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Glucocorticoids improve high-intensity exercise performance in humans


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It was investigated whether oral dexamethasone (DEX) administration improves exercise performance by reducing the initial rate of muscle fatigue development during dynamic exercise. Using a double-blinded placebo controlled randomized crossover design, subjects ingested either 2 × 2 mg of DEX or placebo for five consecutive days. Muscle function 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. 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. Short-term dexamethasone administration increases high-intensity one-legged kicking time to exhaustion and 20-m shuttle run performance, although sprint ability and the initial loss of muscular force generating capacity are similar after DEX and placebo.
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Eur J Appl Physiol
DOI 10.1007/s00421-013-2784-7
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
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
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.
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
N. H. Secher
The Copenhagen Muscle Research Center, Department
of Anesthesia, Rigshospitalet, University of Copenhagen,
Copenhagen, Denmark
Eur J Appl Physiol
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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.
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.
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
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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).
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.
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.
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)
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
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.
The major findings of the present study are that short-term
dexamethasone ingestion increases high-intensity exercise
Eur J Appl Physiol
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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)
Time (s)
Twitch RFD (N x s
Time (s)
Twitch relaxation (N x s-1
Time (s)
0 120 240 360
RMS (% of MVC RMS)
120 ***
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
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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.
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.
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... Skeletal muscle maximal force-generating capacity is gradually lost with exhaustive electrical stimulations (Reid, 1927), repeated voluntary submaximal and maximal isometric contractions in humans (Bigland-Ritchie et al., 1986;Burnley, 2009;Burnley et al., 2012), and sustained maximal voluntary contraction (Place et al., 2007;Carroll et al., 2017;Rodriguez-Falces and Place, 2017). The force-generating capacity is also reduced during/after a dynamic isolated exercise (e.g., dynamic knee-extension; Li et al., 2002;Amann et al., 2013;Froyd et al., 2013;Casuso et al., 2014) and a whole-body exercise (e.g., cycling; Millet et al., 2003;Martin et al., 2004;Ducrocq et al., 2017). Intramuscular fatigue development is highly dependent on exercise intensity, especially around critical torque during isometric exercises (Burnley, 2009), and critical power (CP), where muscle creatine phosphate, lactate, and pH remain stable during exercise below but not above CP (Vanhatalo et al., 2016). ...
... Based on in vitro findings, a plausible mechanistic explanation for the compromised F tw and RFD is a gradual impairment of Ca 2+ release rate (Cheng et al., 2018;Olsson et al., 2020) secondary to inorganic phosphate (P i )-induced sarcoplasmic reticulum (SR) Ca 2+ precipitation and ryanodine receptor 1 (RyR1) inhibition (Allen et al., 2008), even though other possibilities exist, including metabolic acidosis (Fitts, 2008). In humans, a marked reduction of ∼40% in maximal twitch RFD occurs as a consequence of an intense exhaustive exercise in humans (Krüger et al., 2019), and we have previously demonstrated the twitch RFD to be compromised during an exhaustive dynamic exercise (Casuso et al., 2014), but without addressing the impact of intensity. ...
... As an additional measure, RFR is prolonged in fatigued isolated muscle preparations due to slowed Ca 2+ reuptake as well as impaired cross-bridge mechanisms (Allen et al., 1995;Li et al., 2002). Importantly, the marked slowing of relaxation has also been observed in human muscles subjected to fatiguing electrical stimulation (Neyroud et al., 2016) as well as during exercise (Casuso et al., 2014), although very little is known about the effect of intensity. As for RFD, the determination of the intensity-dependent changes in RFR with fatigue development in humans is a feasible way to gain insight to possible underlying mechanisms. ...
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Our aim was to provide an in vivo assessment of human muscle twitch characteristics during and following an exhaustive dynamic exercise to explore temporal alterations of the rate of force development (RFD) and relaxation (RFR). Eleven healthy participants (mean age ± SD: 24 ± 3 years) completed a dynamic knee-extensor exercise in randomized order at three different intensities, eliciting exhaustion after ∼9 min (56 ± 10 W), ∼6 min (60 ± 10 W), and ∼4 min (63 ± 10 W), in addition to a low-intensity (28 ± 5 W) bout. In a novel setup, an electrical doublet stimulation of m. vastus lateralis was applied during exercise (every 30 s) and recovery for frequent evaluation of key contractile properties (maximal force, RFD, RFR, and electromechanical delay) in addition to M-wave characteristics. RFD and RFR remained stable throughout the low-intensity trial but declined in all exhaustive trials to reach a similar level of ∼40% of pre-exercise values at task failure but with the exponential decay augmented by intensity. Following exhaustion, there was a fast initial recovery of RFD and RFR to ∼80% of pre-exercise values within 1 min, followed by a longer suppression at this level. The M-wave characteristics remained unchanged during all trials. In conclusion, this is the first study to quantify the intensity-dependent alterations of RFD and RFR during and after exhaustive dynamic exercise in humans. A hypothesized reduction and fast reversion of RFD was confirmed, and a surprising compromised RFR is reported. The present unique experimental approach allows for novel insight to exercise-induced alterations in human muscle contractile properties which is relevant in health and disease.
... These glucocorticoid-mediated enhancements in the capacity to counter K + shifts may translate into an enhanced exercise performance (111,178). Nordsborg et al. (532) observed that the glucocorticoid-induced improvement of K + transport was associated with enhanced performance during exercise at moderate but not during a subsequent bout at a higher intensity. However, the lack of effect during the high-intensity bout was likely attributed to the greater performance and hence larger work performed during the former bout at moderate intensity. ...
... However, the lack of effect during the high-intensity bout was likely attributed to the greater performance and hence larger work performed during the former bout at moderate intensity. Indeed, a follow-up study showed that a few days of treatment with glucocorticoid enhanced performance during exercise at high intensity by 29% (111). Notably, glucocorticoid treatment also lowers the rate of lactaterelease during exercise (532); an effect that likely reflects a lowered lactateproduction of the exercising muscles and could indicate an augmented contribution from aerobic energy systems. ...
Exercise causes major shifts in multiple ions (e.g., K+ , Na+ , H+ , lactate- , Ca2+ , and Cl- ) during muscle activity that contributes to development of muscle fatigue. Sarcolemmal processes can be impaired by the trans-sarcolemmal rundown of ion gradients for K+ , Na+ , and Ca2+ during fatiguing exercise, while changes in gradients for Cl- and Cl- conductance may exert either protective or detrimental effects on fatigue. Myocellular H+ accumulation may also contribute to fatigue development by lowering glycolytic rate and has been shown to act synergistically with inorganic phosphate (Pi) to compromise cross-bridge function. In addition, sarcoplasmic reticulum Ca2+ release function is severely affected by fatiguing exercise. Skeletal muscle has a multitude of ion transport systems that counter exercise-related ionic shifts of which the Na+ /K+ -ATPase is of major importance. Metabolic perturbations occurring during exercise can exacerbate trans-sarcolemmal ionic shifts, in particular for K+ and Cl- , respectively via metabolic regulation of the ATP-sensitive K+ channel (KATP ) and the chloride channel isoform 1 (ClC-1). Ion transport systems are highly adaptable to exercise training resulting in an enhanced ability to counter ionic disturbances to delay fatigue and improve exercise performance. In this article, we discuss (i) the ionic shifts occurring during exercise, (ii) the role of ion transport systems in skeletal muscle for ionic regulation, (iii) how ionic disturbances affect sarcolemmal processes and muscle fatigue, (iv) how metabolic perturbations exacerbate ionic shifts during exercise, and (v) how pharmacological manipulation and exercise training regulate ion transport systems to influence exercise performance in humans. © 2021 American Physiological Society. Compr Physiol 11:1895-1959, 2021.
... GCs are included in the World Anti-Doping Agency (WADA) Prohibited List because of the health risks associated with their use [4][5][6] and due to evidences of positive effects on exercise performance. [7][8][9] GCs are prohibited during competitions when administered by systemic routes (oral, intramuscular [IM], intravenous, and rectal administrations), and they are allowed by other routes considered of local action (e.g., dermatological, inhalation, and intranasal) for therapeutic purposes. 10 There are no restrictions in the use of GCs in out-ofcompetition periods. ...
... The analysis of urine samples was performed using an extraction protocol previously described by our group with some modifications. 23 Briefly, internal standard (ISTD) solution (40 ng of PRED-d 8 to an ultraperformance liquid chromatographic (UPLC) system, Acquity (Waters Associates), for the chromatographic separation. The drying gas, nebulizing gas, cone gas, or desolvation gas was nitrogen. ...
Prednisolone (PRED) and prednisone (PSONE) are prohibited in sports competitions when administered by systemic routes, and they are allowed by other routes for therapeutic purposes. There is no restriction of use in out‐of‐competition periods. The present study aimed to evaluate the urinary excretion of PRED, PSONE, and their most important metabolites after systemic and nonsystemic treatments in order to verify the suitability of the current reporting level of 30 ng/ml used to distinguish allowed and prohibited administrations and to establish washout periods for oral treatments performed in out‐of‐competition periods. PRED was studied after dermatological administration (5 mg/day for 5 days, n = 6 males) and oral administration (5 mg, n = 6 males; 10 mg, n = 2 males). PSONE was studied after oral administration (10 mg, n = 2 males; 30 mg, n = 1 male and 1 female). Concentrations in urine were measured using an LC–MS/MS method. Concentrations after dermatological treatment were low for all metabolites. After oral administration, concentrations were very high during the first 24 h after administration ranging from 1.6 to 2261 ng/ml and from 4.6 to 908 ng/ml for PRED and PSONE, respectively. Concentrations of most of the metabolites measured were lower than 30 ng/ml from 24 h after all oral administrations. New reporting levels are proposed for PRED and PSONE considering data of our study and other information published after nonsystemic administrations of the compounds. Washout periods of at least 24 h are recommended to ensure no false positives when oral treatments need to be performed in out‐of‐competition periods.
... Eine kurzfristige orale Einnahme von Prednisolon führt unter submaximaler Belastung zu einer Leistungssteigerung durch die Anpassung metabolischer und hormoneller Prozesse [25]. Außerdem wird die Zeit der maximalen Leistungsfähigkeit gesteigert [26]. Die orale Anwendung von Glukokortikoiden ist somit im Wettkampf verboten. ...
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Zusammenfassung Ophthalmologische Medikamente stehen auf den ersten Blick nicht unbedingt im Verdacht, als leistungsfördernde Mittel im Leistungssport angewandt zu werden. Es gibt jedoch einige Beschränkungen, die vor allem bei oraler Einnahme bestimmter Medikamente zu beachten sind. Unter Einbeziehung der aktuellen Maßgaben der Nationalen Anti Doping Agentur Deutschland und der World Anti-Doping Agency wurde eine strukturierte Analyse der Dopingrelevanz ophthalmologischer Medikamente auf Basis einer Literaturrecherche durchgeführt. Eine Anwendung der häufigsten ophthalmologischen Wirkstoffgruppen ist ohne Einschränkungen möglich, vor allem bei topischer Applikation. Eine Ausnahme bildet die orale Einnahme von Diuretika, die jederzeit verboten ist. Bei Glukokortikoiden ist beispielsweise die topische Applikation am Auge erlaubt, jedoch eine orale Applikation innerhalb von Wettkämpfen untersagt. Eine ähnliche Beschränkung gilt bei der Anwendung von Epinephrin, bei der alle systemischen Applikationsformen innerhalb von Wettkämpfen untersagt sind. Bei der Anwendung von Betablockern ist die ausgeübte Sportart maßgeblich, da beim Billard, Bogenschießen, Darts, Golf, Motorsport, Schießsportarten, Skifahren/Snowboarding, Skispringen, Freistil Aerials/Halfpipe und Snowboard Halfpipe/Big Air und Tauchen eine lokale und systemische Anwendung innerhalb von Wettkämpfen unzulässig ist. Beim Schießen und Bogenschießen ist der Gebrauch von Betablockern auch außerhalb von Wettkämpfen untersagt. Sportler*innen mit ophthalmologischen Vorerkrankungen sollten sich vor Anwendung von Medikamenten umfassend von einem Facharzt für Augenheilkunde beraten lassen und gemeinsam einen zulässigen Wirkstoff auswählen, die geeignete Applikationsart beachten und gegebenenfalls, bei obligater Einnahme, einen Antrag auf eine Medizinische Ausnahmegenehmigung stellen. Aktuell ist nicht bekannt wie viele der nationalen und internationalen Sportler*Innen mit Augentropfen behandelt werden müssen.
... The data showed a relatively higher use of glucocorticoids by women vs. men, with a greater number of prednisone and prednisolone samples and a lower number of triamcinolone samples. Only systemic and not local (Kuipers et al., 2008) shortterm administration of corticoids produces significant ergogenic effects during exercise lasting more than 40 min in both man Collomp et al., 2008) and woman (Le Panse et al., 2009) recreationally trained athletes, with a similar gender performance improvement, whereas GC ergogenic effects appear more variable in brief exercise (Nordsborg et al., 2008;Casuso et al., 2014;Zorgati et al., 2014). This was clearly evident in our data by the predominance of GCs in endurance and mixed sports, regardless of gender. ...
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To achieve optimal sports performances, women and men may show specific doping practices because of the physiological and psychological gender differences, but there are few data on this topic. Here, we report the apparent use of prohibited substances and methods by female athletes based on analyses of the doping tests collected by the French Anti-Doping Agency from 2013 to 2019. We compared the frequency of use and the ergogenic and side effects to those of their male counterparts. The results revealed lower use of prohibited substances in female vs. male athletes, with significantly fewer anabolic agents, hormone and metabolic modulators, and cannabinoids. Gender specificity in utilization of substance classes was also shown. Relatively lower use of hormone modulators and cannabinoids and higher use of beta-2 agonists, diuretics and glucocorticoids were found in the woman cohort compared with men cohort, combined with the different choice of substances, possibly because of the altered ergogenic and/or side effects. However, no impact due to gender regarding the sports disciplines was observed, with both women and men showing similar use of anabolic agents, mainly in the anaerobic sports, and EPO and corticoids, mainly in endurance or mixed sports. Further studies are needed to put these French data into a global perspective, comparing uses across countries and exploring possible new developments in the fight against doping in women.
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Introduction This systematic review with meta-analysis investigates the effect of glucocorticoids on maximal and submaximal performance in healthy subjects. Methods We searched for randomised controlled trials investigating the effect of glucocorticoids on physical performance in Web of Science, Scopus, Medline, Embase and SportDiscus in March 2021. Risk of bias was assessed with the revised Cochrane Collaboration Risk of Bias Tool (RoB2). Data from random effect models are presented as standardized difference in mean (SDM) with 95% confidence interval. We included 15 studies comprising 175 subjects. Results Two studies had high risk of bias. Glucocorticoids had a small positive effect on maximal physical performance compared to placebo (SDM 0.300, 95% CI 0.080 to 0.520) and the SDM for the 13 included comparisons was not heterogeneous ( I 2 = 35%, p = 0.099). Meta regression found no difference in the effect of acute treatment vs. prolonged treatment or oral ingestion vs. inhalation ( p > 0.124). In stratified analysis prolonged treatment (SDM 0.428, 95% CI 0.148 to 0.709) and oral ingestion (SDM 0.361, 95% CI 0.124 to 0.598) improved physical performance. Glucocorticoids improved aerobic performance (SDM 0.371, 95% CI 0.173 to 0.569) but not anaerobic performance ( p = 0.135). Glucocorticoids did not change energy expenditure during submaximal performance (SDM 0.0.225 95% CI −0.771 to 0.112). Discussion This study indicates that glucocorticoids improves maximal performance and aerobic performance. Glucocorticoids did not affect the energy expenditure during submaximal performance. The conclusions are based on relatively few subjects leading to limited statistical power and uncertain estimates. Still, these results are consistent and should be of interest to WADA and anyone concerned about fair play. Systematic Review Registration Open Science Framework 2021-04-29 ( ).
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Stress hormones and their impacts on whole organism metabolic rates are usually considered as appropriate proxies for animal energy budget that is the foundation of numerous concepts and models aiming at predicting individual and population responses to environmental stress. However, the dynamics of energy re-allocation under stress make the link between metabolism and corticosterone complex and still unclear. Using ectopic application of corticosterone for 3, 11 and 21 days, we estimated a time effect of stress in a lizard (Zootoca vivipara). We then investigated whole organism metabolism, muscle cellular O2 consumption and liver mitochondrial oxidative phosphorylation processes (O2 consumption and ATP production) and ROS production. The data showed that while skeletal muscle is not impacted, stress regulates the liver mitochondrial functionality in a time-dependent manner with opposing pictures between the different time expositions to corticosterone. While 3 days exposition is characterized by lower ATP synthesis rate and high H2O2 release with no change in the rate of oxygen consumption, the 11 days exposition reduced all three fluxes of about 50%. Oxidative phosphorylation capacities in liver mitochondria of lizard treated with corticosterone for 21 days was similar to the hepatic mitochondrial capacities in lizards that received no corticosterone treatment but with 40% decrease in H2O2 production. This new mitochondrial functioning allows a better capacity to respond to the energetic demands imposed by the environment but do not influence whole organism metabolism. In conclusion, global mitochondrial functioning has to be considered to better understand the proximal causes of the energy budget under stressful periods.
Glucocorticoids are released in by acute aerobic exercise. The objective was to define changes in the expression of glucocorticoid target genes in skeletal muscle in response to acute aerobic exercise at different times of day. We identified glucocorticoid target genes altered in skeletal muscle by acute exercise by comparing data sets from rodents subjected to acute aerobic exercise in the light or dark cycles to data sets from C2C12 myotubes treated with glucocorticoids. The role of glucocorticoid receptor signaling and REDD1 protein in mediating gene expression was assessed in exercised mice. Changes to expression of glucocorticoid genes were greater when exercise occurred in the dark cycle. REDD1 was required for the induction of genes induced at both times of day. In all, the time of day at which aerobic exercise is conducted dictates changes to the expression of glucocorticoid target genes in skeletal muscle with REDD1 contributing to those changes.
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The systemic effect of glucocorticoids (GCs) following injectable routes of administration presents a potential risk to both improving performance and causing harm to health in athletes. This review evaluates the current GC antidoping regulations defined by the World Anti-Doping Agency and presents a novel approach for defining permitted and prohibited use of glucocorticoids in sport based on the pharmacological potential for performance enhancement (PE) and risk of adverse effects on health. Known performance-enhancing doses of glucocorticoids are expressed in terms of cortisol-equivalent doses and thereby the dose associated with a high potential for PE for any GC and route of administration can be derived. Consequently, revised and substance-specific laboratory reporting values are presented to better distinguish between prohibited and permitted use in sport. In addition, washout periods are presented to enable clinicians to prescribe glucocorticoids safely and to avoid the risk of athletes testing positive for a doping test. AIMS
Objective: To determine the effects of glucocorticoids in enhancing athletic performance. Design: At least 2 independent reviewers conducted study selection and extracted demographic and outcome data. Relevant outcomes were stratified by administration time frame and the specific type of drug used. Study quality was assessed using the Cochrane Risk-of-Bias tool and the Cochrane Grading of Recommendations Assessment Development and Education scale. Where appropriate, meta-analyses were performed. Data sources: Embase, MEDLINE, and SPORTDiscus were searched from their beginning to April 2020. Participants: Participants of any sex and training status aged 18 to 65 years were included. Interventions and main outcome measures: Any type of published randomized controlled trial (RCT) that examined any enhancement in sport as well as aerobic, anaerobic, or body compositional parameters for glucocorticoids compared with placebo. Results: There is low-to-moderate evidence suggesting that the administration of glucocorticoids may be more beneficial than placebo in enhancing athletic performance. short-term administration of glucocorticoids significantly improved time to exhaustion, maximal force, and total distance travelled. By contrast, acute administration of glucocorticoids predominantly yielded no changes to athletic performance, except for reductions in total work and maximal power output. Conclusions: Although there is evidence suggesting glucocorticoids have ergogenic effects, these improvements may differ depending on the specific type of drug, dose, and the administration time frame and are also limited by small sample sizes. Therefore, there is a need for large, high-quality RCTs as this may influence future doping policy and athlete care.
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There is considerable conflict within the literature regarding the relevance of isometric testing for the assessment of neuromuscular function within dynamic sports. The aim of this study was to determine the relationship between isometric measures of force development and dynamic performance. Thirty-nine professional rugby league players participated in this study. Forty-eight hours after trial familiarization, participants performed a maximal isometric midthigh pull, with ;120-130- bend at the knee, countermovement jump (CMJ), and a 10-m sprint. Force-time data were processed for peak force (PF), force at 100 milliseconds (F100ms), and peak rate of force development (PRFD). Analysis was carried out using Pearson's product moment correlation with significance set at p < 0.05. The PF was not related to dynamic performance; however, when expressed relative to body weight, it was significantly correlated with both 10-m time and CMJ height (r = 20.37 and 0.45, respectively, p < 0.05). The F100ms was inversely related to 10-m time (r = 20.54, p < 0.01); moreover, when expressed relative to body weight, it was significantly related to both 10-m time and CMJ height (r = 20.68 and 0.43, p < 0.01). In addition, significant correlations were found between PRFD and 10-m time (r = 20.66, p < 0.01) and CMJ height (r = 0.387, p < 0.01). In conclusion, this study provides evidence that measures of maximal strength and explosiveness from isometric force-time curves are related to jump and sprint acceleration performance in professional rugby league players.
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Systemic administration of glucocorticoids (GCs) is banned by the World Anti-Doping Agency (WADA) during competition. Few studies have examined the effects of GCs on exercise performance, but increasing evidence has shown that short-term GC intake enhances performance in animals and humans. However, there are many health risks associated with GC use. Based on the available evidence, as presented in this article, I conclude that GCs are doping agents and should remain on the WADA's list of banned products. Because of the complexity of GCs, however, determining the boundaries between their medical use and abuse (eg, in sports) is a constant challenge for the WADA.
The general linear mixed model provides a useful approach for analysing a wide variety of data structures which practising statisticians often encounter. Two such data structures which can be problematic to analyse are unbalanced repeated measures data and longitudinal data. Owing to recent advances in methods and software, the mixed model analysis is now readily available to data analysts. The model is similar in many respects to ordinary multiple regression, but because it allows correlation between the observations, it requires additional work to specify models and to assess goodness-of-fit. The extra complexity involved is compensated for by the additional flexibility it provides in model fitting. The purpose of this tutorial is to provide readers with a sufficient introduction to the theory to understand the method and a more extensive discussion of model fitting and checking in order to provide guidelines for its use. We provide two detailed case studies, one a clinical trial with repeated measures and dropouts, and one an epidemiological survey with longitudinal follow-up. © 1997 John Wiley & Sons, Ltd.
This study compared the activation pattern and the fatigue rate among the superficial muscles of the quadriceps femoris (QF) during severe cycling exercise. Peak oxygen consumption (VO(2)peak) and maximal accumulated oxygen Deficit (MAOD) were established by 10 well-trained male cyclists (27.5 ± 4.1 years, 71.0 ± 10.3 kg, 173.4 ± 6.6 cm, mean VO(2)peak 56.7 ± 4.4 ml·kg·min(-1), mean MAOD 5.7 ± 1.1 L). Muscle activity (electromyographic [EMG] signals) was obtained during the supramaximal constant workload test (MAOD) and expressed by root mean square (RMS) and median frequency (MF slope). The RMS of the QF, vastus lateralis (VL) and vastus medialis (VM) muscles were significantly higher than at the beginning after 75% of exercise duration, whereas for the rectus femoris (RF), this was observed after 50% of exercise duration (p ≤ 0.05). The slope of the MF was significantly higher in the RF, followed by the VL and VM (-3.13 ± 0.52 vs. -2.61 ± 0.62 vs. -1.81 ±0.56, respectively; p < 0.05). We conclude that RF may play an important role in limiting performance during severe cycling exercise.
Few evidence-based treatment guidelines for tendinopathy exist. We undertook a systematic review of randomised trials to establish clinical efficacy and risk of adverse events for treatment by injection. We searched eight databases without language, publication, or date restrictions. We included randomised trials assessing efficacy of one or more peritendinous injections with placebo or non-surgical interventions for tendinopathy, scoring more than 50% on the modified physiotherapy evidence database scale. We undertook meta-analyses with a random-effects model, and estimated relative risk and standardised mean differences (SMDs). The primary outcome of clinical efficacy was protocol-defined pain score in the short term (4 weeks, range 0-12), intermediate term (26 weeks, 13-26), or long term (52 weeks, ≥52). Adverse events were also reported. 3824 trials were identified and 41 met inclusion criteria, providing data for 2672 participants. We showed consistent findings between many high-quality randomised controlled trials that corticosteroid injections reduced pain in the short term compared with other interventions, but this effect was reversed at intermediate and long terms. For example, in pooled analysis of treatment for lateral epicondylalgia, corticosteroid injection had a large effect (defined as SMD>0·8) on reduction of pain compared with no intervention in the short term (SMD 1·44, 95% CI 1·17-1·71, p<0·0001), but no intervention was favoured at intermediate term (-0·40, -0·67 to -0·14, p<0·003) and long term (-0·31, -0·61 to -0·01, p=0·05). Short-term efficacy of corticosteroid injections for rotator-cuff tendinopathy is not clear. Of 991 participants who received corticosteroid injections in studies that reported adverse events, only one (0·1%) had a serious adverse event (tendon rupture). By comparison with placebo, reductions in pain were reported after injections of sodium hyaluronate (short [3·91, 3·54-4·28, p<0·0001], intermediate [2·89, 2·58-3·20, p<0·0001], and long [3·91, 3·55-4·28, p<0·0001] terms), botulinum toxin (short term [1·23, 0·67-1·78, p<0·0001]), and prolotherapy (intermediate term [2·62, 1·36-3·88, p<0·0001]) for treatment of lateral epicondylalgia. Lauromacrogol (polidocanol), aprotinin, and platelet-rich plasma were not more efficacious than was placebo for Achilles tendinopathy, while prolotherapy was not more effective than was eccentric exercise. Despite the effectiveness of corticosteroid injections in the short term, non-corticosteroid injections might be of benefit for long-term treatment of lateral epicondylalgia. However, response to injection should not be generalised because of variation in effect between sites of tendinopathy. None.
The present study investigated whether short-term oral administration of glucocorticoid would modify performance and selected hormonal and metabolic parameters during submaximal exercise in healthy women. Nine recreational female athletes completed cycling trials at 70-75% VO(2) max until exhaustion after either placebo (Pla, gelatin) or oral prednisone (Cor, Cortancyl, 50 mg per day for 1 week) treatment, according to a double-blind and randomized protocol. Blood samples were collected at rest; after 10, 20, and 30 min of exercise; at exhaustion; and after 10 and 20 min of passive recovery for adrenocorticotrophic hormone (ACTH), dehydroepiandrosterone (DHEA), prolactin (PRL), growth hormone (GH), insulin (Ins), blood glucose (Glu), and lactate (Lac) determination. Cycling time was significantly increased with short-term Cor intake (Cor: 66.4 +/- 8.4 vs. Pla: 47.9 +/- 6.7 min, P < 0.01). ACTH and DHEA remained completely blunted throughout the experiment with Cor versus Pla (P < 0.01), whereas GH and PRL were significantly decreased with Cor after, respectively, 20 and 30 min of exercise (P < 0.05). No significant difference in Ins or Glu values was found between the two treatments but Lac concentrations were significantly increased with Cor versus Pla between 10 and 30 min of exercise (P < 0.05). These data indicate that short-term glucocorticoid intake improved endurance performance in women, but further investigation is needed to determine whether these results are applicable to elite female athletes and, if so, current WADA legislation needs to be changed.
1. It is a clinical impression that some patients given oral corticosteroids develop a sense of wellbeing that is 'inappropriate' to improvements in physical health. This has been termed steroid 'euphoria', but unlike steroid-induced psychosis it has not been documented. 2. To test for the size and frequency of this phenomenon, 20 patients with severe chronic obstructive airways disease (mean FEV1 0.86 l) were given 30 mg of prednisolone for 14 days, after a period of placebo administration in a single-blind study. 3. Lung spirometry and arterial saturation during exercise were measured serially, together with established measures of mood state. 4. No changes in spirometry or arterial saturation during exercise were detected until 7 days of active therapy. 5. Mood state did not change during the placebo period, but small significant reductions in anxiety and depression were measured after 3 days of prednisolone and before any measurable improvement in lung function. Mood state did not then further improve, despite measurable improvements in lung spirometry. 6. This is evidence that prednisolone may produce a mild 'inappropriate' sense of wellbeing within a population receiving the drug, rather than as an occasional idiosyncratic response.
Twelve male subjects were tested to determine the effects of motor unit (MU) recruitment and firing frequency on the surface electromyogram (EMG) frequency power spectra during sustained maximal voluntary contraction (MVC) and 50% MVC of the biceps brachii muscle. Both the intramuscular MU spikes and surface EMG were recorded simultaneously and analyzed by means of a computer-aided intramuscular spike amplitude-frequency histogram and frequency power spectral analysis, respectively. Results indicated that both mean power frequency (MPF) and amplitude (rmsEMG) of the surface EMG fell significantly (P less than 0.001) together with a progressive reduction in MU spike amplitude and firing frequency during sustained MVC. During 50% MVC there was a significant decline in MPF (P less than 0.001), but this decline was accompanied by a significant increase in rmsEMG (P less than 0.001) and a progressive MU recruitment as evidenced by an increased number of MUs with relatively large spike amplitude. Our data suggest that the surface EMG amplitude could better represent the underlying MU activity during muscle fatigue and the frequency powers spectral shift may or may not reflect changes in MU recruitment and rate-coding patterns.
Five subjects exercised with the knee extensor of one limb at work loads ranging from 10 to 60 W. Measurements of pulmonary oxygen uptake, heart rate, leg blood flow, blood pressure and femoral arterial-venous differences for oxygen and lactate were made between 5 and 10 min of the exercise. Flow in the femoral vein was measured using constant infusion of saline near 0 degrees C. Since a cuff was inflated just below the knee during the measurements and because the hamstrings were inactive, the measured flow represented primarily the perfusion of the knee extensors. Blood flow increased linearly with work load right up to an average value of 5.7 l min-1. Mean arterial pressure was unchanged up to a work load of 30 W, but increased thereafter from 100 to 130 mmHg. The femoral arterial-venous oxygen difference at maximum work averaged 14.6% (v/v), resulting in an oxygen uptake of 0.80 l min-1. With a mean estimated weight of the knee extensors of 2.30 kg the perfusion of maximally exercising skeletal muscle of man is thus in the order of 2.5 l kg-1 min-1, and the oxygen uptake 0.35 l kg-1 min-1. Limitations in the methods used previously to determine flow and/or the characteristics of the exercise model used may explain why earlier studies in man have failed to demonstrate the high perfusion of muscle reported here. It is concluded that muscle blood flow is closely related to the oxygen demand of the exercising muscles. The hyperaemia at low work intensities is due to vasodilatation, and an elevated mean arterial blood pressure only contributes to the linear increase in flow at high work rates. The magnitude of perfusion observed during intense exercise indicates that the vascular bed of skeletal muscle is not a limiting factor for oxygen transport.
The effect of propranolol (0.15 mg/kg body wt) on K+ fluxes was investigated in seven healthy males performing 8-min two-legged knee-extension exercise at two different powers. K+ concentration was measured in the femoral vein by a K(+)-selective electrode, and leg blood flow was measured by the dye-dilution technique. During control bouts, rates of change in femoral venous K+ concentration were 38 +/- 10 and 53 +/- 8 mumol.l-1.s-1 at onset of exercise (K+ efflux) and -14 +/- 3 and -34 +/- 3 mumol.l-1.s-1 at cessation of exercise (K+ reuptake) at low and high powers, respectively. This mismatch between K+ efflux and reuptake rates fits with the steady-state K+ loss rate of 0.14 +/- 0.04 and 0.32 +/- 0.09 mmol/min. Propranolol raised K+ efflux rate, did not modify K+ reuptake rate or steady-state K+ loss, but caused transiently increased K+ loss rate at the onset of exercise, thus accentuating the rise of arterial K+ concentration. In conclusion, the continuous muscle K+ loss during steady-state exercise with a small muscle mass is not due to lack of catecholamine stimulation, but beta-adrenoceptor blockade increased the Na(+)-K+ pump lag so that the initial K+ loss at onset of exercise was increased.