Hindawi Publishing Corporation

BioMed Research International

Volume 2014, Article ID 329328, 7 pages
http://dx.doi.org/10.1155/2014/329328

Research Article
The Effect of Prior Upper Body Exercise on
Subsequent Wingate Performance
Marie Clare Grant,1,2 Robert Robergs,3 Marianne Findlay Baird,1 and Julien S. Baker1
1

Institute 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
2
Division of Sport and Exercise Sciences, School of Social & Health Sciences, Abertay University, Bell Street, Dundee DD1 1HG, UK
3
School of Human Movement Studies, Charles Sturt University, Bathurst, NSW 2795, Australia
Correspondence should be addressed to Marie Clare Grant; [email protected]
Received 21 February 2014; Revised 11 April 2014; Accepted 14 April 2014; Published 7 May 2014
Academic Editor: Michael Greenwood
Copyright 2014 Marie Clare Grant et al. This 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. The
aim of this study was to examine the effects of prior upper body exercise on subsequent Wingate (WAnT) performance. Eleven
recreationally active males (20.8 2.2 yrs; 77.7 12.0 kg; 1.79 0.04 m) completed two trials in a randomised order. In one trial
participants completed 2 30 s WAnT tests (WAnT1 and WAnT2) with a 6 min recovery period; in the other trial, this protocol
was preceded with 4 sets of biceps curls to induce localised arm fatigue. Prior upper body exercise was found to have a statistically
significant detrimental effect on peak power output (PPO) during WAnT1 ( < 0.05) but no effect was observed for mean power
output (MPO) ( > 0.05). Handgrip (HG) strength was also found to be significantly lower following the upper body exercise.
These 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 [1, 2]. 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 significantly contribute to PPO [24].
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 [4]. With the current
cycle ergometer design, evidence suggests that the forearm
muscles and therefore the handlebar grip are influential to
overcome high resistive loads to produce an optimum PPO.
This is supported by the findings of Baker et al. (2001) [2]

who found PPO to be significantly greater when a standard

handlebar grip was in place compared to no grip ( < 0.05).
The effects of prior upper body exercise on subsequent
cycling performance have previously been examined [5]. In
this study, blood lactate concentrations [La ] were elevated,
via arm-crank exercise, and dynamic performance during
two 30 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 ] caused an increased uptake in La and H+ by the
inactive leg muscles, leading to an overall performance
decrement. Karlsson et al. (1975) [6] have also suggested that
a period of exhausting anaerobic exercise by the arms or
legs might decrease the performance time of anaerobic effort
in the nonexercising arm or leg region due to the possible
detrimental effects 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 byproducts such as inorganic phosphate (Pi ) [7], Pi is likely to

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Warm-up
0 1 2 3

1 2 3 4 5
Blood

WAnT1

ARF trial
Upper body exercise
HG
(3 10 reps)
30 s recovery
4th set to exhaustion

HG

1 2 3 4 5 6
Blood Blood

HG

1 2 3 4 5 6
Blood Blood

WAnT2

HG

HG

1 2 3 4 5 6
Blood Blood

Figure 1: Schematic representation of both experimental protocols. HG = hand grip; WAnT1 = Wingate Test 1; WAnT2 = Wingate Test 2; and
BS = blood fingertip sample.

play a major role in muscular fatigue during high intensity

exercise. Potential mechanisms whereby high [Pi ] can impair
contractile function thus affecting muscle force production
include hindering crossbridge transition to the strongly
bound high force state; reducing myofibrillar calcium (Ca2+ )
sensitivity; increasing the opening probability of the sarcoplasmic 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 [8]. A rise in metabolic by-products is concomitant
with partial depletion and inhibition of the phosphagen
and glycolytic energy systems [9] during exercise may affect
muscle function in the nonexercising arm or leg [10]. This
effect may contribute to decline in muscular force production
and overall performance. Based on previous research highlighting 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 effective leg
power development [1].
The experimental design of the present study was largely
based on that of Bogdanis et al. [5] with the aim of further
examining the effects of prior fatiguing upper body exercise
on subsequent WAnT performance. A secondary aim was to
investigate if HG strength was correlated with power profiles.

2. Methodology
2.1. Participants. Eleven healthy, recreationally active males
(20.8 2.2 yrs; 77.7 12.0 kg; 1.79 0.04 m) volunteered
to participate in the study. The 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 caffeine and alcohol during the 24 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 48 to 72 hrs.
Participants did not report any muscle soreness before any of
the sessions. The first session was a familiarisation session to
control for the potential effects of learning a novel task and
increase reliability of the results. During this session participants 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 1RM were also determined during this session.
The following two experimental trials were completed
in a randomised order. For the no arm fatigue (NOF)
trial, participants were required to perform two maximal
30 s sprints (WAnT1 and WAnT2) on a cycle ergometer
with a standard handlebar grip, separated by 6 min passive
recovery. In the other arm fatigue (ARF) trial, bicep curls
were completed prior to WAnT1 and WAnT2. Blood [La ]
and handgrip strength were obtained at predetermined time
points throughout the protocols (Figure 1).
2.2. Cycle Ergometry. A leg cycle ergometer (Monark 894E,
Vansbro, Sweden) was used for each experimental protocol.
For each participant the saddle height was adjusted so their
knee remained slightly flexed after the completion of the
power stroke (with final knee angle approximately 170175 ).
Toe clips were used to ensure that the participants feet were
held firmly in place and in contact with the pedals. The cycle
ergometer was connected to a PC to allow for data capture via
the Monark anaerobic test software (version 2.24.2).
Before any experimental testing, each individual completed a standardised warm-up on the cycle ergometer (3 min
at 60 rpm, 2 kg resistance).
For both WAnT1 and WAnT2, participants were given
a rolling start before resistive force application. Once the
subjects had accelerated to 60 rpm the weight basket automatically dropped and participants began to pedal maximally.
Each participant was required to pedal with maximum effort
for a period of 30 s against a fixed resistive load of 75 grams
per kilogram (gkg1 ) total body mass as recommended by
Bar-Or (1987) [11]. 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 handlebar grip. Variables obtained from the Monark anaerobic
test software (version 2.24.2) were PPO (W), relative PPO
(Wkg1 ), MPO (W), and relative MPO (Wkg1 ). For the
population used within the study the WAnT has a high testretest reliability ( = 0.950.97) [11].
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 1RM to be estimated. With each
set the weight was adjusted so that no more than 10 repetitions
could be completed with the final weight. Participants were

BioMed Research International

Table 1: Power output variables recorded during WAnT1 and WAnT2 for both experimental conditions.

NOF
ARF

WAnT1
PPO (W)

WAnT2
PPO (W)

WAnT1
PPO
(Wkg1 )

WAnT2
PPO
(Wkg1 )

WAnT1
MPO (W)

WAnT2
MPO (W)

WAnT1
MPO
(Wkg1 )

WAnT2
MPO
(Wkg1 )

980.0 166.5
929.9 167.7

865.4 168.1
871.7 22.69

12.7 1.5
12.0 1.3

11.2 1.7
11.2 2.0

656.0 84.0
649.3 86.6

589.2 89.3
576.4 81.8

8.5 0.5
8.4 0.7

7.6 0.7
7.5 0.7

This indicates significant differences between WAnT1 and WAnT2 ( < 0.05).

given 2-minute recovery between each set. All participants

were familiar with the exercise; therefore no more than
three sets were required. The Brzycki formula was then used
to estimate 1RM based on the final weight and repetitions
recorded (1) [12]. 70% of the 1RM was subsequently calculated
for each participant to establish the weight required to fatigue
the arms for protocol 2:
1RM =

(weight lifted)
.
[1.0278 (repetitions 0.0278)]

(1)

For protocol 2 (ARF), participants completed 3 sets of

10 repetitions and a 4th set until exhaustion (R30 s between
sets) at 70% 1RM. During the bicep curls, participants palms
were in the supinated position and they were instructed to
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 1 min after
warm-up and 1 min after each exercise bout (Figure 1). Each
maximal static HG test was completed with the participants
dominant hand, while being in a seated position using a HD
dynamometer (Model TKK5001, Takei, Japan).
2.4.1. Blood Sampling. Capillary blood samples (3050 L)
for the measurement of blood [La ] were taken from the
fingertip using standard lancets and capillary tubes. Samples
were taken at rest, 3 min following warm-up and 3 and
5 min following each exercise bout (Figure 1). All samples
were immediately mixed (2 min) and duplicate samples were
analysed to determine the whole blood lactate concentration
(Analox P-LM5, Analox Instruments Ltd, London, UK).
The full protocol for each testing session is outlined in
Figure 1.
2.4.2. Statistical Analysis. Data was statistically analysed
using SPSS (version 20) (IBM, Armonk, NY, USA). For a
single missing data point, data was replaced with a mean
difference adjusted value for the individual compared to
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 (2 [TRIAL] 2
[TEST]) ANOVAs were performed to detect main effect and
interaction effects. For the blood lactate data, a balanced
design was only evident for the postexercise data (3 and
5 min following exercise). For these data, data were analyzed
by repeated measures three-way (2 [TRIAL] 2 [TEST]
2 [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 postexercise (1 min WAnT1 versus 1 min WAnT2) using a repeated
measures two-way (2 [TRIAL] 3 [TIME]) ANOVA. For
all data variables, specific contrasts were performed to test
for mean differences for significant main or contrast effects.
Isolated paired mean differences outside of the balanced
ANOVA designs were assessed by a paired t-test. Pearsons
correlation analysis was used to determine the correlation
between PPO and HG strength. Effect size statistics (ES)
for selected statistically significant t- and F-ratios were also
established. These calculations were based on Cohens (d)
classification of a small (0.2 < 0.5), moderate (0.5 <
< 0.8), and large ( 0.8) ES [13]. Significance was set a
priori at < 0.05. All data is presented as mean standard
deviation (SD).

3. Results
3.1. Cycle Parameters. There was a significant main effect for
the TEST for each of PP0 (W: 1,8 = 19.5, < 0.01,
df = 0.84), relative PP0 (Wkg1 : 1,8 = 22.6, < 0.01,
df = 0.86), and relative MPO (1,8 = 43.8 < 0.01,
df = 0.91) (Table 1), revealing lower power values for WAnT2
compared to WAnT1. Peak power produced in WAnT1 was
lower in the ARF protocol compared to NOF protocol ( <
0.01, df = 0.75); however, no significant interaction was
found ( > 0.05). No significant differences were found in
FI (%) for TEST or TRIAL ( > 0.05) (NOF: 57.0 10.5%
and 57.8 10.7% for WAnT1 and WAnT2, respectively, ARF:
57.3 9.9% and 59.1 9.6% for WAnT1 and WAnT2).
3.2. Blood Lactate. The blood lactate response to each of the
experimental protocols is displayed in Figure 2. There was a
significant TIME effect (1,8 = 15.8, < 0.01, df = 0.81)
and a significant TRIAL TEST interaction ( = 0.041,
df = 0.57). The three-way interaction effect of TRIAL
TIME TEST revealed a trend toward statistical significance
( = 0.089, df = 0.54). Blood lactate was significantly higher
5 min after the arm fatigue exercise in the ARF trial compared
to post-warm-up in the NOF trial ( = 0.001). Based
on the main effect and interaction ANOVA results, blood
lactate was significantly higher throughout the recovery after
WAnT2 than WAnT1. In addition, the interaction effect was
caused by a net decrease in blood lactate between 3 and 5 min
of recovery in WAnT2, whereas blood lactate continued to
increase between 3 and 5 min of recovery after WAnT1.

BioMed Research International

14

60

12

55

10

50

45

Force (kg)

40
35
30

25

Figure 2: Blood [La ] responses prior to and during recovery from

each of WAnT1 and WAnT2. = significant difference between
NOF and ARF.

3.3. Handgrip. The HG strength response to each of the

experimental protocols is displayed in Figure 3. There was a
significant TRIAL effect ( = 0.004, df = 0.81). Therefore,
HG strength was significantly lower at all time points for the
ARF versus NOF trial.
There was a nonsignificant correlation between HG
strength and PPO during NOF ( = 0.29, = 0.38).
However, in the ARF where bicep curls were completed
before WAnT1, there was a meaningful trend of a positive
linear relationship ( = 0.59, = 0.06) between PPO from
WAnT2 and HG strength after WAnT2 (Figure 4).

4. Discussion
The main aim of the present study was to evaluate the effects
of prior fatiguing upper body exercise on subsequent high
intensity cycle ergometer performance. The results demonstrate that fatiguing the upper body had a detrimental effect
on PPO during WAnT1 with nonsignificant 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 2
(Figure 4). Consequently, the functional connection between
HG strength and PPO is more relevant after prior exercise of
the upper body.
In the ARF protocol, HG strength was lower at all measured time points compared to the NOF protocol. Furthermore, PPO was significantly lower ( < 0.05) in WAnT1 in the
ARF protocol compared to the NOF protocol which suggests
that in the absence of leg fatigue, the strength of the grip upon
the handlebar may be influencing PPO. This is in agreement
with the findings of Baker and colleagues (2001) [1] who
found that handlebar grip was essential in the production
of PPO. Perhaps unexpectedly, the only correlation between

6 min after
WAnt2

Sample
NOF
ARF

1 min after
WAnt2

20
1 min after
WAnt1

5 min after
WAnT2

3 min after
WAnT2

5 min after
WAnT1

3 min after
WAnT1

Before

Baseline

Before

Lactate (mmolL1 )

Sample
NOF
ARF

Figure 3: Handgrip strength (kg) measured before and after exercise

for both trials.

PPO and HG strength reaching significance was between

PPO obtained in WAnT2 and HG strength after WAnT2
in the ARF protocol ( = 0.59, = 0.06). A possible
explanation for this finding is that as HG strength shows signs
of recovery following the fatiguing arm exercise (Figure 3),
the relationship between HG strength and PPO becomes
more evident.
The lack of statistically significant differences 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,
it can be speculated that the prior high intensity upper body
2 kinetics facilitating
exercise would have resulted in faster VO
an earlier and greater shift to aerobic metabolism in the
first sprint in protocol 2 (ARF). This shift has the potential
to improve MPO by reducing the O2 deficit and rate of
fatigue induction [14, 15]. This reduction in fatigue can be
highlighted through the lack of difference in FI (%) found
between WAnT1 and WAnT2 in both protocols.
Despite the statistically significant increase in blood [La ]
during high intensity exercise, it is now widely accepted
that La does not have a direct role in muscular fatigue
[16]. However, the rate of blood [La ] accumulation and
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 [17]. During intense exercise, the predominate
mechanism which moves La and H+ out of contracting
muscle is the monocarboxylate transporter system, MCT1
and MCT4 [18, 19], with the transport efficiency dependent
upon various factors including intramuscular and blood pH,
density of MCT1 and MCT4, and on blood flow in working
muscles and other tissues [20]. In the present study, there
was a small increase in the standard deviation values from
3 to 5 min after exercise suggesting participant variability in

BioMed Research International

5
1200

1200

Peak power output (W)

Peak power output (W)

1400

1000
800
600
400

1000

800

600

400
30

35

40

45
Force (kg)

50

55

60

25

30

35

40

45

50

55

60

Force (kg)

(a)

(b)

Figure 4: Correlations between handgrip strength after WAnT2 and peak power from WAnT2 for (a) NOF ( = 0.29, = 0.38) and (b) ARF
( = 0.59, = 0.06).

lactate transport efficiency which reflects possible betweensubject differences in training status.
During ARF, participants commenced the WAnTs with
significantly 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 fibres than the lower
body which in turn causes upper body musculature to be
less efficient in lactate clearance and subsequently also has
a slower recovery [21, 22]. Despite the metabolic benefits
of La production now being widely recognised, there is
a definite association between elevated blood [La ] and
impaired exercise performance [16]. Therefore, this elevated
[La ] in the ARF protocol is likely to be a reflection of other
metabolic disturbances including metabolic acidosis and an
increase in intramuscular Pi and blood K+ thus partially
accounting for the decrease in PPO [7, 23]. 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 effects of H+ on force production
may be largely temperature dependent and may have little
direct effect on human muscle at physiological temperature
[24].
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 production. In terms of energy depletion influencing subsequent
performance, PCr recovery is likely to be a key factor.
Research has shown that after exhaustive exercise, near
complete replenishment of PCr may take from <5 min to in
excess of 15 min, depending on the extent of PCr depletion,
severity of metabolic acidosis (slower if more acidic), and
the muscle motor unit and fibre type characteristics of the
exercised muscle [7]. Therefore, in the present study it is
unlikely that the 6-minute rest period between exercise bouts
would be sufficient for complete replenishment of PCr stores,
thus having a detrimental effect on power profiles obtained

following a previous bout of high intensity exercise. Furthermore as outlined previously, blood [La ] remains elevated,
suggesting intramuscular H+ activity also remains higher,
thus slowing the replenishment process. This is supported
by Bogdanis and colleagues [25] who found that decreased
[PCr] did result in a reduction in power output. However,
it is likely that the detrimental effects of prior exercise on
subsequent performance will be muted when the recovery
period is adequate [26, 27]. For example, when Bouhlel et
al. [10] 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. The 8 min recovery period within this study
suggests that the opposite muscle group is unaffected 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 [5], a
very similar methodology was used. The authors aimed to
elevate [La ] through prior arm exercise (arm ergometry)
and determine the effects of this on subsequent high intensity
cycle ergometry performance. In contrast to our results
they found PPO to be significantly lower during the second
sprint following prior arm exercise but similarly there were
nonsignificant changes in MPO between the two protocols.
It is difficult to directly compare results with Bogdanis et
al. [5] due to differences in equipment, participants, and
experimental procedures employed. We have hypothesised
that the differences between the two investigations may be
due to our upper body exercise (bicep curls) having a directly
fatiguing effect on HG strength which we hypothesised would
be more likely to affect PPO during the initial sprint. We
interpret our results to confirm this hypothesis.

5. Limitations
As with most maximal cycle ergometer tests, prior to the load
being applied there was an initial high rpm. This inertia was

6
not accounted for in the calculation; therefore the considerable energy which had already been accumulated before the
30 s test may have resulted in a possible overcalculation of
PPO and MPO [28].
All participants were physically active and accustomed
to high intensity exercise. However no physiological fitness
testing was undertaken prior to data collection which meant
there was no control over the exercise capacity of each
individual. This is an extraneous variable which may have
led variation in power profiles observed among participants
which was not related to the exercise protocol.

6. Conclusion
In conclusion, this investigation has shown that prior fatiguing upper body exercise has a statistically significant detrimental effect on PPO during the first of two WAnTs. This 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, confirming 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 2 kinetics and therefore increasing
cise resulting in faster VO
the contribution from oxidative metabolism.

Conflict of Interests
The authors declare that there is no conflict of interests
regarding the publication of this paper.

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