slow component was observed, indicat-
ing that muscular acidosis may be causing the decrease in
efficiency. A number of studies, however, suggest that the
relationship is not causal. Raising the lactate concentration
and lowering pH through direct infusion of lactate in work-
ing dogs did not alter V
˙O
2
(99). Likewise, no effect on the
V
˙O
2
slow component was observed after infusion of adren-
aline in humans, which increased blood lactate concentration
and reduced pH (42).
FIGURE 5—Muscle oxygen uptake at selected time points during
30 min of knee extensor exercise at 30 W with an untrained (filled bars)
and a trained leg (open bars). Note that a pronounced slow component
of muscle V
˙O
2
is apparent for the untrained leg (12% from 2 to 3 min
and a further 11% increase from 3 to 30 min) but is absent in the
trained leg. Values are means TSEM (n= 6). Data from Krustrup (80).
V
˙O
2
SLOW COMPONENT: MECHANISMS AND APPLICATIONS Medicine & Science in Sports & Exercise
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7
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Change in the muscle fiber recruitment pattern has been
studied by measurements of single muscle fiber content of
PCr and glycogen. In the study by Krustrup et al. (85), the
glycogen content in type I fibers decreased both during the
moderate and heavy exercise bout, whereas the content in
type II fibers only decreased during the intense exercise
bout where the V
˙O
2
slow component was observed. The PCr
levels in individual fibers from a muscle biopsy taken before
and after 3, 6, and 20 min of exercise provided additional
insight into the fiber recruitment pattern. At rest, approxi-
mately 10% of both the type I and type II fibers were be-
low mean resting values minus 1 SD, and after moderate
exercise, 25% of the type I fibers were below the mean
resting value minus 1SD, whereas little changes were ob-
served for the type II fibers. After 3, 6, and 20 min of the
intense exercise, 37%, 70%, and 74% of the type I fibers,
respectively, and 45%, 83%, and 74% of the type II fibers,
respectively, had PCr levels below mean resting values mi-
nus 1SD. These findings indicate that type I fiber recruit-
ment dominated during moderate-intensity exercise whereas
both type I and type II fibers were involved during heavy-
intensity exercise. Furthermore, the data demonstrate that
more type II fibers were recruited from 3 to 6 min where the
V
˙O
2
slow component was apparent.
As type II fibers seem to be less efficient than the type I
fibers during dynamic exercise in humans, the V
˙O
2
slow
component may be due to the progressive recruitment of
type II fibers (80,84–86). Thus, Krustrup et al. (84) used the
neuromuscular blocking agent cisatracurium (curare analog
(CUR)) to impair the activation of the type I fibers during
10 min of one-legged knee extensor exercise bouts at a mo-
derate intensity (30 W). Measurements of PCr levels in sin-
gle fibers confirmed that fewer type I fibers were active with
CUR infusion compared with the control situation ( F7Fig. 7).
FIGURE 6—Schematic representation of the most likely determi-
nants of muscular efficiency during dynamic exercise. The results ob-
tained in knee extensor exercise and cycle studies (39,82,84–86) suggest
that muscle fiber recruitment influences the O
2
cost as well as ATP
turnover during dynamic exercise, whereas muscle temperature, lac-
tate, and pH in the investigated range had little or no effect. Further
studies are required to elucidate the precise effects of dynamic exercise
on the P/O ratio.
FIGURE 7—A, Thigh V
˙O
2
before and during 10 min of knee extensor exercise at 30 W with (open symbols) and without (full symbols) femoral arterial
injections of a neuromuscular blocking agent (CUR). B, type I (ST) and type II (FT) fiber phosphocreatine (CP) breakdown during CUR and
Control. Values are means TSEM (n= 6). *CUR versus CON. §
AQ1 Significant CP breakdown. #FT versus ST fibers. Data from Krustrup et al. (84).
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Muscle V
˙O
2
was around 100 mLImin
j1
higher with infusion
of CUR and mechanical efficiency was lower (16 vs. 20%)
compared with control, showing that a greater recruitment
of type II fibers leads to a higher muscle V
˙O
2
(Fig. 7).
Additional support for recruitment of type II fibers
playing a crucial part in the development of the V
˙O
2
slow
component is found in a study in which the glycogen levels
were manipulated before whole body exercise (86). Subjects
performed 20 min of moderate-intensity cycling at 50%
V
˙O
2max
on three separate days. On two occasions, the sub-
jects carried out 3 h of low-intensity cycling (40% V
˙O
2max
)
the day before the experiment to lower the glycogen levels
in the type I fibers. On one of these occasions, the subjects
fasted overnight (CHO-DEP), and on the other, they inges-
ted a diet with a high CHO content to examine whether the
exercise the day before influenced the response (CHO-RE).
In the third condition, the subjects rested the day before
testing and had an overnight fast. Analysis of muscle biop-
sies obtained before testing revealed that the prior exercise
and fasting (CHO-DEP) had depleted the glycogen stores of
most type I fibers. Muscle fiber recruitment pattern during
the 20-min exercise bout was assessed by measuring gly-
cogen levels before and after exercise as well as PCr levels
in individual fibers after 0, 3, and 20 min of cycling. A
markedly higher type II fiber recruitment was seen in CHO-
DEP compared with the control condition ( F8Fig. 8A). The
pulmonary V
˙O
2
after 3 min of cycling was higher in CHO-
DEP than in control, and in contrast to the control situation,
aV
˙O
2
slow component (È110 mLImin
j1
) was observed in
CHO-DEP (Fig. 8B). The notion that the V
˙O
2
slow com-
ponent was caused by the exercise performed the day before
testing could be dismissed because the V
˙O
2
response after
the CHO refueling strategy was the same as in the control
condition (Fig. 8B). Thus, these findings underline that the
FIGURE 8—A, Distribution of single-fiber phosphocreatine (CP) content during 20 min of cycling at 50% V
˙O
2max
fortypeI(ST)fibers(left-hand
side) and type II (FT) fibers (right-hand side) in a control condition (CON) and after prior glycogen depletion of ST fibers caused by 3 h of cycling at
40% V
˙O
2max
the day before testing (CHO-DEP). B, Pulmonary V
˙O
2
during cycling at 50% V
˙O
2max
in CON, after the glycogen depletion protocol of
ST fibers (CHO-DEP; n=12,left), and after refueling of the CHO stores (CON-RE, n=6,right). Individual values and means TSEM are presented.
This figure demonstrates the existence of a V
˙O
2
slow component during ostensibly moderate-intensity exercise after glycogen depletion of ST fibers
and consequent increased recruitment of FT fibers. Data from Krustrup et al. (86).
V
˙O
2
SLOW COMPONENT: MECHANISMS AND APPLICATIONS Medicine & Science in Sports & Exercise
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V
˙O
2
slow component during CWR exercise is related to a
greater recruitment of type II fibers. In addition, muscle pH
was not changed during either of the exercise bouts, dem-
onstrating that a V
˙O
2
slow component can be observed
without changes in muscle acidity.
The effect of manipulating the glycogen content of type I
and type II fibers on the V
˙O
2
slow component has been
studied by others. Carter et al. (27) had subjects cycle at a
moderate (80% GET) and heavy intensity (50% of the dif-
ference between GET and V
˙O
2max
) after glycogen deple-
tion of either primarily type I fibers (3 h of cycling at 30%
V
˙O
2max
) or type II fibers (10 1 min at 120% V
˙O
2max
).
After glycogen depletion of the type II fibers, the V
˙O
2
slow
component during heavy exercise was reduced compared
with control, in agreement with Krustrup et al. (86). How-
ever, in contrast to the findings from Krustrup et al. (86),
neither of the manipulations had any effect on V
˙O
2
during
moderate-intensity exercise. One explanation may be that,
in the study of Carter et al. (27), the exercise duration was
only 6 min compared with 20 min used by Krustrup et al.
(86), in which the V
˙O
2
slow component was significant af-
ter approximately 15 min of exercise. Bouckaert et al. (20)
lowered the glycogen content in the type I fibers by having
their subjects eat a meal without CHO (60% fat and 40%
protein) and cycle for 2 h at 60% V
˙O
2max
. Twelve hours
after the exercise without food, the subjects exercised for
9 min at 85% V
˙O
2max
. In comparison with the control con-
dition, the efficiency was reduced after the glycogen deple-
tion protocol with an increase in V
˙O
2
of approximately
140 mLImin
j1
, consistent with the findings by Krustrup
et al. (86). The magnitude of the V
˙O
2
slow component,
however, was not changed by the intervention.
Interestingly, when a transition to a heavy or severe-
intensity work rate is initiated from a moderate-intensity
work rate (as opposed to a baseline of ‘‘unloaded’’ cycling),
the overall V
˙O
2
kinetics is slower and the response gain is
greater, i.e., efficiency is impaired (133,134); reciprocal
effects are observed in the intramuscular [PCr] profiles
(35,72). These effects do not seem to be related to differ-
ences in muscle O
2
delivery (34,36). This ‘‘work-to-work’’
model is useful in exploring differences in fiber-type ener-
getics because it theoretically allows the V
˙O
2
response of
different segments of the fiber-type recruitment hierar-
chy to be isolated (56). The different V
˙O
2
profiles that are
elicited in these conditions (34–36,133,134) also suggest
that type II fibers have slower V
˙O
2
kinetics and lower
efficiency compared with type I fibers. On this basis, a theo-
retical model that attempts to link fiber recruitment patterns
to the different V
˙O
2
profiles in the various exercise intensity
domains, including the delayed and elevated steady state
observed for heavy exercise and the lack of steady state for
severe exercise has been advanced (see Fig. 6 of Wilkerson
and Jones [134]).
Little is known about the mitochondrial P/O ratio during
dynamic exercise in humans. However, there is indirect ev-
idence that the mitochondria play an important role in de-
termining muscular efficiency and it could be speculated that
P/O ratio is changed over time owing to progressive
increases in intracellular Ca
2+
and other electrolytes. Under
ischemic conditions, no changes were observed in muscle
efficiency during a 90-s bout of knee extensor exercise at
30 W, whereas efficiency declined during a similar bout of
exercise in free-flow conditions (82). A gradual lowering
of P/O ratio specifically in the type II fibers, which are
expected to develop higher intracellular Ca
2+
concentra-
tion than type I fibers, may also explain why a higher V
˙O
2
was only apparent after 2 min of exercise in the CUR ex-
periments (84) (Fig. 7).
Overall, it seems that recruitment of additional muscle
fibers and a change in fiber-type recruitment toward type II
fiber scan play an important role in the development of
the muscle V
˙O
2
slow component during intense CWR ex-
ercise, whereas changes in muscle temperature and acidity
seem to be of little importance. In vitro studies using iso-
lated mitochondria from human muscle collected after fa-
tiguing exercise indicate that there are no long-lasting effects
on the mitochondrial P/O ratio (121). However, further
studies are required to elucidate the precise role of the P/O
ratio for the observed difference in efficiency between fiber
types as well as for the development of the V
˙O
2
slow
component during dynamic exercise in humans (105).
V
˙O
2
SLOW COMPONENT: PRACTICAL
SIGNIFICANCE AND APPLICATIONS
Several lines of evidence indicate that the development
of the V
˙O
2
slow component is intimately related to the
muscle fatigue process and that exercise tolerance can be
improved by interventions, which serve to reduce or elimi-
nate the V
˙O
2
slow component. For example, the temporal
profiles of intramuscular [ADP] and [P
i
] (increasing) and
[PCr]and pH (decreasing) are exercise intensity domain-
dependent and, as such, become progressively perturbed in
concert with the development of the V
˙O
2
slow component
(35,71,111). Thus, during severe-intensity exercise, the V
˙O
2
slow component drives V
˙O
2
to V
˙O
2max
and exercise is ter-
minated as dictated by the parameters of the power–time
relationship for high-intensity exercise (i.e., CP and W,
where Wrepresents the finite amount of work that can be
done above CP) (23,68,102). Indeed, it has been suggested
that the magnitude of both the V
˙O
2
slow component and
the Ware a function of the difference between the V
˙O
2
at
CP and the V
˙O
2max
; that is, there is a reciprocal relation-
ship between the development of the V
˙O
2
slow compo-
nent and the progressive reduction in the W(23,122). Given
this relationship between the development of the V
˙O
2
slow
component and the progressive loss of muscle metabolic
homeostasis, it is important to appreciate which inter-
ventions have the potential to reduce the V
˙O
2
slow compo-
nent. This is not only of academic interest in providing
insights into the mechanistic bases to the V
˙O
2
slow compo-
nent; it is also of practical import in devising strategies for
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enhancing performance in athletes and improving exercise
tolerance in the aged or those with pulmonary, cardiovascu-
lar, or metabolic disorders.
Training. Fortunately, several such interventions exist,
and perhaps the most potent of these is endurance exer-
cise training. First, it is interesting to note that the V
˙O
2
slow
component tends to be relatively small in endurance athletes,
presumably as a consequence of the LT and CP occurring
at a high fraction of V
˙O
2max
in this population (66). Second,
it has been established that 6–8 wk of endurance training
results in a significant reduction in the V
˙O
2
slow compo-
nent when subjects are tested at the same absolute work rate
(26,28,137) (Fig. 5). This may also be related to the well-
known effects of endurance training on the LT and CP and/or
be linked to enhanced muscle blood flow (and/or its distri-
bution) or muscle oxidative capacity (63). These latter adap-
tations, in turn, would be expected to improve metabolic
stability, reduce the rate of fatigue development, and attenuate
the requirement for higher-order motor units to be recruited to
sustain power output. Consistent with this, it has been
reported that 5 wk of endurance training results in an atten-
uated fall of muscle pH and a significant reduction in the
amplitude of the intramuscular [PCr] slow component (69).
Given that the termination of exercise in the severe domain
coincides with the attainment of consistently low muscle
[PCr] and pH values (71,122), these data suggest that the
attenuation of the [PCr] slow component (and thus V
˙O
2
slow
component) might be mechanistically linked with enhanced
exercise tolerance after endurance training.
Although it is well established that generalized endurance
training reduces the V
˙O
2
slow component, the specific type
of training (i.e., volume, duration, intensity, etc.) that is
optimal for this effect remains under investigation. For ex-
ample, Berger et al. (18) compared the effects of endurance
training (three to four sessions per week of 30-min duration
at 60% V
˙O
2max
) with work-matched interval training (three
to four sessions per week involving 20 1-min exercise
bouts at 90% V
˙O
2max
)onV
˙O
2
kinetics in previously un-
trained subjects and found that both types of training were
similarly effective in reducing the V
˙O
2
slow component. In
contrast, Bailey et al. (8) reported that just 2 wk (six ses-
sions) of interval training involving 4–7 30-s cycle sprints
significantly reduced the V
˙O
2
slow component and enhanced
severe-intensity exercise tolerance, whereas six sessions of
work-matched, moderate-intensity cycling was ineffective.
Similarly, 3 months of participation in an intense intermit-
tent sport like football resulted in a larger reduction of the
V
˙O
2
slow component compared with moderate-intensity run-
ning in previously untrained men (81). The efficacy of a spe-
cific training intervention will depend on factors such as
initial fitness as well as the duration and other characteris-
tics of the training program (63). Interestingly, it has recently
been reported that 4 wk of pressure-threshold inspiratory
muscle training, which reduced exercise-induced inspiratory
muscle fatigue, significantly reduced the V
˙O
2
slow com-
ponent and enhanced exercise tolerance during severe- and
extreme-intensity exercise (6). This effect may be consequent
to an attenuation of the O
2
and blood flow requirements of
the respiratory muscles for a given rate of pulmonary venti-
lation, thereby attenuating the metaboreflex and enabling an
increased limb O
2
delivery (53). In this regard, it is of interest
that reducing the work of breathing by having subjects inspire
He–O
2
also reduces the V
˙O
2
slow component (31).
Priming. In addition to the chronic interventions of en-
durance or inspiratory muscle training, the V
˙O
2
slow com-
ponent can also be attenuated using an acute bout of heavy
or severe-intensity ‘‘priming’’ exercise (24,43,91). Although
often termed ‘‘warm-up’’ exercise, the effects of prior exer-
cise on V
˙O
2
kinetics during a subsequent bout of high-
intensity exercise cannot be attributed to the elevated muscle
temperature per se (78). Rather, it is likely that enhance-
ments of both bulk muscle blood flow and local matching
of blood flow to V
˙O
2
, as well as an increased activity of
mitochondrial enzymes, after priming exercise retard the
rate of fatigue development and the requirement for ad-
ditional motor unit recruitment to maintain power output
during subsequent exercise (7,21,89). It has been reported
that priming exercise reduces the [PCr] slow component (41,
110), although contradictory data also exist (64). Whereas
the potential for priming exercise to reduce the V
˙O
2
slow
component during subsequent exercise is well documented
(e.g., Bailey et al. [7], Burnley et al. [21,24], Gerbino et al.
[43], Koppo et al. [78], MacDonald et al. [91], and Rossiter
et al. [110]), the effect on exercise tolerance is controver-
sial, with some studies reporting an improvement (22,70)
and others an impairment (38,131) of subsequent exercise
performance.
In a comprehensive recent investigation, Bailey et al. (7)
examined the interaction of previous exercise intensity
(heavy and severe) and subsequent recovery interval (3, 9,
and 20 min) on V
˙O
2
kinetics and severe-intensity exercise
tolerance. The effects on V
˙O
2
kinetics were appreciably
greater when severe (as opposed to heavy) priming exer-
cise was performed. Exercise tolerance was not altered by
heavy-intensity priming exercise. When the recovery inter-
val separating the two severe-intensity exercise bouts was
3 min, exercise tolerance in the second bout was impaired
by 16% relative to the control (no prior exercise) condition.
However, when the recovery interval was extended to 9 and
20 min, exercise tolerance was improved by 15% and 30%,
respectively, relative to the control condition. These data in-
dicate that prior severe-intensity exercise can enhance the
tolerance to subsequent severe-intensity exercise provided
that it is coupled with adequate recovery duration (Q9 min).
This combination, although almost certainly not uniquely
efficacious, presumably optimizes the balance between pre-
serving the positive effects of prior exercise on V
˙O
2
kinet-
ics and providing sufficient time for muscle [PCr] and pH
to recover toward baseline values (38,123). It seems clear
that athletes should carefully consider their precompetition
preparation regimens to benefit from the potential of prim-
ing exercise to enhance performance.
V
˙O
2
SLOW COMPONENT: MECHANISMS AND APPLICATIONS Medicine & Science in Sports & Exercise
d
11
Copyright @ 2011 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
The reduced V
˙O
2
slow component observed after priming
exercise in the study of Bailey et al. (7) was associated with
a blunted increase of the muscle integrated EMG (iEMG)
between 2 and 6 min of exercise. Other studies (21,89) have
also reported changes in iEMG after priming exercise that
may reflect changes in motor unit recruitment profiles. A
diminished rate of fatigue development during exercise af-
ter priming (as a function, for example, of greater muscle
O
2
availability) might limit the requirement for additional
motor unit recruitment. Alternatively, a greater iEMG in
the early minutes of exercise, as has been observed in sev-
eral studies (7,21,35,89), may indicate a reduced metabolic
strain per recruited muscle fiber and may also be conducive
to improved exercise performance. The influence of prim-
ing exercise on motor unit recruitment profiles likely reflects
the balance between the potentially beneficial and detrimen-
tal effects of priming exercise on muscle function, effects
which in turn will be related to the intensity of the priming
exercise bout and the duration of the subsequent recovery
interval (7).
Nutrition. Recent studies have reported that dietary ni-
trate supplementation in the form of beetroot juice, which
increases plasma [nitrite] (an index of increased NO bio-
availability), reduces the amplitude of the V
˙O
2
slow com-
ponent (5,9,88). The mechanistic bases for this effect
remain unclear. The reduced V
˙O
2
slow component is mir-
rored by a reduced intramuscular [PCr] slow component (9)
(F9Fig. 9), suggesting that muscle contractile efficiency is
enhanced by the intervention. Given the important role of
NO in the regulation of blood flow, however, it is also pos-
sible that nitrate supplementation reduces the V
˙O
2
slow
component by improving the matching of O
2
delivery to
V
˙O
2
in active motor units (5,73). Irrespective of the mecha-
nistic bases for the effect, it seems that the attenuated muscle
FIGURE 9—Pulmonary V
˙O
2
(A) and muscle [PCr] measured by
31
P magnetic resonance spectroscopy (B) during high-intensity knee extension
exercise after dietary supplementation with nitrate (closed symbols) or placebo (open symbols). Note the reduced V
˙O
2
and [PCr] slow components after
nitrate supplementation, along with the significantly extended time-to-exhaustion. Data from Bailey et al. (5).
http://www.acsm-msse.org12 Official Journal of the American College of Sports Medicine
Copyright @ 2011 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
metabolic perturbation after nitrate supplementation allows
high-intensity exercise tolerance to be enhanced (5,9,88).
Interestingly, similar effects on the V
˙O
2
slow component and
exercise tolerance have been reported after ingestion of a di-
etary supplement containing L-arginine, the substrate for the
‘conventional’’ NO production pathway catalyzed by NOS
(10), whereas the V
˙O
2
slow component is increased when
NOS is inhibited pharmacologically (73). Collectively, these
data suggest an important role for NO in modulating the de-
velopment of the V
˙O
2
slow component and thus affecting
exercise tolerance.
Another nutritional intervention that has been reported to
influence the V
˙O
2
slow component is sodium bicarbonate
ingestion: in one study, the V
˙O
2
slow component amplitude
was reduced (77), and in another, the onset of the V
˙O
2
slow
component was delayed and end-exercise V
˙O
2
was reduced
(17). This effect is presumably mediated by a greater efflux
of H
+
from muscle to blood, thereby reducing or delaying
muscle fatigue and the recruitment of higher-order motor
units. Consistent with this interpretation, infusion of the drug
dichloroacetate, which activates the pyruvate dehydrogenase
enzyme complex and reduces substrate-level phosphoryla-
tion, results in a reduced amplitude (109) or delayed onset
(65) of the V
˙O
2
slow component.
The previous discussion highlights that the V
˙O
2
slow
component is intimately related to intramuscular events and
to the development of fatigue. In this regard, it is interest-
ing that increasing arterial O
2
partial pressure through the
inspiration of hyperoxic gas mixtures markedly attenuates
the V
˙O
2
slow component (91,130) and also spares muscle
PCr hydrolysis (54,122), an index of metabolic stability. In
contrast, when exercise is performed in the supine posi-
tion (76) and when muscle blood flow is reduced (87), the
V
˙O
2
slow component is increased. Collectively, these ob-
servations indicate that the V
˙O
2
slow component can be
manipulated by altering blood flow or O
2
delivery condi-
tions within the active muscle(s). Again, this is presumably
linked to greater metabolic stability, reduced fatigue, im-
proved efficiency, and changes to fiber recruitment.
CONCLUSIONS
The V
˙O
2
slow component is a fundamental property of
the metabolic response to exercise performed above the LT
that has been excluded from mainstream textbooks and
teaching in exercise physiology, presumably because its
existence presents an inconvenient challenge to our under-
standing of muscle energetics. This is unfortunate given that
the causes and consequences of the V
˙O
2
slow component
are so important for a more complete appreciation of meta-
bolic control, muscle efficiency, and the determinants of
exercise tolerance.
Mechanistically, the progressivelossofmuscleeffi-
ciency represented by the V
˙O
2
slow component is asso-
ciated with the development of fatigue and can be offset
by interventions that enhance metabolic stability (5–8,
9,18,21,26,28,91,130,137). During high-intensity CWR
exercise, the ‘‘conventional’’ V
˙O
2
slow component is as-
sociated with a progressive recruitment of additional
higher-order (type II) muscle fibers, and the low efficiency
of these fibers might well contribute to the increased O
2
cost of exercise (67,84–87,133). However, fatigued fibers
might also become less efficient and require a greater O
2
consumption per unit of ATP turnover and/or a greater
ATP turnover per unit of power output (11,136). Recent
data indicate that muscle efficiency is also lowered
(resulting in a ‘‘mirror-image’’ V
˙O
2
slow component)
during fatiguing high-intensity exercise in which addi-
tional fiber recruitment is debarred (59,124,138). It is im-
portant to recognize, however, that the existence of a V
˙O
2
slow component-like phenomenon in this situation does
not necessarily challenge the strong evidence that the
V
˙O
2
slow component is linked in some fashion to the
recruitment of type II muscle fibers (13,37,67,84–86,
103,104,134), only that the progressive, additional re-
cruitment of these fibers is not obligatory for the slow
component to develop (25,59,124,138). Type II fibers will
be recruited from the onset of fatiguing high-intensity or
all-out exercise and the greater fatigue sensitivity, and
likely slower V
˙O
2
kinetics and impaired efficiency of these
fibers relative to type I fibers might still play a crucial
role in the development of the V
˙O
2
slow component
(104,124,133,138).
From a practical perspective, further study of the mecha-
nistic bases of the V
˙O
2
slow component will be important in
designing interventions for the enhancement of exercise
performance. Although there is an obvious application to
athletes, it is also clear that patient populations and the el-
derly, in whom daily mobility and the quality of life may be
restricted because of a low or limited O
2
transport capacity,
might benefit tremendously from therapeutic strategies that
reduce the V
˙O
2
slow component. This is a worthy goal for
future studies.
There was no funding received.
The results of the present study do not constitute endorsement
by the American College of Sports Medicine.
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... Demnach kann der Einfluss der Atemarbeit bzw. zusätzlicher kardialer Anstrengungen als Ursache des V´O2sc weitgehend vernachlässigt werden(Jones et al., 2011). Innerhalb der potenziell wirksamen Faktoren auf Ebene der Arbeitsmuskulatur scheinen die Temperatur(Krustrup, Söderlund, Mohr & Bangsbo, 2004) und der pH-Wert(Gaesser, Ward, Baum & Whipp, 1994) eine untergeordnete Rolle zu spielen. ...
... Innerhalb der potenziell wirksamen Faktoren auf Ebene der Arbeitsmuskulatur scheinen die Temperatur(Krustrup, Söderlund, Mohr & Bangsbo, 2004) und der pH-Wert(Gaesser, Ward, Baum & Whipp, 1994) eine untergeordnete Rolle zu spielen. Aktuelle Untersuchungen weisen besonders der Faserrekrutierung und einer abnehmenden Effizienz chemischer Prozesse auf kontraktiler Ebene einen entscheidenden Beitrag zum V´O2sc zu(Jones et al., 2011). Konkret deuten Studienergebnisse darauf hin, dass während zunehmender Belastungsintensität der Anteil aktiver Typ II Fasern in der Arbeitsmuskulatur zunimmt, während im niedrigen Belastungsbereich die Aktivierung von Typ I Fasern klar dominiert(Krustrup et al., 2004). ...
... Tatsächlich weisen Studien darauf hin, dass sich durch mehrwöchiges spezifisches Ausdauertraining das V´O2sc in den trainierten Belastungsbereichen reduzieren lässt(Carter et al., 2000;Womack et al., 1995). Auch allgemein zeigt sich, dass ausdauertrainierte Athleten gegenüber untrainierten Probanden eine signifikant reduzierte V´O2sc aufweisen(Jones et al., 2011). Demzufolge kann das Monitoring der Sauerstoffaufnahmekinetik besonders bei Belastungsintensitäten des aerob-anaeroben Übergangsbereichs als zusätzliches Diagnoseinstrument angesehen werden(Jones & Burnley, 2009;Poole, Burnley, Vanhatalo, Rossiter & Jones, 2016). ...
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Die Arbeit beleuchtet den Einsatz algorithmischer Datenbearbeitungen bei sportwissenschaftlichen Spiroergometrien aus praktischen und theoretischen Gesichtspunkten. Die aktuelle Verbreitung von algorithmischen Datenbearbeitungen aus Breath-by-Breath Untersuchungen wird über die Ergebnisse eines Fragebogens und einer systematischen Literaturübersicht dargestellt. Zudem erfolgt die Analyse der durch Algorithmen verursachten Messwertvarianzen der Sauerstoffaufnahme in diskontinuierlichen Belastungsuntersuchungen, bei Jugendlichen und im submaximalen Belastungsbereich.
... The reduced O 2 cost of walking following RMET was exemplified by the lower _ VO 2 levels (during moderate-and heavy-intensity walking) and by the lower _ VO 2 versus time slopes (during heavy-intensity walking) (Fig. 2). No formal analyses of the _ VO 2 kinetics and its different components (Jones et al. 2011) was carried out in the present study, since the patients could perform only one repetition of each exercise. Some data, however, allow us to hypothesize, with reasonable confidence, that the reduced O 2 cost during heavy intensity walking was likely attributable to a reduced amplitude or to the disappearance of the "slow component" of the _ VO 2 kinetics (Jones et al. 2011). ...
... No formal analyses of the _ VO 2 kinetics and its different components (Jones et al. 2011) was carried out in the present study, since the patients could perform only one repetition of each exercise. Some data, however, allow us to hypothesize, with reasonable confidence, that the reduced O 2 cost during heavy intensity walking was likely attributable to a reduced amplitude or to the disappearance of the "slow component" of the _ VO 2 kinetics (Jones et al. 2011). The slope of the linear increase of the _ VO 2 versus time relationship ("excess VO 2 ," characteristic of the _ VO 2 slow component [ (Grassi et al. 2015)]), determined from the third to the 1ast minute of exercise, was indeed substantially decreased following RMET, whereas it was not affected by CTRL. ...
... The slope of the linear increase of the _ VO 2 versus time relationship ("excess VO 2 ," characteristic of the _ VO 2 slow component [ (Grassi et al. 2015)]), determined from the third to the 1ast minute of exercise, was indeed substantially decreased following RMET, whereas it was not affected by CTRL. A smaller amplitude of the slow component of the _ VO 2 kinetics is intrinsically associated with less inefficiency and less fatigue (Jones et al. 2011;Grassi et al. 2015). ...
... About 3 min following the start of an exercise conducted in the heavy-intensity domain above the first ventilatory threshold (VT1), the primary component is superimposed by an elevation ofVO 2 known as theVO 2 slow component (SC).VO 2 SC further delays the stabilisation of the oxidative response and is thought to be related to a deterioration of muscular efficiency. Thus, an increase of the ATP required for a similar power output is observed concomitantly to increases of the ventilatory, cardiac and auxiliary muscles work (Henson et al., 1989;Krustrup et al., 2004;Jones et al., 2011;Korzeniewski and Zoladz, 2015). Accordingly, a theoretical study has recently suggested that changes inVO 2 kinetics may be related to OXPHOS (mitochondrial oxidative phosphorylation system) activity and to additional ATP usage that appears when inorganic phosphate (Pi) exceeds a critical value called Pi crit (Allen and Westerblad, 2001;Korzeniewski and Rossiter, 2021). ...
... This is in agreement with the majority of works examining the effects of blood flow alteration on theVO 2 kinetics during exercise transitions (Koga et al., 1999;Knight et al., 2004). It has been well-documented thatVO 2 SC, which represents an O 2 overconsumption, was related to a deterioration of muscular efficiency in relation to the fatigue process (Henson et al., 1989;Krustrup et al., 2004;Jones et al., 2011). Therefore, the increase ofVO 2 Asc ′ during BFR could have been provoked by Values are means ± SD. ...
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... These experimental conditions (only applied to male subjects) are somewhat different from real race conditions, where higher velocities are maintained from approximately 28 min (10 km) to 145 min (marathon). During this extended time, the energy cost of running may progressively increase, due to slow component increases in oxygen uptake kinetics (Jones et al., 2011) and muscle damage (Assumpcao Cde et al., 2013). The magnitude of elite runners' race time decreases reported in this study is also lower than the ∼4% reported in club and sub-elite runners (Quealy and Katz, 2018). ...
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Running technique has been analyzed since antiquity, and yet the study of gait biomechanics is continually developing and unearthing new insights. This is undoubtedly linked to the great variety of skills required in the running and race walking events, despite their apparent simplicity: a fast but fair sprint start, safe and effective hurdle clearances, negotiation of the tight bends in indoor racing, and coping with changes in gradient in road and cross country running are just a few examples. Increasingly, coaches and governing bodies are looking to sports science to help improve their best athletes and raise participation rates in recreational sport, and need a comprehensive resource on technique, performance and training. Regardless of their standard, competitive athletes strive to improve performance and reduce the risk of injury, and biomechanists are ideally placed to support athletes and coaches in this universal sport.
... Specifically, increased synthesis of NO is proposed to reduce the oxygen cost of ATP resynthesis, lower the ATP cost of cross-bridge formation and promote vasodilation, thereby enhancing skeletal muscle blood flow and oxygen perfusion which may speed oxygen uptake kinetics [8]. These effects may translate to increased endurance exercise performance by improving exercise efficiency, decreasing the oxygen deficit at exercise onset and reducing the VȮ 2 slow component [9]. ...
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... NO production seems to have a powerful effect on the reduction in _ VO 2 slow component amplitude changing of the recruitment type II muscle fibers, which are most active in high-intensity exercise. [41] The loss of mechanic efficiency and fatigue of type II fibers are considered to be responsible for the higher occurrence of the _ VO 2 slow component, [42] and, therefore, BFR may increase the metabolic efficiency of type II fibers, despite not influencing responses during moderateintensity exercise since it mainly requires type I fibers, [37] which can elucidate the potential muscle fiber type-specific effect of BFR on exercise tolerance. ...
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... Since sprint training methodology does not include extensive slow and continuous exercise [84], speed athlete profiles in transition to sports with concurrent aerobic demands may be less familiar or experience discomfort early on with this modality. Even during low-intensity exercise, fast-twitch-dominant athletes (speed profiles), particularly if glycogen depleted (e.g., under recovered/second training session of the day), may place increased reliance on fast twitch fiber motor units [85], which under a continuous low exercise intensity stimulus can increase the VO 2 slow component, making steady-state exercise unattainable [26,86]. The increased dependence on anaerobic metabolism to meet the energetic requirements for the speed profile athlete, in addition to the increased neuromuscular loading with longer high-intensity work, can create unwanted fatigue in the unfamiliar athlete, lowering the quality of subsequent repetitions and potentially future training sessions [74]. ...
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Many individual and team sport events require extended periods of exercise above the speed or power associated with maximal oxygen uptake (i.e., maximal aerobic speed/power, MAS/MAP). In the absence of valid and reliable measures of anaerobic metabolism, the anaerobic speed/power reserve (ASR/APR) concept, defined as the difference between an athlete’s MAS/MAP and their maximal sprinting speed (MSS)/peak power (MPP), advances our understanding of athlete tolerance to high speed/power efforts in this range. When exercising at speeds above MAS/MAP, what likely matters most, irrespective of athlete profile or locomotor mode, is the proportion of the ASR/APR used, rather than the more commonly used reference to percent MAS/MAP. The locomotor construct of ASR/APR offers numerous underexplored opportunities. In particular, how differences in underlying athlete profiles (e.g., fiber typology) impact the training response for different ‘speed’, ‘endurance’ or ‘hybrid’ profiles is now emerging. Such an individualized approach to athlete training may be necessary to avoid ‘maladaptive’ or ‘non-responses’. As a starting point for coaches and practitioners, we recommend upfront locomotor profiling to guide training content at both the macro (understanding athlete profile variability and training model selection, e.g., annual periodization) and micro levels (weekly daily planning of individual workouts, e.g., short vs long intervals vs repeated sprint training and recovery time between workouts). More specifically, we argue that high-intensity interval training formats should be tailored to the locomotor profile accordingly. New focus and appreciation for the ASR/APR is required to individualize training appropriately so as to maximize athlete preparation for elite competition.
... VO 2 kinetics. The on-transient V O 2 kinetics were modelled after four different bouts of 5-min submaximal exercise (10 km·h −1 , moderate intensity, below lactate threshold) to avoid any effect of the slow component phenomenon (Jones et al. 2011). The influence of the inter-breath noise was reduced averaging the results of four identical tests in each participant (Lamarra et al. 1987). ...
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Purpose Continuous incremental protocols (CP) may misestimate the maximum aerobic velocity (Vmax) due to increases in running speed faster than cardiorespiratory/metabolic adjustments. A higher aerobic capacity may mitigate this issue due to faster pulmonary oxygen uptake (V̇O2) kinetics. Therefore, this study aimed to compare three different protocols to assess Vmax in athletes with higher or lower training status. Methods Sixteen well-trained runners were classified according to higher (HI) or lower (LO) V̇O2max. V̇O2-kinetics was calculated across four 5-min running bouts at 10 km·h-1. Two CPs [1 km·h-1 per min (CP1) and 1 km·h-1 every 2-min (CP2)] were performed to determine Vmax, V̇O2max, lactate-threshold and submaximal V̇O2/velocity relationship. Results were compared to discontinuous incremental protocol (DP). Results Vmax, V̇O2max, V̇CO2 and V̇E were higher [(P<0.05,(ES:0.22/2.59)] in HI than in LO. V̇O2-kinetics was faster [P<0.05,(ES:-2.74/-1.76)] in HI than in LO. V̇O2/velocity slope was lower in HI than in LO [(P<0.05,(ES:-1.63/-0.18)]. Vmax and V̇O2/velocity slope were CP1>CP2=DP for HI and CP1>CP2>DP for LO. A lower [P<0.05,(ES:0.53/0.75)] Vmax-difference for both CP1 and CP2 vs DP was found in HI than in LO. Vmax-differences in CP1 vs DP showed a large inverse correlation with Vmax, V̇O2max and lactate-threshold and a very large correlation with V̇O2-kinetics. Conclusions Higher aerobic training status witnessed by faster V̇O2 kinetics led to lower between-protocol Vmax differences, particularly between CP2 vs DP. Faster kinetics may minimize the mismatch issues between metabolic and mechanical power that may occur in CP. This should be considered for exercise prescription at different percentages of Vmax.
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Purpose: Accumulated time at a high percentage of peak oxygen consumption (VO2peak) is important for improving performance in endurance athletes. The present study compared the acute physiological and perceived effects of performing high-intensity intervals with roller ski double poling containing work intervals with (1) fast start followed by decreasing speed (DEC), (2) systematic variation in exercise intensity (VAR), and (3) constant speed (CON). Methods: Ten well-trained cross-country skiers (double-poling VO2peak 69.6 [3.5] mL·min-1·kg-1) performed speed- and duration-matched DEC, VAR, and CON on 3 separate days in a randomized order (5 × 5-min work intervals and 3-min recovery). Results: DEC and VAR led to longer time ≥90% VO2peak (P = .016 and P = .033, respectively) and higher mean %VO2peak (P = .036, and P = .009) compared with CON, with no differences between DEC and VAR (P = .930 and P = .759, respectively). VAR, DEC, and CON led to similar time ≥90% of peak heart rate (HRpeak), mean HR, mean breathing frequency, mean ventilation, and mean blood lactate concentration ([La-]). Furthermore, no differences between sessions were observed for perceptual responses, such as mean rate of perceived exertion, session rate of perceived exertion or pain score (all Ps > .147). Conclusions: In well-trained XC skiers, DEC and VAR led to longer time ≥90% of VO2peak compared with CON, without excessive perceptual effort, indicating that these intervals can be a good alternative for accumulating more time at a high percentage of VO2peak and at the same time mimicking the pronounced variation in exercise intensities experienced during XC-skiing competitions.
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