Detraining

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99
Valoración del paciente: Diagnóstico del
Detraining
Laurent BOSQUET1 & Iñigo MUJIKA2
1Faculty of Sport Sciences, University of Poitiers, France
2Department of Physiology, Faculty of Medicine and Odontology, University of the Basque Country, Leioa, Basque Country
10
Chapter

100
Laurent BOSQUET & Iñigo MUJIKA
Iñigo Mujika earned Ph.D.s in Biology of Muscular Exercise (University of Saint-Etienne, France) and Physical Activity
and Sport Sciences (University of e Basque Country). He is a Level III Swimming and Triathlon Coach. His research
interests include training methods and recovery, tapering, detraining and overtraining. He has performed extensive
research on the physiological aspects associated with endurance sports performance, published over 80 articles in peer
reviewed journals, two books and 13 book chapters, and given over 160 lectures in international conferences. Iñigo was
Senior Physiologist at the Australian Institute of Sport, physiologist and trainer for Euskaltel Euskadi cycling team, and
Head of Research and Development at Athletic Club Bilbao football club. He is Director of Physiology and Training
at USP Araba Sport Clinic, Physiologist of the Spanish Swimming Federation, Associate Editor for the International
Journal of Sports Physiology and Performance, and Associate Professor at the University of the Basque Country.
Laurent Bosquet earned a Ph.D. in Physical Activity Sciences from the University of Montreal (Canada) and a Ph.D.
in Sport Sciences from the University of Poitiers (France). A former Professor at the University of Montreal, Laurent is
a Professor at the University of Poitiers and the Dean of the Faculty of Sport Sciences. His research interest focuses on
the optimization of training methods for dierent populations, including elite athletes, elders or patients suering from
heart diseases. He is the head of the MOVE laboratory (University of Poitiers), associate researcher at the Montreal
Institute of Geriatrics, associate researcher at the Rehabilitation Center of the Montreal Heart Institute, and member of
the research board at the French Soccer Federation.
Iñigo MUJIKA, Ph.D.
Laurent BOSQUET, Ph.D.

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Detraining
Introduction
Endurance performance represents a complex interplay
between several physiological factors, including maximal
oxygen uptake (VO2max), aerobic endurance (AE) and the
energy cost of running (Cr) (Di Prampero et al., 1986).
Endurance training consists therefore in implementing
exercise protocols that will enhance at least one of these
determinants, in order to increase overall performance.
According to the principle of reversibility, training induced
physiological adaptations are transitory and may disappear
when the training load is not sucient. e reasons for
such a scenario are numerous in an athlete’s life: illness,
injury, post-season break or training load adaptation to
recover from a state of overreaching. e consequences
on endurance performance may vary according to the
way training load is altered: training reduction, training
cessation or bed rest connement (Mujika & Padilla, 2000a).
To avoid any confusion with the terminology, a glossary
is given in Table 10.1. is chapter addresses the eect
of training cessation on the physiological determinants
of endurance performance and their underlying factors.
Considering that detraining characteristics may dier
according to the training background, we focus on studies
dealing with well trained to highly trained athletes.
Chapter 10
Detraining
Laurent BOSQUET1 & Iñigo MUJIKA2
1Faculty of Sport Sciences, University of Poitiers, France
2Department of Physiology, Faculty of Medicine and Odontology, University of the Basque Country, Leioa, Basque Country
Detraining A partial or complete loss of training induced anatomical, physiological and performance
adaptations, as a consequence of training reduction or cessation.
Training cessation A temporary discontinuation or complete abandonment of a systematic program of physical
conditioning.
Training reduction A progressive or nonprogressive reduction of the training load during a variable period of
time, in an attempt to reduce the physiological and psychological stress of daily training.
Table 10.1. Glossary.
Maximal Oxygen Uptake
Maximal oxygen uptake represents the maximal amount of
oxygen that can be used at the cellular level for the entire
body. It represents the upper limit of the cardiorespiratory
system and has long been considered as an important
determinant of endurance performance (Saltin & Astrand,
1967). According to the Fick principle, any alteration in
VO2max is the consequence of a modication of maximal
cardiac output (Qmax) and/or maximal arteriovenous
dierence in oxygen (a-vDO2max). It is generally accepted
that the largest part of the training induced increase in
VO2max results from an increase in blood volume, stroke
volume and ultimately Qmax. Nevertheless, the increase in
a-vDO2max, which results from a more eective distribution
of arterial blood from inactive to active muscles together
with a greater oxygen extraction and utilization capacity
by these muscles, plays also an important role in
cardiorespiratory adaptations to endurance training.
Coyle et al. (1984) studied the eect of 12, 21, 56 and 84
days of training cessation on VO2max and its determinants
in 7 well-trained cyclists. Main results are summarized in

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Laurent BOSQUET & Iñigo MUJIKA
Figure 10.1. ey observed a ~15% decrease in VO2max that
followed a roughly exponential kinetics. Very interestingly,
there appeared to be a time sequence in the physiological
mechanisms underlying this loss of adaptation. During a
rst phase lasting 21 to 28 days, a-vDO2max was maintained,
suggesting that the decrease in VO2max was mainly a
consequence of a decrease in oxygen delivery to the muscle.
In fact, Coyle et al. (1985) reported a rapid decrease in
Qmax (~8%) that reached a plateau aer 21 to 28 days of
training cessation. is loss of adaptation resulted from an
important drop in maximal stroke volume (~11%), which
was partly compensated for by a ~5% increase in maximal
heart rate.
e rapid decrease in blood volume aer the rst days of
training cessation observed in several studies is expected
to play a key role in the cascade of events leading to the
decrease in Qmax (Figure 10.2). Once this rst “circulatory
detraining” phase is completed, the ongoing decrease of
VO2max is now the consequence of a continuous decrease in
a-vDO2max (~9%; Figure 10.1). Considering that capillary
density did not decline during the 84 days of training
cessation, this alteration is likely to be the consequence of a
decrease in muscle mitochondrial density or other factors
such as a reduction in muscle blood ow or capillary transit
time (Coyle et al., 1984).
In summary, these results suggest the existence of two
distinct phases in the physiological mechanisms underlying
the continuous decrease in VO2max that is observed in well-
trained endurance athletes once they stop training. During
a rst phase lasting 21 to 28 days, the decrease in VO2max is
mainly the consequence of a loss of central adaptation, as
Figure 10.1. Eect of training cessation on the physiological
determinants of maximal oxygen uptake (VO2max). Q: cardiac
output; a-vDO2: arteriovenous dierence in oxygen; SV: stroke
volume; HR: heart rate. Adapted from the data reported by Coyle
et al. (1984).
Figure 10.2. Eect of training cessation on the blood volume.
shown by a drop in Qmax, while it is peripheral (i.e. specic
to the trained muscles) aerwards. is time sequence has
many practical implications for athletes and coaches that
are discussed at the end of this chapter.
Aerobic Endurance
Aerobic endurance represents the capacity to sustain a high
fraction of VO2max throughout the entire eort duration
(Bosquet et al., 2002). Aerobic endurance is independent
from VO2max, since two individuals with the same VO2max
are not necessarily able to sustain the same fraction of
VO2max for a given eort duration (Peronnet & ibault,
1989). Both factors contribute to set exercise VO2, which
is considered an important determinant of endurance
performance, since the higher the exercise VO2, the higher
the energy provision in the form of ATP resynthesis rate.
Although physiological mechanisms involved in aerobic
endurance are not fully understood, the capacity to sustain
a high fraction of VO2max for a given duration has been
associated with a combination of several factors, including
a high percentage of type I muscle bres, the capacity to
store large amounts of muscle and/or liver glycogen, a high
activity of mitochondrial enzymes and the capacity to spare
carbohydrate by using more fatty acids as energy substrate
(Bosquet et al., 2002).
It is well established that endurance training results in an
increased percentage of type I muscle bres (Pette, 1984). It
is worth noting however that this progressive shi requires
a signicant period of time to take place and the magnitude
of change is oen small (Pette, 1984). As expected, the
eect of training cessation on muscle bre distribution
depends on the duration of the period of inactivity (Mujika
& Padilla, 2001b). While short-term training cessation (i.e.
three weeks or less) is not enough to induce any changes

103
Detraining
(Hortobagyi et al., 1993; Houston et al., 1979), long term
inactivity periods (up to several years) have been associated
with a progressive return to baseline (Coyle et al., 1984;
Larsson & Ansved, 1985).
Non-proteic respiratory exchange ratio (RER) is commonly
used to estimate the respective contribution of fatty acids
and glucose to energy production (Péronnet & Massicotte,
1991). Endurance training has long been associated with
a reduced RER at both maximal and submaximal exercise
intensities, thus suggesting a reduced reliance on glucose
for energy production. Training cessation results in a rapid
increase in RER that appears to reach a plateau within 14
days (Figure 10.3), as well as a rapid decrease in muscle
glycogen stores (up to 20% within 1 week of bed rest or
training cessation) (Costill et al., 1985; Mikines et al.,
1989). e rapid decrease in the glucose transporter
protein GLUT-4 concentration reported aer 6 to 10 days
of training cessation (Vukovich et al., 1996), together with
the important drop of glycogen synthase activity aer just
5 days of training cessation (Mikines et al., 1989) is thought
to play a major role in this process (Mujika & Padilla,
2000a; Mujika & Padilla, 2000b).
Endurance training increases the number and size of
the muscle bre mitochondria, as well as the activity of
oxidative enzymes (Abernethy et al., 1990). One of the
main characteristics of muscular detraining is an important
decrease of this activity (Mujika & Padilla, 2001b). Coyle
et al. (1984, 1985) reported that citrate synthase activity
declined by 23% during the rst 3 weeks of training
cessation in endurance trained athletes, by 23% again from
the 4th to the 8th week and stabilized thereaer. Succinate
Figure 10.3. Eect of training cessation on the respiratory
exchange ratio during exercise. RER: respiratory exchange ratio.
dehydrogenase and malate dehydrogenase followed the
same pattern of disadaptation (Coyle et al., 1984; 1985).
Similar results have been observed in runners (Houmard
et al., 1992; Houston et al., 1979), triathletes (McCoy et
al., 1994) or soccer players (Amigó et al., 1998). Simsolo
et al. (1993) also observed a large reduction of muscle
lipoprotein lipase activity aer two weeks of training
cessation in 16 endurance athletes, which undoubtedly
altered the capacity to spare carbohydrate by using more
fatty acids as energy substrate.
e lactate concentration to a given submaximal exercise
intensity is one of the numerous methods used to
determine aerobic endurance (Bosquet et al., 2002). e
lower its concentration, the better the aerobic endurance.
Considering the short and long term loss of adaptation that
aect some of the physiological factors underlying aerobic
endurance, it is expected that this important determinant
of endurance performance is altered by training cessation.
As shown in Figure 10.4, blood lactate concentration
increases exponentially with training cessation duration,
suggesting that aerobic endurance decreases rapidly when
the training process is interrupted. Although a steady state
value is reached around 21 to 28 days, one can expect a
further decrease in aerobic endurance that results from the
progressive decrease of type I muscle bres.
In summary, aerobic endurance decreases very rapidly
once training ceases, most probably for metabolic reasons.
An additional and delayed decrease remains possible when
the duration of training cessation is long enough to alter
muscle bre distribution.
Figure 10.4. Eect of training cessation on the blood lactate
concentration during exercise.

104
Laurent BOSQUET & Iñigo MUJIKA
Energy Cost of Locomotion
e energy cost of locomotion (Cr) represents the energy
demand to move at a given submaximal power output or
speed. e lower the Cr, especially when body mass is
accounted for such as in running, the lower the energy
expenditure to move at a given velocity and the better
the endurance performance. Factors aecting Cr are
numerous and have been thoroughly reviewed by Saunders
et al. (2004). Some of them are not changeable (e.g. height),
while others can be manipulated (e.g. stride biomechanics,
strength, elastic store-recoil capacity). Numerous
interventions such as plyometric (Berryman et al., 2010) or
high intensity interval training (Saunders et al., 2004) are
eective to decrease Cr and improve performance.
In addition to VO2max and its determinants, Coyle et
al. (1985) also examined the response to submaximal
intensity exercise aer 12, 21, 56 and 84 days of training
cessation. Interestingly, the VO2 response for the same
absolute intensity remained stable during this period,
suggesting that the energy required to develop this power
output was not aected by the lack of training. is is in
agreement with the nding by Houmard et al. (1992) that
Cr was not altered by a 14-day training cessation period in
12 distance runners. As already mentioned, the ability to
store and recoil elastic energy as well as maximal strength
are recognized as important determinants of Cr (Saunders
et al., 2004). We recently performed a meta analysis to
examine the eect of training cessation on maximal force
and maximal power and found that both neuromuscular
qualities could be maintained for up to 3-4 weeks before
declining. is ability to maintain strength performance is
probably related with the ability to maintain Cr.
However, it is important to keep in mind that although
the oxygen demand remains stable, the strategy used
by the subjects to match this energy demand changed
signicantly over time, since the RER increased linearly
with the duration of training cessation (from 0.93 ± 0.01 at
baseline to 1.00 ± 0.01 at day 84, corresponding to a ~8%
dierence). Considering the decrease in VO2max we already
discussed, the relative intensity of this power output
increased with the duration of training cessation from 74
± 2% at baseline to 90 ± 3% at day 84 (~22% dierence).
Perceived exertion logically increased from 12.3 ± 0.4 at
baseline to 17.1 ± 0.4 at day 84 (~39% dierence). In view
of the increase in RER and likely concomitant decrease
in glycogen stores (see the preceding section), one can
easily hypothesize that although Cr is not aected, time to
exhaustion at a given intensity is signicantly altered.
In summary, the oxygen uptake required to run at a given
speed does not appear to be altered by training cessation.
However the concomitant increase in RER and decrease in
VO2max result in a decreased exercise tolerance at a given
speed, since it corresponds to a higher relative intensity
and more glucose is needed for ATP resynthesis while the
glycogen stores are markedly decreased.
Practical Implications
Previous sections described the consequences of training
cessation on the physiological determinants of endurance
performance. It is important for coaches to know whether
an alternative training strategy is ecient to limit these
consequences, particularly when the athlete is injured.
As already discussed, the factors underpinning the
continuous decrease of VO2max depend on the duration
of training cessation. ey are mainly central Qmax during
the rst 3-4 weeks, and mainly peripheral a-vDO2max
aerwards. Considering that central adaptations and
disadaptations are not specic to the trained muscles,
an alternative training can be implemented to avoid or
limit detraining while an athlete is injured. Deep water
running has been shown to be eective for this purpose
(Chu & Rhodes, 2001). For example, Bushman et al. (1997)
found that VO2max, Cr, aerobic endurance and ultimately 5
km performance could be maintained in 11 well-trained
runners who substituted their usual on-land training by
deep water running for a period of 4 weeks. One leg cycling
represents another exercise modality that can be used to
limit the central eect of training cessation in injured
athletes. Olivier et al. (2010) randomized 24 soccer players
with anterior cruciate ligament reconstruction in a control
group that followed a classic rehabilitation program and
an experimental group that added aerobic training of the
untreated leg to the rehabilitation program. Stroke volume
and VO2max were maintained in the experimental group
while they decreased by ~20 and 10% respectively in the
control group. Arm cranking represents an alternative
modality of cardiovascular training that is commonly used
in the conditioning of spinal cord injury patients (Figoni,
1990). Considering that arm VO2max represents roughly
70 to 80% of leg VO2max (Secher & Volianitis, 2006), arm
cranking allows to reach exercise intensities that should be
high enough to maintain (or limit the decrease of) Qmax.
Pogliaghi et al. (2006) provided data that tended to conrm
this hypothesis, since they found in 12 healthy men aged
67 ± 5 years that arm cranking and leg cycling were equally
eective in improving maximal and submaximal exercise
capacity, and that roughly 50% of this improvement was
due to central adaptations. It should be noted however

105
Detraining
that arm cranking appears to be less well tolerated by
athletes than one leg cycling (Olivier et al., 2008). While
other modes of locomotion than the sport-specic one
can also be used as alternative exercises, it is worth noting
that transfer eects between modes are sometimes limited,
particularly when cycling or running are substituted by
swimming (Tanaka, 1994).
Metabolic consequences of training cessation occur rapidly
and aect both substrate utilization and glycogen stores
(Mujika & Padilla 2001a). ese adaptations are peripheral
(i.e. specic to the trained muscles). If it is possible to
implement an alternative training including exercises
that involve the same muscle groups than the competitive
activity, for example deep water running for an athlete
who suers an ankle sprain or an Achilles tendinosis, then
metabolic adaptations should be maintained. Otherwise,
athletes can eventually maintain their VO2max if an
alternative training including exercises that are not specic
to their sport specic muscle groups is implemented,
but their aerobic endurance will dramatically decrease.
Consequently, care should be taken to increase the training
load progressively when athletes resume training, since
they may eventually be able to maintain the same intensity
than before their injury, but not the same volume at this
intensity. Finally, when it is not possible to mobilize trained
muscles for a period longer than 3 to 4 weeks, peripheral
disadaptations will occur and require going through
previous training cycles to restore initial adaptations.
Summary
t .PTU PGUIF QIZTJPMPHJDBM EFUFSNJOBOUT PG FOEVSBODF
performance decline rapidly once the training process
is interrupted, leading to detraining and impaired
performance capacity.
t ,OPXJOH UIF LJOFUJDT PG UIFTF EJTBEBQUBUJPOT BMMPXT
athletes and coaches to implement alternative strategies
limiting the eect of training cessation.
t 702max decreases exponentially with the duration of
training cessation.
t 2max is altered before a-vDO2max, with a cut o duration
of 3-4 weeks.
t .FUBCPMJD EJTBEBQUBUJPOT PDDVS WFSZ SBQJEMZ BOE
negatively aect aerobic endurance.
t ćFFOFSHZ DPTU PG SVOOJOH JT MFTT BČFDUFECZ USBJOJOH
cessation than other determinants of endurance
performance.
t &OEVSBODFQFSGPSNBODFJTEFDSFBTFECZUPEVSJOH
periods of training cessation lasting 3-4 weeks or longer.
t 8IFO UIF USBJOJOH QSPDFTT JT JOUFSSVQUFE NPTU PęFO
because of an injury, athletes and coaches should estimate
the physiological consequences of implementing no
alternative training.
t $IPPTF UIF NPTU BQQSPQSJBUF BMUFSOBUJWF USBJOJOH
according to the cause of training cessation and its
anticipated duration.
t 3FTVNFOPSNBM USBJOJOH QSPHSFTTJWFMZ FWFO XIFO UIF
duration of training cessation is short.
t 8IFOUSBJOJOHDFTTBUJPOFYDFFETUPXFFLTTUSVDUVSBM
disadaptations will occur which require the training
program to go back to the preceding cycle.

106
Laurent BOSQUET & Iñigo MUJIKA
References
Abernethy, P.J., ayer, R. & Taylor, A.W. (1990). Acute and chronic
responses of skeletal muscle to endurance and sprint exercise. A review.
Sports Medicine, 10, 365-389.
Amigó, N., Cadefau, J.A., Ferrer, I., Terrados, N. & Cusso, R. (1998). Eect
of summer intermission on skeletal muscle of adolescent soccer players.
Journal of Sports Medicine and Physical Fitness, 38, 298-304.
Berryman, N., Maurel, D. & Bosquet, L. (2010). Eect of plyometric vs.
dynamic weight training on the energy cost of running. Journal of
Strength and Conditioning Research, 24, 1818-1825.
Bosquet, L., Léger, L. & Legros, P. (2002). Methods to determine aerobic
endurance. Sports Medicine, 32, 675-700.
Bushman, B.A., Flynn, M.G., Andres, F.F., Lambert, C.P., Taylor, M.S. &
Braun, W.A. (1997). Eect of 4 wk of deep water run training on running
performance. Medicine and Science in Sports and Exercise, 29, 694-699.
Chu, K.S. & Rhodes, E.C. (2001). Physiological and cardiovascular changes
associated with deep water running in the young: possible implications
for the elderly. Sports Medicine, 31, 33-46.
Costill, D.L., Fink, W.J., Hargreaves, M., King, D.S., omas, R. & Fielding,
R. (1985). Metabolic characteristics of skeletal muscle during detraining
from competitive swimming. Medicine and Science in Sports and
Exercise, 17, 339-343.
Coyle, E.F., Hemmert, M.K. & Coggan, A.R. (1986). Eects of detraining
on cardiovascular responses to exercise: role of blood volume. Journal of
Applied Physiology, 60, 95-99.
Coyle, E.F., Martin, W.H., Bloomeld, S.A., Lowry, O.H. & Holloszy, J.O.
(1985). Eects of detraining on responses to submaximal exercise.
Journal of Applied Physiology, 59, 853-859.
Coyle, E.F., Martin, W.H., Sinacore, D.R., Joyner, M.J., Hagberg, J.M. &
Holloszy, J.O. (1984). Time course of loss of adaptations aer stopping
prolonged intense endurance training. Journal of Applied Physiology, 57,
1857-1864.
Cullinane, E.M., Sady, S.P., Vadeboncoeur, L., Burke, M. & ompson,
P.D. (1986). Cardiac size and O2max do not decrease aer short-term
exercise cessation. Medicine and Science in Sports and Exercise, 18, 420-
424.
Di Prampero, P.E., Atchou, G., Bruckner, J.C. & Moia, C. (1986). e
energetics of endurance running. European Journal of Applied Physiology,
55, 259-266.
Drinkwater, B.L. & Horvath, S.M. (1972). Detraining eects on young
women. Medicine and Science in Sports, 4, 91-95.
Figoni, S.F. (1990). Perspectives on cardiovascular tness and SCI. Journal
of the American Paraplegia Society, 13, 63-71.
Hortobagyi, T., Houmard, J.A., Stevenson, J.R., Fraser, D.D., Johns, R.A. &
Israel, R.G. (1993). e eects of detraining on power athletes. Medicine
and Science in Sports and Exercise, 25, 929-935.
Houmard, J.A., Hortobagyi, T., Johns, R.A., Bruno, N.J., Nutte, C.C.,
Shinebarger, M.H. & Welborn, J.W. (1992). Eect of short term training
cessation on performance meausres in distance runners. International
Journal of Sports Medicine, 13, 572-576.
Houston, M.E., Bentzen, H. & Larsen, H. (1979). Interrelationships between
skeletal muscle adaptations and performance as studied by detraining
and retraining. Acta Physiologica Scandinavica, 105, 163-170.
Larsson, L. & Ansved, T. (1985). Eects of long-term physical training and
detraining on enzyme histochemical and functional skeletal muscle
characteristic in man. Muscle Nerve, 8, 714-722.
Madsen, K., Pedersen, P.K., Djurhuus, M.S. & Klitgaard, N.A. (1993).
Eects of detraining on endurance capacity and metabolic changes
during prolonged exhaustive exercise. Journal of Applied Physiology, 75,
1444-1451.
McCoy, M., Proietto, J. & Hargreaves, M. (1994). Eect of detraining on
GLUT-4 protein in human skeletal muscle. Journal of Applied Physiology,
77, 1532-1536.
Mikines, K.J., Sonne, B., Tronier, B. & Galbo, H. (1989). Eects of acute
exercise and detraining on insulin action in trained men. Journal of
Applied Physiology, 66, 704-711.
Moore, R.L., acker, E.M., Kelley, G.A., Musch, T.I., Sinoway, L.I.,
Foster, V.L. & Dickinson, A.L. (1987). Eect of training/detraining on
submaximal exercise responses in humans. Journal of Applied Physiology,
63, 1719-1724.
Mujika, I. & Padilla, S. (2000a). Detraining: loss of a training induced
physiological and performance adaptations. Part I. Sports Medicine, 30,
79-87.
Mujika, I. & Padilla, S. (2000b). Detraining: loss of training-induced
physiological and performance adaptations. Part II. Sports Medicine, 30,
145-154.
Mujika, I. & Padilla, S. (2001a). Cardiorespiratory and metabolic
characteristics of detraining in humans. Medicine and Science in Sports
and Exercise, 33, 413-421.
Mujika, I. & Padilla, S. (2001b). Muscular charateristics of detraining in
humans. Medicine and Science in Sports and Exercise, 33, 1297-1303.
Neufer, P.D., Costill, D.L., Fielding, R.A., Flynn, M.G. & Kirwan, J.P. (1987).
Eect of reduced training on muscular strength and endurance in
competitive swimmers. Medicine and Science in Sports and Exercise, 19,
486-490.
Olivier, N., Legrand, R., Rogez, J., Berthoin, S., Prieur, F. & Weissland, T.
(2008). One-leg cycling versus arm cranking: which is most appropriate
for physical conditioning aer knee surgery? Archives of Physical
Medicine and Rehabilitation, 89, 508-512.
Olivier, N., Weissland, T., Legrand, R., Berthoin, S., Rogez, J., evenon,
A. & Prieur, F. (2010). e eect of a one-leg cycling aerobic training
program during the rehabilitation period in soccer players with anterior
cruciate ligament reconstruction. Clinical Journal of Sport Medicine, 20,
28-33.
Péronnet, F. & Massicotte, D. (1991). Table of nonprotein respiratory
quotient: an update. Canadian Journal of Applied Physiology, 16, 23-29.
Péronnet, F. & ibault, G. (1989). Mathematical analysis of running
performance and world running records. Journal of Applied Physiology,
67, 453-465.
Pette, D. (1984). J.B. Wole memorial lecture. Activity-induced fast to slow
transitions in mammalian muscle. Medicine and Science in Sports and
Exercise, 16, 517-528.
Pogliaghi, S., Terziotti, P., Cevese, A., Balestreri, F. & Schena, F. (2006).
Adaptations to endurance training in the healthy elderly: arm cranking
versus leg cycling. European Journal of Applied Physiology, 97, 723-731.
Raven, P.B., Welch-O’Connor, R.M. & Shi, X. (1998). Cardiovascular
function following reduced aerobic activity. Medicine and Science in
Sports and Exercise, 30, 1041-1052.
Saltin, B. & Astrand, P.O. (1967). Maximal oxygen uptake in athletes.
Journal of Applied Physiology, 23, 353-358.
Saunders, P.U., Pyne, D.B., Telford, R.D. & Hawley, J.A. (2004). Factors
aecting running economy in trained distance runners. Sports Medicine,
34, 465-485.
Secher, N.H. & Volianitis, S. (2006). Are the arms and legs in competition
for cardiac output? Medicine and Science in Sports and Exercise, 38, 1797-
1803.
Simsolo, R .B., Ong, J.M. & Kern, P.A. (1993). e regulation of adipose
tissue and muscle lipoprotein lipase in runners by detraining. Journal of
Clinical Investigation, 92, 2124-2130.
Tanaka, H. (1994). Eects of cross training. Sports Medicine, 18, 330-339.
Vukovich, M.D., Arciero, P.J., Kohrt, W.M., Racette, S.B., Hansen, P.A. &
Holloszy, J.O. (1996). Changes in insulin action and GLUT-4 with 6
days of inactivity in endurance runners. Journal of Applied Physiology,
80, 240-244.