Sports Med 2012; 42 (2): 165-168
CORRESPONDENCE
Fatigue during Repeated
Sprints
Precision Needed
I read with great interest the excellent review of
my colleagues O. Girard, A. Mendez-Villanueva
and D. Bishop.[1] While I congratulate the authors
for their detailed work, I wish to comment on,
partly due to recently published data, the relative
importance of (i) parasympathetic reactivation;
(ii)
. muscle (re)oxygenation; and (iii) oxygen uptake
(VO2) kinetics for improved repeated-sprint ability
(RSA).
1. In figure 3 (p. 676[1]), the authors present a
selection of the ‘‘possible physiological mecha-
nisms responsible for fatigue during repeated-
sprint exercise.’’ Among them, parasympathetic re-
activation is mentioned.[2] In contrast to other
suggested mechanisms, however, the possible link
between repeated-sprint (RS) performance and
autonomic activity is not mentioned in their re-
view. For a comprehensive understanding, this
needs to be examined under the context of both
acute fatigue during RS exercise (RSE) [as is the
focus of the present review[1]] and long-term
(training-induced) changes in RS performance.
First, given the great proportion of RS perfor-
mance that is related to neuromuscular parame-
ters,[1] it is difficult to see, from a physiological
perspective, how (central) cardiovascular auto-
nomic adjustments could be considered as a de-
terminant of RS performance. Second, today,
there remains no scientific evidence to suggest that
adjustments in post-exercise autonomic activity
per se play any sort of a significant role ‘during’
RSE. While they share the same acronym (i.e.
Repeated-Sprint Ability and Respiratory Sinus
Arrhythmia [a mechanisms of heart rate variabil-
ity]: RSA), we have consistently failed to find any
direct associations between these variables.[2-5]
In contrast, the current viewpoint today is that
autonomic activity is, rather than a mechanism
regulating fatigue during RSE, more of a promis-
ing marker of training adaptation.[4,5] For instance,
both pre-training parasympathetic reactivation
0112-1642/12/0002-0165/$49.95/0
ª 2012 Adis Data Information BV. All rights reserved.
measures[5] and changes in post-exercise auto-
nomic activity[4] correlated with changes in RS
performance in team sport players. These correla-
tions are likely related to the fact that (i) a high
parasympathetic activity might enable a greater
adaptation to high training loads,[6] and, in turn,
a greater improvement in RS performance; and
(ii) training-induced physiological adaptations
beneficial to the metabolic component of RSA
(e.g. better acid-base regulation, improved oxygen
delivery capacity[1]) are also clearly involved in
the regulation of post-exercise autonomic control
(via changes in the stimulation of metabo- and
baro-receptors[7]).
2. Since a greater between-effort muscle deoxygena-
tion has been shown to be associated with an
impaired physical work capacity, it has been
suggested that muscle oxygenation may be a deter-
minant of high-intensity intermittent[8,9] and RS[10]
performance. Additionally, training-induced accel-
erations in muscle reoxygenation between sprints
has been shown to parallel the improvements in
RSA.[11] However, the lower muscle oxygenation
that was associated with impaired RS perfor-
mance[8-10] was in fact caused by an active between-
effort recovery. It was therefore impossible to
examine whether the impaired RSA was a conse-
quence of the muscle deoxygenation per se, the
increased energetic demands relative to the active
recovery, or both. To examine further, we asked ten
male cyclists to repeat six, 30-second all-out cycling
sprints every 2 minutes; this duration was long
enough to observe a complete muscle reoxygenation
before each successive sprint.[12] Despite this, their
percentage of power decrement was 21%. Along
these lines, arterial occlusion (leading to a com-
plete lack of muscle reoxygenation) after maximal
voluntary contraction of the plantar flexors did not
compromise muscle force recovery to a great extent
(i.e. 89% vs 102% of the initial maximal voluntary
contraction after 5 minutes for occlusion vs control,
respectively[13]). Additionally, muscle oxygenation
and force production capacity during recovery
were only moderately correlated (r = 0.32 [90% CI
0.09, 0.52]; p = 0.02). Therefore, while it is still
possible that incomplete muscle reoxygena-
tion might moderately limit RSA,[13] a complete
muscle reoxygenation/high level of muscle oxygen-
166
ation is not necessarily associated with a preserved
RSA.[12] In fact, a complete muscle reoxygenation
as measured by near-infrared spectroscopy
(NIRS) does not obligatorily reflect a complete
metabolic recovery. Since muscle oxygenation is
directly related to the balance . between O2
delivery to the muscle and local VO2, a complete
muscle reoxygenation . can be observed despite an
increased muscle VO2, as long as O2 delivery
remains elevated following exercise (i.e. hyperae-
mia and increased blood flow). The improved RS
performance observed after endurance training,[11]
might therefore not be related to the acceleration of
muscle reoxygenation per se, but rather to a likely
faster muscle phosphocreatine resynthesis, which
generally parallels the recovery time course of the
NIRS signal.[14]
3. While the physiological rationale for . the
expected relationships between on- and off-VO2
kinetics and RSA makes intuitive sense (i.e. the
lower the O2 deficit and the faster the metabolic
recovery, the better the RSA[1]), recent data ques-
tions this assumption. First, the ability to repeat
sprints depends logically more on recovery mecha-
nisms than on metabolic
. control at the exercise
onset.[15] Second, off-VO2 kinetics might not
accurately reflect muscle metabolism,[16] especially
during successive sprints.[12] For example, Krus-
trup et al.[16] did not find .a relationship between
pulmonary and muscle VO2 recovery kinetics
following exercise. Recent data on highly-trained
young soccer players[17] also suggests that, pro-
bably as a result of the selection process, a large
correlation exists between sprinting speed and
maximal
. aerobic function (to which, in general,
VO2 kinetics are related). Therefore,
. the associa-
tions between RSA and VO2 kinetics observed
exclusively in soccer players[15,18,19] may not reflect
a cause-and-effect mechanism, but instead could
be related to the particular fitness profile of these
players. In support of this latter hypothesis, we
could
. not find any relationship between RSA and
VO2 kinetics in a homogeneous group of moder-
ately-trained cyclists.[12] The lack . of association
between RSA and on- and off-VO2 kinetics was
also confirmed in a subsequent study involving
61 team sport players.[20] The locomotor profile of
the players (i.e. determined by sprinting and
ª 2012 Adis Data Information BV. All rights reserved.
Letter to the Editor
incremental test speed, which is an indirect mea-
sure of maximal aerobic speed[21]) was the exclusive
predictor of RS performance (stepwise regression
analysis).
. ‘Metabolic’ variables
. such as maximal
VO2 and on- and off-VO2 kinetics were excluded
from the model in this study.[20]
To conclude, it is unlikely that parasym-
pathetic reactivation plays a role in regulating
fatigue during RSE. Until new evidences are pro-
vided, the importance. of absolute muscle (re)ox-
ygenation level and VO2 kinetics for improved
RSA also appears limited.
Martin Buchheit
Physiology Unit, Sport Science Department, Aspire,
Academy for Sports Excellence, Doha, Qatar
Acknowledgements
The author has no conflicts of interest that are directly
relevant to the content of this letter.
References
1. Girard O, Mendez-Villanueva A, Bishop D. Repeated-sprint
ability: part I. Factors contributing to fatigue. Sports Med
2011; 41: 673-94
2. Buchheit M, Laursen PB, Ahmaidi S. Parasympathetic re-
activation after repeated sprint exercise. Am J Physiol
Heart Circ Physiol 2007; 293: H133-H41
3. Buchheit M, Duche P, Laursen PB, et al. Postexercise heart rate
recovery in children: relationship with power output, blood
pH, and lactate. Appl Physiol Nutr Metab 2010; 35: 142-50
4. Buchheit M, Millet GP, Parisy A, et al. Supramaximal
training and post-exercise parasympathetic reactivation in
adolescents. Med Sci Sports Exerc 2008; 40: 362-71
5. Buchheit M, Simpson MB, Al Haddad H, et al. Monitoring
changes in physical performance with heart rate measures in
young soccer players. Eur J Appl Physiol. Epub 2011 Jun 9
6. Hautala AJ, Kiviniemi AM, Tulppo MP. Individual re-
sponses to aerobic exercise: the role of the autonomic ner-
vous system. Neurosci Biobehav Rev 2009; 33: 107-15
7. Rowell LB. Human circulation: regulation during physical
stress. New York (NY): Oxford University Press, 1986: 363-84
8. Dupont G, Moalla W, Guinhouya C, et al. Passive versus
active recovery during high-intensity intermittent exercises.
Med Sci Sports Exerc 2004; 36: 302-8
9. Dupont G, Moalla W, Matran R, et al. Effect of short re-
covery intensities on the performance during two Wingate
tests. Med Sci Sports Exerc 2007; 39: 1170-6
10. Buchheit M, Cormie P, Abbiss CR, et al. Muscle deox-
ygenation during repeated sprint running: effect of active
vs. passive recovery. Int J Sports Med 2009; 30: 418-25
11. Buchheit M, Ufland P. Effect of endurance training on
performance and muscle reoxygenation rate during re-
Sports Med 2012; 42 (2)
Letter to the Editor
peated-sprint running. Eur J Appl Physiol 2011; 111:
293-301
12. Buchheit M, Abbiss C, Peiffer JJ, et al. Performance and
physiological responses during a sprint interval training
session: relationships with muscle oxygenation and pul-
monary oxygen uptake kinetics. Eur J Appl Physiol. Epub
2011 Jun 12
13. Ufland P, Lapole T, Ahmaidi S, et al. Muscle force recovery
in relation to muscle oxygenation level [abstract no. PM25-
3 plus poster]. 16th Annual Congress of the ECSS; 2011 Jul
6-9; Liverpool
14. McCully KK, Iotti S, Kendrick K, et al. Simultaneous in vivo
measurements of HbO2 saturation and PCr kinetics after
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15. Dupont G, McCall A, Prieur F, et al. Faster oxygen uptake
kinetics during recovery is related to better repeated sprint-
ing ability. Eur J Appl Physiol 2010; 110 (3): 627-34
16. Krustrup P, Jones AM, Wilkerson DP, et al. Muscular and
pulmonary O2 uptake kinetics during moderate- and high-
intensity sub-maximal knee-extensor exercise in humans.
J Physiol 2009; 587: 1843-56
17. Mendez-Villanueva A, Buchheit M, Kuitunen S, et al. Is the
relationship between sprinting and maximal aerobic speeds
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Sci 2010; 4: 497-510
18. Dupont G, Millet GP, Guinhouya C, et al. Relationship
between oxygen uptake kinetics and performance in re-
peated running sprints. Eur J Appl Physiol 2005; 95: 27-34
19. Rampinini E, Sassi A, Morelli A, et al. Repeated-sprint
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20. Buchheit M. Repeated-sprint performance in team sport
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The Authors’ Response
Part I
To begin, we would like to thank our friend
and colleague, Dr Martin Buchheit, for his in-
terest in our reviews.[1,2] We agree that precision
is always needed, which is one of the reasons that
early in our review we provided a very precise
definition of repeated-sprint exercise (RSE) as
being ‘‘characterized by short-duration sprints
(£10 seconds) interspersed with brief recovery
periods (usually £60 seconds)’’[2] (p. 674). Unfor-
tunately, Dr Buchheit uses data from 30-second
ª 2012 Adis Data Information BV. All rights reserved.
167
sprints and maximal voluntary contractions (MVCs)
to advance his arguments about the potential
determinants of fatigue during RSE. Given the
task-specific nature of fatigue,[3] we believe that it
is often this imprecise definition of RSE that has
led to confusion in the literature.
We respect Dr Buchheit’s expertise in the area of
heart rate variability, and we read with interest his
elaboration on this factor (which was beyond
the scope of our review). However, the argument
in the second paragraph of his first letter is based
largely on a misleadingly truncated sentence from
our review. The actual title for figure 3 was ‘‘Pub-
lished research on the possible physiological
mechanisms responsible for fatigue during re-
peated-sprint exercise’’[2] (p. 676). This does
not convey an endorsement of these factors,
but rather presents a timeline of factors that
researchers have attempted to associate with re-
peated-sprint ability (RSA). In fact, we share
Dr Buchheit’s view that autonomic activity is
unlikely to be associated with RSA (and one of
his papers demonstrating this is included in figure
3[2]). This also explains, as noted by Martin,
why this factor was not further mentioned in our
review.
Dr Buchheit’s second point appears to be that
there is no conclusive evidence that muscle oxy-
genation is a determinant of RSA. We agree, and
in our review we actually wrote that ‘‘the ability
of the subjects to use available oxygen during RSE
may be well preserved’’[2] (p.682). This statement
has recently been supported by two studies demon-
strating that reduced oxygen availability (hypoxia)
has little impact on the muscle oxygenation changes
that typically occur during RSA tests.[4,5] When
matched for initial mechanical work, it is also inter-
esting to observe that women having a lower level of
de-oxygenation exhibited the same work decrement
as men during an RSA test (ten, 10-second cycle
sprints interspersed with 30 seconds of rest), both in
normoxic and hypoxic environments.[5] These find-
ings support the increasing evidence that muscle O2
extraction during sprints is not considered as a lim-
iting factor for RSA, at least when the blood flow to
the muscle is not restricted. Dr Buchheit also adds
that ‘‘a complete muscle re-oxygenation/high level of
muscle oxygenation is not necessarily associated
Sports Med 2012; 42 (2)