A Randomised, Placebo-Controlled, Crossover Study Investigating the Effects of Nicotine Gum on Strength, Power and Anaerobic Performance in Nicotine-Naïve, Active Males
Mündel et al. Sports Medicine - Open
A Randomised, Placebo-Controlled, Crossover Study Investigating the Effects of Nicotine Gum on Strength, Power and Anaerobic Performance in Nicotine-Naïve, Active Males
Toby Mündel 0
Marine Machal 0
Darryl J. Cochrane 0
Matthew J. Barnes 0
0 School of Sport and Exercise, Massey University , Private bag 11 222, Palmerston North 4442 , New Zealand
Background: Nicotine use amongst athletes is high and increasing, especially team sports, yet the limited previous studies investigating the performance consequences of this behaviour have not examined the effects of the principal active ingredient, nicotine, per se. Therefore, we determined whether nicotine gum affected muscular and anaerobic performance. Methods: Nine active males (24 ± 3 years) completed three trials in a random order in which 20 min prior to testing they chewed 2 mg (NIC-2), 4 mg (NIC-4) nicotine or flavour-matched placebo (PLA) gum. Peak and average peak isometric, concentric and eccentric leg extensor torque was measured followed by vertical counter-movement jump height and a 30-s Wingate test. Heart rate was measured whilst capillary blood samples determined pH, HCO3and venous blood confirmed the presence of nicotine. Results: Nicotine was confirmed by the presence of its major metabolite, cotinine and participants reported no side effects with nicotine. Peak and average peak isometric and eccentric torque was significantly affected (NIC-2 > PLA; p < 0.05) whilst peak (NIC-2 > PLA; p < 0.05) but not average peak (p > 0.05) concentric torque was different between trials. Counter-movement jump height was similar across trials (p > 0.05). Anaerobic capacity during the Wingate remained similar across trials (p > 0.05); however, pacing strategy (peak power and rate of fatigue) was different during NIC-2 than PLA. pH was affected by nicotine (NIC-2 > PLA; p < 0.05) and was reduced following the Wingate in all trials. HCO3− showed similar responses across trials (p > 0.05) although it was also reduced following the Wingate (p < 0.05), whilst heart rate was significantly affected (NIC-2/NIC-4 > PLA; p < 0.05). Conclusions: Chewing low-dose (2 mg) nicotine gum 20 min prior to exercise significantly improved leg extensor torque but did not affect counter-movement jump height or Wingate performance compared to a placebo, whilst there were minimal effects of the 4 mg nicotine gum on the performance parameters measured.
Chewing gum; Doping; Stimulant; Performance; WADA
Recent monitoring (urine screening) has determined
that active consumption of nicotine and
nicotinecontaining substances in-competition occurs in
approximately 25–50% of athletes in sports that are
characterised by strength, power and anaerobic
capacity (cf. endurance), e.g. American football, ice
hockey, wrestling, bobsleigh, gymnastics, rugby and
Whilst the World Anti-Doping Agency placed
nicotine onto its monitoring program in 2012, few
studies have determined the performance effects of
nicotine administration, and none without the
confounders of tobacco, withdrawal and tolerance.
The current study has demonstrated that a low-dose
(2 mg) nicotine gum increases leg extensor torque
but counter-movement jump height and anaerobic
capacity remained unchanged when compared to a
These and our previous results indicate that
nicotine per se can improve exercise endurance
and muscular strength, and alongside patterns
of (mis)use future studies should continue to
practically and mechanistically determine the full
extent of this under-researched stimulant in terms
of performance enhancement and athlete health.
The (ab)use of nicotine and nicotine-containing
substances by athletes, especially by professional and elite
status, is prevalent. For example, Marclay et al. 
reported on a one-year monitoring study of 2185 urine
samples from professional athletes in 43 different sport
disciplines. Traces of nicotine and/or tobacco-related
alkaloids were detected in 23% of the samples, with prevalence
of “active” nicotine consumption (cf. passive
environmental exposure) immediately prior to and/or during sport
practice determined at 15% . Of note, cumulative
exposure of >25% (greater than the worldwide prevalence in
the general population, as reported by the World Health
Organization) was reported in American football (56%),
ice hockey (32%), wrestling (32%), bobsleigh (31%),
gymnastics (29%), rugby (28%) and skiing (26%). These
findings were preceded by the alarming observation
that approximately half of the athletes at the 2009 Ice
Hockey World Championships were active nicotine
consumers before and/or during games . Therefore,
the use of nicotine by athletes, regardless of its form
(e.g. snuff, snus), is frequent across many sports and
countries (e.g. [8, 22]).
Athletes’ beliefs are that consumption of nicotine/
smokeless tobacco proves ergogenic by preventing
xerostomia , weight control , improving reaction time
and concentration , helping relaxation and desirable
arousal-attention . These reports are supported by a
meta-analysis determining that the stimulant effects of
nicotine enhance aspects of cognition and attention,
namely motor abilities, attention and memory . The
results are noteworthy as included studies were not
confounded by nicotine’s withdrawal effects, lack of a
placebo control, patient group deficit or elderly decline in
cognition and therefore likely represent true
performance enhancement. However, there are reports that a
dose–response relationship exists whereby lower doses
prove nootropic whilst higher doses do not [25, 26], this
is perhaps due to the known pharmacological and
physiological action of low-dose nicotine as a central
nervous system (CNS) stimulant whilst at high doses, a
depressant or relaxant effect occurs [18, 28].
As the sports and athletes with the most use of
nicotine concern strength, power and anaerobic events (see
above), it follows that performance and research
protocols reflect this. Previous research has shown no
performance enhancement with smokeless tobacco use for
leg extensor force and power , anaerobic
performance [2, 27] or handgrip strength, counter-movement
jump and agility . However, smokeless tobacco
includes many other ingredients that might confound
results and the use of participants that are habitual users
is confounded by withdrawal or tolerance effects, whether
acute or chronic. In an effort to determine the actual
performance effects of nicotine in an acute experimental
setting, in the present study, nicotine-naïve participants
received acute nicotine supplementation, as using this
rationale, we and others have previously demonstrated
physical and cognitive performance enhancement [15, 24]
despite the oft-reported side effects [23, 24].
Nicotine was added to the World Anti-Doping Agency
(WADA) Monitoring Program in 2012, indicating that
WADA wished to detect patterns of misuse .
Concurrently, there should be an increased investigation focusing
on whether nicotine can enhance performance and/or
represents a health threat to athletes in order to inform
WADA on whether nicotine should remain a monitored
substance or even be upgraded to the List of Prohibited
Substances. Therefore, the experimental hypothesis of the
present study was that through its stimulatory effect on
the CNS, nicotine would prove ergogenic at the lower but
not at the higher dose administered compared to a
placebo for measures of leg extensor torque, muscular power
and anaerobic performance.
in team sports and trained (including gym sessions) or
competed regularly ≥3 times per week for at least 2 years.
Each participant was fully informed of all potential risks
and experimental procedures, after which informed written
consent was obtained. All experimental procedures and
protocols were approved by the Institutional Human Ethics
Committee and performed in accordance with the latest
revision of the Declaration of Helsinki.
All testing was conducted in the same laboratory
environment (~20 °C, 600 lx). Participants visited the laboratory
on four occasions, one anthropometric and familiarisation
session and three experimental trials separated by > 2
< 7 days. All participants had previously completed the
measures of performance required for this study;
however, a full familiarisation was still performed before
commencing the experimental trials to minimise learning.
Experimental trials were conducted at the same time of
day (±1 h), and the day of and prior to any experimental
trial was marked by abstinence from alcohol, any exercise
and only habitual caffeine use (as abstinence would in
itself confound from withdrawal effects). Additionally,
participants were asked to replicate their diet during the
first experimental visit for subsequent trials to ensure a
similar metabolic state. For experimental trials, 30 min
prior to performance testing, participants chewed 2 mg
(NIC-2) or 4 mg (NIC-4) nicotine or a flavour-matched
placebo (PLA) gum, the order of which was randomised
using a Latin square design. Immediately following this,
participants completed five voluntary maximal
contractions (MVC) each of isometric (ISO), concentric (CON)
and eccentric (ECC) contractions of the quadriceps
femoris muscle of the dominant leg followed by three
maximal vertical counter-movement jumps (CMJ) and a
30-s Wingate test (WAnT). A 5-min ergometer warm-up
at 100 W preceded the measurement of leg extensor force
and a further 1-min warm-up prior to the WAnT. This
order of tests was kept constant and was <20 min in
duration (Fig. 1).
Experimental Protocol and Measures
On arrival to the laboratory, participants fastened a heart
rate (HR) strap and monitor (Polar, Kempele, Finland) and
were seated for 5 min, after which a baseline HR
measurement was taken. Participants then chewed gum for 20 min
whilst seated before completing a 5-min warm-up on a
cycle ergometer (Monark, Varberg, Sweden) at 100 W,
during which HR measurement was taken in the final
minute before removing the gum. The participant was then
seated on the isokinetic dynamometer (Biodex Medical
Systems, New York, USA) at the previously recorded seat
adjustments so that the femoral epicondyle was aligned
with the dynamometer’s axis of rotation and the ankle
strap positioned 5 cm proximal to the medial malleolus.
Along with the ankle, straps were placed around the chest,
the hips and the leg to be tested in order to isolate the
quadriceps femoris muscle. The lower limb was weighed,
Fig. 1 Upper panel: Schematic of experimental protocol. Seated rest for 5 min and HR measurement followed by chewing gum for 20 min, a
cycle ergometer warm-up at 100 W and another HR measurement. A set of five MVC’s each for ISO, CON and ECC leg extensor force separated
by a 2-min rest. Three maximal CMJ, after a further 1-min cycling at 100 W a capillary blood sample followed by the WAnT and 3-min cool-down
at 100 W ending with a capillary blood sample. Lower panel: Individual plasma cotinine concentration in 2 mg (NIC-2) and 4 mg (NIC-4) gum trials
for the third, sixth and ninth participants to start trials; none detected for PLA. †Significant difference to corresponding NIC-4 value
with the knee fully extended, to account for the action of
gravity. CON and ECC contractions were performed over
a 60° range of motion (from ~110° knee flexion) and ISO
tension measured at 75°. The participant then performed
five MVC of each type with each set separated by 2 min of
passive recovery. CON and ECC torque was measured at
an angular velocity of 30° s−1. Peak and average peak
torque for CON and ECC, and peak and average peak ISO
tension (average calculated from the five contractions)
Participants then performed three CMJ, each separated
by 30 s of passive rest. Participants descended to a
selfselected depth and immediately jumped upward as high
as possible. To exclude the influence of arm swing,
participants were instructed to keep their hands placed on
their hips. Jump height was measured with an electronic
jump mat (Swift Performance, NSW, Australia), and the
peak and average (of three) values were recorded.
Following this, participants completed a further 1-min
cycling at 100 W during which a 50-μL fingertip blood
sample was collected into a heparinised glass capillary
tube, before completing their WAnT. The WAnT was
completed on a friction-loaded ergometer (Monark,
Varberg, Sweden) using a resistive load of 7.5% of body
mass, where cadence was recorded every 5 s and power
output calculated from friction load and flywheel
velocity. The highest and lowest 5-s values were used to
determine peak power (W) and rate of fatigue (%),
whilst the sum of all 5-s values determined the
anaerobic capacity (kJ). Finally, participants cooled down
for 3 min at 100 W at which time collection of a final
50-μL fingertip blood sample occurred. The capillary
blood samples were analysed immediately for
determination of pH and bicarbonate (HCO3−) via an
automated analyzer (Radiometer, Brønshøj, Denmark).
Nicotine Intervention and Verification
Participants were instructed according to the
manufacturer’s recommendations: one piece of gum (2 mg, 4 mg
and placebo; Nicorette Icy Mint, Johnson & Johnson
Pacific, Auckland, New Zealand) was introduced into
the mouth followed by the instructions “chew until there
is a strong taste, then place between your cheek and
gums, and chew again when the taste has faded”, with
this encouraged for 20 min. Participants were not aware
of the research hypotheses, only that on two of the
three occasions they would be receiving nicotine. To
verify the presence of systemic nicotine a resting
(following 20-min chewing but prior to warm-up) venous
blood sample was obtained from every third participant
beginning the study (i.e. n = 3); this reduced sample was
due to resource limitation. Venous blood samples were
obtained from an antecubital vein into a 4-ml lithium
heparin vacutainer tube (Becton–Dickinson, Plymouth, UK)
then placed on ice for 10 min before being centrifuged
(Eppendorf, Hamburg, Germany) at 4 °C for 10 min at
805g. Plasma was removed, aspirated into 500-μl aliquots
and frozen at −80 °C for later analyses using
highperformance liquid chromatography (HPLC). Due to
nicotine’s tendency to fluctuate and relatively short half-life
(~2 h), cotinine, its major (~70%) metabolite with a longer
retention time (~18–20 h) is preferred . Sample
preparation, solid phase extraction and analysis by HPLC
were based on previous methodology  and performed
All statistical analyses were performed with SPSS
software for windows (IBM SPSS Statistics 20, NY, USA).
Descriptive values were obtained and reported as means
and standard deviation (SD) unless stated otherwise.
Levene’s test was used to ensure that data did not differ
substantially from a normal distribution. Baseline/resting
data (for physiological variables) were first analysed
using one-way ANOVA. Data repeated over time (pH,
HCO3−, HR) were analysed by two-way (trial × time)
ANOVA, whilst all other (performance) data were
analysed by one-way ANOVA. Sphericity was assessed and
where the assumption of sphericity could not be
assumed, adjustments to the degrees of freedom were
made (ε > 0.75 = Huynh-Feldt; ε < 0.75 =
GreenhouseGeisser). Following a significant F test post-hoc pairwise
analyses were performed using a paired samples t test
(Bonferroni correction where relevant), with statistical
significance set at p ≤ 0.05. Partial eta-squared (ηp2) is
reported as a measure of effect size, with demarcations
of small (<0.09), medium (>0.09 < 0.25) and large
No order effects were observed (all p > 0.11, ηp2 < 0.16)
and all participants completed the study without
reporting negative side effects; the only comment made was
that most experienced a scratchy/tickly throat during
some (nicotine) trials.
Of the samples screened for blood cotinine concentration
(n = 3; Fig. 1), none was detected during PLA whereas
cotinine concentration increased as a function of dose
(NIC-2: 20 ± 21 ng mL−1, NIC-4: 87 ± 8 ng mL−1; trial:
p = 0.01, ηp2 = 0.97). Resting HR was similar prior to
treatment (trial: p = 0.49, ηp2 = 0.08) but following
treatment differed between trials as a function of time
(trial × time: p = 0.03, ηp2 = 0.34; Table 1) such that
the increase in HR was more pronounced during NIC-2
(6 ± 7 beats · min−1) and NIC-4 (7 ± 9 beats · min−1)
compared to PLA. HCO3− before the WAnT was similar
Heart rate (HR) at rest pre-treatment (Pre) and during cycling at 100 W post-treatment (Post); bicarbonate (HCO3−) and pH before (Pre) and after (Post) WAnT;
placebo (PLA), 2 mg (NIC-2) and 4 mg (NIC-4) trials
aSignificant difference to corresponding Pre value
bSignificant difference to corresponding PLA value
cSignificant difference to corresponding NIC-4 value
between trials (trial: p = 0.40, ηp2 = 0.11) but was decreased
following the WAnT (time: p < 0.01, ηp2 = 0.97), whilst pH
was different between trials (trial: p = 0.03, ηp2 = 0.37) and
across time (time: p < 0.01, ηp2 = 0.90).
Peak and average ISO tension differed between trials
(trial: p = 0.02, ηp2 > 0.37; Table 2) such that NIC-2 >
PLA. Peak (trial: p = 0.05, ηp2 = 0.30) but not average
(trial: p = 0.28, ηp2 = 0.15) CON torque differed between
trials such that NIC-2 > PLA. Peak (trial: p < 0.01, ηp2 =
0.48) and average (trial: p = 0.03, ηp2 = 0.37) ECC torque
differed between trials such that NIC-2 > PLA. Peak and
average CMJ height was similar between trials (trial: p >
0.65, ηp2 < 0.05). During the WAnT (Fig. 2), anaerobic
capacity was similar between trials (trial: p = 0.73, ηp2 =
0.04) although pacing strategy seemed to differ; peak
power differed between trials (trial: p < 0.01, ηp2 = 0.57)
such that NIC-2 < PLA by 6 ± 3% or 49 ± 24 W whilst
the rate of fatigue differed between trials (trial: p <
0.01, ηp2 = 0.59) such that NIC-2 (38 ± 11%) and
NIC4 (37 ± 12%) < PLA (44 ± 10%).
This is the first study to investigate whether nicotine
improves measures of leg extensor torque, muscular power
and anaerobic performance. The main findings from this
study were that (1) low-dose nicotine (2 mg) increased
leg extensor force by ~6% compared to the placebo,
whereas neither low- nor high-dose nicotine affected
counter-movement jump height; (2) during the WAnT,
anaerobic capacity was unchanged although low-dose
nicotine altered the pacing strategy adopted; (3)
physiologically, low-dose nicotine caused a relative alkalosis
and both nicotine doses caused heart rate to be higher
Low-Dose Nicotine Increases Peak and Average Leg
Extensor Torque But Not Muscular Power
Overall, five out of six measures of torque were
significantly improved with NIC-2 (6 ± 5%) with only the average
concentric torque unaffected (4 ± 4%). To our knowledge,
only one previously published study has measured leg
extensor performance. Escher et al.  tested a greater
range of flexion (90°) and angular velocity (250° s−1) than
in the current study using college athletes who regularly
used smokeless tobacco; their participants were tested
following ~12-h abstention from tobacco or having
consumed smokeless tobacco 2 h and immediately prior to
testing. They reported that MVC was lower when using
compared to abstaining from tobacco but commented that
they do not know whether it was the nicotine or any other
substance within tobacco proving ergolytic. However,
cotinine concentration during the tobacco trials in that
study were considerably higher than in our study when
using NIC-4 (~144 vs. ~87 ng mL−1) and therefore it
Table 2 Peak and average leg extensor torque and counter-movement jump height for placebo, 2 and 4 mg nicotine gum.
Values are mean ± SD, n = 9
Leg extensor torque (N m)
ISO isometric, CON concentric and ECC eccentric torque; CMJ counter-movement jump; PLA placebo, 2 mg (NIC-2) and 4 mg (NIC-4) trials
aSignificant difference to corresponding PLA value
Fig. 2 Power output and anaerobic capacity during the WAnT for placebo (filled circle, PLA), 2 mg (grey circle, NIC-2) and 4 mg (open circle, NIC-4)
nicotine gum. Values are mean ± SD, n = 9
remains plausible that in their participants, nicotine
caused a depressant or relaxant effect [18, 28]. However,
our results support those previously obtained when using
another CNS stimulant, amphetamine, albeit by a smaller
Given our results on leg extensor strength, it was
surprising that NIC-2 did not affect CMJ performance. On
the one hand, it might be argued that having produced
more work during NIC-2 than PLA (141 ± 62 J, p < 0.01)
could have produced greater fatigue that would mask
any enhancement during the CMJ, or that the addition
of velocity to force (i.e. power) attenuates any “true”
effect (or single- vs. multi-joint movements). Previous
studies have also found no improvement in CMJ  or
rate of leg extensor force development  with
smokeless tobacco; in fact, Escher et al.  noted an
ergolytic effect when regular users consumed rather than
abstained from tobacco, although this may be due to
nicotine’s biphasic effect at the neuromuscular junction
whereby it exerts excitatory (acutely, when naïve or after
withdrawal) then inhibitory (chronically, when tolerant)
effects [1, 19]. Chandler and Blair  also failed to
demonstrate any effect of amphetamine on leg power. It might
also be that a CMJ is not sufficiently sensitive a test.
Low-Dose Nicotine Affects Pacing But Not Anaerobic
Capacity During the WAnT
Previous studies have failed to detect any difference in
anaerobic capacity during the WAnT when
administering sublingual nicotine in naive participants  or
smokeless tobacco in regular users ; therefore, in this
respect, our results are in agreement. Furthermore, other
CNS stimulants (caffeine, pseudoephedrine) have also
failed to affect WAnT performance [7, 16]. However,
that we observed a reduction in peak power yet an
attenuation in fatigue when administered NIC-2 compared
to PLA was surprising (Fig. 2) and difficult to explain.
We observed a significant relative alkalosis immediately
prior to the WAnT during NIC-2 only whereas the
~2 mmol L−1 higher HCO3− was not significant (p = 0.2,
Table 1); thus, whilst this could provide a mechanism for
reduced fatigue via improved acid–base balance, it does
not explain why the rate of fatigue was equally reduced
during NIC-4. Indeed, as an alkaloid, nicotine is a weak
base (pKa = 8.0) that in gum form, it is buffered to
alkaline pH to facilitate buccal absorption . The authors
feel that further explanation/discussion is not possible,
especially without further mechanistic insight, as this
would be too speculative.
Potential Mechanism(s) of Action
That nicotine that had been sufficiently absorbed
systemically within both NIC-2 and NIC-4 was confirmed
by our measurement of cotinine concentration (Fig. 1),
and that heart rate was elevated during both trials
compared to PLA (Table 1). The sympatho-adrenal
(excitatory) effects of nicotine are well known 
although, given the ergogenic characteristics discussed
here (muscular and anaerobic performance), it is most
likely that nicotine is exerting its effects via stimulating
cholinergic neurotransmission in the basal forebrain
(cortical arousal) and/or enhanced mesolimbic
dopaminergic activity (motivation and reward) .
Nevertheless, a hypoalgesic effect of nicotine should not be
discounted as it has been experimentally demonstrated
to increase the pain threshold , and might therefore
prove ergogenic via antinociception as proposed by
caffeine . The possibility of a placebo effect cannot
be discounted; indeed, it is difficult to mask the effects
such as those from (m)any CNS stimulants. However,
several steps were taken during the study design: (1)
although only single-blind, participants were unaware
of the study hypotheses and only told that they would
be receiving nicotine on two of three occasions, (2) a
flavour-matched placebo was used, and (3) although
participants might have detected the portion of nicotine
swallowed (first-pass metabolism) or the psychoactive/
sympatho-adrenal effects, were a placebo effect is indeed
evident in the current study then it would likely be seen
for NIC-4 also and this was not the case.
Considerations and Future Research
It is acknowledged that a sample size of n = 9 is relatively
small; however, clear and directional statistical results
were observed even with this sample. It is also worth
noting that the finding of the 4 mg gum minimally
affecting the performance measures was not due to side
effects masking or reducing any ergogenic effect(s), as
none were reported. There are many different nicotine
delivery systems commonly available (over-the-counter)
including nasal spray, gum, inhaler, lozenge, sublingual
tablet and transdermal patch. The different delivery
systems result in different nicotine bioavailability and
absorption and therefore pharmacokinetics such that,
for example, peak systemic concentrations are observed
whilst smoking a cigarette, followed by oral snuff and
chewing tobacco with gum being the lowest, possibly
due to the first-pass metabolism and nicotine being
retained in the gum itself . The observed cotinine
concentration from chewing gum was indeed lower than
that observed with oral smokeless tobacco and
transdermal patch [12, 24]; therefore, it would be of interest to
directly compare different delivery systems on the same
experimental sample and performance protocol. There is
also considerable inter-individual variability in nicotine
metabolism (e.g. nutrition, age, sex, medication, ethnicity,
genetics; see ) as we observed for NIC-2 (Fig. 1) and
thus, we cannot be certain that our n = 3 is the
representative of the whole sample. Further, dosing (e.g.
absolute vs. relative) needs to be more carefully considered
for future studies. Finally, as the primary outcome measure
of the present study was performance, future studies should
include further mechanistic insights i.e. motor unit
activation (twitch interpolation, electromyography).
The present study has demonstrated that low-dose (2 mg)
nicotine gum increases leg extensor torque, but
countermovement jump and anaerobic capacity during WAnT
remained unchanged when compared to a placebo, whilst
there were minimal effects of the 4-mg nicotine gum on
the performance parameters measured. Together with our
previous observation , these results indicate that
nicotine per se can improve exercise endurance and muscular
strength, something that WADA should continue to
monitor alongside patterns of (mis)use.
TM contributed to the obtaining funding, conception and design of the work;
data acquisition, analysis, and interpretation; drafting and critically revising
important intellectual content. MM contributed to the design of the work;
data acquisition and analysis. DJC contributed to the design of the work;
critically revising important intellectual content. MJB contributed to the design
of the work; data acquisition; critically revising important intellectual content.
All authors approved the final version of the manuscript. All experimental
procedures were performed in the School of Sport and Exercise, Massey
University, Palmerston North.
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