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Research Article
The Effect of Prior Upper Body Exercise on
Subsequent Wingate Performance
Marie Clare Grant,1,2 Robert Robergs,3Marianne Findlay Baird,1and Julien S. Baker1
1Institute of Clinical Exercise and Health Science, Exercise Science Research Laboratory, School of Science,
Faculty of Science and Technology, University of the West of Scotland, Hamilton ML3 OJB, UK
2Division of Sport and Exercise Sciences, School of Social & Health Sciences, Abertay University, Bell Street, Dundee DD1 1HG, UK
3School of Human Movement Studies, Charles Sturt University, Bathurst, NSW 2795, Australia
Correspondence should be addressed to Marie Clare Grant; marieclare.grant@abertay.ac.uk
Received February ; Revised April ; Accepted April ; Published May
Academic Editor: Michael Greenwood
Copyright © Marie Clare Grant et al. is is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.
It has been reported previously that the upper body musculature is continually active during high intensity cycle ergometry. e
aim of this study was to examine the eects of prior upper body exercise on subsequent Wingate (WAnT) performance. Eleven
recreationally active males (. ±. yrs; . ±. kg; . ±. m) completed two trials in a randomised order. In one trial
participants completed 2×30s WAnT tests (WAnT and WAnT) with a min recovery period; in the other trial, this protocol
was preceded with sets of biceps curls to induce localised arm fatigue. Prior upper body exercise was found to have a statistically
signicant detrimental eect on peak power output (PPO) during WAnT ( < 0.05) but no eect was observed for mean power
output (MPO) ( > 0.05). Handgrip (HG) strength was also found to be signicantly lower following the upper body exercise.
ese results demonstrate that the upper body is meaningfully involved in the generation of leg power during intense cycling.
1. Introduction
High intensity cycle ergometry has been widely employed
in sport and exercise science research to assess indices of
muscular performance [,]. Among these power variables,
the measurement of PPO has received considerable interest.
PPO measurement has traditionally been attributed to the
activity of the lower body musculature. Previous work and
recent investigations in our laboratory have shown that
the upper body may signicantly contribute to PPO [–].
Surface electromyography (sEMG) has revealed that several
upper body muscles (brachioradialis (BR), biceps brachii
(BB), triceps brachii (TB), and upper trapezius (UT)) are
continually active during high intensity cycle ergometry
when a standard handlebar grip is used []. With the current
cycle ergometer design, evidence suggests that the forearm
muscles and therefore the handlebar grip are inuential to
overcome high resistive loads to produce an optimum PPO.
is is supported by the ndings of Baker et al. () []
whofoundPPOtobesignicantlygreaterwhenastandard
handlebar grip was in place compared to no grip ( < 0.05).
e eects of prior upper body exercise on subsequent
cycling performance have previously been examined []. In
this study, blood lactate concentrations [La−]wereelevated,
via arm-crank exercise, and dynamic performance during
two s WAnT was assessed. It was found that prior arm
exercise was related to a decline in PPO during the second
WAnT with the authors suggesting that the resulting elevated
[La−]causedanincreaseduptakeinLa
−and H+by the
inactive leg muscles, leading to an overall performance
decrement. Karlsson et al. () []havealsosuggestedthat
a period of exhausting anaerobic exercise by the arms or
legs might decrease the performance time of anaerobic eort
in the nonexercising arm or leg region due to the possible
detrimental eects of elevated [La−]and[H
+].
Although it is now known that La−per se does not
directly cause muscle fatigue, a rise in other metabolic by-
products such as inorganic phosphate (Pi)[], Piis likely to
Hindawi Publishing Corporation
BioMed Research International
Volume 2014, Article ID 329328, 7 pages
http://dx.doi.org/10.1155/2014/329328
BioMed Research International
HGHGHGHGHG
Warm-up
0123 12345 123456 123456 123456
Upper body exercise
ARF trial
4th set to exhaustion
(3×10 reps)
Blood Blood Blood Blood Blood Blood Blood
WA nT 1
WA nT 2
30 s recovery
F : Schematic representation of both experimental protocols. HG = hand grip; WAnT = Wingate Test ; WAnT = Wingate Test ; and
BS = blood ngertip sample.
play a major role in muscular fatigue during high intensity
exercise. Potential mechanisms whereby high [Pi] can impair
contractile function thus aecting muscle force production
include hindering crossbridge transition to the strongly
bound high force state; reducing myobrillar calcium (Ca2+)
sensitivity; increasing the opening probability of the sar-
coplasmic reticulum (SR) Ca2+ release channels; inhibiting
Ca2+ uptake by the SR; and precipitating with the Ca2+
in the SR, so decreasing the amount of Ca2+ available for
release []. A rise in metabolic by-products is concomitant
with partial depletion and inhibition of the phosphagen
and glycolytic energy systems [] during exercise may aect
muscle function in the nonexercising arm or leg []. is
eect may contribute to decline in muscular force production
and overall performance. Based on previous research high-
lighting the importance of the upper body musculature in
high intensity cycle ergometer performance, it is plausible
that when the upper body is fatigued, it will be less able to
support or stabilize the body to allow for more eective leg
power development [].
e experimental design of the present study was largely
basedonthatofBogdanisetal.[]withtheaimoffurther
examining the eects of prior fatiguing upper body exercise
on subsequent WAnT performance. A secondary aim was to
investigate if HG strength was correlated with power proles.
2. Methodology
2.1. Participants. Eleven healthy, recreationally active males
(20.8 ± 2.2yrs; 77.7 ± 12.0kg; 1.79 ± 0.04 m) volunteered
to participate in the study. e study was approved by the
university ethical committee and all participants completed
an informed consent form and medical history questionnaire.
Participants were instructed to maintain their normal diet
during the days leading up to and on the days of testing and
they were asked to refrain from vigorous exercise and avoid
the consumption of caeine and alcohol during the hours
preceding the testing date. Food was not consumed during
testing and water was available ad libitum.
Participants attended the laboratory on three separate
occasions, at the same time of day, separated by to hrs.
Participants did not report any muscle soreness before any of
the sessions. e rst session was a familiarisation session to
control for the potential eects of learning a novel task and
increase reliability of the results. During this session partic-
ipants were briefed on experimental procedures, instructed,
and familiarised with high intensity cycle ergometry, bicep
curls, and maximal HG testing. Body mass (kg), stature (m),
and RM were also determined during this session.
e following two experimental trials were completed
in a randomised order. For the no arm fatigue (NOF)
trial, participants were required to perform two maximal
s sprints (WAnT and WAnT) on a cycle ergometer
with a standard handlebar grip, separated by min passive
recovery. In the other arm fatigue (ARF) trial, bicep curls
were completed prior to WAnT and WAnT. Blood [La−]
and handgrip strength were obtained at predetermined time
points throughout the protocols (Figure ).
2.2. Cycle Ergometry. A leg cycle ergometer (Monark E,
Vansbro, Sweden) was used for each experimental protocol.
For each participant the saddle height was adjusted so their
knee remained slightly exed aer the completion of the
power stroke (with nal knee angle approximately –∘).
Toe clips were used to ensure that the participants’ feet were
held rmly in place and in contact with the pedals. e cycle
ergometer was connected to a PC to allow for data capture via
theMonarkanaerobictestsoware(version..).
Before any experimental testing, each individual com-
pleted a standardised warm-up on the cycle ergometer ( min
at rpm, kg resistance).
For both WAnT and WAnT, participants were given
a rolling start before resistive force application. Once the
subjects had accelerated to rpm the weight basket automat-
ically dropped and participants began to pedal maximally.
Each participant was required to pedal with maximum eort
for a period of s against a xed resistive load of grams
per kilogram (g⋅kg−1) total body mass as recommended by
Bar-Or () []. All participants were given the same level
of verbal encouragement and instructed to remain seated for
the duration of the test while maintaining a standard han-
dlebar grip. Variables obtained from the Monark anaerobic
test soware (version ..) were PPO (W), relative PPO
(W⋅kg−1), MPO (W), and relative MPO (W⋅kg−1). For the
population used within the study the WAnT has a high test-
retest reliability ( = 0.95–0.97)[].
2.3. Bicep Curls. In a familiarisation session before any
experimental testing, each individual carried out a series of
bicep curls to allow for their RM to be estimated. With each
settheweightwasadjustedsothatnomorethanrepetitions
could be completed with the nal weight. Participants were
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T : Power output variables recorded during WAnT and WAnT for both experimental conditions.
WA nT
PPO (W)
WA nT
PPO (W)
WA nT
PPO
(W⋅kg−1)
WA nT
PPO
(W⋅kg−1)
WA nT
MPO (W)
WA nT
MPO (W)
WA nT
MPO
(W⋅kg−1)
WA nT
MPO
(W⋅kg−1)
NOF 980.0 ± 166.5 865.4 ± 168.1∗12.7 ± 1.5 11.2 ± 1.7∗656.0 ± 84.0 589.2 ± 89.3 8.5 ± 0.5 7.6 ± 0.7∗
ARF 929.9 ± 167.7 871.7 ± 22.69∗12.0 ± 1.3 11.2 ± 2.0∗649.3 ± 86.6 576.4 ± 81.8 8.4 ± 0.7 7.5 ± 0.7∗
∗is indicates signicant dierences between WAnT and WAnT (𝑃 < 0.05).
given -minute recovery between each set. All participants
were familiar with the exercise; therefore no more than
three sets were required. e Brzycki formula was then used
to estimate RM based on the nal weight and repetitions
recorded ()[]. % of the RM was subsequently calculated
for each participant to establish the weight required to fatigue
the arms for protocol :
1RM =weight lied
1.0278 − repetitions × 0.0278.()
For protocol (ARF), participants completed sets of
repetitions and a th set until exhaustion (R s between
sets) at % RM. During the bicep curls, participants’ palms
wereinthesupinatedpositionandtheywereinstructedto
keep the feet a shoulder width apart with their elbows close to
their sides and complete each curl with a continuous, smooth
movement with minimum body disruption.
2.4. Handgrip. HG strength (kg) was measured min aer
warm-up and min aer each exercise bout (Figure ). Each
maximal static HG test was completed with the participant’s
dominant hand, while being in a seated position using a HD
dynamometer (Model TKK, Takei, Japan).
2.4.1. Blood Sampling. Capillary blood samples (– L)
for the measurement of blood [La−] were taken from the
ngertip using standard lancets and capillary tubes. Samples
were taken at rest, min following warm-up and and
min following each exercise bout (Figure ). All samples
were immediately mixed (min) and duplicate samples were
analysed to determine the whole blood lactate concentration
(Analox P-LM, Analox Instruments Ltd, London, UK).
e full protocol for each testing session is outlined in
Figure .
2.4.2. Statistical Analysis. Data was statistically analysed
using SPSS (version ) (IBM, Armonk, NY, USA). For a
single missing data point, data was replaced with a mean
dierenceadjustedvaluefortheindividualcomparedto
the other trial data point. For each of peak power, relative
peak power, mean power, relative mean power, and fatigue
index (FI, %), repeated measures two-way ( [TRIAL] ×
[TEST]) ANOVAs were performed to detect main eect and
interaction eects. For the blood lactate data, a balanced
design was only evident for the postexercise data ( and
min following exercise). For these data, data were analyzed
by repeated measures three-way ( [TRIAL] × [TEST] ×
[TIME]) ANOVA. For HG data, a balanced design was
evident when using the post-warm-up data for the NOF trial
and the post-arm fatigue test data for the ARF trial as the
preexercise data. Preexercise was then compared to postex-
ercise ( min WAnT versus min WAnT) using a repeated
measures two-way ( [TRIAL] × [TIME]) ANOVA. For
all data variables, specic contrasts were performed to test
for mean dierences for signicant main or contrast eects.
Isolated paired mean dierences outside of the balanced
ANOVA designs were assessed by a paired t-test. Pearson’s
correlation analysis was used to determine the correlation
between PPO and HG strength. Eect size statistics (ES)
for selected statistically signicant t-andF-ratios were also
established. ese calculations were based on Cohen’s (d)
classication of a small (0.2 ≤ < 0.5), moderate (0.5 <
< 0.8), and large ( ≥ 0.8)ES[]. Signicance was set a
priori at < 0.05. All data is presented as mean ±standard
deviation (SD).
3. Results
3.1. Cycle Parameters. ere was a signicant main eect for
the TEST for each of PP (W: 1,8 = 19.5, < 0.01,
df =0.84), relative PP (W⋅kg−1:1,8 = 22.6, < 0.01,
df = 0.86), and relative MPO (1,8 = 43.8 < 0.01,
df = 0.91)(Table ), revealing lower power values for WAnT
compared to WAnT. Peak power produced in WAnT was
lower in the ARF protocol compared to NOF protocol (<
0.01,df = 0.75); however, no signicant interaction was
found ( > 0.05). No signicant dierences were found in
FI (%) for TEST or TRIAL ( > 0.05)(NOF:57.0 ± 10.5%
and 57.8 ± 10.7% f o r WA nT a n d WA n T , r e s p e c t i v e l y, A R F :
57.3 ± 9.9%and59.1 ± 9.6% f o r WA nT a n d WA n T ) .
3.2. Blood Lactate. ebloodlactateresponsetoeachofthe
experimental protocols is displayed in Figure .erewasa
signicant TIME eect (1,8 = 15.8, < 0.01,df = 0.81)
and a signicant TRIAL ×TEST interaction ( = 0.041,
df = 0.57). e three-way interaction eect of TRIAL ×
TIME ×TEST revealed a trend toward statistical signicance
( = 0.089,df = 0.54). Blood lactate was signicantly higher
min aer the arm fatigue exercise in the ARF trial compared
to post-warm-up in the NOF trial ( = 0.001). Based
on the main eect and interaction ANOVA results, blood
lactate was signicantly higher throughout the recovery aer
WAnT than WAnT. In addition, the interaction eect was
caused by a net decrease in blood lactate between and min
of recovery in WAnT, whereas blood lactate continued to
increasebetweenandminofrecoveryaerWAnT.
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0
2
4
6
8
10
12
14
Baseline
Before
WA nT 1
WA nT 1
WA nT 2
WA nT 2
Sample
NOF
ARF
Lactate (mmol·L−1)
∗
3min aer
5min aer
3min aer
5min aer
F : Blood [La−] responses prior to and during recovery from
e a c h o f WA nT a n d WA nT . ∗= signicant dierence between
NOF and ARF.
3.3. Handgrip. e HG strength response to each of the
experimental protocols is displayed in Figure .erewasa
signicant TRIAL eect ( = 0.004,df = 0.81). erefore,
HG strength was signicantly lower at all time points for the
ARF versus NOF trial.
ere was a nonsignicant correlation between HG
strength and PPO during NOF ( = 0.29, = 0.38).
However, in the ARF where bicep curls were completed
before WAnT, there was a meaningful trend of a positive
linear relationship ( = 0.59, = 0.06) between PPO from
WA nT a n d H G s t r e n g t h a e r WA nT ( Figure ).
4. Discussion
emainaimofthepresentstudywastoevaluatetheeects
of prior fatiguing upper body exercise on subsequent high
intensity cycle ergometer performance. e results demon-
strate that fatiguing the upper body had a detrimental eect
on PPO during WAnT with nonsignicant impact on any
other power variables. Interestingly, the connection between
prior upper body exercise and PPO was best revealed as a
fair correlation between HG strength and PPO in protocol
(Figure ). Consequently, the functional connection between
HG strength and PPO is more relevant aer prior exercise of
the upper body.
In the ARF protocol, HG strength was lower at all mea-
sured time points compared to the NOF protocol. Further-
more, PPO was signicantly lower ( < 0.05) in WAnT in the
ARFprotocolcomparedtotheNOFprotocolwhichsuggests
that in the absence of leg fatigue, the strength of the grip upon
the handlebar may be inuencing PPO. is is in agreement
with the ndings of Baker and colleagues () []who
found that handlebar grip was essential in the production
of PPO. Perhaps unexpectedly, the only correlation between
20
25
30
35
40
45
50
55
60
Force (kg)
Sample
WA n t 1
1min aer
WA n t 2
1min aer
WA n t 2
6min aer
NOF
ARF
Before
F : Handgr ip strength (kg) measured b efore and aer exercise
for both trials.
PPO and HG strength reaching signicance was between
PPO obtained in WAnT and HG strength aer WAnT
in the ARF protocol ( = 0.59, = 0.06). A possible
explanation for this nding is that as HG strength shows signs
of recovery following the fatiguing arm exercise (Figure ),
the relationship between HG strength and PPO becomes
more evident.
e lack of statistically signicant dierences between the
two protocols in the MPO data is likely to be partly due to the
added variability of this measure compared to PPO. However,
itcanbespeculatedthatthepriorhighintensityupperbody
exercise would have resulted in faster
VO2kinetics facilitating
an earlier and greater shi to aerobic metabolism in the
rst sprint in protocol (ARF). is shi has the potential
to improve MPO by reducing the O2decit and rate of
fatigue induction [,]. is reduction in fatigue can be
highlighted through the lack of dierence in FI (%) found
between WAnT and WAnT in both protocols.
Despite the statistically signicant increase in blood [La−]
during high intensity exercise, it is now widely accepted
that La−does not have a direct role in muscular fatigue
[].However,therateofblood[La
−]accumulationand
removal can be used as a measure of the status of muscle
metabolism with trained individuals reported as having
a greater lactate transport capacity than their untrained
counterparts []. During intense exercise, the predominate
mechanism which moves La−and H+outofcontracting
muscle is the monocarboxylate transporter system, MCT
and MCT [,], with the transport eciency dependent
upon various factors including intramuscular and blood pH,
densityofMCTandMCT,andonbloodowinworking
muscles and other tissues []. In the present study, there
was a small increase in the standard deviation values from
to min aer exercise suggesting participant variability in
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400
600
800
1000
1200
1400
30 35 40 45 50 55 60
Peak power output (W)
Force (kg)
(a)
400
600
800
1000
1200
25 30 35 40 45 50 55 60
Peak power output (W)
Force (kg)
(b)
F : Correlations between handgrip strength aer WAnT and peak power from WAnT for (a) NOF ( = 0.29, = 0.38) and (b) ARF
( = 0.59, = 0.06).
lactate transport eciency which reects possible between-
subject dierences in training status.
During ARF, participants commenced the WAnTs with
signicantly greater circulating blood [La−]. Apart from
the added intense upper body exercise that induced this
increase, it has also been established that the upper body
has a higher percentage of type II bres than the lower
body which in turn causes upper body musculature to be
less ecient in lactate clearance and subsequently also has
aslowerrecovery[,]. Despite the metabolic benets
of La−production now being widely recognised, there is
a denite association between elevated blood [La−]and
impaired exercise performance []. erefore, this elevated
[La−]intheARFprotocolislikelytobeareectionofother
metabolic disturbances including metabolic acidosis and an
increase in intramuscular Piand blood K+thus partially
accounting for the decrease in PPO [,]. It is important
to highlight that despite the common belief that muscle
acidosis is a major cause of fatigue, there is now reasonable
evidence to suggest that the eects of H+on force production
may be largely temperature dependent and may have little
direct eect on human muscle at physiological temperature
[].
In addition to the metabolic disturbances within the
muscles, prior high intensity exercise also causes partial
depletion and inhibition of the phosphagen and glycolytic
energy systems leading to decline in muscular force produc-
tion. In terms of energy depletion inuencing subsequent
performance, PCr recovery is likely to be a key factor.
Research has shown that aer exhaustive exercise, near
complete replenishment of PCr may take from < min to in
excess of min, depending on the extent of PCr depletion,
severity of metabolic acidosis (slower if more acidic), and
themusclemotorunitandbretypecharacteristicsofthe
exercised muscle []. erefore, in the present study it is
unlikely that the -minute rest period between exercise bouts
would be sucient for complete replenishment of PCr stores,
thus having a detrimental eect on power proles obtained
following a previous bout of high intensity exercise. Further-
more as outlined previously, blood [La−]remainselevated,
suggesting intramuscular H+activity also remains higher,
thus slowing the replenishment process. is is supported
by Bogdanis and colleagues [] who found that decreased
[PCr] did result in a reduction in power output. However,
it is likely that the detrimental eects of prior exercise on
subsequent performance will be muted when the recovery
period is adequate [,]. For example, when Bouhlel et
al. [] investigated the possible impact on estimated peak
anaerobic power when a leg test was preceded by an arm
test (or vice versa), they found that subsequent performance
was not reduced. e min recovery period within this study
suggests that the opposite muscle group is unaected by any
continuing metabolic disturbances or other changes from the
preceding bout of exercise if the recovery period is adequate.
In a previous study by Bogdanis and colleagues [], a
very similar methodology was used. e authors aimed to
elevate [La−] through prior arm exercise (arm ergometry)
and determine the eects of this on subsequent high intensity
cycle ergometry performance. In contrast to our results
they found PPO to be signicantly lower during the second
sprint following prior arm exercise but similarly there were
nonsignicant changes in MPO between the two protocols.
It is dicult to directly compare results with Bogdanis et
al. [] due to dierences in equipment, participants, and
experimental procedures employed. We have hypothesised
that the dierences between the two investigations may be
due to our upper body exercise (bicep curls) having a directly
fatiguing eect on HG strength which we hypothesised would
be more likely to aect PPO during the initial sprint. We
interpret our results to conrm this hypothesis.
5. Limitations
As with most maximal cycle ergometer tests, prior to the load
being applied there was an initial high rpm. is inertia was
BioMed Research International
not accounted for in the calculation; therefore the consider-
able energy which had already been accumulated before the
s test may have resulted in a possible overcalculation of
PPOandMPO[].
All participants were physically active and accustomed
to high intensity exercise. However no physiological tness
testing was undertaken prior to data collection which meant
there was no control over the exercise capacity of each
individual. is is an extraneous variable which may have
led variation in power proles observed among participants
which was not related to the exercise protocol.
6. Conclusion
In conclusion, this investigation has shown that prior fatigu-
ing upper body exercise has a statistically signicant detri-
mental eect on PPO during the rst of two WAnTs. is can
be related to a number of factors, including the decrease in
HG strength following the upper body exercise suggesting
the upper body is less able to help overcome the high
resistive loads, conrming results of previous investigations
which suggest that the upper body is crucial in achieving an
optimum PPO. It was also found that MPO was able to be
maintained, which could be explained by prior intense exer-
cise resulting in faster
VO2kinetics and therefore increasing
the contribution from oxidative metabolism.
Conflict of Interests
e authors declare that there is no conict of interests
regarding the publication of this paper.
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