Content uploaded by Rafael A Casuso
Author content
All content in this area was uploaded by Rafael A Casuso on Feb 25, 2015
Content may be subject to copyright.
1 3
Eur J Appl Physiol
DOI 10.1007/s00421-013-2784-7
ORIGINAL ARTICLE
Glucocorticoids improve high‑intensity exercise performance
in humans
Rafael A. Casuso · Lars Melskens · Thomas Bruhn ·
Niels H. Secher · Nikolai Baastrup Nordsborg
Received: 18 September 2013 / Accepted: 26 November 2013
© Springer-Verlag Berlin Heidelberg 2013
Conclusion Short-term dexamethasone administration
increases high-intensity one-legged kicking time to exhaus-
tion and 20-m shuttle run performance, although sprint
ability and the initial loss of muscular force generating
capacity are similar after DEX and placebo.
Keywords Muscle mass · Dexamethasone · Sport ·
Doping · EMG
Abbreviations
CNS Central nervous system
DEX Dexamethasone
EMG Electromyography
MVC Maximal voluntary contraction
RFD Rate of force development
RMS Root mean square
VO2max Maximal oxygen uptake
Introduction
Glucocorticoid injection is used in athletic populations to
suppress inflammation related to, for example, tendinopa-
thy (Coombes et al. 2010) and oral glucocorticoids are pre-
scribed to prevent exacerbation of asthma (Fiel and Vincken
2006). Use of glucocorticoids is banned by the World Anti-
Doping Agency (WADA) due to its possible performance
enhancing effects, but use for medical reasons is allowed.
It has been argued that a performance enhancing effect of
glucocorticoid cannot be proved (Dvorak et al. 2006), but
a recent review indicates a performance enhancing effect
of orally administered glucocorticoid (Duclos 2010). With
the clinical use of glucocorticoids, it is important to evalu-
ate whether glucocorticoids are to be considered as perfor-
mance enhancing drugs.
Abstract
Purpose It was investigated whether oral dexamethasone
(DEX) administration improves exercise performance by
reducing the initial rate of muscle fatigue development dur-
ing dynamic exercise.
Methods Using a double-blinded placebo controlled rand-
omized crossover design, subjects ingested either 2 × 2 mg
of DEX or placebo for five consecutive days. Muscle func-
tion was investigated using one-legged kicking exercise
and whole body performance was evaluated using a 20-m
shuttle run and a 30-m sprint test.
Results One-legged dynamic knee-extensor exercise
time to exhaustion was 29 ± 35 % (mean ± SD) longer
(P < 0.05) in DEX compared to Placebo. Likewise, total
running distance in the shuttle run test was 19 ± 23 %
longer (P < 0.05), whereas 30-m sprint performance was
unaltered. During the initial 75 s of dynamic leg extensions,
peak force and rate of force development determined from
an electrically evoked twitch declined in a similar way in
DEX and placebo. Similarly, the EMG root mean square
was similar with DEX and placebo treatment.
Communicated by Michael Lindinger.
R. A. Casuso
Department of Health Sciences, University of Jaén, Jaén, Spain
L. Melskens · T. Bruhn · N. B. Nordsborg (*)
Department of Nutrition, Exercise and Sport, University
of Copenhagen, Universitetsparken 13, 2nd floor,
2100 Copenhagen, Denmark
e-mail: nnordsborg@ifi.ku.dk
N. H. Secher
The Copenhagen Muscle Research Center, Department
of Anesthesia, Rigshospitalet, University of Copenhagen,
Copenhagen, Denmark
Eur J Appl Physiol
1 3
Oral glucocorticoid supplementation may have direct
effects on skeletal muscle. Glucocorticoids, such as dexa-
methasone, increase Na+, K+ pump capacity and content of
human muscles (Nordsborg et al. 2005). Also, during exer-
cise, the venous K+ concentration is reduced after dexameth-
asone treatment (Nordsborg et al. 2008). These muscular and
systemic effects of short-term oral dexamethasone admin-
istration may alleviate exercise-induced fatigue, because
increased Na+, K+ pump activity and reduced plasma K+
levels appear associated with improved resistance to mus-
cle fatigue during intense exercise (Sejersted and Sjogaard
2000; Nielsen and Clausen 2000; McKenna et al. 2008). In
support, following glucocorticoid supplementation, one-
legged kicking time to exhaustion is not affected at a high
exercise intensity (exhaustion after 1–3 min), but 7 of 9 sub-
jects improved performance for exhaustive exercise lasting
3–8 min (Nordsborg et al. 2008). At lower exercise intensi-
ties and longer duration, treatment with the glucocorticoid
prednisolone increases cycling time to exhaustion at ~75 %
of maximal oxygen uptake by approximately 60 % (from
46 to 74 min) after 1 week (Arlettaz et al. 2007). However,
treatment with dexamethasone did not alter performance dur-
ing an incremental test to exhaustion (Marquet et al. 1999).
Thus, it remains controversial whether whole body exercise
is affected by administration of dexamethasone.
The way glucocorticoid supplementation may affect per-
formance could be unrelated to skeletal muscle function
per se. Glucocorticoids induce an increase of extracellular
dopamine concentration and are associated with increased
locomotor activity in rats (Piazza et al. 1996). Thus, gluco-
corticoids may improve exercise capacity by stimulating the
central nervous system (CNS). This possibility has not been
addressed in humans, but “steroid euphoria” can be observed
after glucocorticoid administration (Swinburn et al. 1988).
To evaluate how dexamethasone may improve perfor-
mance, it is also of importance to address whether the effect
depends on the engaged muscle mass and whether it is related
to local muscular or CNS events. A high temporal resolution
for evaluation of fatigue development during dynamic exer-
cise may reveal underlying physiological events.
The primary aim of the present study was to evaluate
whether dexamethasone administration improves high-
intensity exercise performance by reducing the initial rate
of fatigue development during exercise with a small muscle
mass. The second aim of the study was to evaluate whether
short-term dexamethasone treatment has an effect on whole
body high-intensity exercise.
Methods
Seventeen healthy non-smoking male subjects aged
25.2 ± 2.5 years (mean ± SD) and weighing 78 ± 12 kg
participated in the study after providing their informed
consent. The study conformed to the code of Ethics of the
World Medical Association (Declaration of Helsinki) and
was approved by the Ethics Committee of Copenhagen and
Frederiksberg communities.
Protocol
The subjects ingested 2 mg of dexamethasone or placebo in
the morning (between 7 and 9 a.m.) and evening (between
5 and 9 p.m.) for five consecutive days. Placebo and dexa-
methasone were administered in a randomized crossover
fashion and a double blind protocol was used. Recruitment
and experiments were completed by blinded personnel.
Only one researcher had access to randomization codes
and he did not participate in collecting experimental data.
On the first day after the last intake of dexamethasone or
placebo, muscle function was assessed using one-legged
kicking (n = 17). On the following day, performance was
evaluated for a 30-m sprint (n = 16) and a 20-m shuttle run
test (n = 15). The dexamethasone and placebo trials were
separated by more than 30 days. Participants refrained from
physical activity on the day before the kicking experiment
and on the experimental days subjects refrained from intake
of tea and coffee. Food intake was similar on the day before
and on the experimental day for the two tests.
Muscle function: one-legged knee exercise
All participants completed at least two familiarization trials
on a one-legged kicking ergometer. On the first experimen-
tal day, participants were placed in a seated position with
one foot in a special designed boot that was attached to a
one-legged knee extension ergometer (Andersen and Saltin
1985). Maximal voluntary contraction (MVC) force was
determined as the largest of three 3–5 s maximal contrac-
tions separated by 30 s. During MVC determination, the
knee was in a fixed 90° angle. Force was recorded using
a calibrated strain gauge connected to the heel of the boot
and sampled at 1 kHz. Immediately after (~1 s), a dou-
ble pulse electrical stimulation (400 V, 98 ± 6 mA) was
delivered (2 × 1 ms separated by 10 ms, corresponding to
100 Hz) using a Digitimer DS7AH and DG2A generator
(Digitimer, Hertfordshire, UK) and 5 × 9 cm2 electrodes
(PALS platinum, Axelgaard, Lystrup, Denmark) placed
over the belly of m. rectus femoris. Optimal stimula-
tion intensity was determined prior to the experiment by
increasing stimulation current until a plateau in the twitch
response was observed. This intensity plus 10 % was used
in the experiments.
In five subjects, EMG was recorded from m. vastus lat-
eralis during MVCs and continuously during dynamic exer-
cise. The skin was prepared by shaving, mild sandpapering
Eur J Appl Physiol
1 3
and alcohol rinsing. Electrodes were 2 × 1 cm2 and placed
0.5 cm apart on the belly of m. vastus lateralis. The ref-
erence electrode was placed on the anterior superior iliac
spine. The signal was sampled at 1 kHz with a bandwidth
filter of 15–300 Hz (Grass amplifier, Warwick, USA; AD
instruments Powerlab). EMG is reported as maximal root
mean square (RMS) recorded in a 200-ms window during
contraction normalized to the maximal RMS recorded dur-
ing the MVC prior to dynamic exercise. Reported values
are an average of five consecutive contractions determined
at 5, 15, and 30 s and then every 30 s until exhaustion.
After 30 s of passive movement at 60 rpm, dynamic
knee extensions (60 ± 13 W) were performed until exhaus-
tion defined as a drop from the required 60 to 45 rpm. Mus-
cle twitch response (Fpeak) was evaluated at 5, 15, 45 and
75 s of exercise by applying the described double pulse
electrical stimulation during the passive knee flexion phase
of the kicking cycle. Stimulation was delivered at the exact
same position every time by a custom-built automated trig-
ger system. From the recorded twitches, peak force, rate of
force development (RFD) and rate of relaxation were cal-
culated. Calculations were based on 10 ms averages of the
force tracing recorded at 1 kHz. In pre-trials, it was verified
that repeated stimulations during low-intensity exercise
did not change twitch characteristics. Only subjects who
fatigued between 2.0 and 8.0 min (n = 12) were included
in the analyses because this was the range in which dexa-
methasone appeared to affect performance in our previous
study (Nordsborg et al. 2008).
Performance
On the second experimental day, the participants were
weighed. After warm-up involving sprinting and sub-
sequent 20-min rest, three 30-m sprint tests with stand-
ing start, separated by 2 min were performed. Time was
recorded by photocells (Time It, Eleiko Sport, Halmstad,
Sweden). After another 20 min of rest, a 20-m shuttle run
test was performed (Krustrup et al. 2003). Briefly, 20-m
runs forth and back between a starting, turning, and finish-
ing line were performed at progressively increased speed
guided by audio signals. Between each running bout was
a 10-s active rest period by 2 × 5 m of jogging. After two
failed attempts to reach the finishing line in time, the dis-
tance covered was recorded. Before the test, all subjects
completed a warm-up period consisting of the first four
running bouts in the test.
Statistics
Muscle function variables were analysed by the use of a
mixed model (Cnaan et al. 1997) with factors ‘trial’ (dexa-
methasone, placebo) and ‘sample’ (numerical index, for
example, 1, 2, 3, etc.) and repeated observations for ‘subject’.
If a significant main effect was found, time specific analyses
were performed by Sidak corrected post hoc analyses. Perfor-
mance in the shuttle run and 30-m sprint test was evaluated
by a paired t test. The level of significance was set at P < 0.05.
Results
Dexamethasone and performance
One-leg dynamic knee-extensor exercise time to exhaustion
was 29 ± 35 % longer (333 ± 30 vs. 264 ± 21 s; n = 12;
P < 0.05) in the dexamethasone compared to placebo trial.
Likewise, total running distance in the 20-m shuttle run test
was increased by 19 ± 23 % (P < 0.05) with covered dis-
tance increasing from 637 ± 294 to 731 ± 310 m and total
test duration increasing from 811 ± 594 to 963 ± 663 s.
In contrast, 30-m sprint performance was similar after
dexamethasone (4.5 ± 0.1 s) and placebo (4.6 ± 0.2 s)
treatment.
Dexamethasone and muscle function
The response to electrically evoke muscle twitches during
the passive phase of one-leg dynamic knee-extensor exer-
cise revealed no differences in Fpeak or RFD determined
in the dexamethasone and placebo trials. However, twitch
relaxation was slower (P < 0.05) after dexamethasone com-
pared to placebo treatment after 45 s of exercise (Fig. 1c).
A time-dependent change in all three muscle function
parameters existed (Fig. 1a–c). Compared to the first stim-
ulation response (5 s) during exercise, a lower (P < 0.01)
Fpeak was observed at 75 s in both groups (41 ± 19 vs.
30 ± 15 % after dexamethasone and placebo, respectively).
Similarly, twitch RFD was lower (P < 0.01) at 75 s com-
pared to 5 s (21 ± 16 vs. 20 ± 11 % after dexamethasone
and placebo, respectively). Also, twitch rate of relaxation
was slower (P < 0.01) at 75 s compared to 5 s (47 ± 26 vs.
37 ± 23 %) and at 45 s (P < 0.01) in the dexamethasone
trial.
Dexamethasone and EMG activity
EMG RMS increased (P < 0.05) during exercise in both tri-
als (Fig. 1d) with the change being similar after dexameth-
asone and placebo treatment.
Discussion
The major findings of the present study are that short-term
dexamethasone ingestion increases high-intensity exercise
Eur J Appl Physiol
1 3
performance when evaluated as one-legged kicking time to
exhaustion and 20-m shuttle run test endurance. Further-
more, the gradual reduction of maximal muscular force
generating capacity during the initial 75 s of high-intensity
dynamic exercise was similar with and without dexametha-
sone ingestion. In an anti-doping perspective, banning of
glucocorticoids by WADA should be upheld, as should in-
and out-of competition testing for glucocorticoid misuse.
One-legged kicking performance and possible mechanisms
The observation of an increase in one-legged kicking time
to exhaustion is in accordance with the finding that 7 of the
9 participants experienced an improved performance after
short-term dexamethasone treatment, although this was not
statistically significant (Nordsborg et al. 2008). It may be
that the dexamethasone-induced increase in skeletal mus-
cle Na+, K+ pump expression (Nordsborg et al. 2005) and
reduction in systemic K+ levels during exercise (Nordsborg
et al. 2008) are the primary mechanism responsible for the
improved exercise performance. Thus, it is suggested that
extracellular K+ accumulation is important for the develop-
ment of fatigue (Sejersted and Sjogaard 2000; Nordsborg
et al. 2003) although that remains debated (Allen et al.
2008). Since K+ accumulates rapidly in the extracellular
space at the onset of exercise (Gullestad et al. 1995), it
was evaluated whether the dexamethasone-induced perfor-
mance improvement could be explained by a reduced rate
of muscle function loss during the initial phase of intense
dynamic leg exercise. This evaluation revealed a similar
loss of twitch force in response to a transcutaneous elec-
trical stimulation in control and dexamethasone trials.
Moreover, rate of force development determined from the
evoked twitch was similar between trials. Thus, it appears
unlikely that dexamethasone enhances performance by
slowing the loss of muscle contractility and/or excitability
during the initial 75 s of dynamic contractions. Yet, differ-
ence between trials in the rate of relaxation was observed
after 45 s of exercise, but the importance of that observa-
tion remains unclear. The reason for reduced RFD and
Time (s)
Twitch peak force (N)
0
50
100
150
200
***
**
Time (s)
Twitch RFD (N x s
-1)
1000
1500
2000
2500
**
**
Time (s)
Twitch relaxation (N x s-1
)
-2000
-1500
-1000
-500
0
***
**
#
**
Time (s)
01020304050607080
01020304050607080
01020304050607080
0 120 240 360
RMS (% of MVC RMS)
0
20
40
60
80
100
120 ***
**
*
***
*
A B
C D
Fig. 1 Exhaustive dynamic one-legged knee-extensions to exhaus-
tion were performed after 5 days of either dexamethasone (filled cir-
cles) or placebo (open circles) ingestion. Results are shown for the
first 75 s to include paired measurements for all subjects. Evoked
twitches were generated at 5, 15, 45 and 75 s by transcutaneous
electrical stimulation of m. Quadriceps during the passive phase
in the dynamic contraction cycle. a Twitch peak force (n = 12), b
twitch rate of force development (RFD; n = 12), c twitch relaxation
(n = 12), d root mean square (RMS) of the EMG obtained from m.
Vastus lateralis after 5, 15, 30, 60, 120 s of exercise and 10 s prior
to exhaustion. The RMS value obtained during dynamic exercise
was normalized to EMG RMS from a maximal voluntary contrac-
tion performed before exercise (n = 5). Values are mean ± SD. Sig-
nificant differences from the value at 5 s are denoted by *P < 0.05;
**P < 0.01; ***P < 0.001. Significant differences between trials are
denoted by #P < 0.05
Eur J Appl Physiol
1 3
increased rate of relaxation observed in both trials could
be related to gradual changes in the active muscle mass as
well as changes of intrinsic muscular properties.
It is possible that dexamethasone improved muscle con-
traction ability after the initial 75 s as disturbance of K+
homeostasis becomes gradually more pronounced (Nords-
borg et al. 2008). That possibility was not evaluated in the
present study because of the differences in time to exhaus-
tion and therefore a gradual reduction in the number of
subjects with increasing exercise time.
In addition to local skeletal muscle events that can cause
fatigue, the possibility of fatigue originating from the CNS
has to be taken into account (Gandevia 2001). As a sur-
rogate measure of central motor drive, EMG RMS was
quantified in a subgroup of subjects. EMG RMS increased
during the exercise bout reflecting a gradual increase of
central motor output. This observation is in accordance
with increased EMG RMS during sustained submaximal
isometric contractions (Moritani et al. 1986) as during
high-intensity cycling (Camata et al. 2011). However, it
was not possible to detect a difference in the EMG RMS
increase between the control and dexamethasone trial nei-
ther during exercise nor immediately before exhaustion. Yet
due to the limited number of subjects in the EMG analysis
(n = 5), it has to be considered that an undetected differ-
ence may have existed. In rats, glucocorticoids induce an
increase of extracellular dopamine concentration and loco-
motor activity (Piazza et al. 1996), but the effect of gluco-
corticoids on the human motor cortex activity is unknown.
However, it is well known that glucocorticoids exert effects
on the CNS. For example, prednisolone can induce eupho-
ria (Swinburn et al. 1988) and the impact of dexamethasone
on human central motor drive and voluntary muscular acti-
vation warrants evaluation.
Whole body exercise performance
Whole body exercise performance was evaluated both as
30-m sprint time and 20-m shuttle run endurance. Sprint
performance is related to maximal strength (Wisloff et al.
2004) and rate of force development (West et al. 2011).
The observation that 30-m sprint ability was similar in con-
trol and dexamethasone trials implies that neither maximal
force nor rate of force development was affected by the
dexamethasone treatment. In support of this observation,
performance with a limited muscle mass lasting <2 min is
unaffected by dexamethasone (Nordsborg et al. 2008). It
appears that the primary effect of dexamethasone is related
to maintenance of energy provision for a high metabolic
rate lasting more than 2 min, since 20-m shuttle run endur-
ance was increased. The shuttle run test is characterized by
both high aerobic and anaerobic rates of energy production,
resulting in close to maximal heart rate and high muscle
and blood lactate levels (Krustrup et al. 2006). In agree-
ment with the present results, constant load exhaustive
cycling at 70–75 % of VO2max is prolonged after ingestion
of 50–60 mg Prednisolone (another glucocorticoid ana-
logue) per day for 7 days in both men (Collomp et al. 2008)
and women (Le et al. 2009).
Doping implications
For clinical purposes, dexamethasone is used in the small-
est possible dose, which may be 3.5 mg per day, and thus
similar to the dose used in the present study. Glucocorti-
coid administration is banned by the WADA, although it
is argued that the evidence for a performance enhancing
effect is weak (Dvorak et al. 2006) and suggested that the
ban should be relived (Duclos 2010). However, the present
investigation, in conjunction with others demonstrates the
necessity to maintain focus on potential glucocorticoid
misuse in sports where intense exercise is of importance.
Conclusion
Short-term dexamethasone administration increases time
to exhaustion for high-intensity one-legged kicking and
20-m shuttle run performance. However, sprint ability and
the temporal exercise-induced changes in muscle function
during the initial 75 s of exercise appear unaltered. Thus,
dexamethasone does not seem to affect force generating
capacity or rate of force development. Yet, since the evi-
dence for a performance enhancing effect of glucocorticoid
is supported, a continued effort of anti-doping authorities to
fight their systemic intake is encouraged.
Acknowledgments The present study was supported by Anti-Dop-
ing Denmark.
Conflict of interest The authors declare no conflict of interest.
References
Allen DG, Lamb GD, Westerblad H (2008) Skeletal muscle fatigue:
cellular mechanisms. Physiol Rev 88:287–332
Andersen P, Saltin B (1985) Maximal perfusion of skeletal muscle in
man. J Physiol 366:233–249
Arlettaz A, Portier H, Lecoq AM, Rieth N, De CJ, Collomp K (2007)
Effects of short-term prednisolone intake during submaximal
exercise. Med Sci Sports Exerc 39:1672–1678
Camata TV, Altimari LR, Bortolotti H, Dantas JL, Fontes EB, Smir-
maul BP, Okano AH, Chacon-Mikahil MP, Moraes AC (2011)
Electromyographic activity and rate of muscle fatigue of the
quadriceps femoris during cycling exercise in the severe domain.
J Strength Cond Res 25:2537–2543
Cnaan A, Laird NM, Slasor P (1997) Using the general linear mixed
model to analyse unbalanced repeated measures and longitudinal
data. Stat Med 16:2349–2380
Eur J Appl Physiol
1 3
Collomp K, Arlettaz A, Portier H, Lecoq AM, Le PB, Rieth N, De CJ
(2008) Short-term glucocorticoid intake combined with intense
training on performance and hormonal responses. Br J Sports
Med 42:983–988
Coombes BK, Bisset L, Vicenzino B (2010) Efficacy and safety of
corticosteroid injections and other injections for management of
tendinopathy: a systematic review of randomised controlled tri-
als. Lancet 376:1751–1767
Duclos M (2010) Evidence on ergogenic action of glucocorticoids as
a doping agent risk. Phys Sportsmed 38:121–127
Dvorak J, Feddermann N, Grimm K (2006) Glucocorticosteroids in
football: use and misuse. Br J Sports Med 40(Suppl 1):i48–i54
Fiel SB, Vincken W (2006) Systemic corticosteroid therapy for acute
asthma exacerbations. J Asthma 43:321–331
Gandevia SC (2001) Spinal and supraspinal factors in human muscle
fatigue. Physiol Rev 81:1725–1789
Gullestad L, Hallen J, Sejersted OM (1995) K+ balance of the
quadriceps muscle during dynamic exercise with and without
beta-adrenoceptor blockade. J Appl Physiol 78:513–523
Krustrup P, Mohr M, Amstrup T, Rysgaard T, Johansen J, Steensberg
A, Pedersen PK, Bangsbo J (2003) The yo–yo intermittent recov-
ery test: physiological response, reliability, and validity. Med Sci
Sports Exerc 35:697–705
Krustrup P, Mohr M, Nybo L, Jensen JM, Nielsen JJ, Bangsbo
J (2006) The Yo–Yo IR2 test: physiological response, reli-
ability, and application to elite soccer. Med Sci Sports Exerc
38:1666–1673
Le PB, Thomasson R, Jollin L, Lecoq AM, Amiot V, Rieth N, De CJ,
Collomp K (2009) Short-term glucocorticoid intake improves
exercise endurance in healthy recreationally trained women. Eur
J Appl Physiol 107:437–443
Marquet P, Lac G, Chassain AP, Habrioux G, Galen FX (1999) Dexa-
methasone in resting and exercising men. I. Effects on bioenerget-
ics, minerals, and related hormones. J Appl Physiol 87:175–182
McKenna MJ, Bangsbo J, Renaud JM (2008) Muscle K+, Na+, and
Cl disturbances and Na+-K+ pump inactivation: implications for
fatigue. J Appl Physiol 104:288–295
Moritani T, Muro M, Nagata A (1986) Intramuscular and surface
electromyogram changes during muscle fatigue. J Appl Physiol
60:1179–1185
Nielsen OB, Clausen T (2000) The Na+/K(+)-pump protects muscle
excitability and contractility during exercise. Exerc Sport Sci Rev
28:159–164
Nordsborg N, Mohr M, Pedersen LD, Nielsen JJ, Langberg H,
Bangsbo J (2003) Muscle interstitial potassium kinetics during
intense exhaustive exercise: effect of previous arm exercise. Am J
Physiol Regul Integr Comp Physiol 285:R143–R148
Nordsborg N, Goodmann C, McKenna MJ, Bangsbo J (2005) Dexa-
methasone up-regulates skeletal muscle maximal Na+, K+ pump
activity by muscle group specific mechanisms in humans. J Phys-
iol 567:583–589
Nordsborg N, Ovesen J, Thomassen M, Zangenberg M, Jons C, Iaia
FM, Nielsen JJ, Bangsbo J (2008) Effect of dexamethasone
on skeletal muscle Na+, K+ pump subunit specific expres-
sion and K+ homeostasis during exercise in humans. J Physiol
586:1447–1459
Piazza PV, Rouge-Pont F, Deroche V, Maccari S, Simon H, Le MM
(1996) Glucocorticoids have state-dependent stimulant effects on
the mesencephalic dopaminergic transmission. Proc Natl Acad
Sci USA 93:8716–8720
Sejersted OM, Sjogaard G (2000) Dynamics and consequences of
potassium shifts in skeletal muscle and heart during exercise.
Physiol Rev 80:1411–1481
Swinburn CR, Wakefield JM, Newman SP, Jones PW (1988) Evi-
dence of prednisolone induced mood change (‘steroid euphoria’)
in patients with chronic obstructive airways disease. Br J Clin
Pharmacol 26:709–713
West DJ, Owen NJ, Jones MR, Bracken RM, Cook CJ, Cunningham
DJ, Shearer DA, Finn CV, Newton RU, Crewther BT, Kilduff LP
(2011) Relationships between force-time characteristics of the
isometric midthigh pull and dynamic performance in professional
rugby league players. J Strength Cond Res 25:3070–3075
Wisloff U, Castagna C, Helgerud J, Jones R, Hoff J (2004) Strong
correlation of maximal squat strength with sprint performance
and vertical jump height in elite soccer players. Br J Sports Med
38:285–288
